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CM2001 > PED2006 EXAM PRACTICE > Flashcards

PED2006 EXAM PRACTICE Flashcards

1
Q

What is bacterial conjugation

A

genetic transfer between bacteria that involves direct cell-to-cell contact

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2
Q

how does antibiotic resistance spread

A

transfer of genetic material through bacterial conjugation

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3
Q

what are the four steps in the conjugation process

A

formation of pilus
mating pair formation
transfer of plasmid DNA
separation

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4
Q

what happens during the formation of pilus

A

the donor bacterium, which contains a conjugative plasmid, extends a hair like appendage called a pilus
the pilus attaches to the surface of the recipient bacterium, forming a connection between the two cells

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5
Q

what happens during mating pair formation

A

the pilus retracts, bringing the two bacteria into close contact
a mating bridge forms between the cells, allowing the transfer of genetic material

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6
Q

what happens during the transfer of plasmid DNA

A

the conjugative plasmid in the donor cells is nicked at a specific site called the origin of transfer
one strand of the plasmid DNA is transferred to the recipient cell through the mating bridge
the single stranded DNA in both the donor and recipient cells is replicated to form double stranded plasmids

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7
Q

what happens during separation

A

after the transfer is complex, the mating bridge dissassembles, and the two bacteria separation
both the donor and recipient cells now contain the plasmid

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8
Q

what is required for antimicrobial resistance spread

A

presence of resistance genes
horizontal gene transfer
proliferation of resistance bacteria

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9
Q

what is horizontal gene transfer

A

conjugations allows for the horizontal transfer of R plasmids between bacteria, which can occur when between different species
this means that a non-resistant bacterium can quickly acquire resistance genes from a resistant donor

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10
Q

how does proliferation of resistant bacteria occur

A

once a bacterium acquire a resistance plasmid, it can survive and proliferate in the presence of antibiotics
these bacteria can further transfer the plasmid to other bacteria, spreading the resistance genes within and between bacterial populations

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11
Q

what are the clinical implications of the spread of antimicrobial resistance

A

the spread to antibiotic resistance genes through conjugations can lead to the emergence of multi-drug resistant bacterial strain
this poses a significant challenge for treating bacterial infections, as standard antibiotics become ineffective, necessitating the use of more potent and often more toxic alternatives

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12
Q

what are fluoroquinolone

A

a class of broad-spectrum antibiotics that are effective against a variety of gram positive and gram negative bacteria. they exert their antibacterial effects by targeting bacterial DNA replication and transcription

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13
Q

what is the mechanism of actions of fluoroquinolone

A

inhibitions of DNA gyrase
inhibition of topoisomerase 4

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14
Q

what is the functions of DNA gyrase

A

in bacteria, DNA gyrase is an essential enzyme that introduces negative supercoils into DNA. this is critical for the replication and transcription processes as it prevents the DNA helix from becoming overall tangles and allows it to unwind

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15
Q

what is the action of fluoroquinolone

A

bind to the DNA gyrase-DNA complex, stabilising the enzyme-DNA interaction. this prevents the enzymes from resealing the DNA double strands after they have been cut to relieve the torsional strain

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16
Q

why is the inhibition of DNA gyrase important

A

the interruption of this process leads to the accumulation of double stranded DNA breaks, which ultimately results in bacterial cell death

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17
Q

what is the function of topoisomerase 4

A

this enzyme is involved in the separation of interlinked daughter DNA molecules following DNA replication. it is crucial for proper cell division

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18
Q

how do fluoroquinolone impact toposimerase 4

A

fluoroquinolone interferes with the activity of topoisomerase 4 by stabilising the cleavage complex that the enzyme forms with DNA

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19
Q

why is inhibition of topoisomerase 4 beneficial

A

this action prevents the segregation of replicated chromosomal DNA into daughter cells, thereby inhibition of bacterial cell division and leading to cell death

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20
Q

what are the benefits of fluoroquinolone

A

broad spectrum so effective against a wide range of bacteria
bactericidal effect - they kill bacteria due to irreversible damage they cause to bacterial DNA

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21
Q

drawback of fluoroquinolone

A

resistant mutations can develop in the genes encoding DNA gyrase and toposimerase 4, which are prevent in various bacterial species

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22
Q

what is the posterior lobe of the pituitary gland

A

the posterior lobe of the pituitary gland plays a crucial role in the regulation of various physiological processes

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23
Q

what is the location of the posterior lobe

A

the posterior lobes is located at the base of the brain, attached to the hypothalamus by the pituitary stalk

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24
Q

what is the hypothalamic hypophyseal tract

A

the axons of neurone from the supraoptic and paraventricular nuclei of the hypothalamus extend down through the pituitary stalk into the posterior lobe. these neuron’s synthesise hormone and transport them along their axons to be stored and released from the posterior pituitary

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25
Q

what is the function of the posterior pituitary

A

store and release ADH and oxytocin produced by the hypothalamus

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26
Q

where is ADH synthesised

A

synthesised by the supraoptic nuclei of the hypothalamus

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27
Q

how is ADH released

A

ADH is transported down the axons of the hypothalamic neurone to the posterior pituitary, where it is stored in vesicles and released into the bloodstream in response to specific physiological triggers

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28
Q

what is the functions of ADH

A

ADH primarily acts on the kidneys to promote water reabsorption in the collecting ducts, which helps to regulate the body’s water balance and maintain blood pressure. it also has vasoconstrictive effects on blood vessels, contributing to the blood pressure regulation

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29
Q

where is oxytocin synthesised

A

oxytocin is synthesised in the paraventricular nuclei of the hypothalamus

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30
Q

how is oxytocin released

A

oxytocin is transported along the axons to the posterior pituitary where it is stored and released into the bloodstream upon appropriate stimulation

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31
Q

what is the function of oxytocin

A

labor and deliver - it stimulate uterine contractions during childbirth
lactation - it triggers milk ejections from the mammory glands in response to suckling
social and emotional bonding - oxytocin is also involved in behaviours related to bonding, social recognitions and emotional regulation

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32
Q

what is an ADH agonist, such as desmopressin

A

mimics the action of natural ADH and are primary used to treat conditions like diabetes insipdus and nocturnal enuresis by promoting water reabsorption in the kidneys. their action is particularly significant in the juxtamedullary nephrons, which play a crucial role in the concentration of urine

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33
Q

what is the anatomy of juxtamedullary nephrons

A

juxtamedullary nephrons are located near the border of the renal cortex and medulla. they have long loops of hence that extend deep into the medulla, which is essential for concentrating urine

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34
Q

what is the functions of juxtamedullary nephrons

A

these nephrons are key in creating the osmotic gradient in the medulla necessary for water reabsorption

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35
Q

what is desmopressin

A

is a synthetic analogue of ADH with a longer duration of action and selective V2 receptor activity, which enhances its antiduiretic effects with minimal vasoconstrictive effects

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36
Q

what is the relationship between V2 receptors and desmopressin

A

desmopressin selectively binds to V2 receptors located on the basolateral membrane of the principal cells in the collecting ducts and distal convoluted tubules of the nephrons

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37
Q

what is the relationship between juxtamedullary nephrons and desmopressin

A

juxtamedullary nephrons have a high density of V2 receptors, making them particularly response to ADH and its agonists

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38
Q

how does desmopressin activate the cAMP pathway

A

upon binding to V2 receptors, desmopressin activate adenylate cyclase, increasing the intracellular concentration of cyclic adenosine monophosphate
cAMP acts as a second messenger to activate protein kinase A

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39
Q

how does desmopressin trigger the insertion of aquaporin 2 channels

A

PKA phosphorylation targets proteins that facilitate the translocation of aqauporin 2 water channels to the apical membrane of the principal cells

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40
Q

what are aquaporin 2 channels

A

the channels allow water to move from the lumen of the collecting ducts into the cells

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41
Q

how do aquaporin2 channels affect water reabsorption

A

water is reabsorbed from the filtrate in the collecting ducts back into the surrounding interstitial space and then into the bloodstream, effectively reducing urine volume and concentrating the urine

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42
Q

how do the juxtamedullary nephrons affect the medullary osmotic gradients

A

the juxtamedullary nephrons long loops of henle maintain a high osmolarity in the renal medullar, which facilitates water reabsorption

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43
Q

how does desmopressin affect the medullary osmotic gradient

A

desmopressin enhances the ability of the kidneys to reabsorb water by increasing the osmotic gradient

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44
Q

what are the clinical applications of desmopressin

A

diabetes inspidus
nocturnal enuresis
haemophilia A and von willebrands disease

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45
Q

how can desmopressin be used to treat diabetes insipid

A

desmopressin is used to manage central diabetes inspidus by replacing deficient ADH, thus reducing excessive urination and thirst

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46
Q

how can desmopressin help nocturnal enuresis

A

it helps manage bedwetting by reducing nighttime urine production

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47
Q

how can desmopressin help haemophilia A and von willebrands disease

A

desmopressin is also used to increase the levels of clotting factors in these bleeding disorders

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48
Q

what are the side effects of desmopressin

A

hyponatremia - due to increase water reabsorption, there is a risk of dilution hyponatremia, where the blood sodium levels become too low
headache - caused due to changes in water balance
nausea and abdominal pain

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49
Q

state the hormones released by the posterior pituitary

A

ADH
oxytocin

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50
Q

what is the functions of ADH

A

ADH primarily regulates water balance in the body by increase water reabsorption in the kidneys, thereby reducing urine output. it also has vasoconstrictive properties, which help to increase blood pressure

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51
Q

how is ADH regulated

A

ADH release is stimulated by increased plasma osmolarity and by a decrease in blood volume or blood pressure

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52
Q

what is the role of oxytocin

A

oxytocin plays a crucial role in childbirth and lactation. it stimulates uterine contractions during labor and helps with milk ejections reflex during breastfeeding. additional, oxytocin is involved in social bonding and emotional responses

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53
Q

how is oxytocin regulated

A

oxytocin release is triggered by the distension of the cervix and vagina during labor and by suckling at the breast during breastfeeding. it can be influenced by emotional and social stimuli

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54
Q

give an example of a beta 2 adrenergic agonists

A

albuterol

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55
Q

how does albuterol work

A

albuterol binds to and activates beta2 adrenergic receptors on the smooth muscle cells lining in the airways
activation of these receptors stimulates the enzyme adenylate cyclase, which converts ATP to cyclic AMP
increased levels of cAMP activates protein kinase A, which in turns phosphorylates and inactivates myosin light chain kinase. this leads to relaxation of the smooth muscle cells and bronchodilator

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56
Q

what is the effect of albuterol

A

the rapid relaxation of bronchial smooth muscle results in the widening of the airways, making it easier to breathe and providing quick relief from acute asthma symptoms

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57
Q

when to use albuterol

A

used as a first line treatment for acute asthma attacks due to their rapid onset of action

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58
Q

what are the side effects of albuterol

A

tremors
tachycardia
palpitations
nervousness
hypokalaemia

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59
Q

give an example of anticholinergics

A

ipratropium bromide

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60
Q

how does ipratropium bromide work

A

ipratropium bromide competitively inhibits muscarinic cholinergic receptors on bronchial smooth muscle
by blocking these receptors, ipratropium prevents acetylcholine from binding to them
the inhibitions of acetylcholine binding reduces the intracellular levels of calcium, which is necessary for smooth muscle contractions
this leads to the relaxation of the bronchial smooth muscle and bronchodilation

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61
Q

what is the effects of ipratropium bromide

A

ipratropium provides bronchodilator and helps in reducing mucus secretion, improving airflow and reducing the symptoms of an acute asthma attack

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62
Q

what is ipratropium bromide used for

A

often used in combination with beta2 agonists during acute asthma attacks for a synergistic effect, especially in patients who do not respond adequately to beta2 agonists alone

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63
Q

what are the side effects of ipratropium bromide

A

dry mouth
throat irritations
cough
urinary retention and increase intraocular pressure

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64
Q

what is pain

A

pain is a subjective, unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms such as damage

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65
Q

what are the types of pain

A

acute or chronic
somatic
visceral
neuropathic
psychogenic

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66
Q

what is the function of pain

A

protective mechanism, pain serves as a warning signal for potential or actual damage, prompting individuals to withdraw from harmful situations and seek treatment

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67
Q

what is nociceptions

A

is the neural process of encoding and processing noxious stimuli. it involves the detections of harmful stimuli and the transmission of signals to the central nervous system

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68
Q

what are nociceptors

A

specialised sensory receptors that respond to potentially damaging mechanical, thermal and chemical stimuli

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69
Q

what is the transmission pathway of nociception

A

transduction - noxious stimuli are converted into electrical signals by nociceptors
transmission - these elctrical signals are transmitted via peripheral nerves to the spinal cord and then to the brain
perception and modulation - once the signals reach the brain, they are processed and can result in the perception of pain. the brain can also modulate the signals, altering the perception of pain through various mechanisms

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70
Q

what is the function of nociception

A

is essential for detecting harmful stimuli and initiating protective reflexes, such as withdrawal from the source of harm

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71
Q

what are opioid receptors

A

opioid receptors are a group of g-protein coupled receptors that mediate the effects of opioid drugs. there are 3 primary types of opioid receptors: mu, kappa and delta receptors. each receptor type has distinct roles and is involved in various physiological effects of opioids

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72
Q

what is the role of mu opioid receptors

A

analgesia, euphoria and reward, respiratory depression, sedation, gastrointestinal effects, physical dependence

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73
Q

what are the examples of mu opioid receptor drugs

A

morphine
fentanyl
methadone
oxycodone
heroin

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74
Q

what is the role of kappa opioid receptors

A

analgesia
dysphoria and hallucinations
diuresis
sedation

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75
Q

what are the examples of kappa opioid receptor drugs

A

butorphanol
nalbuphine
pentazocine
dynorphins

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76
Q

what is the role of delta opioid receptor

A

analgesia
mood regulation
neuroprotections
respiratory function

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77
Q

what are the examples of delta opioid receptor drugs

A

deltorphins
enkephalins

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78
Q

what is morphine

A

is a potent opioid analgesic that is widely used for the management of moderate to severe pain. it acts primarily on the central nervous system and the gastrointestinal tract

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79
Q

how does morphine induce analgesia

A

morphine exerts its analgesic effects by binding to and activating mu opioid receptors in the CNS, particularly in the brain and spinal cord. this activation inhibits the release of neurotransmission such as substance p and glutamate, which are involved in the transmission of pain signals

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80
Q

how does morphine induce sedation

A

by activating mu opioid receptors in the brains reward pathways, morphine induces a feeling of euphoria. it also depresses the central nervous system, leading to sedation

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81
Q

how does morphine induce respiratory depression

A

morphien depresses the brainstems respiratory centres by reducing the responsiveness of these centres to carbon dioxides. this action is mediated by mu opioid receptors. this can lead to decreased respiratory rate and volume

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82
Q

how does morphine cause antitussive effects

A

morphine suppresses the cough reflex by acting on the cough centre in the medulla

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83
Q

how does morphine cause gastrointestinal effects

A

morphine increases the tone of the smooth muscle in the GI tract while decreasing peristalsis by binding to opioid receptors in the enteric nervous system

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84
Q

how does morphine cause miosis

A

morphine stimulates the parasympathetic nervous system, resulting in the constriction of the pupils

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85
Q

how does morphine cause cardiovascular effects

A

morphine can cause peripheral vasodilation by releasing histamine and depressing the vasomotor centre in the brain. this can lead to decreased systemic vascular resistance and a drop in blood pressure

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86
Q

what are the effects of morphine inducing histamine release

A

morphine can induce the release of histamine from mast cells. this can cause pruritic, urticaria, and in some cases bronchoconstriction and vasodilation, leading to hypotension

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87
Q

what is schizophrenia

A

schizophrenia is a complex and multifactorial psychiatric disorder characterised by a range of symptoms, including delusions, hallucinations, disorganised thinking and impaired social functioning

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88
Q

what is the dopamine hypothesis for schizophrenia

A

overactivity in mesolimbic pathway -
under activity of the mesocortial pathway

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89
Q

what is the effect of overactivity in the mesolimbic pathway

A

excessive dopamine activity in the mesolimbic pathway is associated with positive symptoms e.g. hallucinations and delusions

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90
Q

what is the effects of under activity in mesocortiyal pathway

A

reduced dopamine activity in the mesocortical pathway is linked to negative symptoms e.g. anhedonia, social withdrawal and cognitive deficits

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91
Q

what is the glutamate hypothesis for schizophrenia

A

NMDA receptor hypofunction - dysfunction of the NMDA-type glutamate receptors contribute to symptoms of schizophrenia. reducing glutamate signalling can affect various neural circuits, leading to both positive and negative symptoms

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92
Q

what is the serotonin hypothesis for schizophrenia

A

5-HT2A receptor involvement - altered serotonin activity, particularly through 5-HT2A receptors, plays a role in modulating dopamine release and can contribute to the symptoms of schizophrenia

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93
Q

what are the structural brain abnormalities associated with schizophrenia

A

enlarged ventricles - indicating loss of brain tissue
cortical thinning - reducing in grey matter volume
hippocampal abnormalities - associated with cognitive impairments and memory deficits

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94
Q

what are the functional brain abnormalities associated with schizophrenia

A

hypofrontality - reduced activity in the prefrontal cortex during tasks requiring executive function and working memory
default mode network dysregulation - abnormal connectivity and activity in the DMN, which is involved in self-referential thought and resting state in the brain

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95
Q

what are the genetic and environmental factors associated with schizophrenia

A

genetic predisposition - schizophrenia has a significant genetic components, with a higher risk among first degree relatives
environmental triggers - prenatal exposure to infections, malnutrition, stress and psychological factors

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96
Q

what are neuroleptics

A

neuroleptics are the main stay of pharmacological treatment for schizophrenia. they are primarily classified into two categories - typical and atypical

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97
Q

what is the mechanism of action of typical antipyschotics

A

dopamine D2 receptor antagonism - these drugs primarily block dopamine D2 receptors, reducing dopamine activity in the brain, particularly in the mesolimbic pathway

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98
Q

what are the examples of typical antipsychotics

A

haloperidol, chlorpromazine

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99
Q

what are the effects of typical antipsychotics

A

reduction of positive symptoms - effective in alleviating hallucinations and delusions

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100
Q

what are the side effects of typical antipsychotics

A

extrapyramidal symptoms such as dystonia, parkinsonism, and tardive dyskinesia due to dopamine blockage

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101
Q

what is the mechanism of action of atypical antipsychotics

A

these drugs block both dopamine D2 and serotonin 5-HT2A receptors, providing a more balanced effect on neurotransmitters

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102
Q

what are the examples of atypical antipsychotics

A

risperidone, olanzapine, quetiapine, clozapine

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103
Q

what are the effects of atypical antipsychotics

A

reducing of positive and negative symptoms - more than typical

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104
Q

what are the side effects of atypical antipsychotics

A

lower risk of EPS but may cause metabolic side effects such as weight gain, diabetes and dyslipidaemia

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105
Q

what are glucocorticoid receptors

A

type of nuclear receptor that upon binding with glucocorticoids, acts as a transcription factor to regulate gene expression

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106
Q

what in the resting state of glucocorticoids

A

in the absence of glucocorticoids, the GR resides in the cytoplasm in an inactive state, bound to chaperone proteins such as heat shock proteins including HSP90 and HSP70

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107
Q

How do glucocorticoids bind

A

glucocorticoids diffuse through the cell membrane and bind to the GR. this binding induces a conformational change in the receptor, causing the release of the chaperone proteins

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108
Q

what happens during nuclear translocation of GR

A

the activate GR translocates from the cytoplasm to the nucleus

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109
Q

what is DNA binding involving GR

A

in the nucleus, the GR dimerises and binds to specific DNA sequences called glucocorticoid response elements located in the promoter regions of target genes

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110
Q

how is gene expression regulated

A

transactivation
transrepression

111
Q

how is GR activity positively regulated through transactivation

A

GR binding to GREs can enhance the transcription of anti-inflammatory and immunosuppressive genes, such as lipocortins 1, which inhibits phospholipase A2, reducing the synthesis of pro-inflammatory molecules like prostaglandin and leukotrienes

112
Q

what enzymes are involved in transactivation

A

tyrosine aminotransferanse, which plays a role in gluconeogenesis

113
Q

how is gene expression negatively regulated through transrepression

A

GR can also interact with other transcription factors, such as NFkB and AP1, to repress the expression of pro-inflammatory cytokines, chemokine and adhesion molecules

114
Q

how can GR interfere transrepression with transcription factors

A

GR can inhibit NFkB and AP1 by preventing their binding to DNA or by recruiting co-repressors, thus reducing the transcription of genes involved in inflammation and immune response

115
Q

what are the drugs involved in anti-inflammatory and immunosuppressive therapies

A

prednisone
dexamethasone
hydrocortisone

116
Q

when are glucocorticoids used

A

used to treat inflammatory and autoimmune conditions such as rheumatoid arthritis, asthma, inflammatory bowel disease and lupus

117
Q

how are glucocorticoid drugs used

A

by mimicking endogenous glucocorticoids, these drugs bind to the GR, leading to the suppression of pro-inflammatory genes and up regulation of anti-inflammatory genes

118
Q

what are the side effects of glucocortoid drugs

A

oestoporosis, muscle weakness, hypertension, hyperglycaemia, and increased risk of infections due to immunosuppression

119
Q

which glucocorticoid drugs can be used in cancer treatment

A

dexamethasone, prednisone

120
Q

when are glucocorticoids used in cancer therapy

A

used as part of chemotherapy regiments for certain lymphomas and leukemias

121
Q

how do glucocorticoids treat cancer

A

these drugs induce apoptosis in lymphoid cells by up regulating pro-apoptotic genes and downregulating anti-apoptotic genes

122
Q

which glucocorticoids are used in adrenal replacement therapy

A

hydrocortisone
cortisone acetate

123
Q

how do glucocorticoids work in replacement therapy

A

used to replace deficient cortisol in conditions like Addisons disease and congenital adrenal hyperplasia
these synthetic glucocorticoids supplement or replace endogenous cortisol, helping to maintain metabolic and immunologic homeostasis

124
Q

which glucocorticoids are used in immunosuppressive therapy

A

prednisone and methylprednisolone

125
Q

how do glucocorticoids work in immunosuppressive therapy

A

glucocorticoids suppress the immune response, reducing the likelihood of the body attacking the transplated organ. used to prevent rejections in organ transplants

126
Q

what is Parkinson’s disease

A

is a progressive neurodegenerative disorder characterised primarily by motor symptoms such as tremors, rigidity, bradykinesia and postural instability

127
Q

what is the pathophysiological basis of Parkinsons Diases

A

dopaminergic neuro degeneration
neuroinflammatory and oxidative stress
genetic factors
non-dopaminergic systems

128
Q

how does dopaminergic neuro degeneration leads to parkinsons

A

PD primarily involves the degeneration of dopaminergic neurone in the substantial nigra par compact, a region of the brain that is part of the basal ganglia. these neuron’s produce dopamine, a neurotransmitter essential for regulating movement
the loss of dopaminergic neurone leads to a significant reduction in dopamine levels in the striatum, a crucial component of the motor circuit in the brain

129
Q

how does neuroinflammation and oxidative stress lead to PD

A

chronic neuroinflammations and increased oxidative stress have been implicated in the pathogenesis of PD. microglial activation and the production of pro-inflammatory cytokines can exacerbate neuronal damage

130
Q

how do genetic factors leads to parkinsons

A

genetic mutations have been identified that increase the risk of developing the disease such as mutations in the SNCA, LRRK2 and PARK2 genes

131
Q

how do non-dopaminergic systems contribute to PD

A

other neurotransmitter systems, including the cholinergic, serotonergic and noradrenergic systems, can also be affected in PD, contributing to non-motor symptoms such as cognitive decline, mood disorders and autonomic dysfunction

132
Q

what are the different types of pharmacological approaches to treating PD

A

dopaminergic therapies
anticholinergic agents
amantadine
adenosine A2A receptor antagonists

133
Q

what is included in dopaminergic therapies for PD

A

levodopa
dopamine agonists
MAO-B inhibitors
COMT inhibitors

134
Q

why is levodopa used in treatment for PD

A

levodopa is a precursors to dopamine that can cross the BBB and is converted to dopamine in the brain. it is usually combined with a peripheral decarboxylase inhibitor to prevent its conversion to dopamine outside the brain, which reduces side effects and increases availability in the CNS

135
Q

why are dopamine agonists used in the treatment for PD

A

these drugs directly stimulate dopamine receptors and can be used alone or in combination with levodopa

136
Q

why are MAO-B inhibitors used in PD

A

monoamine oxidase B inhibitors e.g. selegiline and rasagiline, inhibit the breakdown of dopamine, thereby increasing its levels in the brain

137
Q

why are COMT inhibits used in PD

A

catechol-O-methyltransferase inhibitors e.g. entacapone and tolcapone prevent the breakdown of levodopa, prolonging its effects

138
Q

why are anticholinergic agents used in PD

A

these drugs help to reduce tremors and muscle rigidity by blocking acetylcholine, which is relatively overactive due to the loss of dopamine

139
Q

why is amatadine used in PD

A

has both dopaminergic and anticholinergic properties and may help reduce symptoms, particularly dyskinesia associated with long term levodopa use

140
Q

why is adenosine A2A receptor antagonists used in PD

A

istradefylline is an example of this class, which helps reduce motor symptoms by modulating the activity of the basal ganglia circuits

141
Q

how can cognitive and psychiatric symptoms of PD be treated

A

cholinesterase inhibits can be used for cognitive impairment
antidepressants (SSRIs) and anxiolytics may be prescribed for mood disorders

142
Q

how can sleep disorder be treated in PD

A

medications such as melatonin or clonazepam may be used to manage sleep disturbances

143
Q

how can autonomic dysfunction be treated in PD

A

medications to manage blood pressure, urianry incontinence and gastrointestinal symptoms may be necessary

144
Q

why is hormone replacement therapy used to target oestrogen receptors

A

used in menopausal women to alleviate symtpoms such as hot flushes, night sweats, vaginal dryness and oesteoporosis

145
Q

how does hormone replacement therapy work

A

oesterogen is administered to compensate for the decreased endogenous production

146
Q

what are the agents used in hormone replacement therapy

A

conjugated oestrogen, oestradiol patches, and oesteragens

147
Q

when is selective oestrogen receptor therapy used

A

used in breast cancer treatment and prevention, oesteoporosis preventions, and other oestrogen related conditions

148
Q

what is the mechanisms of selective oestrogen receptor modulators

A

SERMs act as oestrogen agonists in some tissues e.g. bone, cardiovascular systems, and antagonists in other e.g. breast and uterus

149
Q

what are the agents used in selective oestrogen receptor modulators

A

tamoxifens - antagonist in breast, agonist in bone and uterus
raloxifene - antagonist in great and uterus, agonist in bone

150
Q

when are oestrogen receptor down regulators used

A

used in the treatment of hormone receptor-positive breast cancer

151
Q

what is the mechanism of oestrogen receptor down regulators

A

ERDs bind to the oestrogen receptors, blocking its actions and promoting its degradation

152
Q

what is the agent used as oestrogen receptor down regulators

A

fluvestrant

153
Q

when is hormone replacement therapy used to target progesterone receptors

A

combined with oestrogen in menopausal women with intact uterus to prevent endometrial hyperplasia and cancer

154
Q

what is the mechanism of HRT in progesterone therapy

A

progesterone opposes the proliferative effects of oestrogen on the endometrium

155
Q

what are the agents used in progesterone HRT

A

micronised progesterone, medroxyprogesterone acetate

156
Q

when are progestins used in contraception

A

used in various forms of hormonal contraceptions

157
Q

what is the mechanism of progestins in contraceptions

A

progestins prevent ovulations, thicken cervial mucus, and alter the endometrium to prevent fertilisation and implantations

158
Q

what are the agents of progestins in contraception

A

levonorgestrel, norethindrone, etonogestrel, medroxyprogesterone acetate

159
Q

when are selective progesterone receptor modulations used

A

used in emergency contraception, treatment of uterine fibroids and endometriosis

160
Q

what is the mechanism of action of SPRMs

A

they exhibit both agonist and antagonistic effects on progesterone receptors depending on the tissue

161
Q

what are the agents of SPRMs

A

ulipristal acetate (emergency contraception, uterine fibroids), mifepristone (used in combination with misoprostol for medical abortion

162
Q

what treatments can be used in ER positive breast cancer

A

SERMs - tamoxifen
ERD - fluvestrant
aromatase inhibitors - anastrozole, letrozole

163
Q

how does SERMs work in the treatment of ER positive breast cancer

A

block oestrogen receptors in breast tissue, reducing tumour growth

164
Q

how does ERDs work in the treatment of ER positive breast cancer

A

promote the degradation of oestrogen receptors, further decreasing oestrogen signalling in cancer cells

165
Q

how do aromatase inhibitors work in the treatment of ER positive breast cancer

A

reduce oestrogen production, indirectly lowering oestrogen receptor activation

166
Q

what are the treatments for endometriosis and uterine fibroids

A

progestins - medroxyprogesterone
SPRMs - ulipristal

167
Q

how do progestins treat endometriosis and uterine fibroids

A

suppress endometrial tissue growth and reduce symptoms

168
Q

how do SPRMs treat endometriosis and uterine fibroids

A

reduce size of fibroids and control bleeding

169
Q

how do progestins treat menstrual disorders

A

used to manage how heavy menstrual bleeding and irregular periods

170
Q

what are combined oral contraceptives

A

contain both oestrogen and progestin to prevent ovulation and alter the uterine environment

171
Q

what are progestin-only contraceptives

A

suitable for women who cannot take oestrogen, they prevent ovulation and increase cervical mucus viscosity

172
Q

what are the treatments for osteoporosis

A

HRT - oestrogen is used to prevent bone loss in postmenopausal womens
SERMs - preserves bone density by mimicking oestrogens effects on bone without stimulating breast and uterine tissues

173
Q

what are the current strategies for treating antimicrobial resistances

A

antibiotic stewardship programs
combination therapy
newer antibiotics
optimising dosing regimens
vaccinations

174
Q

what is the rationale for antibiotic stewardship programs

A

these programs promote appropriate use of antibiotics to minimise the development of resistance

175
Q

how are ASPs implemented

A

ASPs involve guidelines for proper antibiotic selections, dosing, route of administration and duration of therapy. they emphasise de-escalation based on culture results and use of narrow spectrum antibiotics whenever possible

176
Q

what is the rationale for combination therapy

A

using multiple antibiotics can prevent the emergence of resistance by attacking bacteria through different mechanisms

177
Q

what are the examples of combination therapy

A

combining beta-lactams with beta lactamase inhibits e.g. amoxicillin-clavulanate or using dual antibiotics link vancomycin and rifampicin for certain reistant infections

178
Q

what are the newer antibiotics used for combating antimicrobial resistance

A

linezolid
daptomycin
tigencycline
ceftraoline

179
Q

what is the rationale for optimising dosing regiments

A

proper dosing can ensure effective eradications of bacteria and reduce the risk of resistance

180
Q

how is optimising dosing regimens implemented

A

using pharmacokinetic/pharmacodynamic principles to guide dosing such as prolonged or continuous infusion of beta-lactams

181
Q

what is the rationale for vaccinations

A

vaccines can reduce the incidence of infections and the need for antibiotics

182
Q

what are the examples for vaccinations to prevent antimicrobial resistance

A

vaccines for streptococcus pneumonia and staphylococcus aureus

183
Q

what are the future strategies for treating antimicrobial resistance

A

development of new antibiotics
anti-virulence strategies
bacteriophage therapy
CRISPR-cas systems
antibiotic adjuvants
host-directed therapies
nanotechnology

184
Q

what are the examples of development of new antibiotics

A

oxazolidinone, lipoglycopeptides, and new beta-lactams with enhanced activity against resistant strains

185
Q

what is the rationale for anti-virulence strategies

A

targeting bacterial virulence factors rather than killing bacteria directly can reduce selective pressure for resistance

186
Q

what is the rationale for bacteriophage therapy

A

phages specifically target bacteria, including resistant strains, and can be tailored to individual infections

187
Q

what is the rationale for CRISPR-cas systems

A

gene editing technology can be used to target and destroy resistance genes within bacterial populations

188
Q

what is the rationale for antibiotic adjuvants

A

compounds that enhance the efficacy of existing antibiotics or inhibit resistance mechanism

189
Q

what are the examples of antibiotic adjuvants

A

beta lactase inhibits, efflux pump inhibitors and compounds that disrupt cell wall synthesis

190
Q

what is the rationale for host directed therapies

A

enhancing the hosts immune response to clear infections rather than directly targeting the bacteria

191
Q

what are the examples of host directed therapies

A

immunomodulatory agents
cytokine therapies
vaccines

192
Q

what is the rationale for nanotechnology in targeting antimicrobial resistance

A

nanoparticles can be used to deliver antibiotics more effectively or directly to infection sites, reducing the required dose and minimising side effects

193
Q

what is emesis

A

emesis is a complex reflex that involves multiple systems and is regulated by the body through a coordinated response involved the central nervous system, gastrointestinal tract and various signalling molecules. these process ensures the expulsion of harmful substances from the stomach§

194
Q

what is included in the central regulation of emesis

A

vomiting centre
chemoreceptor trigger zone

195
Q

where is the vomiting centre found

A

located in the medulla oblongata of the brainstem

196
Q

what is the function of the vomiting centre

A

it coordinates the acts of vomiting by integrating signals from various sources and triggering the necessary physiological responses

197
Q

what is the location of the CTZ

A

located in the area postrema, on the floor of the fourth ventricle outside the blood brain barrier

198
Q

what is the function of the CTZ

A

it detects circulating emetogenic substances in the blood cerebrospinal fluid and sends signals to the vomiting centre

199
Q

what receptors are found in the CTZ

A

dopamine
serotonin
neurokinin
opioid

200
Q

what is involved in the peripheral regulation of emesis

A

gastrointestinal tract
vestibular system
higher brain centre

201
Q

what is in the gastrointestinal tract that is involved with emesis

A

mechanoreceptor and chemoreceptors - can detect distension, irritations, and the presence of toxins or pathogens
vagal afferents - send signals to the vomiting centre via the vagus nerve

202
Q

what is the functions of the vestibular system in emesis

A

involved in motion sickness, it detects changes in balance and spatial orientation

203
Q

what is the pathway in the vestibular system

A

signals from the vestibular apparatus are transmitted to the vomtiing centre through the vestibulocochlear nerve and are mediated by histamine and acetylcholine receptors

204
Q

how is the higher brain centre involved in emesis

A

cortex and limbic system - emotional and sensory stimuli, such as disgust, fear, pain and certain smells or sights, can trigger vomiting

205
Q

what is the pathway in the higher brain centre

A

these signals are processed in higher brain centres and then sent to the vomiting centre

206
Q

which receptors are involved in emesis

A

serotonin
dopamine
neurokinin
histamine
acetylcholine

207
Q

what is the location and role of serotonin receptors in emesis

A

found in the CTZ, GI tract and vagus nerve
activation of these receptors by serotonin leads to the initiation of the vomiting reflex

208
Q

what is the location and role of dopamine receptors in emesis

A

prominently present in the CTZ
dopamine agonists can induce vomiting, while antagonists can prevent it

209
Q

what is the location and role of neurokinin receptors in emesis

A

found in the CTZ and vomiting centre
substance P binds to NK1 receptors, playing a crucial role in the vomiting pathway

210
Q

what is the location and role of histamine receptors in emesis

A

in the vestibular nuclei
involved in the vomiting reflex associated with motion sickness

211
Q

what is the location and role of acetylcholine receptors in emesis

A

in the vestibular system and vomiting centre
activation can induce vomiting; anticholinergics can be used to prevent motion sickness

212
Q

what are the phases of emesis

A

nausea - reduced gastric motility and increased tone in the small intestine
retching - contraction of abdominal muscles, diaphragm and intercostal muscles
vomiting - coordinated contraction of the diaphragm and abdominal muscles, relaxation of the oesophageal sphincter, and reverse peristalsis in the stomach and oesophagus

213
Q

what are antiemetics

A

antiemetic drugs target various subtypes to prevent or alleviate nausea and vomiting

214
Q

which antiemetic drugs target serotonin receptors

A

ondansetron, granisetron, palonserton, dolasetron
these drugs block serotonin receptors, preventing the initiation of the vomiting reflex

215
Q

which antiemetic drugs target dopamine receptors

A

metoclopramide, prochlorperazine, promethazine, droperidol
these drugs inhibit receptors, which are involved in the vomiting pathway

216
Q

which antiemetic drugs target neuokinin-1 receptors

A

aprepitant, fosaprepitant, rolapitant, netupitant
these drugs block NK1, preventing the action of substance P a key player in the emetic pathway

217
Q

which antiemetic drugs target histamine receptors

A

diphenhydramine, meclisine, cyclizin, promethazine
these drugs block histamine receptors, particularly used in treating motion sickness and vestibular-related nausea

218
Q

which antiemetic drugs target muscarinic receptors

A

scopolamine
this drug blocks muscarinic receptors, preventing acetylcholine from triggering the vomiting reflex, especially effective for motion sickness

219
Q

which antiemetic drugs target cannabinoid receptors

A

dronabinol, nabilone
these drugs activate cannabinoid receptors, which can inhibit the vomiting reflex, particularly useful in chemotherapy-induced nausea and vomiting

220
Q

which antiemetic drugs target glucocorticoid receptors

A

dexamethasone
believed to exert anti-inflammatory effects and modulate neurotransmitter activity, enhancing the efficacy of other antiemetics

221
Q

when are serotonin receptor antagonists used

A

chemotherapy-induced nausea and vomiting
postoperative nausea and vomiting
radiation-induced nausea and vomiting

222
Q

what are the side effects of serotonin receptor antagonists

A

headache
constipation or diarrhoae
dizziness
QT interval prolongation
serotonin syndrome

223
Q

what are the central targets for antiemetic action of serotonin receptor antagonists

A

chemoreceptor trigger zone
nucleus tractus solitarus
vagal afferents in the gastrointestinal tract

224
Q

when are dopamine receptor antagonists used

A

CINV
PONV
gastroesophageal reflux disease related nausea
gastroparesis-related nausea
general nausea and vomiting

225
Q

what are the side effects of dopamine receptor antagonists

A

extrapyramidal symptoms, such as dystonia and tar dive dyskinesia
sedation
hypotension
anticholinergic effects
prolonged QT interval

226
Q

what are the central targets for antiemetic action of dopamine receptor antagonists

A

chemoreceptor trigger zone
gastrointestinal tract
area postrema

227
Q

when are NK1 receptor antagonists used

A

CINV
PONV

228
Q

what are the side effects of NK1 receptor antagonists

A

fatigue
diarrhoea
hiccups
elevations in liver enzymes

229
Q

what are the central targets for antiemetic action of NK1 receptor antagonists

A

chemoreceptor trigger zone
vomiting centre

230
Q

what are the central targets for antiemetic action of histamine receptor antagonists

A

vestibula nuclei
vomiting centre

231
Q

when are histamine receptor antagonists used

A

motion sickness
vertigo
general nausea and vomiting
PONV

232
Q

when are muscarinic receptor antagonists used

A

motion sickness
PONV

233
Q

when are cannabinoid receptor antagonists used

A

CINV
appetite stimulation in AIDs and cancer

234
Q

when are glucocorticoid receptor antagonists used

A

CINV
PONV

235
Q

what are the side effects of histamine receptor antagonists

A

sedation
drowsiness
dry mouth
blurred vision
urinary retention
constipation

236
Q

what are the side effects of muscarinic receptor antagonists

A

dry mouth
blurred vision
drowsiness
constipation
urinary retention
confusion

237
Q

what are the side effects of cannabinoid receptor antagonists

A

dizziness
euphoria or dysphoria
sedation
dry mouth
increased appetite
potential for abuse and dependency
cognitive impairment

238
Q

what are the side effects of glucocorticoid receptor antagonists

A

hyperglycaemia
increased risk of infection
insomnia
mood swings
weight gain
oesteoporosis

239
Q

what is the mode of action of metformin

A

metformin primarily lowers blood glucose levels by decreasing hepatic glucose production. it also improves insulin sensitivity, enhancing peripheral glucose uptake and utilisation. it has minor effect on slowing intestinal glucose absorption

240
Q

what is the pharmacology of metformin

A

class - biguanide
absorption - oral with bioavailability of 50-60%
distribution - widely distributed in the body tissue
metabolism - not metabolised, excreted unchanged in urine
half life - 4-8hrs

241
Q

side effects of metformin

A

gastrointestinal issues - nausea, vomiting, diarrhoea, abdominal discomfort
lactic acidosis
vitamine b12 deficiency - long term use can reduce b12 absorption

242
Q

what is the mode of action of mealtime insulin therapy

A

involves administering rapid-acting or short acting insulin before meals to manage postprandial blood glucose spikes. these insulins mimic the body’s natural insulin response to food intake

243
Q

what is the pharmacology of rapid acting mealtime insulin therapy

A

types - insulin lisper, aspart, glulisine
onset - 10-30mins
peak - 30-90mins
duration 3-5hrs

244
Q

what is the pharmacology of short acting mealtime insulin therapy

A

types - regular insulin
onset - 30-60mins
peak - 2 hours
duration - 5-8hrs

245
Q

what are the side effects of mealtime insulin therapy

A

hypoglycaemia
weight gain
injection site reactions
allergic reactions

246
Q

mode of action of medications that increase insulin secretion

A

stimulate the pancreas to secrete more insulin. they act on the beta cells in the islets of langerhans

247
Q

classes of medications that increase insulin secretion

A

sulphonylureas - glipizine, glyburide, glimepiride
meglitinides - repaglinide, nateglinide

248
Q

pharmacology of sulphonylureas

A

mechanism - bind to the sulphonylurea receptors on pancreatic beta cells, causing depolarisation and calcium influx, which triggers insulin release
half life - 10-24hours

249
Q

pharmacology of meglitinides

A

mechanism - short action than sulphonylureas; stimulate insulin release by binding to a different site on the sulphonylurea receptors

250
Q

side effects of medications that increase insulin secretion

A

hypoglycaemia - high with sulphonylureas
weight gain
gastrointestinal issues
allergic reactions

251
Q

mechanism of action of anticholinergics as bronchodilators

A

block muscarinic receptors
preventing of acetylcholine - inhibit the parasympathetic nervous systems action
reduced bronchoconstriction - decreased intracellular cyclic GMP levels, leading to relaxation to bronchial smooth muscle and bronchodilation

252
Q

examples of anticholinergics that work as bronchodilators

A

ipratropium
tiotropium

253
Q

when are anticholinergics used as bronchodilators

A

chronic obstructive pulmonary disease
asthma

254
Q

adverse effects of anticholinergics as bronchodilators

A

dry moth
cough
headache
urinary retention
blurred vision

255
Q

mechanism of action of beta 2 agonists as bronchodilators

A

activation of beta2 adrenergic receptors
increased cAMP levels
smooth muscle relaxation - elevated cAMP levels lead to the activation of protein kinase A, which phosphorylates target proteins resulting in the relaxation of bronchial smooth muscle

256
Q

examples of beta2 agonists

A

short acting - albuterol, levealbuterol
long acting - salmeterol, formoterol

257
Q

when are beta2 agonists used

A

asthma
COPD
exercise induced bronchospasm

258
Q

adverse effects of beta 2 agonists

A

tremor
tachycardia
palpitations
hypokalaemia
hyperglycaemia

259
Q

mechanism of action of theophylline as bronchodilator

A

phosphodiesterase inhibition - the enzymes responsible for breakdown of cAMP
increase cAMP levels
bronchodilation - elevated cAMP results in the relaxation of bronchial smooth msucle
anti-inflammatory effects

260
Q

when is theophylline used as bronchodilator

A

asthma
COPD

261
Q

side effects of theophylline

A

narrow therapeutic window index, requiring monitoring of blood levels
gastrointestinal disturbance
central nervous system effects
cardiac arrhythmias
tremors

262
Q

what are the psychological symptoms of anxiety

A

excessive worry
restlessness
irritability
difficulty concentrating
fear
panic attack
sense of impending doom

263
Q

physical symptoms of anxiety

A

increased heart rate
sweating
trembling or shaking
muscle tension
headaches
fatigue
gastrointestinal issues
dizziness
insomnia

264
Q

behavioural symptoms of anxiety

A

avoidance
procrastination
compulsive behaviours
social withdrawal

265
Q

cognitive symptoms of anxiety

A

negative thought
overthinking
indecisiveness

266
Q

examples of short acting benzodiazepines

A

alprazolam
lorazepam
triazolam
midazolam

267
Q

therapeutic uses of short acting benzodiazepines

A

anxiety disorders
insomnia
preoperative sedation - midazolam
panic attacks - alprazolam
seizure control - lorazepam

268
Q

examples of long acting benzodiazepines

A

diazepam
clonazepam
chlordiazepoxide

269
Q

therapeutic uses of long acting benzodiazepines

A

anxiety disorders
seizure disorders - clonazepam and diazepam
muscle spasms - diazepam
alcohol withdrawal - chlordiazepoxide and diazepam
panic disorder - clonazepam

270
Q

what are the factors determining benzodiazepine half life

A

lipid solubility
metabolism
age and liver function
route of administration

271
Q

how does lipid solubility effect benzodiazepine half life

A

higher lipid solubility have a faster onset of action and are rapidly distributed into the central nervous system but may also redistribute into peripheral tissues, prolonging their half life

272
Q

how does metabolism effect half life of benzodiazepine

A

hepatic metabolism
active metabolite - long half life
phase 1 metabolism - long half life
phase 2 - short half lives

273
Q

how does age and liver function effect benzodiazepine half life

A

elderly - metabolism slower so longer half life. can risk to accumulation
liver impairment - longer metabolism = longer half life

274
Q
A

CM2001 (13 decks)

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