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IM FUCKED GOD PLS HELP Flashcards

1
Q

Lofexidine

A

non-substitute detoxification, central ⍺2-agonist, suppresses some components of withdrawal syndrome

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2
Q

Methadone

A

substitution method of detoxification, long-acting drug, no euphoria to morphine

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3
Q

Naltrexone:

A

opioid antagonist, prevents euphoria to opioids, given daily to addicts to prevent relapses, reduces alcohol-induced reward

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4
Q

Buprenorphine

A

partial agonist, substitution method of detoxification

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5
Q

Clonidine:

A

⍺2-adrenoceptor agonist inhibits excessive transmitter release happening during withdrawal

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6
Q

Propranolol

A

β-blocker blocks excessive symp

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7
Q

Acamprosate

A

weak NMDA antagonist interferes with synaptic plasticity, reduces crave

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8
Q

Disulfiram

A

causes accumulation of acetaldehyde making alcohol consumption unpleasant

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9
Q

Nicotine replacement therapy:

A

relieves psychological + physiological withdrawal syndrome + reduces cigarette consumption but not nicotine abstinence

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10
Q

Bupropion

A

Antidepressant blocking monoamine reuptake so NA + DA
Nicotinic antagonist, ↑[DA] in nucleus accumbens
induce seizures, eating disorders, mania (bipolar disorder)

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11
Q

Varenicline (Champix):

A

partial α4β2 nAChR agonist, full agonist for α7 nACHR, more effective than NRT

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12
Q

Withdrawal syndrome

A

physical characterised by abstinence syndrome (LC) sweating, gooseflesh (cold turkey), irritability, aggression
psychological characterised by craving to avoid withdrawal effects

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13
Q

Chronic drug administration

A

homeostatic adaptive changes to oppose drug action, withdrawal –> rebound effect
eg alcohol causes convulsions
amphetamine causes sedation

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14
Q

Mechanism of dependence (DA)

A

Less frontal cortex activity + less striatal D2 binding

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15
Q

Mechanism of dependence (α4β2)

A

Upregulation of α4β2 + rapid development of tolerance – desensitisation of nAch receptors

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16
Q

Impulsive control disorders

A
  • cycle of tension/arousal
  • impulsive acts
  • pleasure/relief/gratification
  • regret/guilt/self-reproach
  • REPEAT via positive reinforcement (natural reward)
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17
Q

Compulsive disorders:

A
  • cycle of anxiety/stress
  • repetitive behaviours
  • relief of anxiety/stress
  • obsessions
  • REPEAT via negative reinforcement (anti reward)
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18
Q

Positive reinforcement:

A

social drug-taking
drug induces pleasurable effect
triggering further drug administration via natural rewards

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19
Q

Negative reinforcement:

A
  • drug
  • tolerance
  • escalating compulsive
  • dependence
  • negative emotional state triggers craving
  • drug administration via aversive, dysphoria experience of withdrawal NOT high
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20
Q

Opioids target

A

Agonist at μ (δ, κ) opioid receptors

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21
Q

Cocaine target

A

Dopamine transporter blocker – indirect DA agonist

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22
Q

Amphetamine target

A

Dopamine releaser – indirect DA agonist

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23
Q

Alcohol target

A

Facilitates GABAA + inhibits NMDA receptor function

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24
Q

Nicotine target

A

Agonist at nACh receptors

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25
Q

Cannabinoids target

A

Agonist at CB1 receptors

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26
Q

Phencyclidine target

A

NMDA receptor antagonist

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27
Q

Hallucinogens target

A

5-HT2A agonists

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28
Q

Cocaine

A

Blocks catecholamine reuptake so↑DA, stimulant effect

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29
Q

Amphetamine

A

Release cytosolic monoamines (DA)

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30
Q

MDMA (ecstasy)

A

-Inhibits monoamine transporters
-Large ↑5-HT
-depletion
↑5-HT –> psychotomimetic effects
↑DA –> euphoria followed by rebound dysphoria

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31
Q

Alcohol

A
  • Potentiates GABA-mediated inhibition like Bz
  • Inhibits presynaptic Ca2+ entry
  • Inhibits transmitter release
  • Disinhibits mesolimbic DAergic neurons (↑ reward)
  • Induces release of endogenous opioid peptides
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32
Q

Nicotine/tobacco

A

-nACh receptors, α4β2 subtype
Receptors, ligand-gated cation channels (pre- + post-synaptic)
-↑NT release + neuronal excitability including opioid peptides
-Cortex + hippocampus (↑cognitive function)
-Ventral tegmental area VTA (where DAergic neuron project to nucleus accumbens reward pathways via DA release)

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33
Q

Barbiturates

A

Positive allosteric modulators

  • ↑Affinity of receptor for agonist
  • ↓GABA required for same response
  • GABA receptor channel opened for longer –> ↑Cl- in less time
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34
Q

Benzodiazepines

A
  • Positive allosteric modulators binding at alpha-gamma interface of pentamer but only bind to alpha 1, 2, 3, or 5
  • Stabilise GABAa receptors in open state so ↑binding of GABA
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35
Q

Flumenazil

A

competitive antagonist at BZD binding site used for OD

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36
Q

Z-drugs

A

Bind at alpha-gamma interface on GABA-A receptors

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37
Q

5HT1A receptors

A

metabotropic,presynaptic membrane, auto-inhibitory

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38
Q

Buspirone

A

For GAD

  • 5HT1A agonist
  • increased activity of receptors
  • body downregulates receptors
  • buspirone still inhibits serotonin release but to a smaller extent than before
  • overall increase in serotonin release in synapse
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39
Q

α1:

A

on postsynaptic membrane couples Gq to activate phospholipase C

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40
Q

α2

A

on presynaptic membrane couples Gi to inhibit adenylate cyclase

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41
Q

β1

A

on postsynaptic membrane couples Gs to activate adenylate cyclase

  • ↑HR, impulse conduction, contraction, ejection fraction
  • ↑Renin release by juxtaglomerular cells
  • ↑Ghrelin release by stomach for hunger
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42
Q

β2

A

on postsynaptic membrane couples Gs to activate adenylate cyclase

  • SM contraction of bronchus, bronchioles, detrusor muscle, uterine muscle
  • Contract urethral sphincter
  • ↑Renin release by juxtaglomerular cells
  • Glucose metabolism: inhibits insulin release, stimulates gluconeogenesis, glycolysis, lipolysis
  • Thickened salivary secretion
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43
Q

Venlafaxine

A
  • 5HT + NA reuptake inhibitor (SNRI)
  • Serotonin transporter > NA transporter
  • ↓appetite due to activation of adrenoceptors
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44
Q

Trazodone

A
  • 5HT2 receptor antagonist blocks reuptake of serotonin
  • α2 antagonist
  • 5HT reuptake inhibitor
  • 5HT2, 5HT3, H1 antagonist
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45
Q

Mirtazapine

A
  • α2 antagonist

- ↑5HT + NA release in synapse

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46
Q

Mianserin

A

α2, 5HT2A, α1 antagonist – cause bone marrow depression

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47
Q

Estrogen

A

treat postpartum depression via monoamine system, GABA system, glutamate system

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48
Q

TCA Amitriptyline

A
  • NA + 5-HT reuptake inhibitor
  • Block Mus so anticholinergic + antimuscarinic –> constipation, blurred vision, dry mouth, drowsiness (reversible)
  • Block H1 –> weight gain + sedation
  • Block α adrenoceptors –> ↓BP, postural hypotension, tachycardia, dizziness
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49
Q

Reversible MAOi

A

Moclobemide

-Accumulation of NA displaces RIMA so degradation of excess NA

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50
Q

MAOA

A

breakdown of 5-HT > NA > DA + tyramine – in cheese + wine

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51
Q

MAOB

A

breakdown DA

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52
Q

Aneuploidy

A
  • Nondisjunction
  • Misscariages
  • Extra chromosome maternal
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53
Q

Sex chromosome aneuploidy

A

Lives :)

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54
Q

Trisomy 21

A

Downs
MOST nondisjunction
Robertsonian translocation
Mosaic

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55
Q

Trisomy 18

A

Edwards
Maternal meiotic nondisjuntction
MOST trisomy
Die

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56
Q

Trisomy 13

A 
Patau
MOST trisomy from maternal nondisjunction
Translocations
Midline defects
Eyes close together
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57
Q

45XO

A 
Turners
Paternal meiotic errors
Can be mosaic
Hands/feet oedema
Webbed neck
Underdeveloped female
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58
Q

47XXY

A 
Klinefelters
Non disjunction paternal/maternal meiosis
Mosaic
Phenotypically MALE
Female fat distribution
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59
Q

47XYY

A

Paternal meiotic non disjunction

Tall

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60
Q

DiGeorge

A

De novo

Commonest deletion syndrome

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61
Q

Williams syndrome

A

De novo + autosomal dominant
Microdeletions
100% penetrant
ELN gene elastin –> CVS disease

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62
Q

Chondrocytes

A

secrete collagen, proteoglycans, hyaluronan

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63
Q

Hyaluronan

A

Tethers aggrecan which is held together by collagen type II fibres
GAG
High viscosity
Highly hydrated
Low load + high velocity (hydrodynamic lubrication)

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64
Q

Aggrecan (GAG):

A

Proteoglycan induces osmotic gel swelling pressure inflates cartilage by creating negative charge

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65
Q

Avascular articular cartilage

A

nutrients from synovial fluid

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66
Q

Type II collagen fibrils:

A

hold it together, resist gel swelling tendency

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67
Q

eg Glycosamino-glycan chain (GAG):

A

chondroitin sulfate, keratan sulfate, hyalauronan

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68
Q

Proteoglycan

A

= GAG + core protein
Has core protein surrounded by GAG chains fixed negative charge + huge osmotic (swelling) pressure from attracted cations – Gibbs-Donan effect

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69
Q

Achieve stability

A
  • Congruity
  • Fibrous capsule + its thickenings into extra-articular ligaments
  • Intra-articular ligaments
  • Packing improves congruity by: menisci: semilunar cartilages, knee, fat pads
  • Muscles acting across joint
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70
Q

Pannus

A

releases metalloproteinases

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71
Q

TIMPS

A

released to inhibit activity of metallopeptidases but low conc to make diff

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72
Q

Collagenases

A

metallopeptidase

cleave collagen type II cleaved + unwind triple helix structure

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73
Q

Metallopeptidases

A

cleave collagen leaving 1/4 + 3/4 fragment

1/4 fragment reveals antibody binding site (neoepitope)

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74
Q

Aggrecanases

A

cleave aggrecan at several points in chain

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75
Q

ADAMTS

A

Aggrecanase

cleave aggrecan at certain points revealing antibody binding sites

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76
Q

DNA ligase

A

attaches Okazaki fragments by forming phosphodiester bonds via complementary nature of “sticky” ends
ATP driven

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77
Q

G-banding

A

Few days
Chromosome number
Translocations
LARGE deletions/dup

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78
Q

FISH

A 
Few days
Suspect gene/region
Chromosome number
Translocations
Deletions/dup
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79
Q

Q-PCR

A

Quick
Suspect trisomy
Chromosome number

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80
Q

aCGH

A

Suspect gene

Point mutations

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81
Q

NGS

A

Point mutations

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82
Q

Gel electrophoresis

A

separate DNA fragments by size

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83
Q

Regulatory factors

A

recognise their target sequence

by interacting through major groove because greater bond variation

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84
Q

TATA box

A

promoter element which allows the binding of RNA polymerase (TBP, TFII, RNAPII)

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85
Q

Telomerase

A

Brings RNA fragment to

restore length of lagging strand

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86
Q

Topoisomerase II

A

molecular clamp unlinks tangled chromosomes using ATP to work clamp

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87
Q

Robertsonian chromosome

A

Fusion of acrocentric chromosomes
45 chromosomes is stable karyotype
46 chromosome is unstable

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88
Q

Deletion:

A

Breakage + loss of acentric fragment

Detected by array CGH/FISH

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89
Q

Haploinsufficiency

A

Deletion in monosomic region

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90
Q

Non-disjunction

A

failure of separation of chromosomes

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91
Q

Mosaicism

A

Presence of 2 genetically different cell lines, derived from same zygote eg production of trisomy

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92
Q

EEG awake

A

HIGH FREQUENCY
Low freq
Desynchronised

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93
Q

EEG sleep

A

Low freq
HIGH AMPLITUDE
Synchronised

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94
Q

Awake

A
  • photoreceptors converge onto retinal GANGLION cell
  • thalamic cells RELAY
  • primary visual cortex
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95
Q

Falling asleep

A
  • thalamic cells DONT RELAY
  • insensitive to retinal input via inhibitory neurone
  • automatically DEPOLARISE
  • fire AP w low frequency synchronously
  • repeat
  • disconnects primary visual cortex from sensory inputs
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96
Q

Serotonin pathway origins/projections

A

Raphe nuclei: projects throughtout CNS –> analgesia

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97
Q

Ach pathway origins/projections

A
  • Pontomesencephalic tegmentum of brainstem projects to thalamus + cerebellum
  • Basal forebrain projects to neocortex + hippocampus
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98
Q

DA pathway origins/projections

A
  • Substantia Nigra projects to basal ganglia

- Ventral Tegmental Area projects to frontal cortex, limbic areas: amygdala, nucleus accumbens

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99
Q

H1 pathway origins/projections

A

Hypothalamus projects throughout cerebral cortex + thalamus

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100
Q

Orexin pathway origins/projections

A

Hypothalamus projects to CNS

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101
Q

NA pathway origins/projections

A

Locus Coerulus of brainstem projects throughout CNS

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102
Q

Extradural haemorrhage

A
  • MMA rupture
  • unconcious
  • lucid as dura takes time to stretch
  • symptoms
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103
Q

Subdural haemorrhage

A

-Trauma
Blood clot between arachnoid + dural meninges
-Rupture of veins crossing subdural space

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104
Q

Subarachnoid haemorrhage

A
  • External brain vessels rupture
  • Berry aneurysm
  • Blood below pia/arachnoid following brain contours
  • Cerebral spasm –> stroke
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105
Q

Multiple petechial haemorrhage

A

-Obstruct small arterioles + capillaries

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106
Q

Watershed zone infarction

A
  • profuse haemorrhage
  • low BF at arterial territories boundaries
  • no O2 to adjacent periphery territory tissue
  • infarction
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107
Q

Cerebral contusion

A

trauma

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108
Q

Microaneurysm

A
  • hypertensive cerebral arteries rupture

- intracerebral haemorrhage

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109
Q

Aortic dissection

A
  • elderly w medial wall degenration

- marfans

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110
Q

Berry sacular

A
  • circle of willis bifurcations rupture

- subarachnoid haemorrhage

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111
Q

AAA

A
  • post atheroma
  • rupture
  • intraperitoneal haemorrhage
  • thromboembolis
  • ischamia + gangrene
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112
Q

cingulate gyrus

A

empathy

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113
Q

mamillary bodies

A

episodic memory

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114
Q

parahippocampal gyrus

A

environmental scenes

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115
Q

amygdala

A

danger detector

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116
Q

orbitofrontal cortex

A

memory + reward

inhibits inappropriate

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117
Q

AMPA receptor

A
  • Ligand gated Glu
  • Activated
  • Allows Na in, Glu binds
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118
Q

NMDA receptor

A
  • Ligand + vg Glu
  • Remains closed
  • Blocked by Mg
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119
Q

Corticospinal tract pathway

A
  • subcortical white matter passing via corona radiata
  • posterior limb of internal capsule - bottleneck
  • crus cerebri - anterior cerebral peduncle
  • basilar pons
  • pyramid of medulla
  • 90% decussate lowest medulla border
  • 10% no decussation
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120
Q

Lateral crossed tract

A

control distal limb for manual dexerity

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121
Q

Anterior uncrossed tract

A

decuss at spinal segment controls proximal limb

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122
Q

UMN cell body

A

in motor/premotor cortex of frontal lobe

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123
Q

UMN axon

A
  • extends spinal cord
  • spinal level muscle
  • synapses LMN
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124
Q

LMN cell body

A

in anterior horn of grey or CN motor nucleus

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125
Q

LMN axon

A

run in peripheral nerve to muscle

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126
Q

M1

A

Voluntary contralateral body

Precentral gyrus, frontal lobe anterior to central sulcus

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127
Q

Premotor cortex

A

Movement plan + preparation

Anterior to M1

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128
Q

Corticospinal

A

voluntary contralateral lib/trunk

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129
Q

Medial surface

A

lower limb supplied by ACA

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130
Q

Lateral superior

A

upper limb + hand

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131
Q

Lateral inferior

A

face + tongue

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132
Q

Corticobulbar

A

CN motor nuclei in brainstem controls jaw, face, tongue, larync, pharynx

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133
Q

Neural tube

A

spinal cord meninges

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134
Q

Neural tube lumen

A

ventricle

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135
Q

Neural epithelial cells

A

cells making up neural tube makes radial glial cell

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136
Q

Morphogen

A

ON/OFF genes in newly formed neuroblast

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137
Q

Microcephaly

A
  • loss
  • uncontrolled mitosis
  • less neuroblast
  • less nerve cells
  • smaller brain learning difficulty
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138
Q

Neurogenesis

A
  • neural plate
  • neural groove
  • neural tube
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139
Q

Ach pathway function of pontomesencephalic tegmentum

A

DESYNCHRONISES thalamus
Inhibits automatic AP firing
Increases thalamic response Restores connection to world

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140
Q

Ach pathway function of basal forebrain

A

RESPONSE STRENGTH + SELECTIVITY PLASTICITY
Awake, attentive
COGNITIVE, LEARNING, MEMORY

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141
Q

Ach pathway dysfunction

A

Damaged basal forebrain in Alzheimer
Gets damaged affecting cholinergic system
Lose cortex cells + Ach which tunes system and aids memory

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142
Q

Aricept

A

Treat Alzeimers

AchE INHIBITORS increase ACh in presynaptic cleft

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143
Q

DA pathway function of substantia nigra

A

voluntary movements

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144
Q

DA pathway function of ventral tegmental area

A

Awake + alert to damaging/rewarding stimuli

ADAPTS BEHAVIOUR towards rewarding stimuli

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145
Q

Ach pathway dysfunction of ventral tegmental area

A

OVER-ACTIVITY SCHIZOPHRENIA (due to amphetamine)

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146
Q

Dopamine Antagonists

A

treating scizophrenia symptoms

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147
Q

NA pathway function of locus coeruleus

A 
AMPLITUDE + SELECTIVITY Plasticity
Awake + vigilant to new stimulus 
Learning + cognitive
Memory consolidation
Mood
Analgesia
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148
Q

NA pathway dysfunction of locus coeruleus

A

ANXIETY + DEPRESSION

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149
Q

Serotonin pathway function of raphe nuclei

A

Quiet waking - zoned out
MOOD + HAPPINESS
Raphe Nucleus Magnus suppresses ascending pain pathway
Impulse-control, patience, relaxing, responses to reward

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150
Q

Serotonin pathway dysfunction of raphe nuclei

A

ANXIETY + DEPRESSION

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151
Q

H1 pathway function of hypothalamus

A

WAKE-PROMOTING circuits

Awake + alert

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152
Q

Orexin pathway function of hypothalamus

A

regulation of sleep/wake cycle, appetite + alertness

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153
Q

Describe wake up

A
  • in HYPOTHALAMUS, HISTAMINE + OREXIN cells activated
  • projections towards BRAINSTEM
  • activate brainstem ARAS (Ascending Rrticular Activating System)
  • includes nuclei of 5-HT, ACH, NA
  • activate basal forebrain
  • projecting to thalamus
  • relay again connecting cortex to world
  • wakefulness
  • DESYNCHORNIZE EEG
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154
Q

Big brainstem lesion

A

COMA since damaged ARAS nuclei so thalamus not desynchronised

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155
Q

promotes sleep

A

Circadian rhythm (SUPRACHISMATIC NUCLEUS)
Tiredness from increased brain activity (ADENOSINE)
Illness (increased IMMUNE BY-PRODUCTS)

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156
Q

Damage to hypothalamic ventrolateral preoptic nucleus

A

damaged GABA cell lesion so insomina

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157
Q

adenosine

A

turns the hypothalamic GABA centre on = sleepy

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158
Q

caffeine

A

ADENOSINE RECEPTOR ANTAGONIST

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159
Q

how to dream

A

-activation of PONTOMESENCEPHALIC TEGMENTUM + BASAL NUCLEUS
-ON cholinergic system:
Higher cortical activity
ON skeletal muscle paralysis

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160
Q

addiction

A
  • enhance DA in

- nucleus accumbens (VT area projects here) = PLEASURE CENTRE

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161
Q

Microglia

A

engulf, digest, destroy pathogens + dead cells

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162
Q

Astrocytes

A 
produce sheath wrapping around nerve cells maintaining ECF at optimal conc for
Na+K+ by AT
Remove used NT
Transport nutrients
Waste products to capillaries
Forms BBB
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163
Q

Electrotonic potential

A

Small
Slow depolarisation
Exponential decay
Graded

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164
Q

De-inactivate

A

reset to original position when at RMP

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165
Q

Absolute refractory period:

A

no AP can be fired as RMP being restored

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166
Q

Relative refractory period:

A

more depolarisation needed to reach threshold so AP firing controlled

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167
Q

Refractory membrane:

A

part of axon in refractory period after AP fired

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168
Q

SM contraction

A
  • Ach binds to M3 Gq in GI, eye, bronchi SM
  • ↑PLC: breaks PIP2 –> DAG + IP3
  • IP3 binds to calcium stores (SR) so calcium release inside cell
  • DAG acts on Na+ channels to depolarise sarcoplasmic membrane so vgcc open, Ca2+ influx
  • Ca2+ binds to calmodulin forming Calcium-calmodulin complex
  • activates MLCK: phosphorylates myosin light chains
  • contraction
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169
Q

Para on eye

A
  • Ach stimulate M3 Gq
  • contracts contrictor pupillae SM
  • miosis
  • opens canal of Schlemm behind pupil
  • drains aq humour
  • reduce intra-ocular pressure
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170
Q

Para on heart

A
  • Ach stimulate M2 Gi
  • ↓SAN freq of pacemaker potentials
  • ↓Conduction
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171
Q

Para on bladder

A 
Symp
-relax detrusor for filling
-contract sphincter to hold
Stretch receptors activate micturtion reflex
-contract detrusor
-relax external spinchter
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172
Q

Para on lungs

A
  • M3 Gq
  • contract bronchi SM cells
  • bronchoconstriction
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173
Q

Ipratopium

A

anti-mus bronchodilator in COPD

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174
Q

Para on GI

A
  • Ach on M3 Gq
  • contract circular + longitudinal SM in GI
  • motility
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175
Q

DAT blocking

A

blocking dopamine transporter so accumulation in synapse eg cocaine

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176
Q

Selegiline

A

selective MAOB inhibitor so no peripheral effect

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177
Q

MAOB inhibitor

A

-block DA metabolism
-protect against MPTP toxicity:
preventing conversion of MPP+ (not neuroprotective) to ↑DA in synaptic bouton
-DA leaks out into synapse

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178
Q

Entacapone

A

COMT inhibitor

slows elimination of L-dopa

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179
Q

Bromocriptine

A

D2 agonists
mimic dopamine effect
1st line young Parkinsons

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180
Q

Ropinirole

A

Newer D2 agonist
Longer duration of action
Lower tendency for dyskinesia

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181
Q

Pramipexole

A

Newer D2 agonist

Antioxidant effects + protective effect on mitochondria

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182
Q

Amantadine

A

antiviral drug, but ↑DA release

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183
Q

Benzatropine

A

For resting tremors
Antimus
Stimulate DA release since Mus receptors inhibits DA nerve terminals

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184
Q

Prochlorperazine:

A

for vestibular dysfunction

Mus, H1, DA antagonists

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185
Q

Promethazine:

A

for vestibular dysfunction

Mus, H1 antagonist

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186
Q

Hyoscine hydrobromide (scopolamine)

A

for vestibular dysfunction

Mus antagonist

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187
Q

Zine, diphenyhydramine (Benadryl):

A

for vestibular dysfunction

H1 antagonists

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188
Q

Monoamine theory FOR

A
  • Overall reduced activity of central NA/5HT systems
  • Reserpine depletes brain of NA +5-HT induces depression
  • Antidepressants increase [amines] in brain
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189
Q

Monoamine theory AGAINST

A
  • Difficult to show deficits in brain [NA] + [5-HT]
  • Plasma responds better to diff AD
  • AD take weeks for effect but ­ in amines acute (secondary adaptive changes more important)
  • Some AD weak on amine uptake (trazodone) so no increase in 5HT + NA
  • Cocaine blocks amine uptake but no AD effect
  • Decrease in 5HT in bipolar linked to aggression not depression
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190
Q

Neuroendocrine theory

A
  • NAergic + 5HT neurons input to hypothalamus
  • hypothalamus releases corticotropin-releasing hormone (CRH)
  • CRH acts on pituitary
  • releases adrenocorticotrophic hormone (ACTH)
  • cortisol release from adrenal cortex in response to ­ACTH in blood
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191
Q

Neuroendocrine theory FOR

A
  • CRH – mimic depressive behaviour
  • ↑[cortisol]plasma in depressed
  • ↑­[CRH] in CSF
  • Genes + environment affect HPA axis hyperactivity
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192
Q

Robertsonian translocation

A
  • Chromosomal rearrangement between chromosomes 14 + 21
  • Short arms of 2 chromosomes break + lost
  • Long arms fuse into single chromosome
  • Produces 3 copies of long arm 21
  • Carrier of robertsonian translocation offspring w Downs
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193
Q

Balanced rearrangements

A

Due to translocations, insertions, inversions
No genetic material lost/gained
No disease
Gametes less likely to have a normal karyotype

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194
Q

Unbalanced rearrangements

A

Due to deletions, duplications, isochromosomes, ring chromosomes, marker chromosomes
DNA gained/lost
Abnormal phenotype

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195
Q

Angelman syndrome

A

Microdeletion
Developmental delay
Speech impairment

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196
Q

Prader-Willi syndrome

A

Microdeletion
Hypotonia in infancy
Small hands + feet
Obesity

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197
Q

Penetrance:

A

proportion of people who will go on to develop a disease if they carry a mutation in a gene - Marfans

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198
Q

Anticipation:

A

worsening of disease severity in successive generations which only occurs in triplet repeat disorders - Huntingtons

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199
Q

Expressivity:

A

variation in severity of a disorder between individuals with same mutation

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200
Q

Imprinting:

A

only maternal or paternal alleles expressed

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201
Q

Autosomal recessive inheritance

A

Genders equally affected
Siblings not parents/offspring
Recurrence risk is 1/4 for each sibling of an affected person
Carrier probability of 2/3 for normal siblings of an affected person
All offspring are carriers

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202
Q

Mosaicism mechanisms

A
  • Post-zygotic nondisjunction: mitotic non-disjunction

- Anaphase lag

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203
Q

Metacentric:

A

p = q

1-3, 16-18

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204
Q

Submetacentric

A

p < q, 4-12, 19-20, X

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205
Q

Synaptonemal complex:

A

lattice of proteins between homologous chromosomes forms at specific locations then spreads to cover entire length of chromosomes

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206
Q

Bivalent:

A

alignment of homologous chromosomes + crossing over

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207
Q

Synapsis

A

tight pairing of homologous chromosomes

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208
Q

Phenylketonuria

A

LOF
Metabolic disorder lack of phenylalanine hydroxylase (PAH)
Homo lack PAH to convert phenylalanine –> tyrosine
SO PKU

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209
Q

De Vivo syndrome

A

Haploinsuffiency
GLUT1 deficiency
Dominant

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210
Q

Marfan’s syndrome

A

Dominant-negative
FBN1 encodes fibrillin-1: forms elastic fibres in connective tissue
Mutant fibrillin-1 forms complex with normal fibrillin-1 blocking normal fibrillin-1

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211
Q

Achondroplasia

A

GOF
Overactive FGFR3 encodes fibroblast growth factor receptor 3
Skeletal development
Dominant

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212
Q

Marfan’s syndrome

A

Dominane-negative
FBN1 encodes fibrillin-1: forms elastic fibres in connective tissue
Mutant fibrillin-1 forms complex with normal fibrillin-1 blocking normal fibrillin-1

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213
Q

Non-synonymous SNP

A

Missense

Nonsense

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214
Q

Synonymous SNP

A

Silent mutation

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215
Q

Promotor SNPs:

A

Changes in the gene promoter may alter level of gene expression eg TATA

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216
Q

Slicing SNPs:

A

Lead to creation/deletion of splice donor, acceptor, branch sites, affecting final mRNA so protein

217
Q

Terminator SNPs

A

Affects termination + polyA of mRNA

218
Q

Euchromatin:

A

extended state dispersed through nucleus, allows gene expression

219
Q

Heterochromatin

A

highly condensed, genes not expressed - centromere

220
Q

Osteoblasts

A

Synthesise + secrete collagen fibres

221
Q

Osteocytes

A

mature bone cells that have stopped making bone and have become buried inside bone tissue

222
Q

Osteoclasts

A

breakdown bone + degrade collagen

223
Q

canaliculi

A

Minute channels in compact bone allow osteocytes to connect throughout bone

224
Q

Osteogenesis imperfecta

A 
Mutated type I collagen gene
Skeletal abnormalities 
Blue sclera
Autosomal dominant
Glycine --> cystine disrupts α helix
225
Q

TGFβ

A

decreases metalloproteinase production + stimulates production of TIMP metalloproteinase inhibitor

226
Q

Achondrogenesis

A

Mutated type 2 collagen

Abnormal development of cartilage + bone

227
Q

Cytokine interleukin-1 (IL-1)

A

Inhibits proteoglycan synthesis
Stimulates metalloproteinase activity
Promote matrix degradation
Stimulates fibroblast growth + bone resorption by osteoclasts

228
Q

Tight junctions:

A

seal
sheet, define membrane
domains

229
Q

Desmosomes

A

Linked to filaments → high

tensile strength

230
Q

DNA Polymerase

A

Synthesises new DNA strands in 5’ to 3’ direction

231
Q

Primase:

A

catalyses short RNA

primers synthesis on single stranded DNA templates

232
Q

DNA Polymerase

A

Synthesises new DNA strands in 5’ to 3’

direction

233
Q

Capped at 5’ end

A

methyl CAP regulates mRNA chain length ensures its stability during translation

234
Q

Polyadenylated tail at 3’ end

A

protect mRNA from degradation by enzymes

235
Q

Capped at 5’ end

A

methyl CAP regulates
mRNA chain length and ensures its stability
during translation

236
Q

Polyadenylated tail at 3’ end

A

→ to protect

the mRNA from degradation by enzymes

237
Q

splicesome:

A

made of 5 snRNA proteins

238
Q

initiation of translation

A

assembly of ribosome on

mRNA together with 1st aminoacyl tRNA (mettRNA)

239
Q

Streptomycin

A

Antibiotic
Acts on small ribosomal subunit
Inhibits initiation
Misreads genetic code

240
Q

termination of translation

A

-link between last AA +
tRNA broken
-polypeptide released from ribosome

241
Q 
Streptomycin 
Erythromycin Large Ribosomal
Subunit
Inhibits translocation
Neomycin Multiple Sites Several effects
A

Antibiotic
Acts on small ribosomal subunit
Inhibits initiation
Misreads genetic code

242
Q

Tetracyclines

A

Antibiotic
Acts on small ribosomal subunit
Inhibits amino-acyl tRNA binding

243
Q

Neomycin

A

Antibiotic
Acts on multiple sites
Several effects

244
Q

Class I anti-arrhythmic

A

Na+ channel blockers

In non-nodal tissue so atria/ventricles ↓upstroke

245
Q

Class II anti-arrhythmic

A

β blockers

nodal + non-nodal tissue

246
Q

Class I anti-arrhythmic

A

Na+ channel blockers in non-nodal tissue so atria/ventricles ↓upstroke

247
Q

Class II anti-arrhythmic

A

β blockers (nodal + non-nodal tissue)

248
Q

Class III anti-arrhythmic

A

K+ channel blockers

(non-nodal tissue) not repolarising quickly, ↑AP length increases refractory period

249
Q

Class IV anti-arrhythmic

A

Ca2+ channel blockers

(nodal + non-nodal tissue) affects upstroke in nodal + plateau in non-nodal

250
Q

Duchenne muscular dystrophy:

A

mutated dystrophin gene Xp21

X linked condition so young men severely affected

251
Q

Myasthenia gravis:

A

Autoimmune
autoantibodies attack nic Ach receptors on muscle so Ach has nothing to bind to on muscle
muscle weakness

252
Q

Radiculopathy:

A

nerve root damaged, caused by arthritis, prolapsed disk (slip disk)
weakness, wasting, radicular nerve root pain

253
Q

Mononeuropathy:

A

nerve damaged distally from trauma or entrapment (compression of nerve)

254
Q

Pyridostigmine:

A

Ach inhibitor blocks Ach breakdown in synaptic cleft to ↑availability

255
Q

Plexopathy:

A

post-infective/traumatic, symptoms dependent on location + extent

256
Q

Erb’s Palsy:

A

during delivery when upper brachial trunk C5 + C6 compressed so lose muscles controlled by upper trunk:

  • Arms adducted
  • Elbows extended
  • Wrist remains pronated
  • Wrist remains flexed
257
Q

Regulatory step in kidney:

A

1α-hydroxylase regulates production of active vitamin D calcitriol

258
Q

Type 1 muscle fibres

A 
ENDURANCE
slow contraction
small motor neuron = red
many mitochondria
resistant to fatigue
259
Q

Type 2a muscle fibres

A

SHORT HIGH INTENSITY
fast contraction
large motor neuron
some mitochondria

260
Q

Type 2b muscle fibres

A 
SHORT MAX INTENSITY
fastest contraction
largest motor neuron - white
low mitochondria
fatigues
261
Q

Marathon runner

A

small muscles
fatigue resistant
dense strong muscles from high oxidative capacity

262
Q

Sprinter

A

rapid powerful contractions
easily fatigues at max efforts
high force per cross-sectional area of muscle
low oxidative capacity via mitochondria

263
Q

Powerlifter

A

muscles hypertrophied
highly glycolytic
fatigue easily

264
Q

Strength training

A

↑type 2 myosins
IGF-1 release
muscle fibre hypertrophy
glycolytic pathway capability

265
Q

Endurance training

A 
low impact CVS training
↑mitochondrial replication
myoglobin content
oxidative metabolic capability 
fatigue resistant
type I slow myosin
266
Q

IGF-1 (insulin like growth factor):

A

initiates skeletal muscle growth
activates satellite cells for muscle fibre growth
↑protein synthesis by activating transcription factors

267
Q

Growth cone in muscle development

A

attracted by high density of AChR clusters

secretes Agrin

268
Q

Satellite cells:

A
  • muscle resident stem cells express Pax7

- postnatal growth + regeneration of muscles

269
Q

Early limb bud:

A

ectodermal jacket surrounding a mesenchymal core

270
Q

Dermatome:

A

subdivision of differentiating somite + skin area supplied by a single spinal nerve + its ganglion forms dermis, subdermal connective tissue

271
Q

Intramembranous ossification:

A

no cartilage intermediate forms flat bones of face, most cranial bones, clavicles

272
Q

Epimere:

A

small dorsal portion formed from somite’s dorsomedial cells
EXTENSOR SPINE
innervated by dorsal primary ramus

273
Q

Hypomere

A

larger ventral portion formed by somite’s dorsolateral cells
FLEXOR SPINE
outer, intermediate, muscles of limbs, inner layers in thorax + abdomen
innervated by ventral primary ramus

274
Q

How somites formed

A

from proliferating pre-somitic mesoderm

275
Q

Somites:

A

mesodermal derivates from paraxial mesoderm

276
Q

Dermomyotome forms

A

Myotome + dermatome

277
Q

Sclerotome forms

A

bones – vertebrae, neural arches, proximal ribs

278
Q

Syndetome forms

279
Q

Myotome forms

A

epimere, hypomere, limb muscle

280
Q

Dermatome forms

A

dorsal dermis

281
Q

Stratum spinosum

A

many desmosomes (junctions) between cells – strong bonds holding epidermis together

282
Q

Stratum basale

A

Stem cells constantly proliferate

283
Q

Stratum granulosum

A

Cells differentiating to form outermost layer
Lamellar bodies contain lipids
‘Keratohyalin’: precursor of keratin

284
Q

Stratum corneum

A

Thick
Squamous cells w/o nuclei
Cornified squamous cells – full of keratin (from keratohyalin granules) so resistant to injury
Nonpolar lipids (waterproof) between cells – from lamellar bodies

285
Q

Melanocytes:

A

synthesises melanosomes, transfers them to basal keratinocytes via long dendrites for UV protection –

286
Q

Keratinocytes:

A

arrange melanin pigment in a cap distal to nucleus especially in basal layer (stem cells)

287
Q

Langerhans cells:

A

immune system, antigen-presenting cells like macrophages, dendritic cells forming network

288
Q

Subsynovium (loose areolar connective tissue):

A

lymphatic drainage of H2O + proteins

289
Q

Type B cell:

A

fibroblastic synoviocyte secretes hyaluronan + lubricin

290
Q

PTH:

A

Stimulates osteoblasts to produce M-CSF + RANK ligand for ↑bone resorption
-↑Ca2+ reabsorption in DCT
-↑Phosphate excretion
↑1-α hydroxylase in PCT

291
Q

Calcium:

A

-Bone growth/remodelling
-Controls PTH secretion
muscle contraction
blood clotting
co-enzyme
stabilization of membrane potentials
second messenger/stimulus response coupling

292
Q

Primary hypoparathyroidism

A

Congenital
DiGeorge
Autoimmune

293
Q

Secondary hypoparathyroidism

A

parathyroid damage

294
Q

Mg hypoparathyroidism

A

co-factor in PTH production

295
Q

Primary hyperparathyroidism

A 
tumour
HIGH Ca2+
single adenoma
diffuse hyperplasia
multiple endocrine neoplasia MEN
296
Q

Secondary hyperparathyroidism

A

-hypocalemia/PTH resistance
-compensatory hyperfunctioning parathyroids
-LOW Ca2+:
renal disease
vit D def

297
Q

Tertiary hyperparathyroidism

A

glandular hyperfunction DESPITE correcting abnormality

HIGH Ca2+

298
Q

Biphosphonates

A

for hyperparathyroidism

maintain existing bone mineralisation

299
Q

Calcimimetics

A

for hyperparathyroidism

Ca2+ too high to active calcium sensing receptor inducing processes to lower Ca2+

300
Q

Granulomatous diseases:

A

characterised by immune responses

cause of hypercalcemia

301
Q

1-alpha hydroxylase:

A

enzyme activates vit D

302
Q

response to hypercalcaemia

A
  • inhibition of 1-alpha hydroxylation of vit D (regulatory step in kidney)
  • PTH production compensates for high Ca2+
  • calcitonin production from thyroid’s C-cells
  • action on bone inhibits PTH action
  • calcitonin reduces Ca2+ - ineffective
303
Q

hypercalcaemia symptoms

A 
CNS depression
RENAL disease
renal STONES
abdominal PAIN
short QT - arrhythmia
304
Q

Frusemide:

A

hypercalcaemia treatment

loop diuretic for insufficient to flush Ca2+ out

305
Q

Bisphosphonates:

A

hypercalcaemia treatment

stop osteoclasts

306
Q

Prednisolone:

A

hypercalcaemia treatment

suppress immune since osteoclast is immuno-stimulated cell

307
Q

Saline rehydration

A

hypercalcaemia treatment

lets Na/Ca exchanger

308
Q

how immobility causes hypercalcaemia

A
  • less osteoblast movement
  • osteoblast slow
  • osteoclast normal
  • BREAKDOWN > filling
  • more Ca2+
309
Q

how thiazide diuretics cause hypercalcaemia

A

increase Ca2+ reabsorption

310
Q

Familial hypocalciuric hypercalcaemia

A
  • Defective calcium sensing gene encodes bone receptor

- HIGH PTH

311
Q

Osteoclast-activating factor

A

produced by lymphoma, multiple myeloma
HIGH PTH
HIGH Ca2+

312
Q

how cancer causes hypercalcaemia

A

lung cancer releases PTH, PTH-RP

313
Q

response to hypocalcaemia

A
  • ↓Ca2+
  • PTH release stimulated
  • ↑activation of 1α-hydroxylase
  • active vit D
  • ↑FGF23
  • ↑phosphate loss in kidney
  • encourages Ca2+ retention
  • ↑vit D increase as intestinal Ca2+ absorption
  • ↑bone resorption
  • ↑serum Ca2+
314
Q

hypocalcaemia symptoms

A 
Paresthesias
Laryngospasm
Bronchospasm --> SOB
Seizures, confusion, hallucinations
Chvosteks sign
Trousseau’s sign
Long QT 
Acute: syncope, congestive HF
Chronic: dry skin, coarse hair, pruritis
315
Q

Pseudohypoparathyroidism

A

produce PTH but defected receptor
HIGH PTH, PO4
low Ca2+, vit D
teddy bear

316
Q

response to vit D def

A
  • ↓Vit D
  • ↓Ca2+ intestinal absorption -↓Ca2+ in blood
  • response is to ↑PTH
  • ↑Ca2+ reabsorption from kidney + ↑bone resorption
  • raise serum Ca2+ normal
  • FGF23 ↓serum phosphate conc
317
Q

FGF23

A
  • produced in bone when high phosphate
  • ↑phosphate excretion from kidney + inhibits activation of vitD by inhibiting 1α-hydroxylase to stop absorbing phosphate from gut
  • ↓serum phosphate conc
318
Q

dietary vit D

A

Take in ergosterol –> ergocalciferol (vit D2)

319
Q

light vit D

A

Hits skin so cholesterol reduced –> cholecalciferol (vit D3)

320
Q

how vit D3 does calcium homeostasis

A
  • ↑Ca2+ absorption in the gut
  • Stimulates CaBP synthesis
  • Synergises with PTH on bone
  • Inhibits PTH synthesis
  • Inhibits 1a-hydroxylase
321
Q

processing location + movement

A
  • magnoceullar input
  • primary visual cortex
  • superior temporal cortex
  • parietal cortex
  • motor/ssc to interact w environment
322
Q

control of saccadic + pursuit movement

A

motor controlled by III, IV, VI nuclei

323
Q

pursuit movement

A

Voluntary

  • pontine nuclei
  • cerebellum
  • vestibular nuclei
  • CN nuclei
324
Q

involuntary saccadic movement

A
  • retina

- SUPERIOR COLLICULUS

325
Q

voluntary saccadic movement

A
  • frontal
  • parietal
  • SUPERIOR COLLICULUS
326
Q

ipsilateral monocular scotoma

A

PARIETAL RETINAL

detach, tumour, infection

327
Q

ipsilateral monocular anopia

A

optic NERVE

tumour, cranial fracture

328
Q

contralateral homonymous hemiaopia

A

optic TRACT

tumour, stroke

329
Q

contralateral homonymous hemiaopia w macula sparing

A

CALCARINE SULCUS

tumour, stroke

330
Q

tunnel vision

A

bilateral retina
GLAUCOMA
intraocular p compresses optic nerve edge

331
Q

central scotoma

A

RETINA

optic nerve, choroid disorder - macular degeneration

332
Q

contralateral homonymous central scotoma

A

bilateral VISUAL CORTEX of macular fibres at occipital cortex

333
Q

bitemporal hemianopia

A

optic CHIASM

pit tumour affects inferior 1st

334
Q

contralateral superior homonymous quadrantopia

335
Q

contralateral inferior homonymous quadrantopia

336
Q

presbyopia

A
  • ageing
  • sclerosed crystalline STIFF lens
  • ciliary weak
  • less accommodation
  • fixed focus
337
Q

vitreous degeneration

A
  • jelly proteins
  • clump
  • low clarity
338
Q

vitreous detachment

A
  • vitreous shrink
  • pulls from retina
  • retinal tear
339
Q

cataract

A

opaque lens proteins

340
Q

type 1a afferent

A

Velocity of muscle STRETCH

spasticity

341
Q

extrafusal fibres

A

driven by α-motor neurones

342
Q

intrafusal fibres

A

driven by γ-motor neurones

343
Q

nuclear bag fibres

A

Type Ia afferents

  • Velocity dependant
  • Monosynaptic
  • Thick fast axons
  • Corrects rapid unintended movements
344
Q

rapid stretch of nuclear bag fibres

A

central portion change length and activate the type Ia afferent

345
Q

nuclear chain fibres

A

Type II afferents

  • Thin slow axons
  • Indirect via excitatory interneurons
  • Maintains limb position
346
Q

type II afferent

A

muscle LENGTH

hypertonia

347
Q

type 1b afferent

A

TENSION

tendon tension from active muscle contraction

348
Q

Golgi tendon organs

A
  • Inhibit rising tone when standing

- Excite muscles when walking (contact α-motor neurone via excitatory interneurone)

349
Q

reciprocal inhibition

A

OFF antagonist α-motor neuron
Gly
QUICK, weak, short lasting

350
Q

presynaptic inhibition

A

OFF antagonist REFLEX arc
GABS
slow, POWERFUL, long lasting

351
Q

Baclofen

A

↑GABAb mimics presyn inhibition

352
Q

GABAa

A

inhibitory + ionotropic

no specific inhibition ALL motor neurons

353
Q

GABAb

A

inhibits spindle fibre REFLEX

354
Q

Tizanidine

A

α2
suppress interneurons
↑NA transmission

355
Q

medial pain pathway

A
  • nociceptors
  • midbrain ALERTNESS
  • non-specific thalamic nuclei
  • anterior cingulate FEAR DISTRESS AVOIDANCE
  • higher cortical areas PERCEPTION
356
Q

lateral pain pathway

A
  • nociceptors
  • VPL nucleus
  • SSC LOCALISE DISCRIMINATE
  • higher cortical areas PERCEPTION
357
Q

delusion

A

A false, unshakeable belief that is out of keeping with the patient’s social and cultural background

358
Q

chemical guidance signals

A

form gradient eg neuroreglin + semaphorins

attract/repel migrating cells

359
Q

marginal zone cells

A

produce reelin via cajal retizius cells

360
Q

reelin

A

Ensure cortical development deep to superficial tissues

Acts as a guidance chemical telling cells to move to the pial surface

361
Q

subplate cells

A

make guidance signals to migrating nerve cells

362
Q

ganglionic eminence

A

becomes inhibitory neurons + oligodendrocytes

363
Q

big pyramidal cells

A

from deep layer
long dendrites to surface
big axons to subcortical structures

364
Q

stellate cells

A

from middle layer

receive info from deep thalamus

365
Q

pyramidal cells

A

from superficial layer

axons to cortical structures

366
Q

lissencephaly

A

mutated reelin

learning difficulties + epilepsy

367
Q

heterotopia:

A 
mutated cytoskeleton
disrupted cortical development
lose doublecortin protein in females
X linked 
unmigrated cell clusters
normal intellect to severe learning difficulties
epilepsy
368
Q

growth cone in axon guidance

A

growth tip of neurites
lamellipodium supported by actin meshwork
fliopodia

369
Q

fliopodia

A

seek guidance signals
attracts actin bundle growth
repels actin bundle shrinkage

370
Q

floor plate signalling proteins

A

attract axon to spinal cord floor + move it to opposite side

371
Q

integrin

A

matching binding molecule

372
Q

laminin

373
Q

cross linking

A

neuroligin-1 + β-neuroxin binds to flipodia forming test synapse

374
Q

active synapses

A
  • ↑Ca2 –> ↑AMPA
  • Dendrite spine grows via cytoskeletal changes
  • Synaptic bouton grows via dendritic signals
375
Q

VPL nucleus

A

info from limb/trunk

376
Q

VPM nucleus

A

info from head/neck

trigeminothalamic pathway

377
Q

dorsal column pathway

A
  • 1st cell body dorsal root ganglion
  • axon enters dorsal root + joins medial/lateral dorsal column
  • 2nd cell body in gracile/cuneate medulla nuclei
  • dessucates internal arcuate fibres at medulla
  • medial lemniscus
  • PON
  • midbrain
  • 3rd cell body thalamic VPN
  • posterior limb of internal capsule
  • SSC
378
Q

medial dorsal column

379
Q

lateral dorsal column

A

> T6
CUNEATE fasiculus
upper limb/chest

380
Q

spinothalamic pathway

A
  • 1st cell body dorsal root ganglion
  • axon enters dorsal root ganglion + synapses
  • 2nd cell body in dorsal root
  • decuss VENTRAL WHITE COMMISSURE:
  • spinothalamic tract some neurons synapse brainstem reticular formation sloww
  • anterolateral medulla
  • pons lateral to medial lemniscus
  • midbrain
  • 3rd cell body thalamic VPN
  • posterior limb of internal capsule
  • SSC
381
Q

lateral inhibition

A

↑spatial discrimination

382
Q

smaller receptive field

A

↑innervation density

383
Q

↓temporal resolution

A
  • receptive field stimulated quick succession
  • mechanoreceptor CANT DEPOLARISE FAST ENOUGH to produce 2 separate potentials
  • potentials SUMMATE
  • LOSE HIGH FREQ INFO
384
Q

all-in-one receptors

A

receptor = afferent
no synapse
somatosensory + olfactory

385
Q

frontal eye fields

A

VOLUNTARY attention, gaze

386
Q

lateral spinothalamic lesion

A

cant localise noxious stimuli

387
Q

stimulate VPL nucleus

A

somatotopically organised

parasthesia

388
Q

descending pain pathway

A
  • orbitofrontal cortex
  • periaqueductal grey
  • nucleus raphe magnus releases 5HT + enkephalin
  • inhibits pain transmission in dorsal horn
389
Q

insular cortex

A

represents body + VISCERA

390
Q

hyperalgesia

A

↑sensitive pain

lose descending inhibitory input

391
Q

allodynia

A

pain w/o noxious

reorganisation

392
Q

neurogenic pain

A

pain independent of tissue damage

long term potentiation between 1st + 2nd

393
Q

anterior cingulate cortex

A

connected to hypothalamus ANS amygdala, frontal cortex (emotion + motivation)

394
Q

anticonvulsant

A

block high freq AP during seizures

↓NT release at potentiated synapses

395
Q

perceptual threshold

A

Minimum stimulus strength that will generate enough action potentials to be detected

396
Q

phantom limb syndrome

A

Afferents innervate stump as though they are the peripheral areas that were previously painful

397
Q

drug dependence

A

Adaptive state due to repetitive drug use resulting in withdrawal symptoms

398
Q

Which pathway is inhibited in addiction

A

Prefrontal cortex and anterior cingulate gyrus to orbitofrontal cortex

399
Q

neuroepithelial cells divide in the vertical plane forming

A

Neuroblast cells

400
Q

REM initiation

A

“higher” cortex produces meaningful but internally generated activity

401
Q

which layer are the bipolar cells found

A

Inner nuclear layer

402
Q

which cone receptors in central vision

403
Q

drusen

A

Fatty plaques form in the retina pigment epithelium

404
Q

Magnocellular cells

A

fast movement and broad outlines

405
Q

associative agnosia

A

Occipito-temporal lobe

lesion

406
Q

Meniere’s disease

A

tinnitus, dizziness, ‘’fullness’’ of ears

407
Q

stereocilia tips are pulled in the direction of the taller one

A

Depolarisation as more ion channels open so more positive charge inside the cell

408
Q

joint

A

Transmit loads

409
Q

odontoid peg

A

pivot joint

410
Q

decrease in Pj

A

after synovial fluid formed

411
Q

aspirin poisoning

A

Hypokalaemia

412
Q

Why is there a higher concentration of ionised aspirin in the blood

A

Aspirin unionised is polar and lipophilic so it can cross the border to donate protons to plasma

413
Q

Where is melanin stored

A

Basal keratinocytes

414
Q

why SNVs arise

A

One base is swapped for another and the mismatch repair system fails to repair this

415
Q

From which layer does the primitive node arise

416
Q

how the clock-wavefront model allows for Somitogenesis

A

Triggers opposing gradient thresholds of signalling molecules stimulate the negative feedback loop of somite protein translation

417
Q

How does thalidomide cause shortened limbs

A

All of the cells in PZ see FGF instead of only half so all re-specify into distal cells

418
Q

Pax7

A

satellite cells allow post-natal growth + regeneration of muscles

419
Q

atopic eczema treatment

A

Dermovate

Ropical calcineurin inhibitors

420
Q

At what point does Actinic Keratosis become Bowen’s

A

Once it involves the full thickness of the epidermis

421
Q

Reciprocal Translations

422
Q

how muscles grow

A

Quiescent muscle cells are simulated to divide into myoblast cells that differentiate into muscle cells and fuse with the injured region

423
Q

pharmacokinetics

A

what the body does to the drugs

424
Q

22q11.2 deletion syndrome

A

cleft palate several immune deficiency + hypocalcaemia

425
Q

myopathy

A

Proximal weakness
Normal reflexes
High CK
Less prominent wasting

426
Q

accuracy of movement

A

muscle increases excitation of the muscle to contract at the same speed as the intrafusal end poles to correct the length of the centre

427
Q

substantia nigra

A

Has cell bodies of dopamine neurones here to control basal ganglia

428
Q

alar plate

A

forms the motor/anterior root

429
Q

anterolateral laminae

A

innervates distal extensors

430
Q

Pyramidal weakness

A

upper limb flexion, lower limb extension and circumduction

431
Q

phase 2 of drug metabolism

A

Makes the metabolites less reactive so that it is removed from the plasma quicker

432
Q

ossicle bones

A

hammer/maleus
anvil/incus
stirrup/stapes

433
Q

oval window

A

membrane covers bone bole

434
Q

middle ear

435
Q

conductive hear loss

A

outer/middle ear dysfunction

436
Q

sensorineural hearing loss

437
Q

endolymph

A

inside cells
K+
fills membranous chamber/cochear duct

438
Q

perilymph

A

surround cells
Na+
fills scala vestibuli + tympani

439
Q

scala vestibule

440
Q

cochlear duct

A

endolymph seprated by vestibular + basilar membrane

441
Q

scala tympani

442
Q

tectorial membrane

A

covers + attaches to spiral organ

roof fixed

443
Q

tip links

444
Q

inner hair cell

445
Q

outer hair cell

446
Q

vibrations on ear drum

A 
tip links pulled
K+ influx
K+ endolymph
K+ into cell via electrochemical gradient
depolarisation
GLUTAMATE 
high f AP
447
Q

basilar membrane

A

base vibrates

448
Q

vestibular membrane

A

contact w scala vestibuli

449
Q

stria vascularis

A

resorps + produces endolymph so normal p

450
Q

endolymphatic hydrodrops

A

increase endolymph p leads to full ear, tinnitus, vertigo

451
Q

outer ear

A

pinna -> tympanic membrane

452
Q

ototoxic drugs

A

fuck stereocilia so less AP
NSAID
cisplatin
aminoglycosides - gentamicin

453
Q

acoustic neuroma/vestibular schwannoma

A

tumours on same nerve diff branches
vestibular + facial nerve run in same meatus
unilateral tinnitus
dizzy + faint

454
Q

presbycusis

A

lose high freq w age

455
Q

Discriminative hearing pathway

A
  • inner hair cells
  • DORSAL cochlear nuclei
  • inferior colliculi
  • thalamic MEDIAL GENICULATE NUCLEUS
  • auditory cortex
456
Q

sound localisation pathway

A
  • inner hair cells
  • VENTRAL cochlear nuclei
  • lateral (high f) / medial (low f)
  • inferior colliculi
  • MEDIAL GENICULATE BODY
  • auditory cortex
457
Q

lateral vestibulospinal tract

A

otolith system
LINEAR movement
postural control

458
Q

medial vestibular tract

A

semilunar canal

ANGULAR head rotation

459
Q

otoconia

A

crystals in saccule + utricle membrane increases inertia + sense gravity

460
Q

utricle

A

horizontal acceleration

461
Q

saccule

A

vertical acceleration

462
Q

cupula

A

gelatinous membrane

bulges towards utricle –> long stereocilia to ON vestibuloreceptors

463
Q

medial longitudinal fasiculus

A

connects ocular CN nuclei to vestibular nuclei

controls ocular muscles

464
Q

vestibulo-ocular reflex

A
  • semicircular canals
  • vestibular nuclei
  • CN nuclei
  • pupil movement
465
Q

purkinje cells

A

large inhibitory GABAergic neurons

inhibits vestibular nuclei so BLOCKS connection between vestibular nuclei + CN nuclei

466
Q

pontine nuclei pathway

A

SHORT TERM POTENTIATION

  • retinal ganglion cell
  • ACCESSORY OPTIC SYSTEM
  • pontine nuclei
  • mossy fibre
  • granule cell
  • parallel fibre
  • purkinje cells -ve
  • vestibular nuclei
  • BLOCK CN
467
Q

olivary nuclei pathway

A

LONG TERM POTENTIATION

  • retinal ganglion cell
  • THALAMIC GENICULATE BODY
  • olivary nuclei
  • climbing fibre
  • purkinje cell -ve
  • vestibular nuclei
  • BLOCK CN
468
Q

voluntary motor loop

A

SMA in medial frontal loop to putamen

469
Q

non motor loop

A

cognition, motivation, addiction

470
Q

caudate-prefrontal connection

A

COGNITION + behaviour

vision attention gaze via projection to frontal eye fields

471
Q

overactive caudate-prefrontal connection

472
Q

limbic loop

A

ventral striatum/nucleus accumbens

opiate receptors = motivation, reward learning, addiction

473
Q

parkinsons

A

substantia nigra pass compacta
bradykinesia = less movement
rigidity = UMN + stretch reflex

474
Q

MPTP heroin metabolite

A

enters via DA transporter

converted to MPP+ via MAOb

475
Q

MPP+

A

oxidative stress on mitochondria

476
Q

retenone pesticide

A

block mitochondria

parkinson symptoms

477
Q

lewbys bodies

A
  • mutated α-synuclein

- protein aggregate ppt

478
Q

why use Domperidone

A

anti-emetic adminstered with L-dopa

479
Q

why ON/OFF parkinsons?

A

rapid oscillations in mobility

rely on L-dopa since all neurons dead

480
Q

dyskinesia

A

sustained contraction via L-dopa from OD

481
Q

akinesia

A

cant initiate movement

482
Q

paradoxial kinesis

A

projections from amygdala to ventral striatum

483
Q

Atropine

A

anticholinergic

484
Q

huntingtons

A

chorea + rigidity

485
Q

Carbidopa

A

DOPA decarboxylase inhibitor

inhibit peripheral metabolism of L-dopa so more can cross BBB

486
Q

cerebellar lesion

A 
intention tremor
ataxia
nystagmus
hypotonia
slur
487
Q

direct pathway to increase planned movement

A
  • striatum
  • globus pallidus internus
  • ACTIVATE thalamus
  • disinhibits ventral anterior thalamus
  • prefrontal cortex signals
488
Q

indirect pathway to inhibit unwanted movements

A
  • striatum
  • globus pallidus exturnus
  • SUBTHALAMIC NUCLEUS
  • globus pallidus internus
  • BLOCKS THALAMUS
  • BLOCKS frontal cortex
489
Q

disinhibition of subthalamic nucleus

A
  • activates globus pallidus internus
  • inhibits ventral lateral thalamus
  • inhibits unwanted movement
490
Q

spinocerebellum

A

vermis + anterior lobe
GAIT, POSTURE, TONE
receives PROPRIOCEPTION info
CORRECTS movement error

491
Q

cerebrocerebellum/pontocerebellum

A

posterior lobe + tonsils
ACCURATE smooth movement
SPEECH articulation

492
Q

vestibulocerebellum/flocculonodular lobe

A

BALANCE
control occular reflexes
receives CN vestibular nerve input

493
Q

dentate nucleus

A

cerebellum outflow pathway

494
Q

granule cells

A

excitatory glutamate neurons

495
Q

basket cells

A

interneurons around purkinje cell bodies

496
Q

golgi cells

A

inhibitory interneurons

497
Q

higher cerebellar functions

A

cognition

language processing

498
Q

how cerebellum receives constant info about intended movement

A

frontal lobe to contralateral cerebellum via pons

499
Q

how cerebellum sends corrective orders

A

brainstem + cerebral motor cortex via thalamus

500
Q

cerebellum role

A

movement INTENT
ACTUAL movement
COMPARES command signals w sensory impulses
sends CORRECTIVE orders

501
Q

lateral cerebellar lesion

A

ipsilateral voluntary extremities

502
Q

medial cerebellar lesion

A

truncal ataxia so broad gait
nystagmus
head tilting

503
Q

hyaline arteriosclerosis

A

damage kidney arterioles
plasma protein exudes into intima
narrows lumen
PINK histology

504
Q

heart response to hypertension

A

LV hypertrophy
Heart dilates + fails
Atrial fibrillation

505
Q

why LV hypertrophy unsustainable

A

STIFFENS myocardium
↑diffusion distance
atherosclerosis in intima

506
Q

chronic kidney disease

A

ischaemic nephron atrophy from hypertension narrowing arteries
small atrophied kidney

507
Q

how does tubulo-interstital inflammation arise from hypertension

A
  • narrow arteries
  • low nephron mass
  • glomerular capillary hypertension
  • ↑glomerular permeability
  • ↑filtration of plasma proteins
  • proteinuria
  • excessive tubular protein reabsorption
508
Q

how fatty plaques form?

A
  • shear stress + Ang II
  • endothelial dysfunction
  • express adhesion molecules
  • activates endothelium
  • recruit infiltarting monocytes + inflammatory cells
509
Q

early hypertensive retinopathy

A

nick retinal veins by overlying arterioles

510
Q

moderate hypertensive retinopathy

A

straight wide capillaries
flame shaped haemorrhage
cotton wool spots
hard exudates around macula

511
Q

late chronic/malignant acute retinopathy

A

optic disc swelling + haemorrhage

512
Q

baroreceptors

A

carotid sinus

STRETCH

513
Q

chemoreceptors

A

carotid/aortic bodies

low O2, ↑CO2, ↑pH

514
Q

what activates RAAS?

A

low perfusion
HIGH Na
sensed by macula densa OR symp via juxtaglomerular apparatus in nephron

515
Q

renin

A

angiotensinogen -> ang I

516
Q

ACE

A

ang I -> ang II

517
Q

11β-hyfroxysteroid dehydrogenase type 2

A

metabolises cortisol -> inactive cortisone

518
Q

how ang II ↑BP?

A 
peripheral vasoconstriction of resistance vessels
aldosterone release 
posterior pit release ASH
thirst
heart hypertrophy
symp 
negative feedback via ANP, BNP
519
Q

baroreceptor reflex

A

vasoconstricts when low BP except brain

520
Q

autoregulation

A

cerebral arteries have tight control w UNCHANGED BP

521
Q

↑PCO2

A

asphyxia
↑cerebral BF
vasodilation

522
Q

↓PCO2

A

hyperventilation
↓cerebral BF
vasoconstriction

523
Q

↓PO2

A

local hypoxia
ADENOSINE
vasodilators
↑cerebral BF

524
Q

defective areas of BBB

A

area postrema brainstem
hypothalamic subfornical organ
hypothalamic periventricular osmoreceptors

525
Q

regional hyperaemia

A

activityyy
depolarisation freq
K+ efflux into environment
vasodilation

526
Q

postural hypotension

A

compliant veins dilate
↓CVP + EDV
↓cerebral BF

527
Q

cerebral spasms

A

UNCONTROLLED vasocontriction -> cerebral ischaemia

528
Q

5HT as local vasoconstrictor

A

from perivascular nerves

529
Q

neuropeptide Y as local vasoconstrictor

A

from perivascular nerves

530
Q

endothelial-1 as local vasoconstrictor

A

from vascular endothelium

531
Q

K+ as local vasoconstrictor

A

from damaged cells

532
Q

Vasospasm treatment

A

Ca2+ channel blocker

ETA blcoker

533
Q

Amlodipine

A

Ca2+ channel blocker
for vasospasm
act on VSMC

534
Q

Bosentan

A

ETA blocker

for vasospasm

535
Q

cushings

A

bradycardia + HIGH BP

536
Q

space occupying lesion

A 
lesion push brain foramen magnum
press on RVLM - symp control
HIGH BP, TPR, HR
stimulate baroreflex
more vagal so bradycardia
537
Q

stroke treatment

A

thrombolysis 4.5hrs evacuate clot
aspirin
Clopidogrel/Ticagrelor

538
Q

cystic space

A

macrophage clears liquefaction necrosis

PPD (8 decks)

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