Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine 4 > Pain > Flashcards

Pain Flashcards

(82 cards)

Start Studying
1
Q

What is nociceptive pain?

A

‘Good pain’ that protects you from potentially damaging stimulus. Autonomic response

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

Describe neuropathic pain

A

Caused by lesion/disease of sensory nervous system. Burning, shooting, pins and needles, numbness

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

Describe dysfunctional pain

A

No noxious stimulus or neuronal damage

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

How do we assess pain?

A

RAT system:
Recognise
Assess
Treat

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

What is the use of uni-dimensional pain assessment scales?

A

Assess intensity (only) and useful for acute pain

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

How do we assess pain in dementia patients unable to communicate?

A

Observation: face, verbalisations, movements, changes in routine/interactions/mental status

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

What is convergence?

A

Single sensory neurone receiving inputs from many sensory receptors

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

What leads to a larger action potential in sensory nerves?

A

Intensity of stimuli
Size of responding receptor population
Number of fibres active

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

Describe the different types of primary afferent fibres

A

Aα - proprioceptor
Aβ - mechanical
Aδ - pain
C - pain

As you go down this list, axon diameter decreases and speed of transmission decreases

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

Describe the tactile pathway of touch afferent fibres

A

Ascend in dorsal columns, synapse in dorsal column nuclei, cross midline in medulla, ascend through brainstem contralaterally, synapse on cells in thalamus, send projections to primary somatosensory cortex

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

Describe the spinal processing route for Aβ and C fibre relayed messages

A

Laminae I and II (most dorsal) are most common site of nociceptor afferent termination. Second order neurones activated. Projection neurones (from lamina I) project to thalamus. Pain signals also set up withdrawal reflexes

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

Describe the C fibre volley

A

Repetitive stimulation of C fibres lead to an increase in number of neuronal spikes

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

How does the brainstem respond to pain?

A

Through spinoreticular tract and branches of spinothalamic tract. Increase in BP, respiration and orientation towards stimulus

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

How does the thalamus respond to pain?

A

Ventral posterolateral nucleus (VPL) acts as final relay before sensory signals reach cortex

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

How does the cortex respond to pain?

A

Consciousness of pain and emotional response of limbic system

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

How does the hypothalamus respond to pain?

A

Response to pain as a stressor - neuroendocrine

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

Where do nociceptive fibres cross the midline?

A

In the spinal cord

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

Describe descending inhibitory control of pain

A

Cortex stimulates periaqueductal grey matter which in turn stimulates Nucleus Raphe Magnus which inhibits pain transmission in the spinal cord

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

What is contained within the brain ventricles?

A

CSF

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

What is the purpose of CSF/

A

Assists in circulating substances, shock absorbant

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

Where is CSF produced?

A

Choroid plexus

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

What is the purpose o the blood brain barrier?

How is it maintained?

A

Interface that ensures the circulation and CSF are kept seperate

Tight junctions between endothelial cells in blood vessels. Pericytes and astrocytes

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

What prostanoids lead to inflammatory response?

A

PGE2

PGI2

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

What is the action of prostaglandins in an inflammatory response?

A

Powerful vasodilators
Cause redness and increased blood flow
Potentiate actions of bradykinin and histamine on blood vessels and nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is bradykinin and what is its function?
Protein made in vasculature and tissue during injury. Activates nociceptors by B1 and B2 receptor. Prostaglandins enhance nociceptor responses to BK
26
What inhibits the actions of COX?
NSAIDs and glucocorticoids
27
What is the antipyretic effect of NSAIDs?
NSAIDs reset body thermostat in fever due to inhibition of prostaglandin production in the hypothalamus
28
How are NSAIDs used as analgesics?
Reduce inflammation and the associated inflammatory pain
29
How do opioid analgesics have their effect?
Open K+ channels and close Ca2+ channels (synaptic hyperpolarisation). Reduce cAMP by inhibiting adenylate cyclase. Overall, prevent synaptic transmission of C-fibres from ventral to dorsal horn in spinal cord. Increase descending inhibitory control of pain
30
How do opioids cause addiction?
Inhibition of synaptic transmission of GABA which lifts its inhibitory effect on dopamine secretion
31
What are the main methods of drug addiction?
``` Increased dopamine release Enhance serotonin (5HT) function NMDA antagonists ```
32
What are the physiological effects of cocaine?
Increase catecholamine neurotransmitter function by preventing re-uptake
33
What are the physiological effects of amphetamines?
Release monoamines from neuronal storage and block re-uptake - increase synaptic dopamine, noradrenaline and 5HT
34
What pharmacological treatment would you use for opiate abuse?
``` Agonist substitution (methadone) Partial receptor agonists (buprenorphine) Anti craving (naltrexone) ```
35
What are the pharmacological treatment approaches to smoking cessation?
``` Nicotine replacement Antagonist treatment (mecamylamine) - blocks rewarding actions of nicotine ```
36
What is meningitis?
Inflammation of the meninges
37
What is encephalitis?
Inflammation of the brain
38
What is myelitis?
Inflammation of the spinal cord
39
What is neuritis?
Inflammation of the peripheral nerves
40
Why is CSF infection difficult to treat?
Low protein Low IgG No lymphatics Blood-brain barrier
41
What are the routes of infection of meningitis?
Blood-bourne Parameningeal suppuration (otitis media, sinusitis) Direct spread through dura (post op, trauma) Direct spread through cribriform
42
What are the symptoms of meningitis?
Headache Neck and back stiffness Nausea Photophobia
43
What are the physical signs of meningitis?
Fever Rash Kernig’s positive (supine position, knee flexed to 90, slowly extended, back pain) Brudzinskis sign (flexing neck also flexes hips and knees)
44
What is the most rapid diagnostic test for meningitis?
Lumbar puncture to obtain CSF and distinguish between bacterial or viral cause (gram stain, PCR, antigen agglutination tests)
45
What are the predisposing factors of meningitis?
``` Immunosuppression Alcohol Diabetes Hyposlenism Myeloma ```
46
What are the complications of meningitis?
``` Death Hydrocephalus Visual deficit Cerebral vein thrombosis Subdural collection Deafness Convulsions ```
47
What are the treatments for meningitis?
Antibiotics (that cross blood-CSF brain barrier) Oxygenation Prevention of hypoglycaemia and hyponatraemia Anticonvulsants Decrease intercranial hypertension
48
What are the different bacterial causes of meningitis?
N. meningitidis H. influenzae type b S. pneumoniae Neonates: E. coli L. monocytogenes Group B streptococci
49
What is a case definition of encephalitis?
Altered level of consciousness, cognition, behaviour or personality lasting more than 24 hours including 2 or more of: Fever Seizures CSF pleocytosis (lots of lymphocytes) EEG findings compatible with encephalitis Abnormal neuroimaging
50
What are the causes of myelitis?
Vasculitis of anterior spinal artery | Infection
51
What are the compilations of myelitis?
Block ascending pathways in spinal cord causing loss of various functions including pain sensation, balance, paralysis etc.
52
How do pathogens enter the CNS?
Initial entry to body: respiratory, GI, subcutaneous, mucosa Then via blood to CNS
53
What is the most common cause of encephalitis?
Herpes simplex
54
What are the 5 stages of a migraine?
Prodrome - yawning, mood or appetite change Aura - initial visual disturbance, peripheral vision ‘shimmers’ Unilateral throbbing headache (4-72 hours) - photophobia, nausea, prostrate Resolution - deep sleep and loss of headache Recovery - exhaustion
55
Describe the genetics of a migraine
Rare autosomal dominant disorder 50 % cases - CACNA1A gene point mutation encoding α1A subunit of P/Q voltage-gated calcium channel (chromosome 19). Altered channel conductance. 30% cases - ATP1A2 gene mutation that encodes Na+/K+ pump α2 subunit
56
What is the vascular origin theory of migraines?
First: Intracerebral vasoconstriction - aura Second: Extracerebral vasodilation - headache
57
What is the cortical spreading depression theory of migraines?
Vasoconstriction and change in blood flow driven by change in metabolic demand. Aura starts with wave of electrical activity in occipital cortex and spreads slowly
58
What is the sensory nerve activation theory of migraines?
Enhanced trigeminovascular neuron activity. Ophthalmic division innervates frontal and parietal cortex
59
How would you diagnose migraine?
Careful history, ruling out other headache causes. Keep diary of migraines to record details: Frequency, length of attack, pain location and character
60
What is the first step to treating/ managing a migraine?
Analgesics and anti-emetics, most effective taken at beginning of attack (often OTC)
61
What are triptans and what is their use? What are their side effects?
Used as primary migraine therapy. 5-HT receptor agonists, cause constriction of cranial blood vessels and inhibit neuropeptide release (available OTC) May cause CVS risks/ chest pain due to coronary artery vasoconstriction
62
What migraine medication is currently in development?
CGRP (calcitonin gene receptor peptide) receptor antagonists and monoclonal antibodies against CGRP
63
What is the role of calcitonin gene receptor peptide (CGRP) in causing migraines?
Vasodilation of blood vessels stimulate trigeminal nerve to secrete CGRP which leads to inflammation and further vasodilation, leading to migraine
64
What are the treatments for severe migraines?
β-blockers, calcium channel blockers, anticonvulsants, amitryptyline
65
Describe the central control of emesis
Generated and coordinated by the vomiting centre - functionally related group of neurones in the medullary reticular formation. Chemoreceptor trigger zone (CTZ) at base of 4th ventricle has multiple receptors. A neurokinin (substance P) is the major output transmitter
66
Where does the vomiting centre receive inputs from?
``` Area postrema - detects blood chemicals Vestibular system - motion sickness Vagal - gag reflex GI afferents Intracranial pressure receptors Descending inputs - sight/smell of vomit ```
67
Why would we purposefully induce vomiting?
If poison is still likely to be in the stomach and not likely to inhale vomit. Can give emetics (ipecacuanha) to induce vomiting
68
What is the most effective single agent therapy for anti-emesis?
Neurokinin-1 antagonist (aprepitant) - inhibits substance P release (major output transmitter)
69
What is the most effective anti-emetic for motion sickness?
H1 and H3 antagonists
70
What combination therapy would you give for chemotherapy-induced emesis?
Neurokinin-1 antagonist, 5-HT antagonist and a corticosteroid
71
How does physical exercise improve memory?
Exercise increases blood flow to hippocampus
72
How does exercise boost neurogenesis and synaptogenesis?
Increases levels of growth factors in the brain
73
How do local anaesthetics work?
Block generation and conduction of nerve impulses at local contact site
74
How do general anaesthetics work?
Alter central neural processing - loss of consciousness with decreased response to painful stimuli and muscle tone
75
Describe the different types of general anaesthetics
``` Inhalation anaesthetics (nitrous oxide) Volatile liquids (halothane) Intravenous anaesthetics (thiopental) Benzodiazepines (diazepam) ```
76
What is minimum alveolar concentration (MAC)?
Inhalation anaesthetics - inhaled dose that prevents movement to a standard surgical stimulus in 50% of patients < MAC number - more potent anaesthetic
77
What is the blood-gas partition coefficient?
The ratio of anesthetic concentrations in the blood and alveolar space when partial pressures in the two compartments are equal
78
Describe the journey of an intravenous anaesthetic
Once in blood stream, some binds to plasma proteins while other remains free Drug transported through venous blood to systemic circulation to cerebral circulation Partial pressure gradient permits entry to brain
79
Describe different intravenous anaesthetics
Propofol - short acting, decrease BP and intracranial pressure, no analgesia Thiopental - fast acting, may cause apnoea/coughing/chest wall spasm... Etomidate - little effects on CVS Ketamine - induces amnesia, unconscious but appears awake
80
What is NaV1.7?
Voltage-gated sodium channels expressed in sensory and nociceptive neurones. Mutations found in people who feel no pain or people who feel constant pain
81
What is erythromelagia?
Genetic condition causing constant pain stimulation. Hypersensitivity of Nav1.7
82
What are cytochrome P450s?
Enzymes involved in drug metabolism and bioactivation found in the liver. Transform drugs into soluble molecules for excretion

Medicine 4 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions