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MD2002 > WEEK 4 > Flashcards

WEEK 4 Flashcards

1
Q

Describe both (i) Fasciculus Gracillis and (ii) Fasciculus Cuneatus.

A

(i) carries information from the lower body extremities
- enters up to T6
(ii) carries information from the upper body extremities
- enters above T6

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2
Q

What are three principal ascending tract systems in the spinal cord?

A
  1. Dorsal column - medial lemniscal pathway
  2. Spinothalamic pathways
  3. Spinocerebellar pathways
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3
Q

For the dorsal medial - lemniscal pathway the pathway for? (HINT: there’s 4)

A
  1. Conscious proprioception
  2. Discriminative touch
  3. Vibration
  4. Pressure
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4
Q

Describe the process of the dorsal column medial - lemniscal pathway. Including what fibres it is composed of.

A

Composed of large A beta fibres
The 1st order neurons ascend ipsilaterally in dorsal columns
At the gracille & cuneatus nuclei (brainstem) they synapse with second order neurons
They then decussate to form the medial lemniscus & project to the ventral posterolateral lobe of the thalamus

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5
Q

Explain the various pathologies of the dorsal column medial - lemniscal pathway.

A
  1. Causes gait ataxia because the brain is deprived of information about the position of the feet
  2. Lesions in cervical region cause upper extremity ataxia
  3. Dorsal column disease causes paraesthesia in the distal parts of the extremities
    - this usually results from ectopic discharge in damaged dorsal column axons, which may be present before any abnormalities are detected on NeuroExam
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6
Q

What are 2 ways you can test the dorsal columns function?

A
  1. Ability to feel changes in position of the toes and fingers (w/out looking)
  2. Ability to feel tuning fork vibrations (w/out looking)
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7
Q

What is the spinothalamic pathway the pathway for?

A

Nociceptive stimuli

- also for mechanical, chemical & thermal detection of coarse or non-discriminating touch as well as pain & temp

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8
Q

Describe the process of the spinothalamic pathway. Including what fibres it is composed of.

A

Composed of small, slow fibres (A delta = non-discriminative touch, heat, cold, sharp pain or C = dull aching pain, itch plus thermal & mechanical)
The 1st order neurons synapse with the 2nd in the dorsal horn
- these then decussate & ascend in either the dorsal OR ventral pathway
In the thalamus they synapse with 3rd order neurons which project into the sensory cortex

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9
Q

What are the (i) Spinothalamic lateral and (ii) Spinothalamic ventral composed of? Explain what happens when there is lesions in the lateral pathway.

A

(i) mix of A delta (temp) and C (pain)
(ii) only C fibres (coarse, non-discriminating touch via mechanosensitive fibres)
Lesions in lateral pathway: result in a decreased perception of pain & temp on the CONTRALATERAL side of the body (always 1 or 2 dermatomes below the lesion)
- can cause paraesthesia, experienced as shooting or electrical pain.
- patients notice it when they experience painless cuts or burns

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10
Q

What is the role of pain?

A

Protects the body

- sense of pain only occurs once in the brain, before this it is simply a code

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11
Q

What is the function of nociceptors? List the various types of nociception. (HINT: there’s 4)

A

They detect noxious stimuli in the world around us and relay signals to the brain
Polymodal - unmyelinated C fibres
- mechanical, chemical, thermal
Mechanical - lightly myelinated A delta fibres
- sensitive to increasing pressure
Chemical - lightly myelinated A delta fibres
- sensitive to histamine, itch feeling
Thermal - lightly myelinated A delta fibres
- sensitive to high/low temperatures

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12
Q

What are the 2 types of pain? Describe them both.

A
  1. Pricking/stabbing = Fast pain, along A delta fibres. Arrive first in the CNS
  2. Burning/Aching = slower pain, along C fibres. Arrives later in the CNS
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13
Q

What is substance P?

A

Modulates peripheral neuron response to noxious stimuli

  • released from pain neurons when stimulated in fast succession
  • increases the sensitivity to noxious stimuli
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14
Q

Describe the mechanism of referred pain.

A

The signals of normal & noxious stimuli enter the spinal cord at the same point
=> cross talk in dorsal horn between modalities is common
- signals from VISCERA get picked up by ascending nerve fibres that are mapped cortically to DERMIS

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15
Q

What is the spinocerebellar pathway composed of? Where does it carry information from? Describe, and name, the route of its two different pathways.

A

Composed of Dorsal (posterior) and Ventral (anterior) routes
- carry info from muscle spindles, GTO, touch receptors.
Both pathways only contain 2 neurons along their path
- the cell bodies of 2nd order are located in dorsal horn of spinal cord & end in vermis of cerebellum
Dorsal tract: ascend ipsilaterally and enter the cerebellum via inferior peduncle
Ventral tract: ascend contralaterally, enter cerebellum via superior peduncle

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16
Q

Explain what condition(s) results from dysfunction of the spinocerebellar pathway. What does this condition result in?

A

Friedreich’s Ataxia
- spinocerebellar tract becomes increasingly ineffective, caused by multiple repeats of the gene for protein Frataxin (which is responsible for iron metabolism in mitochondria)
- results in : uncoordinated arm & leg movements
wide based ‘reeling’ gait
Intention tremor

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17
Q

Define each of the following; (i) fibre (ii) tract (iii) pathway (iv) system.

A

(i) 1 or more adjacent axons travelling in parallel
(ii) large number of axons travelling in parallel within the CNS
(iii) route taken along tracts by sensory OR motor signal (they can cross tracks or just travel along a portion of them)
(iv) complex group of tracts found in a particular portion of the spinal cord OR group tracts serving similar functions

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18
Q

What are the levels of motor control? Describe them. (HINT: there’s 2)

A

UMNs - cortex & brainstem nuclei
- restricted to CNS (don’t contract muscle)
- have an executive function over LMNs (& circuit controlling LMNs)
LMNs - brainstem & spinal cord
- not CNS restricted (stimulate muscle contraction)
- is the motor function to muscles

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19
Q

What are the 2 major classes of descending pathways? Explain what they are controlled by, what they control.

A
  1. Conscious movement - LATERAL pathways
    - controlled by cerebral cortex via 2 corticospinal tracts
    - control voluntary movement
    - mainly control distal muscles
  2. Unconscious movement - VENTROMEDIAL pathways
    - controlled by brainstem
    - posture & rhythmic movements involved in locomotion
    - control axial & proximal muscles
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20
Q

What pathway controls posture? How is posture adjusted? What are the 3 sensory outputs used in controlling posture?

A

Ventromedial pathways
Posture is adjusted by involuntary movement driven both predictively (postural set) and reactively (compensation)
The brain stem is where the postural set is governed
1. Muscle proprioceptors (changes in muscle length & tension)
2. Sense balance derived from head movements relative to the Earth’s gravitational field
3. Visual inputs (movements in visual field representing movement of the body)

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21
Q

What are the two pathways that are ventromedial? Describe their subsets.

A

Vestibulospinal & Reticulospinal
1. Lateral vestibulospinal:
- principle effect is to facilitate extensor MNs & inhibit flexor MNs - innervating ipsilateral medial & axial muscles
- activates alpha MNs & Gamma MNs, causing enhanced muscle spindle mediated stretch reflexes
- their overall effect is that they increase the tone of antigravity muscles
2. Medial vestibulospinal:
- controls head & eye movements
- unplanned head movements activate the vestibular apparatus (which projects to the lateral vestibular nucleus)
- the vestibular nucleus links this info with visual & tectal sensory info & transmits signals to cranial nerves (controlling head, neck & eye movements)
3. Reticulospinal: coordinates movement & posture
by receiving information from multiply sources:
- vestibular nuclei
- cortical areas for voluntary movement
- proprioception, vision etc

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22
Q

Where is the primary motor cortex found?

A

Anterior to the central sulcus

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23
Q

Describe the first branching off from the corticospinal tract.

A

The first branch is the corticobulbar tract
Which goes to:
1. cranial nuclei, UMNs & circuits
2. Influence over unconscious motor output (planned movement)

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24
Q

Describe the second branching off from the corticospinal tract.

A

The second branching is otherwise known as Pyramidal Decussation
90-95% of the corticospinal tract decussates into the Lateral Contralateral Corticospinal Tract - it travels the length of the cord, synapses at each segment & innervates unilaterally
The remaining 5-10% continues as the Anterior Ipsilateral Corticospinal Tract - it ends at L2, decussates at each segment & innervates bilaterally

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25
Q

What does the (i) Anterior Ipsilateral Corticospinal Tract (ii) Lateral Contralateral Corticospinal Tract, provide?

A

(i) postural compensation for movements contralaterally

(ii) fine voluntary control over distal muscles

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26
Q

Explain the various corticospinal lesions (in both UMNs and LMNs).

A

Are quite common as axons are very long (UMNs)
Signs of lesions are presented as +ve or -ve signs
-ve = loss of function
+ve = appearance of an abnormal response
Ex. of a +ve response is the Babinski sign (toes fanning).
- these lesions give rise to UMN syndrome
LMN lesions: cause muscle paralysis, reduced muscle tone, reduced stretch reflex, fasciculation, atrophy
NOTE: in UMN lesions, there’s no atrophy or fasciculation but muscle tone increase often leads to painful spasticity

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27
Q

What is the law of mass of action? Stating the equation, including the equation for the rate of associations and dissociations.

A

[D] + [R] [DR]
k1 = rate constant for associations
k2 = rate for dissociations

rate associations = k1.[D].[R]
rate dissociations = k2.[DR]

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28
Q

What is K(D)

A

The equilibrium dissociation constant
- when the rate of associations = rate of dissociations
It represents the concentration of a drug required to occupy 50% of receptors at equilibrium
It is 1. different for every drug
2. A measure of the affinity of one drug for a receptor

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29
Q

For an agonist, what is the equation to calculate pD2, stating its relationship with a drugs affinity

A

pD2 = -log10(K(D))

the greater the pD2 value, the greater the drugs affinity

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30
Q

What is the overall efficacy equation for an antagonist? (HINT: involves alpha and beta pathways)

A

[D] + [R] [DR] [DR]*
note [DR]* = active
alpha pathway (backwards) = rate constant of receptor inactivation
beta (forward) pathway = rate constant of receptor activation

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31
Q

What are spare receptors?

A

If less than 100% of the receptors are required to evoke a maximum response, then the “extra`’ receptors are referred to as spare receptors

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32
Q

Explain the relationship between the efficacy and the number of receptors required to elicit a response.

A

Very efficacous drugs require to occupy fewer receptors to give a response than less efficacous ones

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33
Q

What are partial agonists?

A

They decrease the response to a full agonist as some receptors will be occupied by partial agonists
- giving a smaller response than if all the receptors were occupied by full agonists

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34
Q

What is competitive antagonist?

A

A competitive antagonist is a drug which interacts/binds reversibly with receptors to form a complex
but this complex does NOT evoke a response

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35
Q

What does a competitive antagonist do to the Log Dose - response curves?

A

It displaces it to the right

- however, the max response to the agonist remains the same

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36
Q

What is the K(A)?

A

The equilibrium dissociation constant for an antagonist,
- The concentration of an antagonist that means you have to add twice as much agonist to produce the same response that would be achieved if no antagonist was present

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37
Q

For an antagonist, what is the equation to calculate pA2?

A

pA2 = -log10 (K(A))

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38
Q

Describe irreversible antagonism, and the effect it has on the graph of an agonist.

A

Binds to the receptor, but dissociates very slowly - if at all!
This results in the slope of the Log dose-response curve being decreased AND the max response being decreased

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39
Q

What is the function of allosteric binding sites?

A

They can modify the affinity OR efficacy of a receptors endogenous ligand or drug.

40
Q

What are the 2 key properties of drugs?

A
  1. AFFINITY = concentration range over which a drug binds to its receptor
  2. EFFICACY = ability of drug to generate/initiate a stimulus once bound to its receptor.
41
Q

Explain the pathogenesis of thrombosis

A
  1. ENDOTHELIAL INJURY
    - formation of thrombi in heart & arteries
  2. ALTERATIONS IN NORMAL BLOOD FLOW
    - tubulence = cardiac & arterial thrombi
    - stasis = venous thrombi
  3. HYPERCOAGUBILITY
    (alteration of blood coagulation which predisposes thrombosis)
    - primary (genetic) = mutation in factor V gene, AFIII deficiency, protein C&S deficiency
    - secondary (acquired) = high risk (bed rest, MI, tissue damage) low risk (myopathy, AF, oral contraceptive, sickle cell anaemia, smoking)
42
Q

What is the role of platelets in thrombosis?

A

after vessel injury, platelets undergo 3 important reactions:

  1. adhesion
  2. secretion
  3. aggregation
43
Q

Identify and explain the morphology of thrombosis

A
  1. mural thrombi:
    - one wall of underlying structure
    - capacious lumina of heart chambers and aorta
  2. arterial thrombi
    - usually occlusive
    - can be mural
    - frequent in: coronary, cerebral, femoral
    - grey, white and friable
  3. venous thrombi (phlebothrombosis)
    - occlusive & dark red
    - veins of the lower extremities (90%)
44
Q

Discuss about clinical features of thrombosis

A
  1. Arterial
    - loss of pulses distal to thrombosis
    - areas become: pale perishing cold, painful, paraesthesia
    - eventually results in tissue death & gangrene
  2. Venous
    - superficial: congestion, swelling pain, tenderness
    - deep: foot & ankle oedema, asymptomatic (recognise only once embolised)
45
Q

What is used as a treatment for thrombosis?

A

Stockings is used as a prevention mechanism

Anticoagulant drugs are used to prevent clot growth

46
Q

Discuss the different classes of embolism.. (HINT: there’s 5)

A
  1. Pulmonary embolism
    - arise from DVT (95%)
    clinical course = result in respiratory & haemodynamic compromise
  2. Systemic embolism
    - through arterial system
    - 80-85% come from within heart
    - almost always = infarction
    major sites = lower extremities, brain, viscera, UL.
  3. Air Embolism
    - bubbles of air/gas within circulation obstruct vascular flow and damage tissues = BAROTRAUMA
    arise from: pneumothorax, caissons disease, delivery/abortion, lung/chest wall injury
  4. Fat Embolism
    - due to fractures of long bone shafts or soft tissue trauma/burns
    - characterised by: pulmonary insufficiency, neurologic symptoms, anaemia & thrombocytopenia
    - symptoms after latent 24-72 hrs
    sudden onset of: trachypnoea, dyspnoea, tachycardia, irritability & restless -> deriulium & coma
  5. Amniotic Fluid Embolism:
    - labour complication = maternal mortality (86%)
    - infusion of amniotic fluid into maternal circulation
    - clinical presentation = respiratory difficultly (deep cyanosis & CV shock) -> convulsions -> coma
47
Q

What are the causes of infarcts?

A 
Thrombosis & embolism
Vasospasm
Atheroma expansion
Twisting of vessels
Traumatic rupture
48
Q

What are the types of infarcts?

A 
Red (haemorrhagic)
- venous occlusions
- in loose tissues
- tissues w. dual circulation
White (anaemic)
- arterial occlusions
- solid organs
Septic or Bland
49
Q

Discuss the morphology of infarcts.

A

Haemorrhagic:
- ovarian = venous, dark blue & haemorrhage
- lung = loose tissue, wedge shaped, red & haemorrhagic
- SI = dual circulation, red & haemorrhagic
Anaemic
- spleen = wedge shaped, white
- kidney = wedge shaped, white

50
Q

What factors influence infarcts?

A
  • single vascular supply vs dual
  • rate of occlusion development
  • vulnerability to hypoxia
  • lack O2 content in blood = faster infarction (anaemic/cyanotic)
51
Q

The ANS is a 2 neuron system. Explain this statement.

A

Pre ganglionic fibres originate from the CNS

Post ganglionic fibres originate from the autonomic ganglia

52
Q

Explain the relationship of the ANS to the eye.

A
  1. Pupillary dilator muscle
    - sympathetic innervation
    - mydriasis
  2. Pupillary constrictor muscle
    - parasympathetic innervation
    - miosis
53
Q

Describe the sympathetic innervation of the adrenal gland

A
  • pre ganglionic fibres synapse on chromaffin cells and release adrenaline (80%) and noradrenaline (20%) into the systemic circulation
    => eliciting a widespread tissue response
54
Q

List the various neurotransmitters of the ANS.

A 
Parasympathetic:
- pre = NACh
- post = MACh
Sympathetic:
- pre = NACh
- post = NA (note: some release ACh i.e. sweat glands)
55
Q

What are the root values of the musculocutaneous, axillary & radial nerves - including what they innervate (both motor AND sensory).

A

MUSCULOCUTANEOUS (C5, 6, 7): motor to flexors of the arm (BBC) & sensory as the lateral cutaneous nerve of the FA
AXILLARY (C5, 6): motor to the deltoid & teres minor & sensory to the skin over the lower part of the deltoid (as the superior lateral brachial cutaneous nerve)
RADIAL (C5-T1): motor to extensor muscles of the arm & FA & sensory to posterior skin of arm, FA & hand.

56
Q

What are the locations and trajectories of the axillary, musculocutaneous and radial nerves including important relations and muscles and skin innervated

A

AXILLARY: passes posteriorly through the quadrangular space & lies on the surgical neck of the humerus with the posterior circumflex humeral artery
MUSCULOCUTANEOUS: pierces coracobrachialis & eventually becomes the lateral cutaneous nerve of the forearm (C6,7) where it terminates by exiting lateral to the biceps running with the cephalic vein near the cubital fossa. Then descends the lateral FA anteriorly to the wrist
RADIAL: passes posteriorly through the lower triangular space with profunda brachii artery. Passes posterior to humerus & descends arm in the radial groove between the lat & med heads of triceps. Enters cubital fossa by piercing lat inter-muscular septum. Divides into a superficial cutaneous branch & a deep motor branch once in the FA

57
Q

What are the root values of the gluteal, sciatic, common fibular, and femoral nerves of the lower limb?

A 
SUPERIOR GLUTEAL (L4, L5, S1)
INFERIOR GLUTEAL NERVE (L5, S1, S2)
SCIATIC (L4, L5, S1, S2, S3)
COMMMON FIBULAR (L4, L5, S1, S2)
SUPERFICIAL FIBUALR (L5, S1, S2)
DEEP FIBULAR (L4, L5)
FEMORAL (L2, L3, L4)
58
Q

What are the locations and trajectories of the gluteal, sciatic, common fibular, and femoral nerves? including important relations and muscles and skin innervated.

A

SUP GLUT: enetrs sciatic foramen above piriformis & runs laetrally between gluteus med & min & splits into a sup branch (glut med) & an inf branch (glut min & tensor fasciae latae)
INF GLUT: enters sciatic foramen below piriformis & runs deep to glut max - innervating it
SCIATIC: enters gluteal region via greater sciatic foramen & runs below piriformis & deep to glut maximus, midway between the ischial tuberosity & greater trochanter, behind hip joint. Terminates as tibial & common fib at apex of pop fossa. Innervates muscles in posterior thigh, all muscles in leg & foot & articular branches to all LL joints.
COMMON FIB: Runs inferiorly & laterally following medial border of the biceps, passing over the lat head of gastroc & winding round neck of fibula where is terminates as superficial fib (lat compartment) & deep fib (ant compartment). Innervates lateral aspect of the knee joint
FEMORAL: descends in abdomen then travelling through the pelvis to midpoint of inguinal lig. Then traverses behind the inguinal lig into thigh. Passes through femoral triangle & gives off articular branches to hip and knee joints. Terminal cutaneous branch of the femoral nerve=saphenous
nerve which continues(with the femoral artery and vein) through the adductor canal to the leg. Innervates muscles of ant thigh

59
Q

What are the clinical complications & symptoms for the gluteal nerves?

A

Injury to superior = compromised hip joint with interrupted medial rotation & abduction of the thigh. Would transfer to the centre of gravity over the supporting lower limb ‘glut medius limp’
When glut medius & minimus are affected, pt has Trendelenburg gait. Compensated for by producing waddling gait (raising pelvis to allow clearance of the foot moving forward) Can also arise from dislocation of the hip or fracture of the greater trochanter.

60
Q

What are the clinical complications & symptoms for the axillary nerve?

A

Injury results in reduced abduction (beyond 15 degrees) & muscular atrophy (flattened shoulder)
Injuries can occur upon fracture of the surgical neck or dislocation of the GH joint
Injury will also affect sensation over the lateral proximal arm area near the inferior deltoid because of loss of innervation through the superior lateral cutaneous nerve of the arm

61
Q

What are the clinical complications & symptoms for the musculocutaneous nerve?

A

Injury would result in paralysis of the BBC muscles causing weak flexion of the shoulder & GH joint, elbow joint & weak supination
Would also cause loss of sensation to the lateral FA

62
Q

What is the contents of the cubital fossa (from medial to lateral)

A

Median nerve
Brachial artery
Biceps tendon
Radial Nerve

63
Q

What are the clinical complications & symptoms for the radial nerve?

A

Injury commonly presents as ‘wrist drop’. Wrist partly flexed due to the flexor muscles still being intact. Extension of wrist & fingers at MCP joints compromised.
Injury in post. FA: extension of thumb & MP joint compromised
Testing for radial nerve integrity = ask pt to extend MP joints against resistance (if intact long extensor tendons will show)

64
Q

What are the clinical complications & symptoms for the sciatic nerve?

A

Compression of the nerve can occur due to its trajectory under the piriformis muscle (including muscle spasms). Is more common in athletes & woman
Direct injury/trauma would eliminate extension of hip & thigh & flexion of leg.

65
Q

What are the clinical complications & symptoms for the common fibular nerve?

A

Susceptible to injury in dislocation of knee joint or upon fibular fracture.
Severe injury of nerve paralyse muscles in lat & ant compartments of leg => foot drop (loss of dorsiflexion of ankle & foot evertors). Toes don’t clear the ground during walking, requiring compensation, but resulting in foot slaps
Loss of sensation can occur in anterolateral aspect of leg & dorsum of foot

66
Q

What are the 3 ways that bloodborne pathogens are transmitted?

A
  1. Direct contact with infected blood fluids
  2. Infection via contaminated needles, syringes, or other unsterilised instruments
  3. Direct infection into the bloodstream by arthropod vectors (e.g. mosquitoes)
67
Q

What are the 3 routes in which HIV occurs?

A
  1. Via blood/blood products ro contaminated needles
  2. Sexually (virus is present in semen & vaginal secretions)
  3. Perinatally (transplacentally during delivery, ingestion of breast milk)
68
Q

How is HIV treated? (HINT: there’s 3 inhibitors used)

A

Nucleoside reverse transcriptase inhibitors (NRTIs)
Non- nucleoside reverse transcriptase inhibitors (NNRTIs)
Protease inhibitors (PIs)

69
Q

How is HIV diagnosed?

A

ELISA
Western Blotting

NAAT used to detect viral RNA in serum
NOTE that an initial neg test should always be followed up

70
Q

How is the Hepatitis B Virus (HBV) transmitted?

A

Blood or blood products
Contaminated needles & equipment used by IV drug users
Association with tattooing, body piercing & acupuncture

71
Q

What are the various antigens associated with HBV?

A 
HBsAg = surface antigen
- indicates infectivity
- Anti-HBsAg provides immunity & appears late
HBcAg = core antigen
- appears early in infection
HBeAg = pre core antigen
- indicates high tansmissibility
72
Q

What are the clinical features of HBV?

A 
Pre-icteric(jaundice) stage:
- malaise
- anorexia
- nausea
- pain in R upper quadrant (tender liver)
Icteric stage
- jaundice
- Bilirubin (dark urine)
73
Q

What is the treatment of HBV?

A 
Pegylated interferon (peginterferon) is superior compared to alpha-interferon in sustaining suppression of viral replication
- antiviral activity of nucleoside analogues may be successful even in chronic HBV pts
74
Q

What are the viral features of HCV?

A 
Flavivirus
Single stranded RNA genome
Enveloped
Replicates primarily in hepatocytes
Destroys liver cells
Virus can't be cultured
75
Q

How is HCV transmitted?

A

Blood & blood products
Tattooing, body piercing & acupuncture
Haemodialysis

76
Q

What are the clinical features of HCV?

A 
Usually asymptomatic
Fatigue
Nausea
Weight loss
May rarely progress to cirrhosis
Small proportion may develop hepatocellular carcinoma
77
Q

What is the treatment of HCV?

A

None that is specific
Interferon reduces liver transaminases in 80% of pts
Ribavirin works well in combo with pegylated alpha inferferon
Monitor viral load by NAAT
No vaccine yet available

78
Q

What is the cause of malaria?

A

Caused by 5 species of the genus Plasmodium
- P.falciparum
- P.vivax
P.ovale
P.malariae
P.Knowlesi
Female Anopheles mosquito injects sporozoa into the bloodstream (zoonotic disease)

79
Q

What are the clinical features of malaria?

A

Fever
Flu-like symptoms
P. falciparum infection can rapidly progress to death. It affects ever organ and has a wide range of complications
- e.g. cerebral malaria, circulatory shock, hepatitis

80
Q

How is malaria diagnosed?

A

At least 3 blood films (both thick and thin, thin identifies species whilst thick tells you how much is there) obtained from different times for microscopy
NAAT = useful for detecting drug resistance

81
Q

What is the treatment for malaria?

A

Chemo kills the blood stages of the parasite
Resistance means treatment advice should be changed regularly
Combination therapy is the norm:
- Quinine, Chloroquine(issues w.resistance, Doxycycline, Proguanil, Malarone, Artemether

82
Q

How is malaria prevented?

A 
Sleep under bed nets
Cover exposed skin between dusk & dawn
Use of mosquito repellants
Prophylaxis
Vaccines currently being developed
83
Q

What is the course and distribution of the median nerve? State its root values.

A

C6, C7, C8, T1
Supplies muscles of anterior compartment of forearm except FCU and half of FDP (that to the ring & little finger)
Anterior to brachialis & lower humerus in cubital fossa, posterior to bicipital aponeurosis, medial to brachial artery & biceps tendon
Passes between 2 heads of PT to lie in the plane between FDS & FDP
Reappears at the wrist lateral to the tendons of FDS, between them and FCR
Before entering the carpal tunnel it gives (Superficial) Palmar Cutaneous Branch that passes superficial to the Flexor Retinaculum to supply the skin of the central palm

84
Q

What are the clinical complications & symptoms for the median nerve?

A

Injury common at cubital fossa by elbow dislocation, or by supracondylar fractures of humerus
Flexion of thumb & index & middle fingers lost & these digits can’t be made into a fist (pronation lost & ulnar deviation on wrist flexion)
Injury to ant IO nerve causes loss of flexion of distal IP joints of thumb & index finger, the “OK” sign cannot be made

85
Q

What are the clinical consequences of carpal tunnel syndrome?

A

May affect median nerve progressively to cause tingling over the Thenar eminence & radial 3.5 digits
The central palm is spared due to the more proximal origin of the palmar cutaneous branch
Eventually there may be sensory loss with weakness & wasting of the thenar muscles

86
Q

What is the course and distribution of the ulnar nerve? State its root values.

A

C7, C8, T1
Passes immediately post to med epicondyle of humerus
Passes between 2 heads of FCU, to pass distally in FA between FCU & FDP
At wrist, comes superficial, lying just medial to the ulnar artery & passes through the Ulnar (Guyon’s) Canal, then anterior to flexor retinaculum to enter the palm

87
Q

What are the clinical complications & symptoms for the ulnar nerve?

A

Common at medial epicondyle of humerus, causes senosry loss of both palmar & dorsal surfaces, of the medial hand & of the medial 1.5 digits.
Loss of FCU causes difficulty in adduction of wrist & there is radial deviation upon wrist flexion
Loss of FDP to ring & pinky fingers means their distal IP joint cant be flexed & flexion is now weakened in those medial fingers - now difficult for them to make a fist
AT WRIST: loss of adductor pollicis (& deep head of FPB) Test: clasp sheet of paper between thumb & palm. Pt will use thumb abduction & flex of distal IP joints (giving a +ve Froment’s sign). Also test the IO
ULNAR CLAW:MCP extension, IP flexion => hand looks like a claw BUT the radial 2 lumbricals are still acting (median) so the claw is restricted to the ring & little fingers. (NOTE: the claw is less pronounced if the injury is at elbow as flexing affect of FDP is lost = ulnar paradox)

88
Q

What is the course and distribution of the deep fibular nerve? State its root values.

A

L4 - S3
Deep to biceps tendon, crosses fibular head & then around its neck, where it divides, deep to fibularis longus. Then divides into:
SUPERFICIAL FIB: started between fibularis longus & brevis, but now subcutaneous & on its way to skin of lower, lateral leg & dorsum of foot (except 1st cleft)
DEEP FIBULAR: passing through EDL to lie on the IO membrane, supplied all 3 muscles of ant compartment & descends towards ankle. Passes anterior to the tibia into dorsum of foot to supply ED & HB & the skin of the 1st cleft

89
Q

What are the clinical complications & symptoms for the common fibular nerve? (HINT: compartment syndrome)

A

Most common at head/neck of fibula, where it may be injured by fracture of fibula
But it is also subcutaneous & => susceptible to direct trauma
Loss of ankle & digit dorsiflexors, and evertors, causing Footdrop & loss of sensation of the lateral leg & dorsum of the foot.
COMPARTMENT SYDROME = oedema & raised pressure occurring w/in any leg compartment as the result of muscle over-use or crush injury (or too tight ski boots)
The pressure compromises muscle action, vascular supply & nerve supply. Passive movement causes xs pain in the affected compartment.
If the deep fib is involved = loss of sensation at the 1st cleft (dorsum)

90
Q

What is the course and distribution of the tibial nerve? State its root values.

A

L4 - S3.
Supplies all muscles of the superficial & deep posterior compartments
Leaves the popliteal fossa, lying on popliteus, & passing deep to gastrocnemius & soleus.
It divides into the medial & lateral plantar nerves deep to the flexor retinaculum (witht he post tibial artery & its venae comitantes) & they supply the skin of the sole.
MED = abductor hallucis, flexors digitorum & hallucis brevis & the lumbrical to the 2nd digit
LAT = all other muscles of sole (incl. quadratus plantae)

91
Q

What are the clinical complications & symptoms for the tibial nerve?

A

Due to its deep position, injury to the Tibial nerve is rare, but if it occurs, it causes loss of ankle & digit plantarflexion & loss of sensation to the sole

92
Q

What is the course and distribution of the medial plantar nerve?

A

Supplies more skin than muscles in sole
Equivalent to median nerve in palm
Enters sole deep to Abductor Hallucis (which it supplies) & lies between abductor & FDB, which it also supplies.
Ends by sending cutaneous branches to the medial sole & 3.5 digits, inc. nail beds after supplying the 1st lumbrical & FHB

93
Q

What is the course and distribution of the lateral plantar nerve?

A

Enters sole deep to Abductor Hallucis & then lies between FDB & quadratus plantae (which it also supplies) before emerging into the sole & dividing into deep & superficial branches.
The deep branch (like the ulnar) supplies those muscles in the sole not supplied by the medial planar (remaining 3 lumbricals, all interossei, all muscles to pinky toe & adductor hallucis)
Superficial branch ends by sending cutaneous branches to the lat sole & 1.5 digits, inc. nail beds

94
Q

What are the clinical complications & symptoms for the medial plantar nerve?

A

May be compressed deep to flexor retinaculum and/or abductor hallucis giving aching, numbness or tingling (paraesthesia) along the medial aspect of the sole (not unlike carpal tunnel syndrome)

95
Q

What are the clinical complications & symptoms for the lateral plantar nerve?

A

Also like the ulnar, injury to the lateral plantar may cause a claw foot deformity

MD2002 (17 decks)

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