Tentir+DMS+week+3

Dermato-Musculoskeletal Module TENTIR Week III

The following document contains the TENTIR of FMUI 2012

1 May the odds be ever in your favor

Table of Content

LECTURE 18 (Patophysiology of Pain and Itch) 2

Anatomy 3 (Muscle of Upper Extremeties) 24


LECTURE 18 (Patophysiology of Pain and Itch) (Michelle)

PATHOPHYSIOLOGY OF PAIN AND ITCH

OUTLINES 1. Definition and Classification 2. Pathophysiology

Theories / Basic Mechanism Peripheral Mechanism Central Mechanism Sensitization Modulation

3. Dermato-musculoskeletal Pain 4. Pain and Itch (Similarities, relation, etc)

DEFINITION: 1. PAIN: unpleasant sensory and emotional experience associated with actual or potential

tissue damage, or described in terms of such damage (International Association for Study of Pain, 1979)

2. ITCH: unpleasant sensation that elicits the desire or reflex to scratch

Pain usually elicits the reflex to avoid the stimulus or the cause of tissue damage, subjective, influenced by past & present experiences and the emotional state of the individual

CLASSIFICATION: PAIN:

- Duration: o Acute o Chronic (>3-6 months)

- Clinical: o Nociceptive caused by stimulation of peripheral nerve fibers that respond only

to stimuli approaching or exceeding harmful intensity o Inflammatory associated with tissue damage, inflammation mediators and

inflammatory cells infiltrate o Neuropathic the system affected is the nervous system so actually there are no

stimuli but it feels painful because the nerve is damaged. Sometimes it is also called phantom pain


o Psychogenic also known as psychalgia, pain that is caused, increased, or prolonged due to emotional, mental, or behavioral factors

o Mixed has two components, nociceptive and neuropathic. For example, low back pain may originally resulted from mechanical injury (trigger nociceptive pain) that leads to nerve compression (produce neuropathic pain)

o Idiopathic as the name, it occurs without known cause

- General classification of pain: Fast pain & Slow pain (Table 1)


ITCH:

- Duration: o Acute o Chronic (> 6 weeks)

- Clinical: o Pruritoceptive caused by peripheral stimulation of itch nerve fibers, usually

caused by skin disease o Neurogenic / systemic because of systemic disease (for example: Hepatitis,

chronic liver disease, chronic renal disease); induced centrally with no neural damage, mostly associated with increased exogenous opioids and possibly synthetic opioids

o Neuropathic same concepts with neuropathic pain but for itch o Psychogenic same concepts with psychogenic pain but for itch o Mixed same concepts with mixed pain but for itch

Figure 1 Examples of

Clinical Pain Classification


Table 2 Clinical Classification of Itch

PATHOPHYSIOLOGY Basic mechanisms of pain:

1. Transduction 2. Transmission 3. Modulation (happens in CNS) 4. Perception

Theories of itch:

Intensity = explain that the itch is the same as pain however the intensity is much less. This theory is no longer acceptable as specific receptor for itch is found

Specificity = itch sensory modality has its own pathway, sensory, and brain areas Selectivity = modification of specificity theory. Some agents are able to stimulate itch

and pain and nerve overlapping neuron can carry both sensations. The interpretation of stimuli, whether it is pain or itch, depends on several factors

Figure 2 From Stimulus to Perception


Stimulus will be received by receptor and the signals will be conducted by 1st order sensory neuron to the spinal cord (transduction). The process happens in the peripheral nerve system. The central mechanism begins from the 2nd order sensory neuron which will continue the stimulus into the brain through the 3rd sensory neuron first. In central mechanism coding & processing (modulation) happens but the perception comes from brain.

PATHOPHYSIOLOGY OF PAIN

Figure 3 pathway of pain transmission

As explained before, this is just a picture of the 4 basic mechanisms of pain: transduction and transmission in 1st order neuron modulation in the spinal cord carried by the spinothalamic tract (anterolateral pathway) to the thalamus 3rd order neuron (thalamocortical) to the cerebral cortex to be perceived

4 basic mechanisms of pain: (from table in Lecture 19 slide 11)


Transduction: the process by which afferent nerve endings participate in translating noxious stimuli (e.g, a pinprick) into nociceptive impulses

Transmission: The process by which impulses are sent to the dorsal horn of spinal cord and then along the sensory tracts to the brain

Modulation: The process of dampening or amplifying pain-related neural signals, primarily in the dorsal horn of the spinal cord, but also elsewhere, with input from ascending and descending pathways

Perception: The subjective experience of feeling pain that results from interaction of transduction, transmission, modulation, and psychological aspects of individual

Difference between adaptation & modulation:

Adaptation: its like wearing a watch. At first we realize its there but after sometime we get used to it and forget its there until we have to use it again. This happens in receptor (example: Paccinian corpuscle)

Modulation: it can be described as less feeling. For example if we feel pain and we rub it, the pain feels less painful but the receptor doesnt adapt. This happens in central mechanism.

The fibers that carry pain are categorized into 2: unmyelinated C fibers for slow pain & myelinated A fibers for fast pain

Pain receptors or nociceptors can be categorized into three:

Mechanical nociceptors: mechanical damage (crushing, pinching, cutting) Thermal nociceptors: temperature extremes, especially heat Polymodal nociceptors: all kinds of damaging stimuli, even irritating chemicals released

from damaging stimuli

In general, mechanical and thermal type of stimuli elicits fast pain while slow pain can be elicited by all three types.

Bradykinin, serotonin, histamine, potassium ions, acetylcholine, etc are some example of the chemicals that can excite chemical type nociceptors. Some are released from damaged tissue,

Figure 4 Pathophysiology of Pain Peripheral Mechanism


some from leukocytes, etc. Prostaglandins and substance P do not directly excite pain but greatly enhance the sensitivity of pain endings. The chemical substances plays major role in stimulating slow pain that occurs after tissue injury.

Figure 6 Pathophysiology of Pain (Central)

The signals are carried by A or C fibers to the dorsal root of spinal cord and terminate in different regions, according to particular fiber (e.g, A terminate in lamina marginalis). The fibers then crossed through anterior commissure and goes up to the brain through the anterolateral pathway. In Some fast pain & most

Figure 5 Chemical Mediators in

Pain Conduction


slow pain fibers terminate in reticular nuclei/reticular formation (spinoreticular tract), periaqueductal gray region, and tectal area of mesencephalon (superior colliculi in pictures, but some sources mention inferior colliculi as well) (spinomesencephalic tract). The rest of the fiber, however, continue and pass through the thalamus. There, they diverge into 2 different paths:

Medial system (for emotional component): the paleospinothalamic tract pass through DM (dorsomedial) Intralaminar Nuclei of the thalamus limbic system / anterior cingulate cortex (insula, amygdala, hypothalamus)

Lateral system (for discriminative localization of pain): neospinothalamic tract pass through VPL (ventral posterolateral) & VPM (ventral posteromedial) nuclei of thalamus primary somatosensory cortex

Figure 7 Pain Pathophysiology Peripheral Sentisization

CGRP: Calcitonin gene-related peptide (CGRP) is a vasodilator neuropeptide that is expressed in a subgroup of small neurons in the dorsal root ganglion (DRG), trigeminal, and vagal ganglia, which respond to noxious, thermal, or visceral input. Figure 8 Pain Pathophysiology Central Sensitization


Glutamate is the NT responsible for transmission of fast pain. C fibers also release glutamate, however substance P plays important role in slow pain transmission. More Na+ channels & blockade of K+ channels more depolarization nociceptors more positive

Figure 9 Central Sensitization

Hyperalgesia: excessive sensitivity to pain, may include a decrease in threshold and an increase in suprathreshold response in this case the nociceptor is affected. This happens for example in burned skin in which. Whe

Allodynia: pain produced by a non-noxious stimulus, small stimulus (even touch) feels painful. In this case, the nerve is not supposed to detect noxious stimuli. Refers largely to pain evoked by A-bers or low-threshold A- and C-bers


Theories that try to explain why these conditions happen: alter gene & protein synthesis Happens in between I & II sensory order neuron (already in CNS). There are various NT released from afferent nere fiber. NMDA-R & AMPA-R continuously being stimulated will increase calcium ions and trigger gene alteration blockade of K+ channels and more Na+ channels nerve become more sensitized (refer to Figure 8) CHEMICAL MEDIATORS ACTIVATING NOCICEPTORS: (not included in lecture, nice to know)

1. GLOBULIN AND PROTEIN KINASES which are released by damaged tissue. These two are suggested to be the most active pain-producing substances. Very little amount of globulin injection can induce severe pain.

2. ARACHIDONIC ACID is also released during tissue damage and will then be metabolized into prostaglandins. All types of nociceptors can be sensitized by the presence of prostaglandins and the prostaglandins enhance the response of receptor to noxious stimuli greatly1. Basically, it will hurt more when prostaglandins are present1. Prostaglandins are a special group of fatty acid derivatives that are cleaved from the lipid bilayer of plasma membrane and act locally on being released1. They block potassium efflux from nociceptors, causing additional depolarization, leading to lower threshold of nociceptors. However, prostaglandin doesnt directly excite pain3. Aspirin works by blocking the conversion of arachidonic acid to prostaglandin4.

3. HISTAMIN that is released to surrounding area by mast cells who are stimulated by tissue damage. It excites nociceptors.

4. NERVE GROWTH FACTOR (NGF) which release is triggered by inflammation or tissue damage. Binds to receptors on surface of nociceptors and activate them.

5. SUBSTANCE P (SP) & CGRP (CALCITONIN GENE-RELATED PEPTIDE) that are released by injury. Both produce vasodilation and cause the spread of edema around the beginning location of damage. Substance P, however, increase sensitivity of nociceptors but does not directly excite them, just like prostaglandins3.

6. POTASSIUM (K+) whereas their extracellular concentration increase resulting from tissue damage. Local K+ concentration correlates with pain intensity

7. SEROTONIN (5-HT), ACETYLCHOLINE (ACh), LOW pH, and ATP which are released with tissue damage it shows that very small subcutaneous injections of these substances excite nociceptors.

8. MUSCLE SPASM & LACTIC ACID (minute subcutaneous injection excite nociceptors)

PAIN MODULATION Pain modulations are divided into two: afferent & descending Figure 10 Pain Modulation: Afferent


a. In absence of input from C fibers, tonically active inhibitory interneuron suppresses pain

pathway no signal to brain b. With strong pain, C fiber stops inhibition of the pathway, allowing strong signal to be

sent to the brain strong painful stimulus to brain c. Pain can be modulated by simultaneous somatosensory input (touch or nonpainful

stimulus) Painful stimulus decreased If theres pain, the inhibition from inhibitor interneuron will stop. When the area is rubbed (for example) A fiber (tactile but not noxious stimuli) is connected to the inhibitory interneuron release NT stimulate inhibiting interneuron C fiber is partially inhibited but we still can feel pain

Figure 11 Pain Modulation: Afferent


Originate from the periaqueductal gray matter. Basically the picture tells us that there are endogenous opiate that is being released from the inhibitory interneuron in the dorsal horn and the opiate helps in modulating pain

PATHOPHYSIOLOGY OF ITCH

Figure 12 Pathway of Itch Conduction

Pathophysiology of itch is similar to pain. The stimuli are also polymodal. The stimuli is received by pruriceptive afferent fibers dorsal root of spinal cord pruriceptive projection neurons thalamus insula & anterior cingulated cortex (suffering); orbitofrontal & prefrontal (compulsive scratching); motor response (scratching); spatial, temporal, and intensity aspects (localization)

Figure 13 Pathophysiology of Itch Peripheral Mechanism


Pathways of itch are divided into two: histamine dependent & histamine independent. Itch has lots of mediators, including NGF, Histamine, IL (interleukin), brain-derived nerve factor, etc. They are transmitted by 2 distinct systems that both use C-fibers. Because not all itches are histamine dependent, so for several types of itch, anti-histamine doesnt work.

Table 3 The Mediators of Itch (I dont think we have to memorize all)


Table 4 The Mediators of Itch

Figure 14, 15 Pathophysiology of Itch Peripheral Mechanism


Sensitization of itch causes the release of mediators such as NGF, Histamine, etc. The stimuli will then be carried by the first order neuron to the spinal cord and synapse with the second order neuron. The NT that plays role includes IL-31RA, GRPR, NK-1R. The second order neuron cross the spinal cord and goes up to the brain. The second order neuron will then synapse with third order neuron and the brain will perceive itch

PATHWAY FOR PAIN AND ITCH

The two

pictures basically show the pathway for pain and itch. The blue one illustrates pathway for pain


while the red one illustrates itch. The pathophysiology are similar and the stimulus for both are polymodal (responding to several different forms of sensory stimulation). Sprouting: production of new processes (outgrowths) by nerve cells, for example by embryonic neurons undergoing primary differentiation or by adult neurons in response to nervous system damage). Sprouting causes the nerve ending to cover more area

PATHOPHYSIOLOGY OF ITCH MODULATION

Inhibition of itch:

Counter stimuli by other somatosensory modalities:

Pain Heat/cold Electric Capsaicin (this substance can actually be found in chili)

In pain, periaquaductal gray area helps in pain modulation by releasing endogenous opiates. In itch, such mechanisms is still questioned.


In the figure above, picture (b) shows the modulation of itch by pain. So when we scratch, the nociceptor is stimulated. Nociceptor will transmit the feeling of pain to the brain while at the same time it excites BhIbh5 (interneuron) that inhibit itch.


The figure above is just another illustration (B) of itch modulation by pain through the interneuron BhIhb5. Picture (A) illustrates the selectivity theory. When the nociceptive population is stimulated the brain will perceive pain while when the itch selective population is stimulated, the brain will perceive itch.

DERMATOMUSCULOSKELETAL PAIN Because of the very limited time and power and ability to write this, Im so sorry but most of this part will

only be copy-pasted from the slides as it is already in form of texts

So Dermato-musculoskeletal pain is categorized as nociceptive pain. It is very important to be treated because if its not treated correctly it will lead to viscous cycle as shown below

The table below shows the difference between superficial somatic pain (skin and integumentary), deep somatic pain (musculoskeletal), and visceral pain. The highlighted in this module is the superficial somatic pain and deep somatic pain

TYPES OF MUSCULOSKELETAL PAIN:


Special muscle pain ISCHEMIC:

Happens in contraction with reduced blood supply Prolonged contraction Major problem in elderly with peripheral vascular disease (intermittent claudication = pain caused by too little blood flow to the muscles which is typically felt during walking (or exercise), called intermittent because it comes and goes with exertion and rests)

Ischemic muscle pain from the heart angina Several metabolic diseases can cause exercise induced ischemic pain

CRAMP: Due to ischemia Can be due to locally generated contractions (contractures) in some metabolic diseases

Usuallly exercise induced (EIC) EAMS (Exercise Associated Muscle Cramps) Excessive contraction driven by motor nerve firing Occurs in fatigue muscle Can sometimes be relieved by stretch when theres no ATP the actin-myosin cross-bridge cant pull apart and so stretching helps release actin-myosin binding

DOMS (delayed onset muscle soreness): Arise 8 hours post exercise until several days Associated with eccentric contraction (example: running downhill) Reduced on repetition of exercise Probably triggered by slowly developing inflammation (and) or microtear of the muscle fibers

Inflammation ARTHRITIS (table showing the difference between RA and OA):


Uncertain cause (chronic): low back pain, neuropathies, fibromyalgia

FIBROMYALGIA: Considered a syndrome (it has more than 1 symptoms, A group of symptoms that collectively indicate or characterize a disease, psychological disorder, or other abnormal condition)

Clinical manifestation: o Chronic widespread muscular pain (>3 months) o Chronic fatigue o Widespread tenderness (hyperalgesia)

Not common in Indonesia, more common in Western countries


In

figure (a) the ascending nociceptive pathway is replied by descending inhibitory pathway that modulates the pain. In figure (b) hyperalgesia occurs as the levels of NT that augment pain transmission in CNS increase while the descending analgesia decrease (deficient) causing more severe pain.

LOW BACK PAIN: Most common chronic pain problem Possible causes:

o Disc herniation o Spinal problem (spondylosis) o Tumor/cancer o Osteomyelitis of the spine o Trauma/injury (ex: fracture, compression) o Osteoporotic disease

Often no obvious pathology Often work-related

REPETITIVE STRAIN INJURY: Nearly as common as low back pain Affets a relative young age group


Suspected to be work related but is still debatable (patients often blame keyboard or light industrial work)

Stress fractures

RELATION OF ITCH AND PAIN Conclusion, pain and itch appears to be independent sensations INVERSELY RELATED: Itch reduced by nociceptive counter-stimuli (example: scratching) Pain analgesic opioids often have the adverse side effect of producing itch

SIMILAR Itch-producing agent activate nociceptive primary afferent fibers and can generate simultaneous pruritic and nociceptive sensations

Perception of itch and pain depends on which neuron stimulate the nerve Similar modulations, same tract, share several mediators

In the figure above, stimuli located more to the left (red) stimulate pain while if its more to the right (blue) it stimulates itch.


Anatomy 3 (Muscle of Upper Extremeties) (christy)

There are three groups of muscles on upper extremity: shoulder cuff, upper arm, forearm, and hand

Shoulder cuff

Classifications:

Thoracoclavicularis muscles thorax between clavicula Thorachohumeralis muscles between thorax and humerus Scapulohumeralis muscles between scapula and humerus

Anterior View

Posterior View


1. Musculus thorachoclavicularis M. sternocleidomastoideus

o Origo: head of sternum. Insertion: processus mastoideus on os temporal o Function: flexion of vertebral column, head extension involving articulation atlanto-

occipital, one-sided flexion of neck and head, lateral rotation M. subclavius

o Origo: first costae. Insertion: inferior of os clavicula o Function: shoulder depression

2. Musculus thoracoscapularis M. trapezius

o Origo: os occipital, ligamentum nuchae, and processus spinosus from thoracal vertebra. Insertion: clavicula and scapula.

o Function: stabilizer of deltoid and latissimus dorsi during arm abduction M. rhomboid major and M. rhomboid minor

o Rhomboid major: Origo processus spinosus vertebra thoracal superior and Insertion scapula

o Rhomboid minor: Origo: processus spinosum C7-T1 and Insertion: scapula o Function of both rhomboid major and minor: Abduction of scapula and downward

rotation M. serratus anterior

o Origo: at the edge between anterior and posterior costa 1-. Insertio: anterior surface of scapula

o Function: Upward rotation of scapula >< antagonistic with rhomboid major and minor

M. pectoralis minor


o Origo: anterior and posterior surface of costa 3-5. Insertio: processus coracoideus of scapula. This muscle is located beneath the pectoralis major

o Function: it works together with m. subclavius for depressing shoulder position M. homohyoideus

o Origo: superior scapula. Insertio: Hyoid bone o Location: right and left side of the neck, beneath the layer of

sternocleidomastoideus and on the lateral side of m. sternohyoideus

3. Musculus Thoracohumeralis

M. pectoralis major o Origo: cartilage of costae 2-6, sternum and medial side of clavicula.

Insertio:tuberculum majus of os humerus. o Function: flexion, adduction, and shoulder medial rotation

M. latissimus dorsi o Origo: processus spinosus vertebra thoracal inferior and all of processes spinosus at

lumbal, costae 8-12, fascia thoracolumbal. Insertio: sulcus intertubercularis of humerus

o Function: Extension, adduction, and endoration of shoulder. 4. Musculus Scapulohumeralis

M. deltoid o The most superficial muscle on humerus. o Origo: os clavicula and os scapula (acromion and spina scapulae). Insertio:

tuberositas deltoidea on os humerus o Function: agonist of shoulder abduction. The anterior side is used for flexion and

endorotation. The posterior side is used for extension and lateral rotation M. subscapularis

o Located on the anterior part of scapulae o Origo: fossa subscapularis. Insertio: mminus on shoulder o Function: endorotation of shoulder

M. suprapinatus and infraspinatus o Posterior part of scapulae o Both of them are separated by spina scapulae. Above the spina scapulae fossa

supraspinata. Below the spina scapulae fossa infraspinata origo of m. infraspinata. Insertio of both the muscles: tuberculum major of os humerus

o Function: supra shoulder abduction. Infra endorotation


M. teres major

o Origo scapula. Insertio sulcus intertubercularis of os humerus. M. teres minor, origo: margo lateralis of os scapulae, insertion: tuberculum majus of os humers

Palm

Classification: Thenar (lateral), intermediate, Hypothenar (medial). From the the most profound layer

M. opponens pollicis: profound thenar M. interossei palmares:

o Origo: os metacarpal (except, metacarpal III). Insertio: proximal phalange (all digits except metacarpal III)

o Function: adduction and flexion of all digits except metacarpal III (articulation metacarpophalangeal) and extension of digits (articulation interphalangeal)

M. interossei dorsales o Origo: metacarpal. Insertion: proximal phalanges o Function: abduction of digits II-IV (articulation metacarpophalangeal), flexion of

digits II-IV (articulation metacarpophalangeal), and extension of all digits (articulation interphalangeal)

M. lumbricales manus o Origo: lateral side of the tendon of m. flexor digitorum profundus. Insertio: lateral

side of m. extensor digitorum communis on proximal phalanges o Function: flexion for all digits (articulation metacarpophalangeal) and extension of

digits (articulation interphalangeal) M. opponens digiti minimi hypothenar


More superficial muscle

M. abductor pollicis brevis o Origo: flexor retinaculum and os trapezius. Insertion: lateral side of proximal phalange o Function: abduction of thumb (articulation carpometacarpal)

M. flexor pollicis brevis o Origo: flexor retinaculum, os trapezium, capitatum, and trapezoid. Insertio: lateral side

of proximal phalange of thumb o Fucntion: flexion of thumb (articulatio carpometacarpal and articulation

metacarpophalangeal) M. adductor pollicis

o Origo: capitatum and metacarpal II-III. Insertio: medial side of proximal phalange of index finger

o Function: adduction of thumb M. opponens pollicis:

o Origo: flexor retinaculum. Insertion: lateral side of metacarpal I

Intermediate Layer

M. lumbricales manus M. abductor digiti minimi


o Origo: os pisiform and tendon of m. flexor carpi ulnaris. Insertio: medial side of proximal phalanges of little fingers

o Function: abduction and flexion of little fingers M. flexor digiti minimi brevis

o Origo: flexor retinaculum and hamatum. Insertion: medial side of proximal phalanges of little fingers

o The location is more superficial than m. opponens digiti minimi M. opponens digiti minimi (quinti)

o Origo: flexor retinaculum and hamatum. Insertion: medial side of proximal phalanges of little fingers

o Function: moving little finger in order to meet the thumb M. palmaris brevis

o Located on subcutaneous


Thats the end of the Tentir for Summative 2 Growth and Development Module lectures! Happy studying guys and bunch of thanks to those who made and edited the tentirs, wish you all

the luck for the summative, cheers!

SiePend FMUI 2012 Compiler & Editor: Aqila Sakina Zhafira

Layout: Filbert Riady Adlar

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