Musculoskeletal System

 Inflammation in gout is due to recrutiemtn fo neutrophils, phagocytosis of

theurate crystals → release of cytokines → neutrophil activation and further
chemotaxis
 Patients of APS may be isolated or associated with other automimmune
disease like SLE, many of them don‟ t have the clinical syndrome
Dermatology

Melanoma :
 Risk factors : + sunlight exposure,
dysplastic nevi, light skin
 Melanomas with radial growth
has low metastatic risk, Vertical
growth → highly risk of
metastasis (Breslow‟ s depth is the
most prognostic indicator in
malignant melanoma)
 Histopathology: poorly formed
cells with large irregular nuclei,
clumped chromatin & prominent
nucleoli
 Lentigo maligna→ multinucleated
 giant cells, common in elderly considered melanoma in situ
 Actinic keratosis :
o Erythematous papules with overlying whitish
scale, felt more than seen whith sandpaper like
rough architecture.
o May form keratin horn, its size rarely exceed 1
cm
o Occur in response to excess sunlight → occur
more in face, scalp, ear
o It is regardedas premalignant
Ephelides (freckles), solar lentigines Acrochorda (skin tags)
Freckles → ↑↑ melanin production Locations of most frictions e.g. axilla
Lentigines → ↑↑ melanocytes (larger, adults)

 Urticaria (Hives)
 Either due to (1) IgE mediated mast cell degranulation (2) non IgE mediated
degranulation e.g. contrast, opiates, physical urticarial (3) mast cell independent
mechanisms e.g. hereditary
 Characterized by superficial dermal edema. DD angioedema → edema involve
deep dermis, SC tissues
 Acanthosis : ↑↑ S. Spinosum → acanthosis nigricans, seborrheic keratitis,
psoriasis
 Spongiosis: intercellular epidermal edema → ↑↑ spaces between cells ,
eczematous dermatitis (spongiotic dermatitis)
 Glomus tumor (glomangioma) :
o DD of painful tumor underneath nail bed; either subungal melanoma or glomus
tumor.
o Glomus body: numerous small encapsulated neuro-vascular oragns present in
dermis of nail bed, pad of finger & ear.
o it composed of afferent arteriole connected to innervated muscular AV
anastomosis → efferent vein
o Modified smooth muscles are arraged around these channels to shunt the blood
away from the skin in cold temperature & vice versa.
Clinical association with dermatomyositis:
- May occur as part of para neoplastic syndrome in cancers of ovary, lung
adenocarcinoma and NHL (usually parallel with the course of the cancer)
- Patients who develop dermatomyositis > 50 years have ↑↑ risk for occult
malignancy
Describe the gross & microscopic features of Kaposi sarcoma:
- Gross: multiple blue-violet dermal plaques first appear on the feet and legs
before spreading proximally, later mucosal involvement ad organ spread
- Microscopic: spindle and endothelial cell proliferation, RBCs rxtravasation and
inflammation

Describe the clinical picture of actinic keratosis : Small, scaly, erythematous lesions
with sandpaper texture occurring on non-exposed area
 Describe the histological findings in actinic keratosis :
 Hyperkeratosis, parakeratosis, atypical keratinocytes with pleomorphic nuclei
→ so AK is considered pre malignant lesions, although they on‟ t invade the
dermis  they may progress to be squamous cell carcinoma rather
than BCC
Describe the clinical picture of dermatitis herpetiformis:
 They appear as erythematous pruritic papules, vesicles & bullae → bilateral,
symmetric, extensor surface of elbows & knees, may occur in the back,
buttocks
 The lesions are clustered and grouped like the herpes viral infection

L/M of shingles:
- Intranuclear inclusions in keratinocytes, with multinucleated giant cells
- Acantholysis of keratinocytes and intra epidermal vesicles
 L/M of molluscum contagiosoum → eosinophilic cytoplasmic inclusions (molluscum
bodies) in infected cells.
 L/M of dermatitis herpeticformis→ micro-abscesses contain fibrin & neutrophils at
the dermal papillae tips

Describe the clinical picture of Erythema multiforme:

 Usually affect the extremities, trunk, face, neck, +/- oral mucosa in EM major
 Usually, target lesion with central dusky area
 Mechanism & commonest causes of Erythema multiforme: cell mediated immunity
(CD8 cytotoxic cells), commonly associated with HSV & mycoplasma
Difference between Erythema multiforme & SJS : SJS commonly associated with
systemic findings, associated with medications
Mention the different types of nevi: Junctional, compound, intradermal nevi
 Histological appearance of xanthelasma. It consists ofmacrophage laden with fat
cells (foam cells), lies in the superficial dermis → yellowish discoloration

Histological and gross features of different types of melanocytic nevi

 Junctional nevi → flat, black to brown pigmented macules with central darker
coloration
 Compound nevi → raised papules with uniform brown to tan pigmentation
  Intradermal nevi → older lesions, skin to tan colored, dome shaped and
pedunculated
Pemphigus vulgaris:
 Clinical picture of Pemphigus vulgaris: painful flaccid bullae and erosions
of the skin (easily ruptured so erosions are the main presentation) & mucus
membranes (mostly oral mucosa), with Nikolsky signs positive new blister
formation by gentle traction or rubbing, Asboe-Hansen sign positive bullae
spread laterally when pressure is applied on the top.
 Diagnosis of Pemphigus vulgaris: epidermal intra-cellular IgG & C3 deposits, anti-
desmoglein antibodies in the serum
Capillary hemangioma :
- Other names of Capillary hemangioma: infnaitle, superifical, strawberry angioma
- Characters of Capillary hemangioma: appear during 1st week of life gow rapidly
but frequently regress spontaneously by late childhood (5 – 8 years), near the
epidermis
Effects of chronic application of topical steroid on the skin.
 ↓↓ production of EC matrix collagen & GAGs  Dermal atrophy , cracking
 SC tissue & fat atrophy
 Clinical picture of vitiligo: arise in 2nd – 3rd decade of ife with variable sized absent
pigmented macules more on face, extremities, axillae, umbilicus and genitalia, dark
colored people are more prone to this
 Describe the pathophysiology of albinism → melanocytes cannot produce melanin
pigments due to defective tyrosine kinase
 Describe the pathophysiology of post-inflammation hypopigmentation →
redistribution of the melanin along the skin with diminished spread to skin.
Causes & Clinical picture of contact dermatitis:
 Highly pruritic, erythematous rash with papules & vesicles, signs of excoriation.
Mostly affect the exposed areas with linear distribution
 Caused by contact to plants like poison ivy, sumac, oak → produce urushiol (act
as hapten)
 Describe the pathophysiology of café au lait patches → ↑↑ melanosome aggregates
within the melanocyte cytoplasm
Cherry angioma:
- Other names of cherry hemangiomas: senile hemangioma
- Character of Cherry angioma: appear in 30 - 40s, don‟ t regress spontaneously,
multiple with age, always superifical
- Histo-pathological features of Cherry angioma: shrpely circumscribed areas of
congested capillaries & post-capillary venules in the papillary dermis
 Ecchymosis:
 Petechie (< 5mm), purpura (5 mm – 1 cm), ecchymosis (≥ 1 cm)
 They are extravasated hematoma, not blanch during compression.
 Palpable purpura is usualy indicative of leukocytoclastic vasculitis.
 Ecchymosis may be due to superficial blleding or more
commonly due to deep hematoma
 Seborrheic keratosis:
 Describe gross picture of Seborrheic keratosis:
benign, brown epidermal tumor commonly in middle
aged people, flat macules → warts with velvety surface,
well demarcated border, stuck – on appearance
 Describe microscopic picture of Seborrheic
keratosis: small cells resembling basal cells,
hyperkeratosis (↑↑ stratum corneum), keratin
containing cysts.
Cutaneous small vessel vasculitits:
 Affect skin only, palpable non-blanching
cutaneous purpura affect mainly lower limbs
 Caused by exposure to drugs, pathogens
including penicillins
 L/M: markedly inflamed BV + fibrinoid necrosis
→ with neutrophils invade perivascular space (leukocytoclastic vasculitis) older
lesions → mononuclear cells
Atopic dermatitis:
 Clinical picture of Atopic dermatitis:
- mostly present by age 5 years
- red crusty lesions involve face, scalp, extensors and sparing of the diaper area
- marked History of exacerbation & remission
- older children present with lichenification in the flexural distribution,
- the most important finding is intense pruritis
 Lab findings in Atopic dermatitis: high serum IgE, eosinophilia, ↑↑ cAMP PDE in
WBCs.
 Site of affection in Atopic dermatitis : red crusty lesions involve face, scalp,
extensors and sparing of the diaper area, older children present with
lichenification in the flexural distribution,
Eczematous dermatitis:
 Acute allergic contact dermatitis (ACD)
 - Type IV hypersensitivity, due to CD4 activation → inflammatory response in
24 hours after re-exposure
- L/M:
 spongiosis (accumulation of edema fluid in the inter-cellular spaces in
theepidermis)
 may be marked to form intra-epidermal vesicles
 +/- peri-vascular infiltrates of lymphocytes & eosinophil (either
in superficial dermis or deeper)

- On chronic exposure → lesion become less edematous, weepy → thickening of

stratum spinsosuum & stratum corneum → to form plaques
Acanthosis nigricans:
 Commonly associated with skin tags.
 Sudden appearance in middle aged or elderly may suggest malignancy
Effect of Ultraviolet A rays on the skin:
UV A rays cause photoaging by → ↑↑ O2 species → ↑↑ inflammation of the skin → ↓↓
collagen fibrils & ↑↑ matrix metalloproteinase  ↓↓ type I, III, elastin
deposition.
Why photaged skin appeared wrinkled ??
- Changes occur in :
 Epidermis → thinning
 Dermis → ↑↑ crosslinking of the collagen & deposition of the collagen breakage
products
 Dermo-epidermal junction → flattened rete ridges
 SC fat → atrophic
 Psoriasis :

 Pathogenesis: APCs (dendritic cells) → CD4 activation and CD8 T-cells in

epidermis  production of cytokines & keratinocyte growth factor
 Clinical picture: sharply demarcated salmon colored plaques. Covered with
loosely adherent silvery scale. Commonest in elbow, knees
 L/M: hyperkeratosis, acanthosis, elongation of reter ridges, mitotic activity above
the epidermal basal cell layer, ↓↓ absent stratum granulosum.
- Associated with Auspitz sign → thinning out of the epidermis superior to
dermal papillae
- Munro micro-abscesses → neutrophils may form clusters in the superficial
dermis & stratum corneum.

Embryology

Osteogensis imperfecta:
 Defective synthesis in type I collagen by osteoblast
 Blue sclera → ↓↓ CT → transparent vessels
 Small malformed teeth
Anatomy
 Glans penis & popliteal lymph nodes → drain in the deep inguinal lymph nodes,
Cause & clinical picture of common peroneal nerve injury:
 May be injured due to external compression due to prolonged immobility
 Plantarflexion & inversion posture
 Loss of sensation of anterolateral leg & dorsum of the foot
 Foot drop with high steppage gait
Clinical signs point to patellar fracture:
  Acutely swelling with focal tenderness
 Inability to extend the knee against gravity
 Palpable gap in the extensor mechanism
 Mention the anatomy of psoas muscle : anterior surface of transverse process, lateral
surface of the vertebral body at T12 – L5, it unite with ilacus to insert in the lesser
trochanter.
 Mention the anatomical composition of Guyon‟ s canal: it is formed by hook of
hamate & pisiform bone and covered by fibro-osseous tunnel.
Describe the squeal of inter-scalene nerve block: anesthesia is given in the scalene
triangle, with paralysis of brachial plexus, all patient undergo interscalene
nerve block have ipsilateral diaphragmatic paralysis. All muscles of UL are
innervated by brachial plexus except trapezius & SCM .
Where is the safest place for intra-muscular injection: most injection should target
the anterolateral gluteal area (Von Hochstetter triangle) to minimize possibility of
nerve damage

Femoral nerve (origin, course, motor & sensory):

- Origin: largest branch of femoral plexus form L2 – L4 → pass between the psoas
& iliacus → pass under the inguinal ligament (lateral to the femoral artery)
- Motor: innervate quadriceps muscle → extension of the knee & flexion of the hip
- Sensory: skin & muscle of anterior thigh femur, knee, + saphenous nerve
(terminal branch of femoral nerve) → sensation in the medial leg below the knee
 Mechanism of femoral nerve block: best is done by injection in the inguinal crease
lateral to the femoral artery (injection at the femoral canal is not appropriate as
femoral nerve is not content of femoral sheath)
Histology of bone :
o Functional unit consists of central
arteriole, surrounded by Havarsin
canal & lamellae.
o Each lamella consists of bony matrix
with lacunae inside it, small canaliculae
is connecting the lacunae together.
o Osteocytes harbor the lacunae with its
cytoplasmic process pass through the
lacunae from which signaling & waste
products interchanged by gap
junctions
o Osteocytes maintain the activity of
osteoblast, short term control of
calcium homeostasis. Its activity is
maintained directly by the serum
calcium level & indirectly by PTH, it
also help regulate bony remodeling
Ankle joints and ligaments :
o Lateral (weaker): calceneo-fibular, anterior & posterior talo-fibular ligaments
(ant. talofibular ligament is the most prone to injury)
o Maedial (very strong): deltoid complex → ant & post. tibio-talar, tibio-calceneal,
tibio-navicular )
o Subtalar joint → reinforced by talo-calceneal ligament
o Tibia & fibula → syndesmotic structures e.g. interosseous membrane, tibio-
fibular ligament (ant, post, transverse)
Junctional complexes ‫ بال ترت يب‬:
1) Tight junction 2) adherenes junctions 3) desmosomes
Sciatic nerve anatomy :
o The pelvic outlet is divided by sacro-spinous ligament into greater & lesser sciatic
foramen
o Boundries greater sciatic foramen :
 Antero-lateral: greater sciatic notch of
ilium
 Inferiorly : ischial spine & sacro-
spinous ligament
 Superiorly :anterior sacro-iliac ligament
 Postero-medial : sacro-tuberous
ligament
o Most of the greater sciatic foramen is
occupied by piriformis muscle (origin
form anterior sacral pieces, insertion at
greater trochanter, action is external
rotation of extended thigh & aduction of
the flexed thigh)
 o Structures pass above the pyriformis: superior gluteal vessels &
nerves
o Structures pass below the pyriformis: inferior gluteal vessels &
internal pudendal vessels & sciatic nerve
o Hypertrophy or injury of piriformis muscle → compress sciatic
nerve  sciatica like findings pyriformis syndrome
(tenderness with deep palpation or stretching with adduction
and internal rotation)
o Obturator internus muscle → pass throuuhgt the lesser sciatic
foramen, same action as pyriformis muscle

Sensory supply of lower limb & groin

o
 Pudendal nerve block :
o Course: it arise from S2-S4 between coccyges muscle & pyriformis muscle → exit
from greater sciatic notch then re-enter the pelvis near to ischial spine from lesser
sciatic notch
o Complication : injection in internal pudendal artery, inferior gluteal artery →
hematoma , arrhythmia
o Landmark : intra-vaginally identify ischial spine & sacro-spinous
ligament (from sacrum to ischiual spine) → inject very close to ischial spine
o Pudenal nerve injury may occur during prolonged second stage of labour → stretch
injury (due to its curved course) → cause fecal& urinary incontinence, perineal
pain, absent ana wink
o Compare with cauda equine syndrome  bilateral radicular pain, saddle
anesthesia, hyporeflexia (LMNL)
 Lumbo-sacral apoplexy → foot drop & numbess of lateral foot due to compression of
lumbo sacral trunk.
Serratus anterior muscle :
o Origin : side of the chest along 1st – 8th ribs, insert at the medial border of the
scapula
o Important as chest tube insertion pass through it … it must be inserted either in
4th or 5th intercostal space along the mid / anterior axillary line to traverse the
serratus anterior & intercostal muscle
Radial nerve :
o Course medial to the surgical neck of the humerus, deep to teres major muscle →
enter the radial groove of the humerus
o # at the axilla → ↓↓ triceps reflex (as nerve damage the muscle before entering
the groove)
o More distal damage → intact triceps reflex
o Preacher‟ s hand  Pope‟ s blessings
Ulnar nerve :
o Pass in Gyuon‟ s canal between hook of hamate & pisiform

o
Anatomy of sarcomere :
o M line → myosin, correspond to A band (thin & thick) & H band (only myosin)
o Z line (darkest line) → actin, corrospod to I band (only thin filaments)
o HIZ sortened during muscle contraction


Damage to lower brachial plexus trunk
(C8 – T1) →
a) Damage to both ulnar nerve &
medial nerve → total claw hand
deformity
b) Damage to sympathetic chain (T1) →
Horner syndrome
Microscopic histology of the muscle
fiber:
 T-tubule contain L-type Ca channel
(DHP) coupled with ryanodine
receptors on the sarcoplasmic
reticulum → ↑↑ Ca release
throughout the muscle fibril 
coordinated synchronized
muscle contraction
Anatomy of sarcomere: ZI-MA
 Z-line → bind to actin to form I-band
 M-line → bind to myosin to form A-band (overlap)
H (homogenous) – band → contain myosin only
 Z-line and M-line are formed of structural proteins which bind the actin & myosin
to them e.g. titin & α-actinin
 Groin hernia :
a) Direct & indirect hernia occur above the inguinal ligament, while the femoral
hernia occur below it
Direct hernia Indirect hernia
Protrusion through triangle of Hasselbach. Failure of obliteration of process vaginalis
Less prone to incarcerate More common, more on Rt. side
Less prone to descend to scrotum Better felt by tip of finger
Best felt with pulp of finger
b) Femoral hernia is more common in ♀ & tend to occur on the right side.
Superficial inguinal lymph nodes drain all skin below the umbilicus except testis
(para-aortic) & posterior calves, glans penis (deep inguinal LNs)
Compartment syndrome :
 Caused by long bone fractures, crush
injury, thermal injury, non-traumatic
causes e.g. bleeding
 Clinical picture include severe pain out
of proportion of injury degree +/-
weakness & sensory loss … urgent
fasciotomy
 In evaluating the nerve injury,
notice if the main trunk or its
distal branches are only affected,
don’t forget compartment
syndrome
Common peroneal nerve :
 It I the lateral branc of the sciatic nerve,
it divide at the upper border of the
popliteal fossa → traverse laterally to come in contact with fibular neck
(commonest site of injury) where it divide into:
a) Deep peroneal nerve: supply anterior compartment of the leg (e.g. tibialis
anterior, extensor digitorum longus, extensor halluces longus) → dorsiflexion
b) Superficial peroneal nerve: supply muscle for eversion e.g. peroneus
longus & previs , more sensory supply of dorsum of foot and lateral of leg
Tibial nerve :
 It traverse the popliteal fossa → deep to soleus muscle → enter tarsal tunnel
 Proximal injury → cause dorsiflexion & eversion
 Divide into lateral & medial branches → sensation to sole & motor to intrinsic foot
muscle  distal injury → sensory loss only with intact muscle action
 Ilio-inguinal vs. ilio-hypogastric nerves:
 Both arise from L1
 Ilio-hypogastric nerve: arise from lateral border of psoas major muscle,
behind the kidney , in front of the Quadraus lamboroum → supply the
anterolateral abdominal wall muscles.
o Anterior branch :emerge aove the superficial inguinal ring to innervate the
skin over the pubic region  may be injured during appendectomy
o Lateral branch : descend over the iliac crest to innervate the gluteal region
 Ilio-inguinal nerve : accompany the spermatic cord through the superficial
inguinal ring → upper and medial thigh & parts of external genitalia
Anatomical snuffbox :
o Bounded medially by extensor pollicis longus tendon, laterally by abductor
pollicis longus & extensor pollicis brevis tendons
o Floor is formed by scaphoid & trapezium
o Persistant pain & tenderness → suspect scaphoid fracture (supplied by dorsal
scaphoid branch of radial artery)
Anterior shoulder dislocation (associated findings)

o Flattening of the shoulder

o Fullness at anterior axilla
o Prominence of the acromion bone
o Damage of the axillary nerve
Supra-condylar fracture of the humerus :
o Three structures pass in front the humerus; median nerve, brachial artery,
radial artery
o Antero-medial displacement of the proximal segments → damage of the median
nerve & basilar artery.
o Antero-lateral displacement of the proximal segments → damage of the radial
nerve.
Median nerve :
o Arise from lateral & medial cord fibers, course with brachial artery in groove
between biceps & brachialis
o Enter forearm in a foramen in the antecubital fossa → between two heads of
pronator teres muscle → between FDS & FDP → deep to flexor retinaculum
o distal injury to median nerve (e.g. CTS, suicide) → preserved flexion of 2nd & 3rd
digits, normal sensation over the thenar eminence  the nerves arise more
proximally
Latissmus dorsi muscle :
 Origin: iliac crest, lumbar fascia, spinous process of T7 – T12, lower ribs
 Insertion : Bicipital groove of the humerus
 Innervation: Thoraco-dorsal nerve (C6 – C8)
 Function: extension, adduction, internal rotation
Thoracic outlet syndrome (TOS):
 TOS may be due to cervical rib or scalene abnormalities.
 Most commonly occur in the scalene triangle in the neck bounded by scalene
muscles and 1st rib
 Anterior scalene muscle: originate from C3 – C6 and attach to the scalene tubercle
of the 1st rib.
 Middle scalene muscle: originate from C2 – C7 and insert into posterior 1st rib.
 Brachial plexus & subclavian artery pass between the 2 scalene muscles.
Subclavian vein runs anteromedial to triangle
Psoas abscess & psoas muscle :
o Origin : transverse process of T12 – L5, descend in front of the hip joint & deep to
the inguinal ligament
o Insertion: shared tendons with ilacus to insert in lesser trochanter.
o Action: major flexors of the hip joint
o Abscess → psoas sign: pain exacerbate by stretch the psoas muscle as extension
of the hip
o Risk factors : IV drugs, DM, HIV,
 Anatomical relation of different parts of duodenum:
- 1st part → pass horizontally over L1, intra-peritoneal
- 2nd part → pass inferiorly from L1 – L3, related to head of pancreas, CBD,
ampulla of Vater
- 3rd part → horizontally over L3, related to aorta, IVC, SMA, uncinate process
- 4th part → pass superiorly to the left of L2 – L3, Ligament of Treitz
 Horizontal transection of the rectus abdominus carry the risk of? Superior
& inferior epigastric arteries supply the rectus abdominus, inferior artery pass
posterior to the rectus abdominus at the level of the arcuate line → injury lead to
significant hematoma due to loss of the the supporting posterior rectus sheath.
Musculo-cutaneous nerve:
 Arise from C5 – C7, lateral cord of the brachial plexus.
 It innervates the major flexors of the forearm, coracobrachialis.
 The nerve continues as lateral cutaneous nerve of the forearm to provide sensory
innervation of the lateral forearm.
Serratous anterior muscle:
 Origin: surface of the 1st 8 ribs
 Insertion: medial border of the scapula
 Function: stabilize & rotate the scapula upward
 Innervation: long thoracic nerve (C5 – C7)
 Injury: winging of the scapula, inability of shoulder abduction above the
horizontal level.
Mention blood supply of the femoral neck & importance of each of them:
  Medial circumflex femoral artery : (main blood supply) it give the ascending
cervical & retinacular branches (most vulnerable fro damage)
 Lateral circumflex femoral artery : they contribute to the trochanteric
anastomosis, minor contiution to the femoral head
 Acetabular branch of obturator artery : not clinically significant

Femoral attachement of ACL & PCL : (PM AL)
- Posterior CL : medial condyle of the femur (antero-lateral)
- Anterior CL: lateral femoral condyle (postero-medial aspect)
Trapezius injury:
- Supplied by CN XI which pass superficially in the posterior triangle of the neck,
supply sterno-mastoid & trapezius
- The nerve prone to injury dueing neck dissection. Proximal inury cause paralysis in
both muscles.
- Origin: cerviacal & thoracic vertebrae till T12
- Insertion on the shoulder & clavicle
- Injury cause drooping of the shoulder, winging of the scapula, inability to
abduct the shoulder above horizontal level (don‟ t confuse with serratus
muscle)
 Superior gluteal nerve injury may occur due to pelvic trauma, hip surgery, buttock
injection.  notice the gluteus medius lurch

Fall on outstretched hand may cause scaphoid fracture, lunate dislocation (ususally
exist together), distal radius fracture
Flexor retinaculum = transverse carpal ligament
Femoral triangle:
 Femoral artery → mid-inguinal point (midway between pubic tubercle, ASIS)
 Femoral vein cannulation → ~ 1 cm below the inguinal ligament, ~ 1 cm medial to
femoral artery pulsation
Common iliac artery branches (before passing inguinal ligament) :
 Inferior epigastric artery (pass medially, superiorly)
 Deep circumflex iliac artery (pass laterally)
Obturator nerve (L2-L4):
 Pass postero-medially to the iliopsoas muscle, along the lateral aspect of the lesser
pelvis → then pass through the obturator canal
(only nerve pass through it) → one it enter the
thigh it gives obturator externus muscle, and
divide into 2 branches → to give the thigh
adductors, cutenous branch (medial thigh)
 The nerve is commonly damaged by pelvic
trauma, tumor (bladder), surgery
Ilio-psoas muscle:
 Iliacus originate from the concavity of the pelvic
bone, common insertion in lesser trochanter
Cricothyrotomy: incision is
done through these structures
1) Skin
2) Superficial cervical fascia
(SC fat, platysma)
3) Deep cervical fascia
(investing & pre-tracheal)
4) Cricothyroid membrane
Histological difference
between osteoblast &
osteoclasts:
 Osteoblasts: single nucleus,
mesenchymal origin, found
in periosteum & BM
 Osteoclasts: multinucleated
cell (2 – 5 nucleus) (formed
by several precursor cells
fuse to create multinucleated cells), mononuclear origin
 Differentiation of osteoclasts need Macrophage colony stimulating
factor (M-CSF) & receptor for activated NF-κB (RANK-L)
 In Paget disease, osteoclast are very large may harbor > 100 nuclei
Bone physiology:
 OPG from osteoblasts → block RANK on osteoclasts → ↓ osteoclasts
 Ratio between OPG / RANK-L control the remodeling process of the bone (↑↑
OPG / ↓RANK-L) → ↑↑ osteoblasts
 Estrogen act by ↑↑ OPG by osteoblast, ↓↓ expression of RANK →maintain bone
mass
Types of bone:
- Trabecular bone: compose only 15% of the skeleton, metabolically more active
In intial phases of osteoporosis; trabecular thinning & perforation with
loss of inter-connecting bridges
- Cortical bone: affected in advanced osteoporosis
Supra-spinatous (mechanism of empty can test):
- Action of supra-spinatus can be isolated by empty can test.
- Abduction of the arm 90, forwd flexion of the arm 30 degree, full supination of
the arm by pointing the thumb downward → abduction in front of resistance =
supra-spinatus
Notice:
- Lateral trunk of the brachial plexus give rise to → musculo-cutaneous nerve
- Medial trunk of the brachial plexus give rise to → ulnar nerve
- Posterior trunk of the brachial plexus give rise to → radial nerve (the largest)
& axillary nerve
Course of the radial nerve in the forearm:
- Pass anterolateral to the lateral humeral condyle → give deep & superfifica
sensory branch → deep branch pass between the 2 heads of supinator muscle
(damaged by repetitive supination & pronation) to be posterior
interosseous nerve
Radial nerve injury levels (axilla, humerus, supinator):
 axilla: finger & wrist drop, absent triceps reflex, sensory loss on the arm,
forarm, hand
 Mid shaft humerus: sparing of the triceps reflex, sensory loss on the forearm
, hand only
 Supinator canal: finger drop only, intact extensor carpi radialis longus, no
sensory loss
Axillary nerve :
 Arise from the posterior cord of the brachial plexus and pass deep oin the axilla in
the Quadrangular space (bound medially by long head of triceps, laterally by
humerus, superiorly by ters minor, inferiorly by teres major muscle)
Lumbar puncture:
 Spinal cord end at L1/L2 (in infants L3/L4), dura end at S2
  Highest point of the iliac crests correspond to L4 vertebral body ,
optimal location is at L3/L4 or L4/L5 space
Changes following fracture clavicle:
 Medial part: displaced superiorly by
sternomastoid
 Lateral part : displaced inferiorly by
weight of the arm
 Attachment of muscles to clavicle 


Physiology

 Types of muscle fibers “don’t be confuse”:

o Type I : for sustained postural muscles r.g paraspinal
o Type IIa : intermediate between type I & type IIb → use aerobic glycolysis
o Type IIb : use anaerobic glycolysis
 Ach, Substance P, serotonin, Bradykinin → endothelial receptors → ↑↑ Ca →
Arginine + O2 → citrulline + NO2
Dimethyl arginine is an endogenous analogue of arginine → ↓↓ NO synthetase
 Mention the physiological role of Fibronectin: glycol-protein produced by
fibroblast, bind to integrin, matrix collagen GAGs → cell adhesion and migration.
Mention the physiological role of integrin:
- Integrin: transmebrane protein receptor with extra-cellular portion and
intracellular portion.
 Extracellular portion: bind with collagen, laminin, fibronectin
 Intracellular portion: bind with microfilaments (actin), intermediate
filaments(keratin)
Lachman test indicate ?? ACL injury
Explain the role of ATP, ADPin skeletal muscle contraction:
 ATP → when attached to myosin, it induce release from myosin, in death, loss
of ATP → persistant contraction  rigor mortis
 ADP → ATP hydrolysis cause ADP → attachment of myosin with actin
Why rheumatoid arthritis have higher risk of neurological manifestations &
complications??
 RA usually involve cervical spine & atlanto-axial joint → joint destruction 
atlanto-axial sublaxation.
 As C1 has higher mobility relative to C2
 Chronic symptoms → neck pain, stiffness & neurological findings.
 Endotracheal intubation → acutely worsen the sublaxation & cause compression
of the spinal cord  spinal shock
Describe primary active transport, examples:
- Carrier molecules are enzymes that hydrolyze ATP (ATPase).
- Ex.: Na/K ATPase, H/K ATPase (proton pump), Ca ATPase
What sit he determining factors for resting membrane potential:
 In the resting state, permeability of the membrane for K (through non gated
channels) is much higher than for Na → so the RMP is approaches the
equilibrium potential of the K
 There are small number of channels that allow flow of Na into the cell → push
the RMP toward the positive side → so the RMP is not exactly equal to the
equilibrium of K, but less negative than of K
 Although the RMP = the RMP of Cl- , the chloride have little role in the
determination of the membrane potential
What determine the membrane potential (in general):
 The direction (+ / -) membrane potential is the intra-cellular potential
(intracellular – extracellular).
 At rest, there is negative charges (-70) at the inner membrane.
 Passage of Na, Ca into the cells → making it more positive
 Passage of Cl into the cells, or K out of the cell make the membrane potential
more negative.
Define & explain Equilibrium potential: e.g. as K pass out of the cells, negative
ions inside the cells pull K again, but K still pass down to its concentration gradient,
till it make a gradient big enough that amount of K pulled into the cells = amount of
K pass out of the cell (net diffusion across the membrane is zero)
Action potential of membrane :
 Resting potential: ~ - 70 due to non-gated channels of K channels
 Hyperpolarization: because voltage gated K channels remain open for short time
after repolarization is complete till it reach to ~ -85
Some cytokines :
 Osteopetrogene (OPG) : decoy receptor, ↓↓ binding of RANK-L to RANK → ↓↓
differentiation & survival of osteoclasts
- Loss of function mutation → juvenile Paget disease
 FGF : reglate chondroblasts & osteoblasts
 IGF-1 : ↑↑ osteoblast replication & collagen synthesis, inhibit matrix
metalloproteinase – 13 (MMP-13) → ↓↓ collagen degradation
Foreign body granuloma appear as tender erythematous lesion
Granuloma is due to Th1
 Pathology

 Rickets → un-mineralized osteoid matrix :

- Causes :
 ↓↓ conversion into active form e.g. dark skin, ↓ sun exposure (UV B radiation)
 ↓↓ Intake of vit. D → maternal Vitamin D deficiency, exclusive breastfeeding
- Effect of vitamin D

Markers of bone remodeling :

 Osteoblasts: alkaline phosphatase; ALP produced from bone, placenta, liver,
intestine.
- Total ALP is not beneficial, so differentiation between bone & hepatic ALP is
important by
1) Electrophoresis, specific mono-clonal antibodies
2) Heat denaturation (bone ALP is easily denaturated by heat)
 Osteoclasts:
- acid phosphatase : not commonly used as marker for osteoclastic activity
- urinary hydroxyproline: destruction of collagen produce hydroxyproline,
but it can ↑↑ by meat eating
- urinary deoxypyridinoline: pyridinoline cross link collagen fibers, it is the
most important marker for osteoclastic activity.
Avascular necrosis :
 Other causes : (+) fat emboli, vasculitis
 Microscopic analysis :
- Dead bone = clear empty lacunae
- Fat necrosis
Treatment of rheumatoid arthritis:
 The foundation of treatment is DMARDs (1st
is MTX)
 Response to antibiotics usually take several
weeks → must be bridged by steroids / NSAIDs for rapid relief
Polymyositis:
  Elevated muscle enzymes e.g. aldolase
 Elevated anti Jo1 antibody → anti histidyl tRNA synthetase
 Biopsy → endomysial mono-nuclear inflammatory infiltrate, patchy necrosis
 Anti-smooth muscle antibody → autoimmune hepatitis
Achondroplasia :
o Although it is AD disease, 90% of cases are De novo, 10% only are inherited
o FGFR3 normally inhibit excess chondrocyte proliferation inendochondral
ossification; it is excessively activated here.
o Normally, endochondrial ossification … … chondrocyte in the growth plate
continue to proliferate through-out childhood → then calcified and invaded by
osteoblast to become woven bone, then maturated to be compact bone cause
Patent procuss vaginalis cause indirect inguinal hernia & communicating
hydrocele which is seen connected to the peritoneal cavity, unlike non
communicating hydrocele (as in adults)
Rheumatoid arthritis Vs. osteo-arthritis:
o Hard nodules in OA resembles bony osteophytes

Rheumatoid arthritis :
o Pathogenesis:
 Auto-immune antibodies aginst type II collagen, citrullinated
vimentin  activate CD4 Th cells
 CD4 Th cells → synthetize rheumatoid factor (bind IgG), anti-
citrullinated protein antibody (bind self protein) → form immune
complex deposition in synovium & joints → chronic inflammation.
Polymyositis:
o Muscle weakness may be painful / painless
o Biopsy : ↑↑ MHC-I on sarcolemma, ↑↑ CD8 cells → myocyte destruction.
o Associated with restrictive lung disease, myocarditis
Acute osteomyelitis:
o Children → usually affect long bones (LL)
o Adults → + vertebral involvement + predisposing to bacteremia
o Usually vague and need high index of suspicion.
 Von Hipple Lindau → AD disease, contained cysts inside the liver, kidney, pancreas
Melanoma : commonly metastasize to brain (high incidence), GIT (not bone), liver,
lung
Complications varicose veins : impaired woud healing, infection, chronic edema,
stasis dermatitis and skin ulceration (medial malleoulus)
 Phlegmasia alba dolens → massive iliofemoral DVT → incinc. Venous pressure in leg
→ ↓↓ arterial flow → painful white “milk leg”
 Pathogenesis of Paget disease: caused by environmental factors and gene mutations
affecting RANK, OPG → ↑↑ activation of RANK & OPG → ↑↑
osteoclastic activity so initial phase is usually osteolytic  large
no. of osteoclasts (abnormally large with ↑inc number of
nuclei)
o At early stages; osteoclasts release cytokines → ↑↑ fibroblast proliferation
(highly vascular stromal tissue) → cause AV shunting & high COP faillure
o Osteosclerotic phase : dense hypo-vascular mosaic pattern of
lamellar bone with irregularly haphazardly oriented sections separated by
prominent cement lines
o ↑↑ activity of fibroblast & osteoblast → ↑↑ risk of osteosarcoma.
Commonest cause is Staph. Aureus, strept. pyogenes.
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Dermatology ∷ psoriasis :
Keratinocyte hyperplasia
(hyperkeratosis)
Persistence of nuclei in
eratinocytes (para-keratosis)
Absemt stratum granulosus
Hyperplastic dermal papillae
(rete ridges)
 Anti-ds DNA & anti smith antibody (anti snRNPs) → are diagnostic for SLE, but
therie absence don‟ t rule out the disease
Difference between gout and pseudogout in the pattern of oint affection:
- Pseudo gout → > 50% of cases knee is involved
- Gout → more affect the 1st meta-tarsophalangeal joint
Difference of osteomyelitis in adults & children.
- In children , the site of infection is metaphysis of long bone, slow flow,
sinusoidal vasculature
- In adults, the vertebral body is the most common location in adults.
Clinical picture of Reiter syndrome (reactive arthritis)

 These symptoms are due to immune complex deposition

 Keratoderma blennorrhagicum → hyperkeratotic vesciles on palm & sole
(syphilis cause popular or pustular rash not vesicular)
 Circinate balanitis → serpiginous annular dermatitis of the glans penis
Mention causes of myopathy
Causes of myopathy with normal CK level, how to differentiate
Mention the function of COX-1 & COX-2 enzymes:
 COX–1: housekeeping functions→ platelets aggregation, gastric mucosal,
vascular homeostasis
 COX–2: inflammation → inducible enzyme during inflammation as it is
induced by IL-1 & TNF-α
 CNS manifestations of Sarcoidosis: Sarcoidosis will cause infiltrating masses in
the brain/ pituitary lead to ↓↓ dopamine → ↑↑ PRL
Causes of myopathy with elevated CK

Characters of hypothyroid myopathy

- Associated with signs of hypothyroidism, proximal muscle weakness
- Myoedema → focal muscle contraction at site of percussion, due to ↓↓ uptake of
Ca from SR
- Hung up reflexes → delayed relaxation phase of deep tendon reflexes
Clinical picture of Bursitis:
 Normal passive ROM, decreased & painful active ROM
 Severe pain with point tenderness
 Swelling of the superifically seated bursae
 Anserine bursitis → obesity, athletetes
Temporomandibular joint dysfunction (TMD):
 Constellation of symptoms including jaw pain, facial pain & ear discomfort
 May be due to derangement of the mandibular branch of CN V → which supply
the face, cheeks + tensor tympani in the middle ear, so TMD associated with
otologic symptoms
 Osgood Sclatter disease (OSD):
 Overuse injury of the secondary ossification center (apophysis) of the tibial
tubercle
 Due to repetitive quadriceps contraction & chronic avulsion cause the proximal
patellar tendon to separate from the tubercle → callous formation → elevation &
prominence of the tuberosity
Tennis elbow (lateral epicondylitis):
 Due to repetitive minor trauma to extensor carpi radialis brevis (ECRB) → excess
fibroblast & neovascularization (no true inflammation)
Spinal canal stenosis:
 Most commonly in lumar region, mainly due to degenerative arthropathy > 60
years.
 ↓↓ height of the inter-vertebral discs → ↑↑ load on the posterior spinal part →
thickened ligamentum flavum , facetal arthropathy
 Clinical picture: neurogenic claudication, posture dependant pain (↑↑ by
straightened spine, ↓↓ on leaning forward)
 Radial head sub-laxation (nursemaid‟ s elbow):
 Most common elbow injury in children
 Mostly at age of 1 – 4 years (at age of 5, the annular ligament become strong)
 Due to vigorous axial traction on the forearm, especially extended pronated elbow
 Due to tear occur in the annular ligament of the radius.
Viral arthropathy (Parvovirus B19):
 Initial non-specific symptoms of viral diseases (associated with high viremia,
viral shedding)
 Erythema infactiosum, acute arthropathy (due to active immune complex
deposition, with minimal viremia)
 Acute polyarthropathy: occur in adults, cause symmetrical polyarthopathy
involving PIP, MCP, knees, elbows. Self-limited & non destructive
Keloid :
 Pathogenesis: normally, in proliferative phase, contraction of actin filaments in
myofibroblasts occurs to approximate wound edges. TGF-β help differentiation of
fibroblast into myofibroblasts & this process should diminish after healing
 In keloid, unregulated ↑↑ in TGF-β → extension beyond borders of scar
 It occur after minor trauma & major trauma, may be painful, pruritic, raised
  L/M of keloid show haphazardly arranged of thick, pink collagen bundles

Gout
 Synovitis (acute joint pain, tenderness, limitation ROM) → best next step is
diagnostic arthrocentesis to rule out septic arthritis (true medical emergency),
gouty arthritis, hemarthrosis, rheumatic disease (even serum Uric acid level is
inconclusive is diagnosis acute gouty arthritis)\
 Crystal induced arthropathy → microscopic analysis is conclusive for crystals,
synovial WBCs 20 – 100,000
 WBCs in the synovium > 100,000 → septic arthritis
Gout :
 Causes : (+) myeloproliferative disorder (↑↑ turn over)
 Urate crystal prefer the areas with lower temperature (which favour crystal
formation) especially in the distal lower limb (MTP, knee ankle).
 Neutrophils take up the crystal → free radicle release → cytokine production &
joint inflammation

 Takayasu arteritis : ♀ < 40 years, GCA → >50 years.
The distinction is usually made by age as both histologies are the same with medial
granulomas , GCA → affect carotid branches, while Takayasu affect reminder
branches of aorta. GCA if occur in young age, it is usually considered as a part of
Takayasu arteritis.
Ankylosing spondylitis:
 Some extra-skeletal manifestations :
1) CVS → ascending aortitis  dilatation of the aortic ring & AR
2) Anterior uveitis
3) Involvement of the thoracic spines & costo-vertebral & costo-chondral junction
→ limit chest wall expansion & hypoventilation
Chest wall expansion is usually used to detect the progression of
patients with AS
 Pharmacology
 MTX is the 1st line for moderate – severe RA, preferentially inhibit growth of rapidly
growing cells e.g. neoplastic & inflammatory

 Hydroxychloroquine → most important side effect is irreversible retinopathy

Isotretinoin therapy :
 Isotretinoin is a synthetic isomer of natural all trans retinoic acid
 (+) → condom used as 2nd contraceptive method, monthly pregnancy test is
advised
 Side effects :

 Mechanism of action:
- Isotretinoin → enter cell as retinon → retinal→ retinal receptor  bind to
retinoic acid response element (RARE) → change transcription of genes →
1) ↓↓ sebum production
2) ↓↓ size of sebaceous glands & ↑↑ cell turn-over
3) ↓↓ follicular epidermal keratinization → loose keratin plugs & facilitate their
expulsion
Drug induced lupus (DILE):
 Anti-histone antibodies (very common in DILE, 50% SLE)
 Anti dsDNA antibodies (rare in DILE, 80% SLE)
 ANA are found in both
 Biological agents for RA :
 Eternecpt: fusion protein → link “TNF-α + Fc portion of humanized IgG1” →
act as decoy protein.
 Certo-li-zu-mab pegol : (pegol) pegylated (zu) humanized (mab)monoclonal
antibody, act as (li) immunomodulator that target TNF-α → it lack Fc protion so
preventing complement activation
Acute gouty arthritis:
 NSAIDs are the 1st drugs → if contraindicated : give colchicine
 Probenecid & allopurinol is contraindicated in acute attack → precipitate uric acid
& worsen the condition.
Difference of molecular action between aspirin & celecoxib:
The main difference is on COX-1 inhibitor → COX-1 is responsible for platelets &
GIT manifestations:
- Platelets → no ↓↓ TxA2
- GIT → no ↓↓ PGI2 → no peptic ulceration and erosions
Manifestations and treatment of tumor lysis syndrome :
- Rapidly damaging cells → release of potassium, phosphorus, urate
- Rasburicase (recombinant form of urate oxidase, not normally present in human)
transform the uric acid into soluble form (allantoin)
Mechanism of action of bisphosphonates:
1) Bind to hydroxyapatite → ↓↓ binding of osteoclast on bone surfaces
2) ↓↓ osteoclast proton production
3) ↑↑ osteoclast apoptosis
4) ↓↓ recruitment of osteoclast precursor
 The net result is slow the rate of bone loss, minimal ↑↑ bone density
Mention the differentiating characters of back pain due to degeneration


Mention the differentiating characters of back pain due to radiculopathy:

Mention the differentiating characters of back pain due to spinal stenosis

 Mention the differentiating characters of back pain due to spondyloarthropathy

Mention the differentiating characters of back pain due to metastasis

 May be associated with systemic symptoms

Mention the differentiating characters of back pain due to osteomyelitis

 Indications of uric acid lowering drugs (prophylaxis): → best is XO inhibitor

1) Frequent gouty arthritis attacks
2) Uric acid kidney stones
3) Chronic joint destruction by gout
4) Prescence of gouty tophi
Colchicine bind to intra-cellular tubulin prevent its polymerization to microtubules,
important side effects are Diarrhea , not used in renal impairment
Describe the Acid base status in aspirin toxicity & mechanism:
 Early: respiratory alkalosis as salicylates directly stimulates the medullary
respiratory center.
 Later > 12 hr.: mixed acidosis, as uncoupling, ↑ heat → ↑↑ accumulation of organic
ketones in the blood (not due to compensation)
Mention different drugs used for osteoporosis:
Adverse effects of succinylcholine :

 As succinyl choline bind to ligand gated nicotinic channels (non selective for Na
only) cause hyperkalemia → exaggerated hyperkalemia & life threatening
arrhythmia occur in crush / burn injury, denerving injury (e.g. GBS),
myopathy.
Describe the mechanism of action of succinyl choline:
 Phase I block: when the drug is bound to the end-plate channels (cannot be
degraded by ACEchE) → continuous depolarization with no repolarization →
blockage of the Na channels in inactivated state → flaccid paralysis
 Phase II block: continuous depolarization fo the end-plate channels →
desensitization to the effect of succinylcholine → similar to non-depolarizing
block