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Anatomy – MSK, GI,

Resp, GU
Musculoskeletal
and Rheumatology

1
Musculoskeletal Anatomy
Radial Artery and Radial Nerve Bony Anatomy of the Hand
•Arterial Pathway of Upper Extremity

•With fracture of midshaft humerus


Risk of injury to:
•Radial nerve (wrist drop)
•Deep brachial artery (travel together)

•Radial nerve (think extension!) innervates most of


the forearm
•Extensors of the elbow (triceps, anconeus)
•Brachioradialis and Supinator muscles
•Wrist extensors
•Innervates the extrinsic extensors of the digits

•Radial artery branches off Brachial art. at elbow


•Diverges into: radial art. and ulnar art. passed
the elbow 2 3

Carpal Bones

Trapezoid
H
Trapezium C
P
S Triquetrum
L Tenderness in Anatomic Snuff Box
Thumb Spica
Cast
4 5
Venous Arch of Hand
Arterial Arches of the Hand

6 Most Common Arch Anatomy 7


(variants do exist)

NECK
• Several muscles insert on the clavicle:
– Pectoralis Major (medial)
– Deltoid (lateral inferior)
– Subclavius (lateral inferior)
– Trapezius (lateral superior)
– Sternocleidomastoid (medial superior)

Note: Sternocleidomastoid muscle is responsible for the upward traction on the


medial section of the fractured clavicle - deltoid/pectoralis pull lateral portion down
*SCM is Innervated by CN XI (spinal accessory nerve) – also
innervates trapezius muscle
• SCM functions to turn the head in the opposite direction
– L SCM turns head right
– R SCM turns head left

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Sciatic, Superior gluteal nerve

Superior and Inferior gluteal nerves


go through greater sciatic foramen

ABC Order
Medial Lateral Sciatic Nerve

1) Injury to the superior gluteal nerve weakness of the glut. medius + glut. minimus
- produces (+) Trendelenburg test
2) The inferior gluteal nerve innervates gluteus maximus
Injury of the inferior gluteal nerve difficulty rising from A seated position
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and climbing stairs. 11

Femoral Circumflex Artery – Femoral head & neck blood supply

Femoral neck fractures are common in elderly patients


with osteoporosis s/p fall

Femoral head and neck derive their blood supply from


the Deep Femoral Artery
-Medial and lateral femoral circumflex arteries
-these vessels together form the trochanteric
anastomosis

Medial femoral circumflex artery makes the largest


contribution to the blood supply to femoral head
(+ )Trendelenburg Sign: - Vulnerable to damage from femoral neck fractures due
Drop of pelvis when lifting to its close association with the posterior aspect of the
leg opposite to weak gluteus femoral neck.
medius - Injury or thrombosis of this vessel can occur and result in
Avascular necrosis (AVN) of the femoral head

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15
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Knee Joint

Most sensitive test


for ACL tear?
Lachman Exam

Most sensitive test for


PCL tear?
Posterior Drawer Exam

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Collateral Ligaments

Varus stress is ValGus stress is


abnormal in LCL abnormal in MCL
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injury injury 19

• A 24yoM comes to a physician 24hrs after an injury to the right • A 24yoM comes to a physician 24hrs after an injury to the right
knee while playing soccer. He can walk, but he limps on the knee while playing soccer. He can walk, but he limps on the
right side. He states he was hit by another player on the lateral right side. He states he was hit by another player on the lateral
side of his right knee, but did not feel a snap or pop at the time side of his right knee, but did not feel a snap or pop at the time
of the incident. On exam, the right knee appears normal but on of the incident. On exam, the right knee appears normal but on
palpation of the medial joint line there is tenderness. Increased palpation of the medial joint line there is tenderness. Increased
laxity is observed with valgus stress exam at 30 degrees. laxity is observed with valgus stress exam at 30 degrees.
Lachman and posterior drawer tests are negative. Which is the Lachman and posterior drawer tests are negative. Which is the
most likely diagnosis? most likely diagnosis?
• (a) Meniscus injury (a) Meniscus injury
• (b) sprain of LCL (lateral collateral ligament) (b) sprain of LCL (lateral collateral ligament)
• (c) sprain of MCL (medial collateral ligament) (c) sprain of MCL (medial collateral ligament)
• (d) tear of the ACL (d) tear of the ACL
• (e) tear of the PCL (e) tear of the PCL

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II. Gastrointestinal Anatomy:
Abdominal Aorta Branches

1)Ulcer posterior wall of stomach


External Iliac a. erosion of splenic artery
2)Ulcer of posterior wall of
duodenum Gastroduodenal art.
Internal Iliac a. 3)Ulcer of less curvature of stomach
left gastric artery
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SMA and IMA Anatomy SMA Syndrome


• SMA leaves the aorta at the level of L1
• Supplies the intestine from the duodenum & pancreas to the left colic flexure
• Transverse portion of the duodenum lies horizontally at the level of L4
– Between the aorta and superior mesenteric artery
• SMA and aorta normally form ~45° angle

• “SMA syndrome” is caused by compression of the 3rd portion of the duodenum


by the overlying abdominal aorta and SMA
– Very rare
– Leads to symptoms of partial intestinal obstruction
-- patients usually have low mesenteric fat (less cushion) or
pronounced lumbar lordosis
• Low body weight or recent weight loss
• Loss of mesenteric fat due to burns or other catabolic states (cancer)
• Prolonged bed rest – spinal cord injury, patients in body casts, etc.
Superior Rectal
Artery

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Gastrointestinal CT Anatomy

1 – Esophagus
3 – Trachea
7 – Aorta
8 - Scapula

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1 – Right Lung
2 – Right Hepatic Vein
3 – Liver
4 – Left Hepatic Vein
5 – Stomach
6 – Splenic flexure of
colon
7 – Spleen
8 – Left Lung
9 - Aorta

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1 – Inferior vena cava
2 – Right kidney
3 – Aorta
4 – Left Renal vein
5 – Left Kidney
6 – Superior mesenteric artery
7 – Superior mesenteric vein
8 – Gallbladder
9 – Liver

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4 – IVC
5 – Psoas Muscle
6 - Aorta

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A 63 year old male with a h/o gastrointestinal bleed has developed a sudden onset A 63 year old male wit a history of gastrointestinal bleed has developed a sudden onset
shortness of breath. Evaluation shows pulmonary embolism. A filter placement is planned shortness of breath. Evaluation shows pulmonary embolism. A filter placement is planned
to prevent further embolization. The filter will most likely be place in which of the to prevent further embolization. The filter will most likely be place in which of the
following structures? following structures?

A – duodenum
B – IVC
C – Aorta

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Duodenum
Gallstone Ileus
--Mechanical obstruction resulting from passage of a large (>2.5cm) stone into the bowel
The first part of the duodenum – Occurs in patients with long standing cholelithiasis (gallstone dz)
• Emerging from the pylorus of the stomach – Middle-aged to elderly females (4Fs: female, flatulent, forty, fertile)
• Horizontally oriented and overlies the first lumbar vertebra
• ***Only part of the duodenum that is NOT retroperitoneal!!!*** –A cholecystenteric fistula forms between the gallbladder & adjoining gut tissue
-secondary to persistent pressure on these tissues
The second part of the duodenum - obstruction usually occurs at ileocecal valve
• Courses inferiorly from the level of L1 toL3
• Close relation to the head of the pancreas Diagnosis: Classic signs/symptoms SBO – abdominal pain, vomiting, +TTP
Ampulla of Vater = Site where the pancreatic and common bile ducts provide their secretions Abdominal XR shows SBO and pneumobilia (gas in biliary tree)
Upper GI barium contrast study shows no passage of contrast into large intestine

The third part of the duodenum


• Courses horizontally over L3 vertebra, abdominal aorta, & IVC Treatment:
• Close association with the uncinate process of the pancreas & the SMA (sma syndrome) – Laparotomy with Surgical removal of the offending stone
- Puts these structures at high risk for direct invasion – Cholecystectomy and repair of the fistula
Example: tumor in the third part of the duodenum
The fourth part of the doudenum
• Courses superiorly and to the left of the L2 and L3 vertebrae & becomes the jejunum 36 37
past the ligament of Treitz
Choledocholithiasis and Cholangitis
choledocholithiasis: Obstruction of the cystic duct or common bile duct by a gallstone

PE: biliary colic, jaundice, and cholangitis


- increased Alkaline Phosphatase
- increased Bilirubin

Cholangitis (bacterial infection of biliary tree secondary to obstruction):


•Fever/Chills + Jaundice + RUQ pain Charcot’s Triad
•Inspiratory pause during RUQ palpation (Murphy’s sign)
•Right upper quadrant ultrasound - stones in the biliary duct
NOTE: ERCP diagnostic and therapeutic
- sphincterotomy and decompression

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Retroperitoneum

Peritoneal Organs – mobile organs which have mesentery and fully enclosed in peritoneum
Retroperitoneal Hematomas
Retroperitoneal Organs – fixed organs partially covered in peritoneum
Retroperitoneal hematomas
Retroperitoneum includes the following structures: –Commonly associated with abdominal and pelvic trauma
1. Major vessels: – Develop in up to 50%of patients with blunt abdominal trauma
– Abdominal aorta, inferior vena cava and their branches
2. Solid organs: Pancreatic injury with formation of a retroperitoneal hematoma
– Pancreas (except the tail), kidneys, adrenal glands • Severe blunt or penetrating abdominal trauma
3. Hollow organs: •Caused by direct abdominal blows from:
– Parts 2 & 3 and 4 of the duodenum –mal positioned seat belts
– Ascending and descending colon (secondarily retroperitoneal),
– Rectum –steering wheels during MVCs
– Ureters and bladder
- Pancreatic injury can cause mild symptoms or be symptomatic
- Abdominal CT scan obtained in blunt abdominal trauma to exclude
retroperitoneal hematoma

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LSB 4th Intercostal space- RV
A penetrating injury at the left sternal border in the fourth intercostal space (level of
the nipple) will pass through the following layers:
1.Skin and subcutaneous layers
2.Pectoralis major muscle
3.External intercostal muscle
4.Internal intercostal muscle
5.Internal thoracic artery and veins
6.Transversus thoracis muscle
7.Parietal pleura
8.Pericardium
9.Right ventricular myocardium

Right lateral retroperitoneal hematoma


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shown displacing the right kidney

The Lung: CXR


Lower border of pleura Midclavicular line Midaxillary line Paravertebral line
Right 7th rib Upper border of 10th rib 12th rib

left 7th rib Lower border of 10th rib 12th rib

•Thoracentesis should be performed :


•between 5th and 7th ribs midclavicular line
•7th and 9th ribs along the midaxillary line
• 9th and 11th ribs along the paravertebral line

•If the needle is inserted higher, there is a risk of lung injury


•Insertion of the needle below the 9th rib at the midaxillary
line on the right may cause liver injury

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Pneumothorax

Tension Pneumothorax is commonly tested:


-Condition where air enters the pleural cavity during inspiration, but not expelled during exhalation
-An increasing volume of air accumulates with the pleural space (blowing up balloon)
RIGHT tension
***Deviation of the lung and mediastinum to the opposite side of the chest*** pneumothorax
Increased pressure within the chest cavity causes decreased SVR to the heart leading to decreased
cardiac output. Tracheal deviation away
from affected side
Signs/Symptoms Tension Pneumothorax:
Tachycardia, hypotension, tachypnea
Hypoxia and absence of breath sounds
Hyperresonance to percussion on the affected side

Chest X-ray: can be used to confirm diagnosis but…

Treatment Emergent needle thoracostomy! Then chest tube (after needle decompression)

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TYPE II Pneumocytes
To Review: TYPE II Pneumocytes Alveolar marcrophages
Regenerate alveolar lining & produce surfactant •Lung’s first line of defense against foreign
particles in the air (bacteria, debris, etc.)
•Accumulate within alveolar spaces in disease
•The alveolar surface is predominantly (95%) covered states
by flat type I pneumocytes
Goblet cells
•The interspersed cuboidal type II pneumocytes are • Rarely found in the respiratory epithelium
the source of pulmonary surfactant and are also the beyond the level of the smallest bronchi
main cell type responsible for replacing the alveolar (normally absent from terminal airway)
epithelium after alveolar injury. • differentiated mucin-producing cells.
–Type II pneumocutes are unique in their ability to proliferate in
response to injury.
Pseudostratified columnar ciliated epithelium of
the tracheobronchial tree REMEMBER:
•Clara cells are non-ciliated, secretory constituents of
Changes to Simple cuboidal ciliated epithelium at Type II pneumocytes have two
the terminal respiratory epithelium.
the level of the respiratory bronchioles important functions:
Cilia are absent from the lining of the terminal 1) regeneration of the alveolar
alveolar ducts and alveolar sacs lining following injury
2) surfactant production
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Horseshoe Kidney
The Heart: Coronary Vessels This intravenous pyelogram (IVP) shows the kidneys joined
at their lower poles. This is the most common variant of
horseshoe kidney (90%)
•Right & left main coronary arteries arise directly (In the other 10% of cases the fusion occurs at the upper poles)
from the root of the aorta
–Provide the blood supply to the heart muscle
Horseshoe kidney is found in approximately 1:500
•Left main coronary artery divides into: autopsies, and may lead to urinary tract obstruction and
(1) left anterior descending (LAD) artery the development of hydronephrosis.
(2)Circumflex artery
–Supply most of the anterior and left lateral surfaces of the
heart
During embryogenesis, the kidney goes through the stages of pronephros, mesonephros, and
•85%-90% of individuals (“right dominant
metanephros.
circulation)
– Right coronary artery gives rise to the posterior descending Fetal metanephros is initially located in the sacral region,
artery while in the adult the mature kidney is located at vertebral levels T12-L3
•Approximately 10% of patients (“left dominant
***The RIGHT kidney sits LOWER than the left kidney***
circulation”)
–Posterior descending artery arises from the circumflex branch Right coronary artery also gives rise
of the left main coronary artery to the SA and AV nodal arteries in This relative ascent of the kidneys from the sacral region to their normal anatomic position
most patients results from the disproportionately rapid growth of the caudal part of the embryo.
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Urethral Injuries – Retrograde Urethrogram • A 19yoM is involved in a motorcycle accident in


(never pass Foley catheter!!) which he sustains a closed fracture of his right femur
and a pelvic fracture. In addition to the obvious
deformity in his leg, physical exam is remarkable for
If vignette states “blood at urethral
the presence of a scrotal hematoma and blood in the
meatus” or “high-riding prostate” suspect rectal exam, but the prostate cannot be felt. The
bladder rupture or urethral injury patient states that he feels the need to void, but
cannot do so. Which is the most appropriate next step
in Dx?
REMEMBER:
Test to rule out urethral injury?
Retrograde cystourethrogram • (a) CT scan of pelvis
(look for urine extravasation)
(b) scrotal sonogram
(c) IV pyelogram (IVP)
(d) retrograde cystogram via Foley catheter
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(e) retrograde urethrogram
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• A 19yoM is involved in a motorcycle accident in
which he sustains a closed fracture of his right femur Explanation
and a pelvic fracture. In addition to the obvious
deformity in his leg, physical exam is remarkable for • The hallmark of a urologic injury is a trauma
the presence of a scrotal hematoma and blood in the
rectal exam, but the prostate cannot be felt. The patient with blood in the urine. When blood is
patient states that he feels the need to void, but visible at the meatus and you add the scrotal
cannot do so. Which is the most appropriate next step hematoma, the “vanishing” prostate, and the
in Dx? inability to void: you’re looking at a urethral injury.
The LAST thing you want to do is put in a Foley
• (a) CT scan of pelvis catheter. A retrograde urethrogram is the best
(b) scrotal sonogram choice
(c) IV pyelogram (IVP)
(d) retrograde cystogram via Foley catheter
(e) retrograde urethrogram
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Painless Scrotal Swelling


Gonadal Drainage

REMEMBER:
REMEMBER: Left testicular/ovarian vein
Right
1) Hydrocele – remnant of processus vaginalis
comes directly off the left renal
testicular/ovarian vein (+) transillumination
vein comes off the
IVC
2) Varicocele – “bag of worms” (left testicle > right testicle)
-- dilation of pampiniform plexus
(-) transillumination

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• A 14yoM presents to the ED with very sudden and
Painful Scrotal Swelling severe pain in the right testicle. There is no h/o
trauma or recent mumps. He is afebrile, and a
1) Epididymitis urinalysis shows no pyuria. The testis is swollen,
- Infection of epididymis (often secondary to STD)
- Testicular pain, fever, redness
exquisitely painful, high in the scrotum, and riding in
- Pain may decrease with scrotal elevation a horizontal position. Which is the most appropriate
next step in management?
2) Testicular Torsion
- spermatic cord twists resulting in ischemia • (a) ice packs, analgesics, careful observation
- (-) cremasteric reflex
(b) sonogram of the testicle
- acute scrotal pain
- pain not improved by scrotal elevation (c) IV antibiotics
- Doppler US shows decreased flow to testes • (d) Testicular biopsy
- urgent treatment: manual detorsion vs. surgery
• (e) Emergency surgery
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• A 14yoM presents to the ED with very sudden and • An otherwise healthy 24yoM presents in the ED with
severe pain in the right testicle. There is no h/o very severe pain of recent onset in his right scrotum.
trauma or recent mumps. He is afebrile, and a The pain is constant and began about 3 hours prior to
urinalysis shows no pyuria. The testis is swollen, his arrival. Exam shows a temp of 103 degF. The
exquisitely painful, high in the scrotum, and riding in testis on the affected side is in the normal position
a horizontal position. Which is the most appropriate but appears swollen and is exquisitely tender to
next step in management? palpation as is the cord above the testis. Urinalysis
• (a) ice packs, analgesics, careful observation shows pyuria. Which of the following is the most
(b) sonogram of the testicle appropriate next step in management?
(c) IV antibiotics • (a) antiviral medication started within the hour
(d) Testicular biopsy (b) scrotal sonogram and antibiotics
(e) Emergency surgery (c) cystoscopy and bladder irrigation
Explanation: the vignette describes a patient with classic testicular torsion, a true urologic (d) trans-scrotal biopsy and appropriate resection
emergency requiring immediate de-torsion manually or via surgery. Sonogram of the
testicle is indicated when the diagnosis is unsure to determine if there is flow to the testis. 60
(e) emergency surgery and bilateral orchiopexy
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• An otherwise healthy 24yoM presents in the ED with very Female Reproductive Anatomy
severe pain of recent onset in his right scrotum. The pain is
constant and began about 3 hours prior to his arrival. Exam
shows a temp of 103 degF. The testis on the affected side is
in the normal position but appears swollen and is exquisitely
tender to palpation as is the cord above the testis. Urinalysis
shows pyuria. Which of the following is the most
appropriate next step in management?
• (a) antiviral medication started within the hour Ligaments of the uterus
Suspensory ligament of the ovaries Contains the ovarian vessels
(b) scrotal sonogram and antibiotics
(c) cystoscopy and bladder irrigation
Transverse cervical (cardinal) ligament Contains the uterine vessels
(d) trans-scrotal biopsy and appropriate resection
(e) emergency surgery and bilateral orchiopexy Round ligament of uterus Contains no important structures
Travels through the inguinal canal (like spermatic cord in male)
Explanation: the clinical picture describes acute epididymitis, which is treated Attaches distally to the labia majora
with antibiotics. So that testicular torsion (an emergency) is not missed, a Broad ligament Contains the round ligaments of the uterus
sonogram should be performed to rule out torsion with certainty. Ovaries 63
62 Fallopian tubes

Arthrocentesis
Musculoskeletal/ Rheumatology WBC Crystal/Polymerization
• Osteoarthiritis <2000 OA (Asymmetric: DIP, PIP)
(DJD)

• Inflammatory
(RA, Gout, CPPD) 25,000-50,000 RA (Symmetric: MCP, PIP)
*Gout – needle shaped
(-) birefringence
*Pseudogout – rhomboid shaped
(+)birefringence

• Septic Arthritis >50,000 Staph aureus most common

64 65
Osteomyelitis – infection of bone
• Most common organism:
• Prosthetic replacement
– Staph. aureus -S. aureus
• Sexually active -S. epidermidis (biofilm)
– Neisseria gonorrhea (rare)
• Vertebral Osteo
– Septic arthritis more • -Mycobacterium TB
common (Pott’s disease)
• Diabetics and drug addicts
• Cat and dog bites or scratches
– Pseudomonas aeruginosa -Pasteurella multocida
• Sickle cell
– Salmonella

• Elevated CRP & ESR (Nonspecific)


• MRI (detect bone changes)
66 67

Osteoarthritis =“Obesity” Rheumatoid Arthritis:


“Degenerative” Joint Disease (NO inflammation )
“Morning Stiffness” > 30m: Symmetrical joint involvement(MCP, PIP)
Asymmetric: DIP,PIP, Crepitation

• Deteriorated articular cartilage from injury/use


• No increase ESR (not inflammatory) • Anti-cyclic citrullinated peptide (anti-CCP)
Antibodies more specific than RF
• Normal strength, reflexes, & sensation
• RF is IgM Ab against Fc of IgG
• Pain worsens with use (throughout day) • Pain worse when first wake up then improves
with use
• XRay:
– Bony spurs “osteophytes” (degeneration) • Synovial hypertrophy + Pannus formation
–Joint narrowing + thickened subchrondral bone • Causes erosion of cartilage, bone, tendon, ligament
• HLA-DR4 is a risk factor
Treatment:
-PT, NSAIDs, losing weight
-advanced DJD may require joint replacement for
• X-ray: Narrowing of joint space & juxta-articular erosions
pain relief

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Rheumatoid Arthritis:
“Morning Stiffness” > 30m: Symmetrical joint involvement(MCP, PIP) Osteoarthritis Rheumatoid

• Autoimmune disease:
Diagnosis:
1. Rheumatoid factor and Anti-CCP Ab
2. Increased ESR

Treatment (Next step management):


1.NSAIDS, DMARDs - MTX, hydrochloroquine, 5-
ASA, infliximab, etanercept
2.COX-2 inhibitors
3.Corticosteriods
Ulnar deviation of digits in
patient with RA

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Primary Bone Tumor Locations

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Gout/CPPD (Pseudogout)
“Pain, swollen JOINT after eating Protein”
“Punched out erosion of cortical bone”
DNA Purine (Production) Uric Acid (Excrete it out, Uric acid stone )

Gout: Pseudogout:“Large Joints”


“1st toe MTP(Podagra)/Tophus”
– Hyperparathyroidism,
• MCC
Hematochromatosis
–Lesh Nyhan syndrome
–PRPP excess
– Hypophosphatemia
–Uric acid excretion – Hypomagnesemia
–von Gierke’s dz Dx: Arthrocentesis
–Calcium Pyrophosphate crystals
Dx: Arthrocentesis – (+) Birefringent
- uric acid crystals –Rhomboid shaped
- (-) birefringence ↑Uric Acid (Hyperuricemia: Renal Insufficiency)
- Needle shaped Increase production
• Xanthine oxidase Inhibitors:
Next Step (Management)
Acute gout/pseudogout: • Allopurinol
• NSAIDS Decrease excretion
• Colchicine (Neutrophil chemotaxis/microtubule) • Don’t use with kidney stone
Chronic Gout/pseudogout: • Decrease Tubular Reabsorption:
• Hydration •Pobenecid (inhibits PCN secretion)
• Probenacid, Allopurinol •ASA (high dose)
• Increase Secretion: 75
74
• Diuretics , ASA (low dose)

Seronegative Spondyloarthropathies
“Exercise improves Pain”
Morning Stiffness >2H
(Absence of RF: rheumatoid factor)
Reiter’s Triad: “Can’tSee,
“Can’t See, Can’t
Can’t Pee,Pee, Can’t
Can’t Climb
Climb a Tree”
a Tree”

1. Conjunctivitis (anterior uveitis)


1. Ankylosing spondylitis
– Associated with IBD, Aortic insufficiency, 3rd degree HB 2. Arthritis
2. Reactive arthritis (Reiter Syndrome) 3. Non gonococcal urethritis
– Non Gonnococcal (Chlamydia)
3. Arthritis with inflammatory bowel disease
–Most common Asymmetrical inflammatory arthritis of LE in young men
– IBD(UC/Crohn’s) flare ups: Pyoderma gangrenosum + Erythemia Nordosum
–Reiter’s reactive arthritis occurs several weeks after a GU (nonGC urethritis) or GI (bacterial
– Avoid NSAIDS (↑ Leukotrienes = not good for Crohn’s=Proinflammation ) enteritis) infections
4. Psoriatic arthritis –Autoimmune reaction by urethritis (Chlamydia trachomatis) or Enteritis (Salmonella,
– DIP + Skin: Nail Pitting, Sausage Shaped Digits, Shigella, Campylobacter, Yersinia)
– Tx: MTX (like RA)- very destructive –Synovitis (knees, ankles, feet)
Common S/S: –Extraarticular manifestations (conjunctivitis, cardiac conduction, AR, balanitis)
–Seronegative –Skin lesions (soles, feet) Vesicles that become pulstules followed by keratotic scales
–Involves Back/ Sacroiliac Joints (keratoderma)
–Have higher incidence of HLA B27 (MHC class I) –Axial involvement (sacroilitis)
–Extra-articular Manifestations (Reiter’s)

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Systemic Lupus Erythematosus
Ankolosing Spondylitis “Multiple Systems”
• Chronic inflammatory disease of sacroiliac joints
& axial skeleton leading to fusion of affected “I’M DAMN SHARP” or “DOPAMINE • False (+) Syphylis due to
joints RASH” antiphospholipid antibody
• Young & middle age men Immunoglobulins (anti-ds DNA, ani-Sm, – RPR/VDRL
antiphospholipid)
• HLA-B27 in 90% Malar rash (butterfly on face)
• Death from Renal Failure:
• Morning stiffness & LBP that improves with Discoid rash – Immune Complex Deposition
• Nephrotic –wire loop: Nonsclerosing
activity Antinuclear (ANA) antibody
Mesangial
• Associated with IBD, Aortic insufficiency, 3rd Mucositis (oropharyngeal ulcers) • Renal Failure =MCC of Death
degree HB, Anterior uveitis Neurologic disorders
Antinuclear antibodies (ANA)
Serositis (pleuritis, pericarditis)
• Sacroiliac joints +TTP bilaterally - Sensitive but not specific for SLE
Hematologic disorders Anti-dsDNA Ab very specific, poor prognosis
• Spine may have decreased range of motion Arthritis Anti-Smith antibodies (anti-Sm) very specific,
“Bamboo Spine”
Vertical syndesmophytes Renal Disease but not prognostic
Photosensitivity Antihistone antibodies- drug induced SLE

78 79

GRAIN:
Sarcoidosis Gammaglobulinemia
SLE • African American Females
Rheumatoid arthritis
ACE increased
• Immune-mediated Interstitial fibrosis
• Hypercalcemia (20%) Noncaseating granulomas
Drugs causing drug-induced lupus:
– Elevated conversion of vit D to active form in epitheloid Macrophages
*(Hyperuricemia-50%)
“HIP” – hydralazine, isoniazide, – Nephrocalcinosis (CRF = end stage)
procainamide
• Widespread Noncaseating Granulomas
*Remember: Anti-histone Ab • Elevated serum ACE
• CXR:
– Interstitial Fibrosis & Bilateral Hilar lymphadenopathy
Neonatal SLE: anti-Ro – “potato nodes”
Abs from mother to fetus • Systemic Disease: Bell’s palsy, restrictive lung dz, Heart block, Anemia, etc.

80 81
Polymyalgia Rheumatica Scleroderma “Collagen”
Antinuclear antibody + scl-70
• Pain & Stiffness in Shoulders & Hips • Inflammation causes progressive tissue fibrosis with increased type 1 and 3 collagen
• Skin tightness (face, hands, esophagus)
– Trouble rising from chair or lifting arms overhead • Raynauds (Pain with exposure to cold)
Anticentromere Ab:
specific for CREST
– NO muscular weakness Two Forms:
Anti-Scl-70 Ab
1.Progressive systemic sclerosis – diffuse type
• Usually elderly women •Most common cause of death: Renal Failure (antitopoisomerase 1) in
• Renal Artery Sclerosis (Constriction ↑↑Renin) diffuse dz with poor
• Fever, malaise, weight loss • Management (no treatment for collagen): prognosis
– ACEi (blocks renin), Cough side effect (due to bradykinins)
– Patients > 50
– ARBs: Losartin
– Associated with Temporal (Giant cell) Arteritis 2.CREST syndrome -- limited form
Calcium Deposits, Raynauds, Esophageal dysmotility, Sclerodactyly, Telangiectasias
• Aortic aneurym 2. Treatment:
• ↑ESR with normal CK – Calcium channel blockers,
– ACE-I, ARB
• Treatment: low dose prednisone – D-Penicillamine

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Polymyositis
Sjogren’s Syndrome • Symmetric proximal muscle weakness
–Immune mediated muscle inflammation
(1) Increased CK
• Dry Eyes, Mouth (Exocrine glands), arthritis, usually females 40-60yo • Infiltration of muscle endomysium by macrophages & CD8 lymphocytes
(2) Anti-Jo-1 Abs
• Schirmer’s serology (also in SLE): (3) Muscle bx shows
• Increase Neonatal Heart Block • Muscle Biopsy for diagnosis: Inflammation (CD8) of myofibils
inflammation
– Anti-Ro (SSA) • Pharmacologic management: Steroids
– Anti-La (SSB)

Dermatomyositis
• Similar to polymyositis with additional
• Heliotropic rash
• “Shawl sign” – rash of back shoulders, chest
• Gottron’s papules – scales on dorsal hands
• Associated with malignancy: Lung + Breast CA

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Vasculitides (Type III):
MCTD(Mixed Connective Tissue) Vascular “deposition” of immune complexes

Raynauds, Arthralgia, Myalgia, Fatigue, Esophageal hypomotility 1. Polyarteritis Nodosa


– HBsAg + in 30%
– Involves NS, GI tract, kidney, heart (not lung)
Combination of all connective disorders: – Cyclophosphamide + Steroids

1. Sjogren disease 2. Churge Strauss Syndrome


Hypersensitivities:
Type 1 : anaphylaxis, hay fever
2. Polymyositis - affects lung, spleen, kidney Type 2 : “Cy-2-toxic”
-asthma, eosinophilia, granulomas Type 3 : circulating immune
3. Dermatomyositis - p-ANCA (+) complexes
Type 4 : delayed hypersensitivity
4. RA/SLE/Sleroderma (CREST) (tuberculosis)
3. Wegener Granulomatosis
Antinucleotide Protein Antibodies against - Nose, lungs, sinuses, kidneys
– URI (sinusitis),nasal septum perforation, LRI
ribonucleprotein (+RNP) U1RNP Ab (Hemoptysis, Granuloma), Kidney (Hematuria)
– 3C’s For Wegener:
Management: Steroids • Cyclophosphamide + C-ANCA + Crescentic
glomerulonephritis

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Vasculitides (Type III): Vasculitides (Type III):


Vascular “deposition” of immune complexes Vascular “deposition” of immune complexes

7. Temporal Arteritis (giant cell arteritis)


4. Goodpasture’s Disease - most common vasculitis
• Antiglomular basement membrane antibodies • >60yo F with increasing HA, facial pain
(IgG) • Polymyalgia Rheumatica in 50%
• Flu-like symptoms
• URI 1-2wks prior to kidney dz
• 1st give steroids (Prevent Blindness)
• LRI (Hemoptysis/Granuloma), Kidney
(Hematuria) • Biopsy of Temporal Artery for dx

8. Kawasaki Disease
5. Henoch- Schoenlen Purpura
• Acute Necrotizing vasculitis in Kids
• “Palpable Purpura” (nonblanching in BUTTOCKs
• “Strawberry Tongue”, Fever, erosions of oral mucosa,
and legs),
maculopapular skin rash
• Abdominal pain, diarrhea • Aortic Aneurysm, coronary arteries affected in 70%
• MC childhood systemic vasculitis
• Circulating IgA immune complexes 9. Beurgers (Thromboangitis Obliterans ) Disease
• Male Smoker, fingers can turn gangrenous
6. Takayasu Arteritis (“pulseless dz”) • Intermittent Claudication
• Cold sensitivity (Raynaud’s)
• Young asian ♀ + Hand pain
• Smoking cessation mandatory to decrease progression
• Narrowing of arterial walls with stenosis
• Hand Pulse↓↓ compared to Aorta
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• Treatment: Steroids
Autoantibodies to Know for Exam!
Autoantibody Disorder Disorders of the Neuromuscular Junction
Aninuclear antibodies (ANA) SLE
Anti-ds DNA, anti-smith Specific for SLE
Antihistone Drug-induced lupus
• Myasthenia gravis:
Anti-IgG (rheumatoid factor) Rheumatoid arthritis – Most common NMJ disorder
Anticentromere Scleroderma (CREST) – *Autoantibodies to postsynaptic ACh receptors
Anti-Scl-70, Antitopoisomerase I Scleroderma (diffuse) – Ptosis, diplopia, and proximal muscle weakness
Antimitochondrial Primary biliary cirrhosis – Associated with thymoma
Antigliadin Celiac disease
– *Symptoms worse with muscle use*
Anti-basement membrane Goodpasture’s
– Treatment: anticholinesterases (pyridostigmine), Prednisone
Anti-epithelial cell Pemphigus vulgaris
Antimicrosomal, anti-peroxidase, Hashimoto’s thyroiditis • Lambert-Eaton syndrome: paraneoplastic autoimmune dz
antithyroglobulin
– *Autoantibodies to presynaptic Ca2+ channel
Anti-Jo-1 Polymyositis,
Dermatomyositis – Results in ↓ Ach release leading to proximal muscle weakness
Anti-SS-A (anti-Ro) Sjogren’s syndrome – *Associated with SMALL CELL LUNG CA
Anti-SS-B (anti-La) – *Symptoms improve with muscle use*
Anti-glutamate decarboxylase Type 1 diabetes • Secondary to repetitive nerve stimulation (incremental response)
c-ANCA Wegener’s granulomatosis – Treatment: treat the CA +/- medications
p-ANCA Vasculitides (Churg-Strauss) 90 91

Miscellaneous Info
Guillan-Barre Syndrome (GBS): Viral Vaccines: Live vs. Killed
– Acute demyelinating autoimmune dz of peripheral nerves

– T-lymphoctye & Mφ infiltration of peripheral nerve tissue


• Live attenuated
– Induces both humoral + cell mediated immunity
– Ascending muscle weakness
• **Begins is distal lower extremities**
– MMR V. TROY (VZV, Tetanus, OPV(Sabin),
• CSF Analysis: increased protein w/ normal cell count Yellow fever
– Assoc. w/ Campylobacter jejuni infection (also HSV, Mycoplasma)
• Killed (RIP)
– Only induces Humoral (B cell) “STABLE”
Treatment: respiratory support, Plasmapharesis, IVIG – Increases host Humoral response to make Ig against
HA of virus via receptor mediated endocytosis
• RIP.HAV (Rabies, Influenza, Polio (salK)
92 93
Capsular Polysaccharide Attached
Vaccines to Exotoxin (Toxoid) for Vaccine:
• Tetanus Vaccine – Toxoid (Inactive Form)
• Hib (H. Influenza type b) vaccine
• Acellular Pertussis Vaccine –Bordetella Pertussus (Detoxified – Contains bacterial capsular polysaccharide conjugated with diptheria toxoid
Toxoid) – Encapsulated Bacteria (polycapsule component can be covalently) bound to protein carriers
– Used as vaccine antigens
• HBV vaccine – Purified Inactivated HBsAg (DNA recombination) – Carrier protien converts polysacharide
– T cell independent to T cell dependent antigens
• VZV vaccine –Live Attenuated varicella virions • Approved carrier proteins:
• BCG –Live Attenuated vaccine (M. Bovis) – Diptheria Toxin,
– Tetanus toxoid
• Polio 2 types: – C. Botulium Toxin
– Sain/Salk – N.M (outer membrane )

– Sabin (OPV)- Live attenuated • Encapsulated (Capsular polysaccharide)-vaccine Antigen Activates CMI (TH1 CD4 to
recognize organism & activate IL2)
– SalK (IPV) –Killed inactivated virions – Strep Pneumonia
– Only IPV is approved in the US – Salmonella
– Klebsiella
– H. Influenza
– Pseudomonas
94 – Neisseria Meningitis
– Citrobacter, Cryptococcus 95

Endotoxin
Bacterial Defense
• Polysaccharide capsule expressed by some bacterial organism
–(SSKHPNC= Strep Pneumonia , Salmonella, H. Influenzae, Proteus, Neisseria, Cryptococus neoformus)
–Act to inhibit phagocytosis of these organisms by macrophages & neutrophils
–Recognition of encapsulated leads to opsonization by antibody & complement leads lysis of cell

• B- lactamase conveys resistance to PCN


- B- lactamase inhibitors *(Clauvinic Acid, Tazobactam, Sulbactam)

• Coagulase – Molecule on surface of Staph aureus


–Reacts with Prothrombin: converts Fibrinogen Fibin
–Fibrin –coats the organism
• Resistance to phagocytosis
• Lecithinase (Clostridium perfringens)
–Alpha toxin or phospholipase C
–Destroys erthrocytes, platelets, leukocytes & endothelial cells
–Rapid tissue necrosis in clostridial myonecrosis (GAS GANGRENE)

96 97
• Salmonella Enterobacteriacea
Encapsulated Bacteria • Shigella
• Klebsella
• Polysaccharide Capsule • Enterobacter
– Antiphagocytic Virulence factor
• Quelling • Serratia
• Strep pneumo – Capsule swells with anticapsular antisera (Abx
• Salmonella exposure) • Proteus
• Klebsiella • N.MG
• H. influinzae • Capsule serves as Antigen in Vaccine
• Proteus – Pneumovax, HiB, meningococcal vaccines • Citrobacter
• Neisseria
• Cryptococcus
• C3 deficiency • COFFE
– Recurrent pyogenic infections
• C5-9 deficiency
– Capsule
– Neisseria infections – O antigen
• (Endotoxin polysacharide= Lipid A released during bacteria lysis - Abx treatment)
Asplenic patients have increased – Flagella
risk of infection by encapsulated – Ferment glucose
organisms – Enterobacteriaeae

98 99

Transplant “HAC.G”
Transplant Rejection : MHC • Hyperacute rejection “NOW/ on Table”
– Preformed recipient antibodies against the host: Type II-
– ABO antibodies & anti-HLA
– Immediate perfusion of transplanted organ by recipient blood
• Immediate molting of the organ
β₁
– Spasm & occlusion of graft vessels occur
• Ischemia and necrosis
– (Host/ Recipient) Antibodies against ABO antigen (Donor)
• Acute “ICU: 1-4weeks”
– Cytotoxic T reacts against foreign MHC
APCs: “B. M. D” – Dense infiltrate of mononuclear cells
• B cell – Reversible with cyclosporin, OKT3
• Macrophage
• Dendritic cell • Chronic “At home”: > 4wks
MHC II = HLA- DR, HLA-DP, HLA-DQ – Antibody Mediated Vascular damage
MHC I = HLA- A, HLA-B, HLA-C
– Fibrosis of graft stroma & blood vessels
1. α, β polypeptides [Transmembrane] 1. Heavy chain & β2 Microglobulin – Irreversible
2. Antigen Presetation to CD4+ 2. Presents antigen to CD8 cytotoxic • GVHD “Any time”:
3. T Helper [Th1, Th2] Activation • Loading of RER (viral antigens)
• Donor CD4 & CD8 destroy host (TNFα)
• Stimulates Humoral 3. Apoptosis of Presented Cell
• Cell mediated responses • Severe organ failure
• Skin, liver, kidney, gut:
4. Graft rejection
100 • Diffuse macular eruption (palms, back, neck) 101
• Severe with whole body generalization & bulla formation
Transplant “HAC.G” Transplant “HAC.G”
• GVHD
• Acute heart rejection 2 out of 5 pts – After allogeneic bone marrow transplantation of organs rich in lymphocytes (liver),
– CMI: – Transfusion of non irradiated blood
– Anti-donor host antibodies & cases of humoral rejection are diagnosed by direct – Host is generally severely immunodeficient due to primary dz or immunosupressant
immunoflourescence medicaiton
– Time frame “1 to 4 weeks” following transplant – Immunocompetent T cells within DONOR tissue recognizes host MHC antigens as
– Dense infiltrate of mononuclear cells usually composed primarily of T lymphocytes foreign & attacks them
– Acute cellular rejection of transplanted organ is mediated by host T lymphocyte – Donor CD4 & CD8 destroy host
sensitized against foreign MHC antigens – Most severely targeted: skin, liver, GI but can be any tissue
– Acute rejection is usually diagnosed before symptoms set in because of close – Liver damage: Jaundice, increased ALT , AST, ALP (alkaline phosphatase) & billirubin
surveillance of these patient
– GIT: diarrhea, intestinal bleeding, abdominal cramping
– Symptoms consistent with progressive rejection include those found in heart failure
(systolic dysfunction) such as dyspnea on exertion or PND – Skin(severe) Desquamation GVHD
– GVHD competent donor T cells are transplanted into patients who does not possess a
• Acute & Chronic: Host T cells sensitized against MHC antigen functional immune system
– Acute rejection manifest as vascuilitis of graft vessels – SCID receiving whole blood transfusion containing T lymphocyte

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