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2009-07-02T20:06:00.006+06:00

Supracondylar Fractures of the Humerus in Children

2009-06-25T21:47:00.007+06:00

Anatomy:

The distal humerus resembles a triangle, with the medial and lateral columns making up the sides and the trochlea forming the base (270° arc). The lower end of the humerus is expanded from side to side, and has articular and non-articular parts. The articular part includes the Capitulum which articulates with the head of the radius and the Trochlea which articulates with the trochlear notch of the ulna. The non-articular part includes: the medial epicondyle (related to the ulnar nerve), the lateral epicondyle, the medial and lateral supracondylar ridges, the coronoid fossa, the radial fossa, and the olecranon fossa.

Supracondylar fractures of the humerus are common in young age. They are produced by a fall on the outstretched hand. The distal fragment is mostly displaced backwards, so that the elbow is unduly prominent, as in dislocation of the elbow joint. However, in a fracture, the three bony points of the elbow form the usual equilateral triangle.

Ossification:
The humerus ossifies from one primary center and 7 secondary centers. The primary center appears in the middle of the diaphysis during the 8th week of development.
The upper end ossifies from 3 secondary centers: one for the head, one for the greater tubercle, and one for the lesser tubercle. These 3 centers fuse together during the sixth year to form one epiphysis, which fuses with the shaft during the 20th year. The upper end is the growing end of the humerus.

The lower end ossifies from 4 centers which form 2 epiphysii. The centers include: one for the capitulum and the lateral flange of the trochlea (first year), one for the medial flange of the trochlea (9th year), and one for the lateral epicondyle (12th year). All three fuse during the 14th year to form one epiphysis, which fuses with the shaft at about 16 years. The center for the medial epicondyle appears during 4-6 years, forms a separate epiphysis, and fuses with the shaft during the 20th year.

Supracondylar Humeral Fractures:

Much of the difficulty encountered in treating distal humerus fractures lies in the complex anatomy of the elbow joint. The highly constrained nature of the elbow joint causes it to absorb energy following direct trauma. Consequently, articular comminution may occur.
The following observations were made in a study by Wilkins studying 4,520 fractures:
1) 97.7% of the fractures were of the extension type, and only 2.2% were of the flexion type; 2) most occurred in males and especially in between the ages of 5 and 8 years; 3) Volkmann’s ischemic contracture occurred in 0.5% of the fractures; and 4) the radial, median, and ulnar nerves were involved in that order of frequency.

Dameron has listed, depending on the type of fracture, four basic types of treatment: 1) side arm skin traction; 2) overhead skeletal traction; 3) closed reduction and casting, with or without percutaneous pinning; and 4) open reduction and internal fixation.

Classification:
Most distal humerus fractures can be classified into 2 etiologic groups: those resulting from a high-energy mechanism, such as a motor vehicle accident, and those resulting from a low-energy injury, such as a fall while walking.

Gartland has proposed a further classification for supracondylar fractures: Type I, undisplaced; Type II, displaced with intact posterior cortex; and Type III, displaced with no cortical contact; his classification also notes whether the fracture is displaced posteromedially or posterolaterally.

The type I undisplaced fracture can be satisfactorily treated closed with external fixation, such as a plaster cast. The type II fracture is displaced and is difficult to reduce and to hold reduced by external methods. The type III fracture is displaced posteromedially or posterolaterally with no cortical contact and the periosteum may be stripped; reduction is difficult, and maintaining reduction is almost impossible without some form of internal fixation. The fracture should be reduced in extension and reduction should be maintained through the use of the triceps bridge by holding the elbow in flexion if the pulse and vasculature tolerate it.

Angular Deformities associated with Supracondylar Humeral Fractures:

Previously cubitus varus or cubitus valgus were thought to occur because of growth arrest of the distal humeral epiphysis, rather than because of malreduction of the fracture.

Cubitus varus is the most common angular deformity that results from supracondylar fractures in children. Cubitus valgus, although causing tardy ulnar nerve palsy, is rarely seen and occurs more often from nonunion of lateral condylar fractures.

Cubitus varus and cubitus valgus should be prevented by obtaining proper anatomic reduction. Of the two, cubitus varus produces a distasteful cosmetic deformity, yet only rarely any limitation of motion. A big problem noted in the prevention of these abnormalities is obtaining satisfactory roentgenograms to determine whether any cubitus varus or valgus is present.

The three most common reasons for residual cubitus varus or valgus deformity are:
1) the inability to interpret poor roentgenograms and therefore, acceptance of a less than adequate reduction; 2) the inability to interpret good roentgenograms because of a lack of knowledge of the pathophysiology of the fracture; 3) loss of reduction.
Whether external mobilization or pin fixation is used, the forearm should be placed in the pronated position to decrease the lateral tilt and resultant cubitus varus.

Imaging Studies:

The bone quality, fracture pattern, level of comminution, articular involvement, displacement, and associated injuries, must be understood completely before treatment is attempted. Multiplane radiographs, including anteroposterior (AP) and lateral views, are appropriate.

AP radiographs should be obtained with the elbow flexed approximately 40° and with the radiographic beam directed perpendicular to the distal humeral surface. This allows disengagement of the olecranon from its fossa and permits a better view of the distal humerus.

In the pediatric population, the Baumann angle (the angle between the lateral condylar physeal line and the axis of the humerus) is often measured using AP radiographs. It must be compared to the contralateral side.

A computed tomography (CT) scan can be obtained of the distal humerus to further analyze the fracture pattern. Duplex Doppler ultrasonography or angiography can be performed to check vascular status.

Closed Reduction and Percutaneous Pinning:

Closed reduction is difficult not only to achieve, but also to maintain because of the thinness of bone of the distal humerus between the coronoid and olecranon, where most supracondylar fractures occur.

Fowles and Kassab noted that ulnar nerve lesions are common in displaced flexion fractures. The reduction is more difficult, the results are worse than in extension fractures, and these anteriorly displaced fractures should be considered for accurate reduction and percutaneous pinning.

Percutaneous fixation after closed reduction has the advantage of providing excellent stability of the supracondylar fracture in any position of the elbow. However, the ultimate result will be only as good as the initial reduction, and does not depend on the placement of the pins. If the fracture is not satisfactorily reduced and is held in an unsatisfactory position with pins, the outcome will be unsatisfactory, just as if no pin fixation were used.

A 5-year-old girl fell onto her outstretched hand and sustained a Gartland Type II supracondylar humerus fracture with medial impaction. (A) Lateral preoperative radiograph. (B) Anterior/posterior (A/P) preoperative radiograph. (C) Lateral radiograph after closed reduction and percutaneous pin fixation (cross-wire technique). (D) A/P postoperative radiograph. (E) Lateral radiograph taken four weeks postoperatively. (F) A/P follow-up (4 wks) radiograph. There is good evidence of healing.

Technique:
Place the patient prone or supine on a fracture table. Prepare and drape the elbow. Outline the posterior triangle of the elbow joint (the medial and lateral epicondyles and the olecranon). Reduce the fracture by applying longitudinal traction, extending the fracture, and manipulating with the thumbs to correct lateral tilt, medial impactation, or posterior displacement. Flex the elbow to neutral. Crisscross two smooth Steinmann pins through the condyles and metaphysic, one to exit above the medial epicondyle and one to exit above the lateral epicondyle. Be careful to avoid the ulnar nerve. Following engagement of the shaft, use an image intensifier to make sure the pin engages the opposite cortex proximally. Cut the pins off beneath the skin and bend their ends so they will not migrate proximally but can be easily retrieved in the office. Check and note radial pulse.

Aftertreatment:
A long arm posterior plaster splint is worn for 3 weeks. Ulnar, radial, and median nerve function should be checked after anesthesia. The pins are removed at 3 weeks and another posterior splint is applied. At 4 weeks, intermittent active range of motion exercises are started at home after being taught by a physical therapist to the child and parent. Passive motion or forceful manipulative motion must be avoided in children because they will decrease the range of motion and may frighten the child.

Open Reduction and Internal Fixation:

Open reduction and internal fixation of supracondylar fractures are indicated when closed reduction is unsatisfactory. In a type III displaced fracture with no cortical contact and completely detached periosteum, and with the fracture fragment penetrating the skin (compound fracture), a satisfactory closed reduction may not be possible, if, after one or two attempts at closed reduction with the child under general anesthesia, the fragments cannot be reduced and held by percutaneous pinning, open reduction and internal fixation are indicated. Also if the elbow is so severely swollen that a closed reduction cannot be maintained, then olecranon traction may be used for several days, followed by closed or open reduction as necessary. Other indications for O.R.I.F. include open (compound) fractures that require irrigation and debridement and those fractures complicated by vascular injury, mysositis ossificans excessive callus formation with residual stiffness, and decreased range of motion.

If open reduction and internal fixation are to be carried out, they should be performed after the swelling has decreased, but no later than 5 days after that time because the possibility of mysositis ossificans increases after that time.

Gruber and Hudson treated 31 difficult fractures with open reduction and internal fixation and observed satisfactory results even in the most severe ones.

Technique:
Prepare and drape the arm in the usual fashion with the patient supine. Make a curved incision over the lateral humeral epicondyle. Dissect the soft tissue, including the anconeus and common extensor origins, and retract these anteriorly and posteriorly respectively. Make sure the radial nerve is retracted posteriorly to avoid injury. Observe the supracondylar fragment, and note its alignment with the proximal fragment. Use a small curet to remove any hematoma at the fracture site. Note any interdigitations on the ends of the bone and by matching them, reduce the fracture. Use two crossed Steinmann pins in a manner similar to that described for percutaneous pinning. Cut the pins percutaneously for easy removal later. Close the incision in layers.

Aftertreatment:
A posterior plaster splint is applied and the radial pulse and neurological function are checked following anesthesia. The pins are removed at 3 to 4 weeks and an active, not passive, range of motion program is started.

Complications:

Supracondylar fracture of humerus being the most common fracture in children needs proper treatment to prevent complications like compartment syndrome, neurovascular compromise (Volkmann’s ischemic contracture), elbow stiffness (mysositis ossificans) and angulations.

Injuries to nerves or blood vessels are much more serious than the fracture itself. The early recognition of such complications is imperative. Early and adequate treatment of acute vascular complications is necessary, even though it means surgical exploration of the antecubital fossa and resection of the injured segment of the brachial artery. Adequate and early treatment of acute vascular injuries usually ensures a good prognosis, but delay may lead to serious and permanent disability.

Gartland type I supracondylar fracture can be early treated with casting alone but displaced (Gartland type II, III) can be treated with casting, ORIF or percutaneous Pinning (PCP). Close reduction and casting is an old treatment modality that is still practiced in developing countries due to limited facilities. Close reduction and casting has its own advantages and disadvantages. Its advantages are no need of metal insertion, least costly, safe, time effective, bearing less morbidity. Disadvantages are loss of reduction, compartment syndrome and cubitus varus.

References:

Campbell’s Operative Orthopedics, 4 volume set
Human Anatomy: Regional and Applied. B.D. Chaurasia
www.emedicine.com
www.wikipedia.com

The Diabetic Patient: A Clinical Approach

2009-06-07T19:15:00.000+06:00

Diabetes Mellitus is a metabolic disorder affecting millions of people across the globe. We as doctors and medical students should know these patients from A-Z. The following is a quick review of points to remember when approached by someone with diabetes in your clinic.

History: Take a normal history as with any other patient, but keep these points in mind...

Hypoglycemia- tremors, fatigue, palpitations, sesting, coma
Neuropathy- calf muscle pain, burning muscles, "losing shoes"
Nephropathy- decreased urine output, frothy urine, periorbital swelling, recurrent UTI
Cardiovascular- pain, dyspnea, loss of breath
Retinopathy- blurry vision, halos, spots
Autonomic- orthostatic hypotension, GIT disturbances, recurrent infections
Dermopathy- poor wound healing

Investigations: (for the known diabetic)

Fasting blood sugar- <110>125 is established diabetes
Lipid profile- ALT and SGPT every 6 months
Urine DR in special regards for microalbuminuria (<200>200 is irreversible).
Creatinine clearance
Serum creatinine and Urea
ECG
Fundoscopy

Examinations: Perform foot, abdominal, CVS, respiratory, 3rd 4th 6th 7th cranial nerves, and check of dehydration.

Particularly in Foot examination:
Inspection- look for discoloration, ulcers, callus', skin changes, loss of shin hair, cuts, and bruises. Pay special attention to the intertarsal spaces.
Palpation- pedal edema, vibration (this is usually the first sense to be compromised in 'diabetic foot'- diabetic neuropathy), proprioception, temperature, touch, reflexes, pulses.

Diet: The following diet pertains particularly to those patients from the Indian subcontinent. Please refer to a diabetic book for patients of other ancestry.

Contraindications- bakery sweets, white bread, white a'ata (use chokaar instead), rust, cold drinks (sodas), sharbaats, gosht, biryani, mattar plow, biscuits, jam, jelly, honey, red meat.

Foods that help- chaana with chai, boiled eggs, akhroat, dhalia, omega 6 fatty acids (fish and walnut).

Keep in mind- eating 1/2 cup rice is okay but only once a day, oil should be decreased in all foods, dhai with no sugar or malai, only 1 fruit is allowed per day.

Management:
Management of diabetes varies from patient to patient. Please refer to medicine books for details.

Diabetic Emergencies:

Diarrhea and vomiting can cause uremia leading to hiccups.
Acute renal failure
Diabetic ketoacidosis- Patient is usually young with Type I DM.
Hyperosmotic nonketotic diabetic coma causes high bloog glucose levels and dehydration

Plasma osmolarity can be calculated by the following equation: (normal is 275-290 mmol)
Plasma osmolarity = (sodium x 2) + (BUN / 2.8) + (blood glucose / 18)

Managed initially by I/V insulin and isotonic saline. Followed by dextrose with insulin to allow for intracellular free water absorption.
Check blood pressure for orthostatic hypotension.

Further investigations: CBC, blood culture, urine culture, head to toe examination for signs of infection.

Note: The following was just a quick review of what to expect when dealing with a patient with known diabetes mellitus. Please refer to a textbook for further details.

Pathology- Female reproductive MCQ's

2009-06-01T23:10:00.004+06:00

1) Which one of the following endometrial lesions is associated with the highest risk of developing endometrial carcinoma?

A. Chronic endometritis
B. Complex hyperplasia with atypia
C. Complex hyperplasia without atypia
D. Simple hyperplasia
E. Squamous metaplasia

The correct answer is B. In general, any condition characterized by excessive estrogenic stimulation is associated with some degree of endometrial hyperplasia and increased risk of endometrial cancer. Endometrial hyperplasia is a histologic precursor of endometrial adenocarcinoma.The most severe changes are present in complex hyperplasia with atypia. Disorganization and crowding of glands, high mitotic activity, and nuclear atypia characterize this change. 25% of women with this form of hyperplasia develop adenocarcinoma.

2) a 36 year old gravid female notes vaginal bleeding. Ultrasound reveals small grape-like cystic structures witout evidence of a developing embryo. A diagnosis of complete hydatidiform mole is made at the hospital. Further analysis is most likely to reveal that:

A. hCG levels are markedly increased
B. serum levels of alpha fetoprotein are elevated
C. the genotype of the mole is 46,XX and is completely paternal is origin
D. the genotype of the mole is triploid
E. two or more sperm fertilized the ovum

The most correct answer is C. A complete hydatidiform mole is characterized by elevated hCG and grape like cystic structures filling the uterus with no detectable embryo on ultrasound. The genotype of a complete hydatidiform mole is purely paternal, caused by fertilization of an egg that has lost its chromosomes. Hydatidiform mole is associated with increasing maternal age, and may be a precursor to choriocarcinoma.

hCG levels are increased relative to normal values for dates, rathar than decreased, in a molar pregnancy (choice A).

Alpha fetoprotein (choice B) is a marker for endodermal yolk sac tumors, embryonal tumors in men, and hepatocellular carcinoma. It is made by the fetus, hence not detectable in a complete hydatidiform mole.

Triploidy and even tetraploidy are characteristics of partial moles (choice D). Partial moles are thought to be due to fertilization of an egg with two different sperm, one with an X and one with a Y chromosome, typically leading to triploidy.

Two or more sperm may fertilize an ovum, leading to a triploid fetus and a partial mole (choice E).

3) A 37 year old woman complains to her gynecologist of discomfort during intercourse and placement of a tampon. Physical examination demonstrates flocculent swelling below the skin of the posterolateral part of one labium majora. Which of the following is the most likely diagnosis?

A. Bartholin's gland cyst
B. Condylomata acuminatum
C. Lichen sclerosis
D. Vestibular adenitis
E. Vulvar squamous hyperplasia

The correct answer is A. This is a Bartholin's gland cyst, which is a relatively common lesion occurring when Bartholin's duct becomes obstructed, typically a sequela to a previous infection. The cysts can enlarge to 3 to 5 cm in diameter.They are lined by either transitional or metaplastic squamous epithelium. Treatment is by excision or marsupialization (permanent opening).

Condylomata acuminatum (choice B) usually produces a papillary lesion (venreal wart).

Lichen sclerosis (choice C) usually produces gray, parchment-like thinned epidermis.

Vestibular adenitis (choice D) usually produces an exquisitely tender posterior introitus with focal ulcerations.

Vulvar squamous hyperplasia (choice E) usually produces a white plaque.

4) A 39 year old woman has cyclical premenstrual pain. Her breasts have a "lumpy bumpy" texture on palpation. A biopsy is performed. The histopathologic features include small cysts lined by epithelial cells with apocrine metaplasia, calcium deposits, areas of fibrosis, increased number of acini (adenosis), and foci of florid hyperplasia of ductal epithelium. Which of these changes increase the risk of breast cancer?

A. Adenosis
B. Apocrine metaplasia
C. Calcium deposits
D. Cysts
E. Epithelial hyperplasia

The correct answer is E. Fibrocystic changes usually come to clinical attention by causing pain (often cyclical, in premenstrual phase), palpable lumps, or mammographic densities and calcifications. A "lumpy-bumpy" texture is caused by cysts and fibrosis. Epithelial hyperplasia is defined as an increase in the number of epithelial cell layers in the ductal epithelium. Florid epithelial hyperplasia leads to an increased risk of developing carcinoma, especially is these is associated cellular atypia (atypical ductal hyperplasia).

Adenosis (choice A) refers to an increase in the number of acini and can be observed in fibrocystic changes as well as in other breast conditions, such as sclerosing adenosis.

Apocrine metaplasia (choice B) describes a benign change of breast epithelial cells that come to resemble the apocrine epithelium of sweat glands.

Calcium deposition (choice C) is a nonspecific finding that mar occur in a number of both benign and malignant breast change, including fibrocystic changes, ductal carcinoma in situ, and invasive carcinoma. Calcification is not clinically significant except for its diagnostic value.

Cysts (choice D) are frequent in fibrocystic changes and result from dilatation of ducts. A classic gross description is that of blue-dome cysts, which appear brown to blue because of their turbid fluid content.

5) An 83 year old female has a biopsy of an ulcerated nipple lesion that is interpreted as Paget's disease. A biopsy of the underlying breast tissue will most likely show which of the following?

A. Acute mastitis
B. Ductal carcinoma in situ
C. Intraductal papilloma
D. Invasive lobular carcinoma
E. Normal breast tissue

The correct answer is B. Paget's disease of the breast is a form of ductal carcinoma in which neoplastic cells involve the squamous epithelium of the skin by direct extension through the lactiferous ducts.

Acute mastitis (choice A) is a disease of nursing women in which bacteria (S. aureus) gain entry to the breast tissue via cracks in the traumatized nipple. It is characterized by acute inflammation and tissue necrosis.

Intraductal papilloma (choice C), a papillary mass arising within the ducts, usually presents as a single subareolar tumor that may produce a bloody or serous nipple discharge.

Invasive lobular carcinoma (choice D) is a tumor of the terminal ductules of the breast. It presents as a poorly circumscribed, rubbery breast mass. Lobular carcinoma does not produce Paget's disease.

Paget's disease of the breast always reflects underlying ductal cancer. This is in marked distinction from extramammary Paget's disease, which may arise without an identifiable malignancy (choice E).

GLAUCOMA

2009-04-13T07:06:00.003+05:00

Glaucoma: group of diseases in which increased IOP (intraocular pressure) in an eye produces optic disc cupping and visual field defects.

Normal IOP: 10-21 mm Hg
- Usually slightly high in the morning and slightly deceased at night.

PRODUCTION OF AQUEOUS HUMOR:
(a) Active Secretion: 80% ultrafiltration & 20% diffusion
(b) Drainage: 90% through the Trabecular pathway & 10% through the Uveo-scleral pathway
(c) Level o episcleral venous pressure

CLASSIFICATION:
A. Developmental aka. Congenital: Children present with BUPTHALMOS (increased corneal diameter)
- Primary
- Rubella
- Secondary to other ocular causes such as aniridia
B. Acquired
1. Open angle
- Primary – chronic open angle
- Secondary
2. Closed angle
- Primary – Acute and Chronic closed angle
- Secondary – Due to trauma, raised episcleral venous pressure, steroid induced, associatd with other ocular disease such as uveitis

TONOMETRY (measurement of tension or pressure, particularly IOP)
1. Goldmann tonometer
2. Schiotz tonometer
3. Perkin’s tonometer
4. Air Puff tonometer
5. Tono pen

EYE EXAM:
1. Check IOP
2. Look for optic disc cupping
3. Test field of vision

GONIOSCOPY (examination of anterior chamber of the eye to demonstrate ocular motility and rotation)
- Done to identify structures in the irideo-corneal angle.
- Use a triple-mirror GONIOLENS to visualize the angle and the periphery of the retina
- Opening of the angle is graded (Grades 0-4)
Grade 0: Closed angle
Grade 1:Narrow angle
Grade 2: Moderately narrow angle
Grade 3: Open angle
Grade 4: Widest angle

OPTIC NERVE HEAD CHANGES SEEN IN GLAUCOMA:
1. Retinal nerve fiber changes
2. Concentric expansion of optic disc cup
3. Localized expansion of optic disc cup (notching at inferior or superior pole)
4. Narrowing of neuro-retinal rim
5. Pallor
6. Splinter hemorrhages on disc margin
7. Deepening of optic cup
8. Nasalization of vessels
Note: Papillomacular area is spared and tunnel vision is preserved!!

PERIMETRY:
Visual field: an island of vision surrounded by a sea of darkness.
Normal visual field:
- Superiorly 50 degrees
- Inferiorly 70 degrees
- Nasally 60 degrees
- Temporally 90 degrees

VISUAL FIELD DEFECTS SEEN IN GLAUCOMA:
1. Arcuate Scotomas
2. Isolated paracentral scotoma
3. Nasal step
4. Temporal wedge
5. Ring scotoma

PRIMARY OPEN ANGLE GLAUCOMA:
1. Adult onseT
2. IOP > 21mm Hg at some point in the course of the disease
3. An open angle of normal appearance
4. Glaucomatous optic nerve damage
5. Visual field defect

RISK FACTORS for the development of glaucoma:
1. Age > 40 years
2. Race (higher incidence in Black people)
3. Family history
4. Diabetes
5. Hypertension
6. Myopia
7. Prolonged use corticosteriods (oral or topical)

SYMPTOMS: Usually symptomless & diagnosed on routine eye examination!!
- Patient with Acute closed angle Glaucoma may present with : photophobia, and painful eye, loss of vision, watering of the eye

SIGNS:
1. Increased IOP
2. Fluctuating IOP
3. Optic disc changes
4. Glaucomatous field change

TREATMENT:
1. Medical :
- Alpha-2 agonists eg. Apraclonidine
- Beta Blockers eg. Timolol, Carteolol
- Carbonic anhydrase inhibitors eg. Brinzolamide, Dorzolamide
- Prostaglandins eg. Latanoprost, Travaprost
- Sympathomimetic and Parasympahtomimetic agents eg. Adrenaline, Pilocarpine

2. Laser cyclophotocoagulation

3. Surgery (has a lot of complications and is therefore the last resort of treatment!)
- Argon Laser trabeculoplasty
- Trabeculectomy (a fistula is created between the angle of the anterior chamber and sub Tenon’s space to allow drainage of the fluid)
- Cryotherapy of ciliary body

Management of TRABECUECTOMY FAILURE:
1. Adjunctive Antimetabolites- such as 5-FU and Mitomycin
2. Artificial drainage shunts
3. Cyclodestructive procedure using Lasers OR Cryotherapy

LOW-TENSION GLAUCOMA:
- Also known as Normotensive Glaucoma
- The intraocular pressure is normal but optic disc cupping and field defects are present

OCULAR HYPERTENSION: IOP > 21 mm Hg but there’s no cupping and visual field defects

Cataract

2009-04-12T19:24:00.004+05:00

Any congenital or acquired opacity in the lens capsule or substance, irrespective of the effect on vision, is a cataract. Cataract is the commonest cause of treatable blindness in the world.

Lens: The lens is biconvex and transparent. It is held in place behind the iris by the suspensory ligament whose zonular fibers are composed of protein fibrillin which attach its equator to the ciliary body. Disease may affect structure, shape and position.

Normal lens: 4-5mm thick and approx. 10 mm in diameter.
Outer: cortex.
Inner: Nucleus

Classification:
I. According to Age
- Congenital
- Infantile
- Juvenile
- Pre-senile
- Senile

II. According to Morphology
- Capsular
- Sub-capsular
- Cortical
- Nuclear

III. According to Etiology
- Age related: example senile cataract
- Traumatic cataract
- Metabolic cataract: due to diabetes mellitus, hypoparathyroidism
- Toxic cataract: due to use of steroids, and other medications
- Complicated cataract: secondary to some other eye disease such as chronic anterior uveitis, acute angle closure glaucoma, pathological myopia

IV. According to Maturity
- Immature cataract
- Mature cataract
- Hypermature cataract: Proteins are liquefied and the permeability of the capsule is increased. This results in leakage of proteins and deposition of calcium.

Example: MORGAGNIAN CATARACT (Cortex liquefies and the nucleus sinks down)

Intumescent cataract: Lens is swollen due to water retention. Maybe immature, mature or hypermature.

Symptoms:
1. Blurred vision (most important symptom)
2. Glare
3. Monocular diplopia
4. Haloes around light
5. Improvement in near vision

Signs:
Depend on the state of maturity of the cataract
1. Decreased visual acuity
2. Change in the colour of the pupil
3. Iris shadow
4. Abnormal red reflex

Management:
(There is no medical treatment for cataract!)
1. Surgery (Goal of cataract surgery: to leave the patient emmetropic)
2. Glasses

Indications for Cataract Surgery:
1. Visual improvement
2. Medical indication eg. The patient develops glaucoma or diabetic retinopathy,r etinal detachment
3. Cosmetic indication

Pre-operative Assessment:
1. Complete ocular exam
2. Macular function test
3. Optic nerve function test
4. Biometry
5. Investigations:
- CP & ESR (complete blood picture and erythrocyte sedimentation rate)
- FBS (fasting blood sugar)
- UDR (urine detailed report)
- Hep B and C virology

Anaesthesia:
1. Facial Block
2. Retrobulbar block

Surgical Techniques:
1. ECCE (Extra Capsular Cataract Extraction)
2. ICCE (Intra Capsular Cataract Extraction)- not used anymore
3. Phacoemulsification – the newest method

Disadvantages of ICCE (Intra Capsular Cataract Extraction):
1. Large incision
2. Posterior capsule is removed and so the vitreous gel may come out
3. Posterior capsule is removed and therefore, there is no support for the IOL (intraocular lens)

Advantages of Phacoemulsiication:
1. Small tunnel incision
2. Quick recovery
3. Early visual rehabilitation
4. Useful for the removal of soft cataract (nucleus is soft)

Complications of Cataract Surgery:
1. Operative complications
- Rupture of posterior capsule
- Vitreous loss
2. Post-op complications
- Iris prolapse
- Corneal edema
- Uveitis
- Endopthalmitis
- Post-op Astigmatism
- Cystoid macular edema
- Retinal detachment
- Posterior capsule opacification

Congenital Cataract
- Opthalmological emergency!!!!
- Bilateral congenital cataract results in a significant effect on visual acuity and results in nystagmus and amblyopia.
Nystagmus: involuntary rapid movement (horizontal, vertical, rotatory or mixed i.e. of two types) of the eyeball.
Amblyopia: dimness of vision without detectable organic lesion of eye.

Age-Related Macular Degeneration

2009-04-09T14:07:00.000+05:00

It is the leading cause of irreversible blindness in developed countries.
Complex multifactoral progressive disease with genetic and environmental influences.

PATHOGENESIS:
Not well understood but it is believed that oxidative stress is the key component of retinal pigment epithelial (RPE) degeneration. Progressive diffuse thickening of the Bruch's membrane (retinal layer that provides nourishment and oxygen to the RPE and the outer layers of retina, including the rod and cone cells) causes hypoxia----> choroidal neovascularisation---->weak new vessels leak serous fluid/blood---->distort central vision and reduce clarity of central vision.
Alternatively death and atrophy of RPE also occurs.

DRUSEN BODIES: visualized clinically as yellow deposits situated within Bruch's membrane. Vary in size and shape/maybe discrete or confluent. Either collagen-based or granular lipid rich.

ESSENTIALS OF DIAGNOSIS:
Older age group (>55year)
Gradual progressive simultaneous or sudden sequential deterioration of central vision in both eyes affecting reading and recognising faces.
Distortion or abnormal size of images (demonstrated by Amsler chart)
No pain or redness.
Macular abnormalities seen by ophthalmoscope.

Suggested Associated Risk Factors:
famale sex
smoking history
family history
hypertension
hypercholestrolemia
history of exposure to UV light
hypermetropia
cataract surgery

Dry ARMD/ Atrophic Degeneration 85%:
Gradual progressive bilateral visual loss of moderate severity.
Atrophy and degeneration of outer retina and RPE.
Variable and may result in severe visual impairment over a span of 5-10 years.
In advanced stages it is possible to see underlying choroidal vessels.

Treatment: No specific treatment but patients benefit from visual rehabilitation (refraction and low vision assessment). Peripheral fields and hence navigational vision are always maintained.

Wet ARMD/ Exudative Degeneration 15%:
Aggressive form of the disease.
Rapid clinical course and 75% of the patients have marked reduction in vision over 3 years.
Disease characterized by choroidal neovascularisation----> fluid leakage and bleeding in the macular region.

Treatment: is aimed at closing off blood flow through the area of choroidal neovascularisation to allow resolution of exudative changes. It is based on which of the following categories (as seen in Fundus Fuorescien Angiography) the disease falls in:
Classic only- neovascularisation fully delineated
Predominantly classic with little occult- ≥50% classic with some occult
Minimally classic- ≤ 50% but >0% classic
Occult only- full extent of neovascularisation not visible

Laser Photocoagulation: occludes neovascular regions of retina
Done for classic-extrafovealand juxtafoveal conditions but also causes considerable to adjacent retina.

Photodynamic Therapy: light activated agent, verteporfin, is given IV. Laser is then used at a particular wavelength to activate the photosensitizer which causes local vessel occlusion without damage to nearby retina. Needs to be repeated every 12 weeks.
This too is used for the subfoveal type of the classic lesion.

Antiangiogenic Agents:
Inhibitors of vascular endothelial growth factor(eg synthetic steriods) which would reverse neovascularisation.
Have to be administered every 4-6 weeks with risks of intraocular infection, inflammation and retinal detachment.
These can be used for both classic and occult.

Submacular Surgery:
Microsurgical viterectomy + retinal incision and then removal of vessels.
Suitable for selected cases.

Macular Rotation:
Macular region of retina is physically moved to overlie another place where the RPE is healthy followed by strabismus surgery. The procedure is complicated and carried significant risk.

Pathology- GIT MCQ's

2009-04-09T01:45:00.001+05:00

1) A 60 year old man presents to his physician because of progressive dysphagia, first for solids, then for liquids. Endoscopy reveals a large fungating mass 2 cm above the gastroesophageal junction. Biopsy of the mass demonstrates glands, extending into the muscular layer, containing cells with large hyperchromatic nuclei. Which one of the following conditions is most likely associated with the development of this mass?

A. Barrett's esophagus
B. Esophageal rings
C. Esophageal webs
D. Scleroderma
E. Sliding hernia

The correct answer is A. Biopsy is consistant with esophageal adenocarcinoma which usually arises in aread of gastric or intestinal metaplasia (Barrett's esophagus) in the lower or middle one third of the esophagus. The prognosis for adenocarcinoma is poor, unless caught very early.

Esophageal rings (choice B) are rims of fibrovascular tissue found in the lower esophagus.

Esophgeal webs (choice C) are mucosal ledges in the upper esophagus.

Scleroderma (choice D) can cause fibrosis and impaired motility of the esophagus.

In sliding hiatal hernias (choice E), part of the stomach protrudes above the diaphragm.

2) A 30 year old man with a 15-year history of ulcerative colitis develops intermittent cholestatic jaundice. Ultrasonographic examination fails to reveal gallstones. Liver biopsy demonstrates a large bile duct obstruction. Which of the following would most likely be seen on endoscopic retrograde cholangiopancreatography (ERCP)?

A. Beading of transhepatic bile ducts
B. Markedly dialted common bile duct containing irregular radioluscent masses
C. Mass at the ampulla of Vater
D. Moderately dilated intrahepatic bile ducts and stricture in the bile duct at the lower end of the common bile duct

The correct answer is A. The most likely diagnoses is primary sclerosing cholangitis, a disorder with a probable autoimmune component that is associated with ulcerative colitis (66% correlation). The disease is characterized by inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts, producing alternating strictures and dilatation of the structures. These changes are seen as "beading" on ERCP.

Gallstones in the biliary tree produce irregular radiolucent masses (choice B).

Choice C describes the findings associated with carcinoma of the ampulla of Vater.

Choice D describes the findings associated with carcinoma of the extrahepatic bile ducts.

Choice E describes the findings associated with carcinoma of the pancreas.

3) A patient has had years of intermittent diarrhea and abdominal pain, but has never consulted a physician. Eventually he begins to pass fecal material in his urine and he seeks medical attention. Which one of the following diseases is most likely to cause this complication?

A. Celiac disease
B. Crohn's diease
C. Diverticulitis
D. Ulcerative colitis
E. Whipple disease

The correct answer is B. Passing fecal material in urine strongly suggests the possibility of a fistula between the bowel and bladder. Of the diseases listed, only Crohn's disease commpnly produces fistulas. Fistulas are produced in Crohn's disease because the disease affects the entire thickness of the bowel wall, rathar than being restricted to the mucosa (e.g., ulceratice colitis).

Celiac disease (choice A) is a mucosal disorder of the small intestine caused by intolerance to certain components of gluten from wheat and other grains.

Diverticulitis (choice C) can cause bowel perforation with peritonitis but does not usually cause fistula formation.

Ulcerative colitis (choice D) is much less commonly associated with fistula formation than is Crohn's disease.

Whipple's disease (choice E) is a small intestinal disorder caused by infection with Tropheryma whippelii.

4) A 40 year old man complains of increasing difficulty in swallowing in the past 3 years. He reports a feeling of pressure in the chest occurring 2-3 seconds after swallowing a solid bolus. He also experiences regurgitation of undigested food eaten hours previously. A radiograph taken after swallowing barium shows a distended esophageal body with a smooth tapering at the lower esophageal sphincter. Manometry shows the absence of esophageal peristalsis and a lower esophageal sphincter that fails to relax. What is the most likely diagnosis?

A. Diffuse esophageal spasm
B. Incompetent lower esophageal sphincter
C. Oropharyngeal dysphagia
D. Scleroderma
E. Achalasia

The correct answer is E. Achalasia is an acquired esophageal motility disorder that slowly develops. The motility is abnormal due to the loss of inhibitory enteric neurons of the esophageal body and lower esophageal sphincter. Both vasoactive intestinal peptide and nitric oxide function as inhibitory neurotransmitters here, and the presence of both is decreased in achalasia. Radiographs typically show a dilated esohpagus that tapers at the lower esophageal sphincter, producing the so called "bird's beak". Because of the poor motility, ingested food is regurgitated and can lead to aspiration symptoms. Manometric demonstration of absent peristalsis in the esophageal body and poor relaxation of the lower esophageal sphincter with a swallow confirm the diagnosis.

The primary complaint with diffuse esophageal spasm (choice A) is mid-sternal pain that can be misdiagnosed as cardiac pain. The pain is caused by prolonged contraction of the entire esophageal body. Symptoms can be brought on by eating certain hot or cold meals. A manometric study may show poor peristalsis in the smooth muscle portion of the esophageal body, but lower esophageal sphincter function is unaffected.

The primary complaint with incompetant lower esophageal sphincter (choice B) is heart burn and regurgitation due to gastroesophageal reflux. Endoscopic examination of the esophagus may reveal inflammation, erosions, and even ulcers. A manometric study would show lower than normal resting tone in the lower esophageal sphincter.

The fact that the patient's symptoms do not occur until 2-3 seconds after a swallow suggests that oropharyngeal dysphagia (choice C) is not the diagnosis. The presence of cogh, Hoarseness, or nasal regurgitation commonly occurs with this disorder. Oropharyngeal dysphagia is often due to neurological or muscle disorders like stroke, amyotrophic lateral sclerosis, muscular dystrophy, or myasthenia gravis.

Scleroderma (choice D) is a connective tissue disease in which esophageal smooth muscle is gradually replaced by dense collagenous material. Manometry woud show poor esophageal peristalsis and decreased lower esophageal sphincter tone. Significant acid reflux with resultant esophagitis is almost universal.

More questions to come soon...

Diabetic Retinopathy

2009-04-06T20:39:00.003+05:00

Diabetic Retinopathy is one of the commonest cause of blindness in the world. Diabetics are at 25% more risk to be blind than normal people. Also, almost half of the diabetics at some stage develop eye disease. Hence, diabetes is a major predisposing factors to ophthalmic pathology.

Ocular diseases that are associated with Diabetes include:

a- Diabetic Retinopathy
b- Cataract
c- Glaucoma
d- Infections

(Delayed healing is also a result of diabetes)

Pathogenesis:

The major factor in the pathogenesis of Retinopathy in diabetics is a microangiopathy of vessels supplying the retina )or a part of it(.

The main vascular damage can be divided into two parts: a) Leakage; b) occlusion

a) Endothelial cells rely exclusively on glucose for nutrition and insulin helps in the transport of glucose into them. Thus, when there is absence of insulin or a resistance to it, the cells start becoming undernourished. And overtime they suffer injury (and most likely cell death). The dead cells result in a leaky and weakened vessel wall. The leaky vessel wall leads to edema of the retina, followed by hemorrhage and finally WBC infiltration - thus resulting in damage to the retina.

b) As the vessel continues to weaken, microaneurysms form in the vasculature which over time can get occluded and thus lead to infarction of the retina supplied distally to the occlusion.
As the retina is denourished due to thrombosis of the vessel supplying it, there is release of Vascular Angiogenesis Factor (VAF). Under the influence of VAF, new blood vessels are formed to keep the retina nourished but that is to no avail as the new vessels leaky and weak and thus more hemorrhage and edema occurs, resulting in further loss of vision.

Risk Factors:

a) Duration of diabetes
b) Control of Diabetes
c) Pregnancy and other diabetogenic conditions
d) Anemia
e) Hypertension - DM and HTN go hand in hand
f) Smoking
g) Obesity and Hyperlipidemia

Symptoms:

This form of retinopathy is asymptomatic initially. Although some people might complain of dark areas in their vision.

Signs:

On Ophthalmic examination, red (hemorrhagic) and white (exudative) dots are seen. Exudates are of two types: hard and soft. Hard exudates contain protein, have marked edges and are small and discrete. the soft exudates on the other hand are of a lighter colour. They appear softer and have less marked edges with fuzzy borders.

Classification:

Diabetic Retinopathy are classified in two types depending on vascular proliferation. They are as follows:

a) Non-proliferative: they don't grow from the initial lesion and there is no neovascularization, or only minimal.

b) Proliferative: there is dangerous level of neovascularization and they appear as fronds. These vessels might bleed into the Vitreous and give rise to opaque membranous plaques which can then result in retinal detachment.
If all the above is present along with glaucoma, the condition is called Advanced Diabetic Eye DIsease (ADED).

Diagnosis:

It is based on positive history of Diabetes and Ophthalmoscopic examination.

Complications:

a) Vitreous hemorrhage
b) Retinal detachment
c) Formation of opaque membranes
d) Burnt-out stage

Treatment:

Specific: is to get rid of the new vessels being formed and removing the occlusion
Non-specific: control Diabetes and Hypertension; avoid ischemia

Screening:

Screening is an important tool in preventing the development of Retinopathy in cases with high index of suspicion. Diabetics should be examined at least once a year and the frequency should increase with every decade.

Common Nose Emergencies - Their Management.

2009-04-05T01:07:00.011+05:00

Foreign Body in the Nose? Outline your management.

History/examination

Plain X ray of the nose in lateral and anteroposterior view (when necessary)

Removal of the foreign body (depending on the type):

*Flattened FB (eg piece of paper) -----> Removal by pair of Crocodile forceps

*Ireggular rounded FB ------>Removal by a rounded Hook or Probe (do NOT attempt by Crocodile forceps as it may cause the fb to be lodged deeper in the nose).

Treating Epistaxis?

Pinching ---->if unresponsive-----> Anterioir Nasal Packing ---->if unresponsive--- >Posterior Nasal Packing ----->if unresponsive-----> Cautery by Silver Nitrate.

*the patients presenting with severe epistaxis must be immediately made hemodynamically stable by:

maintaining ABGs, Vitals, Topical Decongestants and Normal Saline.

Sedation of the patient is necessary in most cases.

Blood should be arranged for trasnfusion.

If a patient is a known case of HTN, it must be controlled immediately to prevent further blood loss and plasma expanders to be infused.

*patients with posterior nasal packing are usually admitted in the ICU because the PNP may cause oxygen desaturation.

Simplest method for Posterior Nasal Packing?

14 FR Foley's Catheter

Management of Complicated Sinusitis (usually involving the eye and sometimes, the brain also)?

(In order of importance):

History/Examination

Call for assistance from Opthalmology/Neurology

IV antibiotics infusion (Ceftriaxone works best)

Observe for 24 hours, if sympotoms persist then proceed with surgery (Functional Endoscopic Sinus Surgery or External Ethmoidectomy) after a CT scan.

Trauma leading to fracture of the nose, outline the treatment?

History/Examination

X- ray (it has great medicolegal importance)

Analgesics.

Reduction of the fracture ---> ONLY if the patient is brought in within 2 hours of the trama.

*If, however, the patients comes to you 2 hours after the trauma and edema is present then do NOT reduce the fracture then. Give analgesics and send the patient home, call after 7 days (aftet the edema has settled) to reduce the fracture.

Treatment of Septal Hematoma?

Make an incision on one side

Drain the blood

Leave a small drain (to prevent re accumulation)

Pack the nose on both sides (remove after 48 hours)

Start prophylactic Systemic Antobiotics.

Management of post Septoplasty (or any other nasal surgery) Septal Hematoma?

Re-open the already present surgical incision.

Drainage ----> leave the drain in for 1 day ----> Pack the nose

Give an Anti biotic cover.

Treating Septal Abscess?

Incision on the most dependent part of the abcess

Evacuate the pus

(any necrosed cartilage will also be removed)

Place a small drain

Do nasal cavity packing

Send the pus was C/S and till the report comes in keep the patient on broad spectrum antibiotics.

*nasal pack should be removed daily and any pus accumulated should be drained for a few days till the condition subsides.

-Sources: Udairpuwala, Dr. K.I - HOD ENT department ZMUH KDLB, Dr. K.M - Professor of ENT department ZMUH KDLB.

ENT: Acute Airway Problems

2009-03-31T20:26:00.017+05:00

Classification

Congenital
Choanal Atresia, Laryngomalacia, Vocal Cord Paralysis, Laryngeal Webs.

Acquired
Acute Laryngitis, Supraglotittis, Croup, Foreign Bodies, Laryngotracheal Trauma.

Choanal Atresia
Congenital condition due to the persistence of the Buconasal membrane.
Unilateral or Bilateral
Emergency treatment is to provide an oral airway.
Definitive treatment by correcting the atresia.

Laryngomalacia
Most common cause of stridor
In infants and congenital abnormalities
Stridor is due to prolapse of supraglottic structures
Prolapse into laryngeal inlet during inspiration
Mechanism unknown

Clinical features:
Symptoms mild at beginning and then gradually peak
Inspiratory stridor is croaking in character
Symptoms exacerbated during sleep, crying, and in various positions (supine vs prone)

Signs:
Tachypnea, intercostal/subcostal recessions
Severe cases – cyanosis, apneic episodes, failure to thrive, pulmonary HTN

Evaluation:
Flexible Endoscope- Omega shaped epiglottis.

Treatment:
Self limiting
Severe cases:
Surgical (10%)- supraglottoplasty

Vocal Cord Paralysis
Congenital/Acquired, Unilateral/Bilateral, Adductor/Abductor

Pathology:
Malignant diseases (30%), Iatrogenic (25%), External trauma (15%), Idiopathic (15%),
Other (15%)

Vocal Cord Positions:
A- median B- paramedian C- cadaveric D- fully abducted (heavy inspiration)

Clinical Features:
Hoarseness of voice
Weak cough
Aphonia
Inhalation of food leading to respiratory tract infections
Dyspnea
Stridor

Evaluation:
Confirm stability of airway
Bronchoscopy
MRI

Treatment:
Unilateral
Compensatory position of normal cord
Speech therapy
Surgical procedures
Bilateral
Tracheostomy
To clear secretions and prevent inhalation of food (adductor paralysis).
To relieve respiratory obstruction (abductor paralysis).

Laryngeal Webs
Due to incomplete recanalization of larynx
Most common– anterior glottis

Symptoms: weak cry, aphonia, stridor, hoarseness.

Diagnosis: direct laryngoscopy

Treatment:
Thin webs are excised with micro scissors or CO2 laser. Thick webs require excision via laryngofissure and placement of a silicon keel.

Acute Laryngitis
Infectious- S. pneumoniae, H. influenza, S. aureus
Non-Infectious- vocal abuse, allergy, thermal/chemical burns, laryngeal trauma (endotracheal intubation).

Clinical Features:
Hoarseness of voice, pain in throat after talking, dry irritating cough worse at night, and general fever symptoms.

Treatment:
Vocal rest, Avoidance of smoking and alcohol, Steam inhalations, Cough sedative, Antibiotics, Analgesics, Steriods

Supraglotittis (Acute Epiglottitis)
Inflammatory condition confined to supraglottic structures, i.e. epiglottis, aryepiglottic folds and arytenoids.
Children – age 2-7
Due to H. influenzae type B
High mortality if not diagnosed and treated

Symptoms/Signs:
Rapidly progressing diseases
Presentation within a few hours
Fever, dyspnea, odynophagia, drooling
Irritable child, muffled voice
Inspiratory stridor – late feature (airway completely obstructed)

Evaluation:
Minimal investigations
X-ray: Swollen epiglottis shown as ‘thumb sign’

Treatment:
Hospitalization
Antibiotic therapy
Steriods
Hydration & Humidification
Tracheostomy

Laryngotracheobronchitis
Commonly known as croup
Most common infectious cause of airway obstruction in children
Viral – parainfluenzae virus

Symptoms/Signs:
Gradual onset; after URTI
Barking cough + hoarseness + stridor
Inspiratory stridor

Evaluation:
History and examination
X-rays

Treatment:
Hospitalization
Antibiotics
Humidification
Parenteral fluids
Severe cases – steroids + racemic epinephrine via a respiratory bronchidilator
If no response – endotracheal tube

Acute Airway Problems Assessment:
Examinations
Medical Treatment
Resuscitation and appropriate airway management.
02 ventilation
Antibiotics
Steroids
Surgical Treatment
Surgical correction
Tracheostomy
Cricoid split
Laryngeal reconstruction

Schizophrenia

2009-03-21T21:11:00.004+05:00

Schizophrenia is a disorder in which patient have psychotic symptoms and social and occupational dysfuntion that persists atleast for 6 months.

Epidemiology:it affects 1% of population..and typical onset is early 20s for men and late 20s for females.
Riskfactors:
Positive family history is one of the most important risk factor for scizophrenia others include prenatal or postnatal factors such as difficulties,infections during prenancy or delivery or low premorbid IQ,cannabis use,migration to different culture.

Etiology:
exact etiology is unknown but ''dopamine hypothesis'' is most widely accepted theory according to this theory it is beleived that schizophrenia is due to hyperactivity in brain's dopimenergic pathway..and anothers fact that support this theory in that the drugs that block dopamine receptors shows great imporvement in this disease..postmortem studies have shown higher number of dopimergic receptors in subnuclei of cortex in schizophrenic patients.

According to DSM IV 2 or more symptoms should be present for atleas 6 months
Positive symptoms
1:Hallucinations
2:Delusion
3:bizzare behaviuor
4:Unusal thoughts,behaviour with social and occupatonal dysfuntion
Negative symptoms(5A's)
1:Anhedonia
2:Alogia
3:Apathy
4:Affect flattening
5:Asociality

There are five subtypes of schizophrenia(according to DSM IV)
1:paranoid(Paranoid delusions,frequent auditory hallucinations affect not flat)
2:Catatonia(motoric immobility,or excessive purpossless movement,maintence of rigid posture)
3:Disorganized(disorganized speech,behaviour,flat or inappropriate affect)
4:Undifferentiated(Delusions,Hallucinations,disorganized speech,catatonia behaviuor,negative symptoms not met the criteria for paranoid,catatonis or disorganized)
5:residual(resolved but some symptoms persist)

Treatment:
Antipsychotic agents:these include typical and atypical antipsychotic agents...
Psychosocial treatment:it includes stable reality oriented psychotherapy,family support, psycho-education,social and vocational skills training...

Congestive Heart Failure: Brief Introduction

2009-03-21T12:56:00.005+05:00

Congestive Heart Failure is a condition or rather a syndrome, in which heart is unable to maintain adequate blood circulation in the body to meet its demand due to a problem with the structure or function of the heart.

Types:

Systolic:
1. Low Ejection Fraction
2. Due to myocardial infarction, alcohol, drug abuse
Diastolic:
1. Normal Ejection Fraction
2. Decreased ventricular compliance
3. Due to long-standing hypertension
4. S4 characteristic
High output failure:
1. Ex: Thyrotoxicosis, anemia, AV fistulas, sepsis.
Low output failure:
1. Ex: Most forms of heart diseases fall under low output failure.

Clinical Findings in Congestive Heart Failure
*Left Ventricular Failure*	*Right Ventricular Failure*
Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Frothy blood-tinged sputum Bilateral basal crackles Pulsus alternans S3 gallop	Edema of lower extremities (Gravity-dependent region) Congested liver (Nutmeg liver, cardiac cirrhosis) Distended jugular vein Hepatomegaly Pitting edema Pulsus paradoxus S3 gallop

Chest X-ray Findings

Butterfly pattern opacity around hilum, referred to as "bat wings" appearance.
White horizontal lines visible as a result of interstitial edema called Kerley B lines.
Enlarged heart silhouette.
Prominent upper lobe vessels.
Pleural effusion.

Ear, Nose & Throat (ENT) Download

2009-03-10T19:45:00.000+05:00

100 Cases in Ear, Nose & Throat (ENT)
By
Prof. Dr. Hassan Wahba
Professor of Otorhinolaryngology
Faculty of Medicine Ain Shams University

Format: PDF
Download Link: 100 Cases in Ear, Nose & Throat (ENT)

Brachial Plexus Branches

2009-03-10T19:19:00.004+05:00

Brachial Plexus Branches
Nerve	Innervation	Damage to Nerve leads to:
Musculocutaneous	Flexors of arm Flexors of forearm	Weak arm & forearm flexion Weak forearm supination
Axillary	Deltoid	Failure to abduct arm
Radial	Extensors of Forearm Wrist Proximal phalanges Thumb	Unable to extend arm, forearm, proximal phalanges, thumb Unable to extend wrist: Wrist-drop Unable to supinate, abduct
Median	Flexors of Wrist Hand	Flexor, pronator, thenar muscles paralysis; Unable to flex the index and middle fingers leading to: Benediction sign
Ulnar	Flexors of Wrist Hand Extensors of Phalanges	Unable to flex the flexors, 4^th and 5^th phalanges: Claw-hand Unable to adduct thumb

Mnemonic for Brachial Plexus Branches: "My Aunt Raped My Uncle"

From Lateral to Medial: Musculocutaneous, Axillary, Radial, Median, and Ulnar nerves

Long thoracic

Serratus anterior

Winged-scapula (scapula alata)

Transmural infarcts - Flash Card Series

2009-03-08T13:32:00.001+05:00

Kartagener Syndrome - Flash Card Series

2009-03-08T12:13:00.004+05:00

Pharmacology Flash Cards - PowerPoint Format

2009-03-04T19:23:00.001+05:00

Absolute great review of the entire discipline of Pharmacology.
Excellent concise flashcards.
Detailed, thorough and key-points highlighted.
Printer friendly.
Covers all major systems.
Includes General Pharmacology revision.
Format: PowerPoint Presentation.
A must have for anyone taking Pharmacology and proves to be a great USMLE review aid.

Contributed/Authored by Anonymous

Download Link: Pharmacology Flashcards

Renal Corpuscle

2009-03-01T01:37:00.003+05:00

Renal Corpuscle is a part of the nephron.

It consists of:

Glomerulus
Bowman’s capsule

Source: http://www.siumed.edu/

1. Glomerulus

The glomerulus is the tuft of capillaries extending into Bowman’s capsule.
It is made of endothelial cells forming the inner layer of capillary walls, which possess large fenestrations (60-90 nm in diameter)

It has a basal lamina made up of:
a. Lamina externa: Contains heparin sulfate (glycosaminoglycan) that prevents negatively charged proteins from entering Bowman’s space.

b. Lamina densa: Contains type IV collagen that prevents large molecules from entering Bowman’s space.

c. Lamina interna: Contains heparin sulfate (glycosaminoglycan) that prevents negatively charged proteins from entering Bowman’s space.

The mesangium is the interstitial tissue between capillaries, which is made of mesangial cells and Extracellular Matrix. Mesangial cells are phagocytic, can contract, have receptors for angiotensin II and atrial natriuretic peptide.

2. Bowman’s capsule

It has a parietal layer made up of simple squamous epithelium.
It has a visceral layer made up of modified simple squamous epithelium called podocytes.
Podocytes have primary processes and secondary processes called pedicels. There are slits between adjacent pedicels, which are bridged by diaphragms.
The space between the visceral and parietal layers is called the Bowman’s Space.

OBGYN: Cardiotocograph

2009-02-23T20:18:00.000+05:00

CTG (Cardiotocograph)

- Graphical record of fetal heart sounds, uterine contractions and fetal movements.

The CTG Machine:

- Has 1 screen and 3 probes

Cardio probe: to detect fetal heart sounds.
Toco Probe: detects strength and frequency of uterine contractions
Fetal movement probe: The mother is asked to press a button each time she feels her baby move.

Fetal heart rate (FHR):

- Normal: 120-160 beats/min (Range of the baseline fetal heart rate)

- FHR < style="">Bradycardia

- FHR > 160 beats/min is Fetal Tachycardia

Acceleration: An increase in FHR of at least 15 beats/min lasting for at least 15 seconds

Deceleration: A decreased in FHR of at least 15 beats/min lasting for at least 15 seconds. There are three types of deceleration, Types I, II and III.

Toco: Uterine Contractions:

- Range: 0 to 100 mm H₂O

- 20 to 40 mm H2O- Mild contractions

- 40 to 60 mm H2O- Moderate contractions

- 60-100 mm H2N- Severe contractions

Note: Uterine contractions are recorded at # of contractions/10 minutes.

The time between two dark red lines on the CTG paper is taken as 10 minutes.

Indications for CTG:

Done at the time of admission
Done again at the time of induction of labor

OBGYN: Postpartum Hemorrhage

2009-02-23T19:57:00.000+05:00

PPH (Postpartum Hemorrhage)

- Excessive blood loss from the female genital tract starting at the time of the 3^rd stage of labor until 42 days after the delivery of the baby.

Note: Normal blood loss after NVD: upto 500 ml

Normal blood loss after a C-Section: upto 1000 ml

Primary PPH: Blood loss within 24 hours of the 3^rd stage of labor.

Secondary PPH: Blood loss starting after 24 hours of the delivery of the baby until 42 days post-partum.

Causes of Primary PPH:

I. Uterine atony (accounts for 90% of the cases of Primary PPH)

- Myometrial and Placental causes of Uterine atony.

II. Genital tract trauma (7%)

III. Coagulopathies (3%)

I. Uterine Atony: The uterus is unable to contract.

Myometrial causes of Uterine atony:

In multipara females, the uterus is over-distended as a result of multiple pregnancies.
The uterine muscle is replaced by fibrous tissue in some areas.
Prolonged 1^st and 2^nd stage of labor
Fibroid uterus

Placental causes of uterine atony:

Placental retention
Placenta Accreta
Placenta Previa
Placenta Abruptio

II.Genital tract trauma (Accounts for 7% PPH cases)

Deep episiotomy
Perineal tears
Cervical tears
Uterine tears
Wound dehiscence

III.Coagulopathies (Account for 3% PPH cases)

Thrombocytopenic purpura
DIC
Pre-eclampsia
HTN

OBGYN: Mechanism of Labor

2009-02-23T19:32:00.000+05:00

Mechanism of Labor

- Series of changes in the attitude and position of the presenting part of the baby during its passage through the birth canal.

Attitude: relationship of parts of the baby to one another.

Position: Relationship between the fixed part of the maternal pelvis and the fixed part of the baby.

Denominator: Baby’s fixed part (varies with presentation).

Example: the chin is the denominator when the presentation is the face, sacrum is the denominator when the presentation is breech and occiput is the denominator when there is vertex presentation.

Note: Iliopectineal line is taken as an ANTERIOR point.

Sacroiliac joint is taken as a POSTERIOR point.

Pelvic Inlet:

- AP diameter = 11.5cm

- Transverse diameter = 13.5cm

- Therefore, Trasverse diameter > AP diameter (at the pelvic inlet)

- And so the baby enters the pelvis in the trasverse position

Pelvic Outlet:

- AP diameter = 13.5cm

- Transverse diameter = 11.5 cm

- AP diameter > Transverse diameter (at the pelvic outlet)

- The baby is delivered in the AP position

Steps of the Mechanism of Labor:

Descent and engagement
Flexion
Internal Rotation
Extension
Restitution
External Rotation

= Delivery of the baby!!!

OBGYN: Patient with c/o Menorrhagia

2009-02-23T19:30:00.000+05:00

Questions to ask from a patient who presents to the clinic with complains of Menorrhagia:

- Since when? (onset)

- How many pads does she use each day? (Assess flow)

- How soaked are they?

- Is there any soaking of clothes?

- Does she see any clots?

- How many days does she bleed?

- Is there any dysmenorrhea?

- Does she get weak? Feel dizzy?

- How do her heavy periods affect her daily life: Is she still able to continue with her house chores? Does she miss school or work because of her periods?

D/Ds of Menorrhagia:

Uterine fibroids (doctor might feel a mass in the abdomen on examination)
Endometriosis
Endometrial hyperplasia/ cancer
IUD contraceptive use
Hormone producing tumor of the ovary
PID (pelvic inflammatory disease)
Anticoagulant therapy (Ask about easy bruisiblity)
Vitamin K deficiency
Von Willebrand factor deficiency
Hormonal imbalance such as Cushing’s or Thyroid abnormalities (Ask the patient about recent weight gain? Weight loss? Heat and cold intolerance?)
Stress

GYN: History Taking

2009-02-23T19:28:00.000+05:00

GYN: History taking

Name:

Husband’s name:

Age:

Time since marriage:

Address:

LMP:

Parity:

Presenting Complaint:

Examples

- Amenorrhea: secondary amenorrhea is when the patient hasn’t had her periods for more than 6 months.

- Menorrhagia: Heavy menstrual flow but normal duration.

- Dysmenorrhea: painful periods.

- Oligomenorrhea: cycle is prolonged (more than 35 days)

- Polymenorrhea: the cycle is less than 21 days and so the patient has periods more than once in one month.

Normal Menstrual Cycle is approx: 21-35 days long

Normal amount of blood loss: 5-80 ml

Length of periods: 1-8 days

HOPC:

- onset

- duration

- associated symptoms

- aggravating and relieving factors

Menstrual History:

- Age at menarche

- Cycle

- Flow

- Dysmenorrheal?

- Intermenstrual bleeding?

- Post-coital bleeding?

- Contraceptive use?

- Has she ever had a PAP Smear taken?

- LMP

Obstetrics History:

- Ask about each pregnany: Duration of pregnancy? Complications? Outcome?

- Ask about each delivery: Mode of delivery? Place of delivery? Complications at the time of delivery?

- Ask about each baby: Birth weight of baby? Was the baby breast fed?

Past History:

- Past medical: HTN, Diabetes, TB, Seizures, Asthma etc..

- Past Surgical

- Blood Transfusions

- Is her vaccination up-to-date?

Personal History:

- Appetite

- Sleep

- Bowel

- Micturition

- Recent weight gain/weight loss

- History of any addictions (such as smoking, naswaar, hooka etc..)

- History of any allergies to foods or medicines?

Family History:

- Is the marriage consanguineous?

- History of breast cancer, ovarion cancer, uterine cancer etc..

- History of HTN, Diabetes etc..

Social History:

- # of family members

- # of earning members

- Approximate income?

- Use of boiled water at home?

Obstetrics: History taking

2009-02-23T19:25:00.000+05:00

Obstetrics: Science and art of dealing with a pregnant female.

Obstetrics: History Taking

Name:

Husband’s Name:

Time since marriage:

Gravida:

Parity:

LMP:

EDD:

Presenting Complaint:

- Gestational age in weeks

- Reason for coming today?

History of Presenting Complaint:

- Was the pregnancy planned and spontaneous?

- How did she know she was pregnant?

- How did she confirm the pregnancy?

1^st Trimester

- Ask about nausea? vomiting?

- Other associated symptoms such as fever? Abdominal/pelvic/back pain? Burning micturition?

- Vaginal discharge?

- Bleeding per vaginum?

- Use of folic acid tablets? (small yellow colored pills)

- Was an ultrasound done at 6 or 7wks (Dating scan)

2^nd Trimester

- Ask about regular use of folic acid, iron and calcium supplements?

- Ultrasound at 18-22wks (Anomaly scan)?

- Quickening: fetal movements? (normally felt around 20 weeks gestation)

- Fever? Rash? Abdominal pain?

3^rd Trimester

- Tetanus toxoid vaccine at 28 wks and 32 wks?

- Regular doctor checkups?

- Ultrasound?

- Booked case?

Post-natal History:

- Are you breast feeding the baby?

- Have you passed feces and urine?

- Ask about lotia/bleeding?

- How is the baby doing?

- How is the mother doing?

Past Obstetrics History

Pregnancy:

- Gestational age at time of delivery?

- Outcome of preganancy?

Labour/delivery:

- Normal vaginal delivery? C-section?

- Labor- Normal? Prolonged?

- Length of labor?

- D&E?

- D&C:

- Place of delivery? (at home or at the hospital?)

- Any other complications?

Perperium:

- Any complications?

Baby:

- Gender of baby?

- Age of baby?

- Breast fed? Length of breast feeding?

- Birth weight?