Category: Module

Renal Trauma

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Renal Trauma

RENAL INJURY

  • Renal trauma is due to-

a) Minor injuries- blunt trauma (RTA, falls, assaults & sporting injuries)

b) Major injuries – penetrating trauma (knife or gunshot wounds)

  • Blunt trauma is much more common than penetrating trauma.
  • Renal injuries are classified as follows-

1. Grade I-

  • Contusion or non-enlarging subcapsular perirenal haematoma, and no laceration.

2. Grade II-

  • Superficial laceration

3. Grade III-

  • Laceration >1 cm without extension into the renal pelvis or collecting system (no evidence of urine extravasation).

4. Grade IV-

  • Laceration extends to renal pelvis or urinary exrravasatlon.
  • Vascular: injury to main renal artery or vein with contained haemorrhage.
  • Segmental infarctions without associated lacerations.
  • Expanding subcapsular haematomas compressing the kidney.

5. Grade V-

  • Shattered kidney.
  • Avulsion of renal hilum: devascularisation of a kidney due to hilar injury.
  • Ureteropelvicavulsions.
  • Complete laceration or thrombus of the main renal artery or vein.

 

 

Clinical features-

  • Hematuria is the most important sign of renal injury.
  • Loin bulge due to perinephric haemtoma.
  • Bruising of soft tissue in the loin.
  • Retroperitoneal haematoma –> abdominal distension.
  • systolic blood pressure ≤90 mmHg

Investigations-

  1. Intravenous pyelography (IVP) can shows (An IVP is done urgently to assesss the damage to the kidney and to know the functioning of the other kidney)-
  • Intrarenal extravasation
  • Extrarenal extravasation
  • Function of injured kidney

2. CT scan with contrast is the IOC

3. USG

Treatment-

  • Blunt trauma are treated conservatively
  • Penetrating injuries, small & major lacerations- surgical exploration.

Exam Important

  • Renal injuries are classified as follows-

1. Grade I: contusion or non-enlarging subcapsular perirenal haematoma, and no laceration.

2. Grade II: superficial laceration

3. Grade III: laceration >1 cm without extension into the renal pelvis or collecting system (no evidence of urine extravasation).

4. Grade IV

  • Laceration extends to renal pelvis or urinary exrravasatlon.
  • Vascular: injury to main renal artery or vein with contained haemorrhage.
  • Segmental infarctions without associated lacerations.
  • Expanding subcapsular haematomas compressing the kidney.

5. Grade V:

  • Shattered kidney.
  • Avulsion of renal hilum: devascularisation of a kidnev due to hilar injury.
  • Ureteropelvicavulsions.
  • Complete laceration or thrombus of the main renal artery or vein.

 

 

Clinical features-

  • Hematuria is the most important sign of renal injury.
  • Loin bulge due to perinephric haemtoma.
  • Bruising of soft tissue in the loin.
  • Retroperitoneal haematoma –> abdominal distension.
  • systolic blood pressure ≤90 mmHg

 

Investigations-

  1. Intravenous pyelography (IVP) can shows-
  • Intrarenal extravasation
  • Extrarenal extravasation
  • Function of injured kidney

2. CT scan with contrast is the IOC

3. USG

 

 

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Odontogenic Keratocyst

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Odontogenic Keratocyst

                                ODONTOGENIC KERATOCYST

  • OKC arises from residual strands of epithelium from dental lamina.
  • Forms a cyst in the jaw in tooth bearing area.
  • Lined by keratinized squamous epithelium.
  • It is locally aggressive and high rate of recurrence
  • OKC –> ameloblastoma –> malignant lesion (SCC)

Clinical features-

  • Patient between 10- 40 years are affected.
  • Common in males.
  • Site 3rd molar tooth (posterior mandible)
  • Pre malignant jaw cyst

Treatment-

  • Osteotomy with enucleation with chemical cautery (Cornoy’s sign)
  • Recurrence rates for inadequate removed lesions can reach 60%.

Exam Important

Clinical features-

  • Patient between 10- 40 years are affected.
  • Common in males.
  • Site 3rd molar tooth (posterior mandible)
  • Pre malignant jaw cyst
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Pediatric burn injury

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Pediatric burn injury

INTRODUCTION:

  • Burns and scalds account for 6% of peadiatric injuries.
  • The majority involve pre-school children,burns being most common between 1-2 yrs,flame burns bet 5-18 yrs.
  • Children have nearly 3 times BSA:BM ratio of adults.
  • Consequently greater fluid requirements and more evaporative water loss than adults.
  • Children
  • Burn that may appear partial thickness may instead be a full thickness burn.
BURNS:
Wounds caused by exposure to:
  • Excessive heat
  • Chemicals
  • Fire/steam
  • Radiation
  • Electricity
DEPTH OF BURN:
  • Partial thickness burn = involves epidermis
  • Deep partial thickness = involves dermis
  • Full thickness = involves all of skin
DEGREE OF BURN:

1st DEGREE BURN:

  • Involves only epidermis
  • Tissue will blanch with pressure
  • Tissue is erythematous and often painful
  • Involves minimal tissue damage
  • Sunburn

2nd DEGREE BURN:

  • Partial thickness burns 
  • Involve the epidermis and portions of the dermis 
  • Often involve other structures such as sweat glands, hair follicles, etc. 
  • Blisters and very painful 
  • Edema and decreased blood flow in tissue can convert to a full-thickness burn

3rd DEGREE BURN:

  • Referred to as fullthickness burns 
  • Charred skin or translucent white color 
  • Coagulated vessels visible 
  • Area insensate – patient still c/o pain from surrounding second degree burn area 
  • Complete destruction of tissue and structures

4th DEGREE BURN:

  • Involves subcutaneous tissue, tendons and bone
MAJOR BURNS:
  • PT and FTB with affected BSA>10% under 10yrs age. 
  • PT and FTB with affected BSA>20% over 10 yrs age. 
  • FTB with affected BSA>5%. 
  • PT or FTB involving face,hands,feet,perinium or major joints. 
  • PT or FTB involving an inhalational burn. 
  • PT or FTB involving an electrical or chemical burn.
BURNS EXTENT:
  • Burn extent is calculated only on individuals with second and third degree burns
  • Palmar surface = 1% of the BSA
MEASUREMENT CHARTS:
  • Rule of Nines: Quick estimate of percent of burn
  • Lund and Browder:
    • More accurate assessment tool
    • Useful chart for children – takes into account the head size proportion.
  • Rule of Palms: Good for estimating patches of burn wound
RULES OF NINES:
  • Head & Neck = 9%
  • Each upper extremity (Arms) = 9%
  • Each lower extremity (Legs) = 18%
  • Anterior trunk= 18%
  • Posterior trunk = 18%
  • Genitalia (perineum) = 1%
MANAGEMENT:

URGENT:

  • High flow o2 face mask with reservior bag.
  • Cervical collar (injury spine )
  • Cooling burn wound –cold running water for 15-20 min,avoid making pt hypothermic.
  • Prevent hypothermia
  • Insert min 2 peripheral cannula in unburnt skin
  • Fluid resusitatation
  • Insert urinary catheter in all pts>20% BSA.
  • Fast the pt and insert NG tube for all pts with>20% BSA,all intubated pts,head and neck burns,younger children >10%BSA.
  • Adequate analgesia-IV opoids.
  • Emergency wound management e.g.,cling film or clean non-adhesive dressing.
  • Escharotomy if indicated e.g., circumferential burns around limbs or trunk.

PARKLAND FORMULA:

  • 4 ml R/L x % burn x body wt. In kg. 
  • ½ of calculated fluid is administered in the first 8 hours 
  • Balance is given over the remaining 16 hours. 
  • Maintain urine output at 0.5 ml/kg/hr.  
  • If evidence of extensive tissue damage then aim for a higher UO 1-2 ml/kg/hr. 
  • Monitor sr electrolytes esp for hyponatremia. 
  • In younger children calculate the maintenance fluids and add this to the resusitation fluids

Surgeries and Dressings:

  • Escharotomy may be needed for circumferential burns to limbs,neck or trunk. 
  • Early surgical debridement of nectrotic tissue is preferred as early grafting is associated with improved outcome. 
  • Scrubbing of affected skin is also frequently undertaken. 
  • Blood loss during operative sessions can be large.

Escharotomy:

  • Circulation to distal limb is in danger due to swelling. 
  • Progressive loss of sensation / motion in hand / foot. 
  • Progressive loss of pulses in the distal extremity by palpation or doppler. 
  • In circumferential chest burn, patient might not be able to expand his chest enough to ventilate, and might need escharotomy of the skin of the chest.

Exam Important

  • According to Parkland formula, the initial orders for choice of fluid and rate of infusion should be Ringer’s lactate, 1250 ml/h for 71/2h
  • Burn injury with the body parts involved: face including scalp, both buttocks and circumferentially around both thighs TBSA 0.35
  • Burns in children assessed by Lund and Browder
  • Head and neck burns in infant constitute 18 of burns
  • Parkland formula for burns is for Ringer lactate

 

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Atherosclerosis

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Atherosclerosis

ATHEROSCLEROSIS

  • Atherosclerosis is an thickening & hardening muscular arteries which is characterised by soft gramous lipid cores (atheromatous plaque).
  • It is the commonest & most important arterial disease.
  • Most commonly affected are aorta, coronaries & cerebral arterial system.
  • Most commonly coronoary circulation affected is – Left anterior descending artery

Etiology–

Pathogenesis-

  • Most widely accepted theory for atherosclerosis is inflammatory response to endothelial injury.
  • According to this hypothesis, atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to endothelium.
  • Hyperlipidemia, hypertension, smoking can cause endothelial injury.
  • Foam cells are formed when macrophages & smooth muscle cells accumulated oxidised LDL.
  • Chlamydia Pneumoniae presents the strongest association with human atherosclerosis.

Morphological features-

1. Fatty streaks & Dots- are the earliest lesions composed of intimal collections of foamy macrophages & smooth muscle cells.

  • Prominent in the aorta (often in posterior wall)

2. Gelatinous lesions- develop in the intima of the aorta.

3. Artheromatous plaques (arthemaous lesions/ fibrous plaque)-

  • Most severely affected is the abdominal aorta.
  • Involves iliac, femoral, carotid, coronary & cerebral arteries.
  • Superficial luminal part of the fibrous cap (convex) composed by smooth muscle cells.
  • Cellular area under fibrous cap composed of macrophages, foam cells, lymphocytes.
  • Deeper central soft core consists of cholesterol clefts, fibrin, necrotic debris & lipid- laden foam cells.

4. Complicated plaques-

  • Calcification- occurs more commonly in advanced athermatous plaques.
  • Ulceration
  • Thrombosis- superimposed thrombi
  • Haemorrhage

Clinical features-

Major clinical effects of atheroscelrosis are-

  1. Heart (coronary artery disease, IMD, MI)
  2. Brain (stroke)
  3. Aorta (aneurysmal dilatation)
  4. Intestine (ischaemia, infarct)
  5. Lower extremities (gangrene)
  • Blood vessels affected by atherosclerosis- abdominal aorta (most commonly), Circle of Willis (least commonly affected)

Exam Important

  • Most commonly affected are aorta, coronaries & cerebral arterial system.
  • Most commonly coronoary circulation affected is – Left anterior descending artery

Etiology–

Pathogenesis-

  • Most widely accepted theory for atherosclerosis is inflammatory response to endothelial injury.
  • According to this hypothesis, atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to endothelium.
  • Hyperlipidemia, hypertension, smoking can cause endothelial injury.
  • Foam cells are formed when macrophages & smooth muscle cells accumulated oxidised LDL.
  • Chlamydia Pneumoniae presents the strongest association with human atherosclerosis.

Morphological features-

1. Fatty streaks & Dots- are the earliest lesions composed of intimal collections of foamy macrophages & smooth muscle cells.

  • Prominent in the aorta (often in posterior wall)

2. Gelatinous lesions- develop in the intima of the aorta.

3. Artheromatous plaques (arthemaous lesions/ fibrous plaque)-

  • Most severely affected is the abdominal aorta.
  • Involves iliac, femoral, carotid, coronary & cerebral arteries.
  • Superficial luminal part of the fibrous cap (convex) composed by smooth muscle cells.
  • Cellular area under fibrous cap composed of macrophages, foam cells, lymphocytes.
  • Deeper central soft core consists of cholesterol clefts, fibrin, necrotic debris & lipid- laden foam cells.

4. Complicated plaques-

  • Calcification- occurs more commonly in advanced athermatous plaques.
  • Ulceration
  • Thrombosis- superimposed thrombi
  • Haemorrhage
  • Blood vessels affected by atherosclerosis- abdominal aorta (most commonly), Circle of Willis (least commonly affected)
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Mitochondrial DNA

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Mitochondrial DNA

Mitochondrial DNA (mtDNA)

  • It is a separate genome located in the cytoplasm of nearly all eukaryotic cells
  • Is closede circular, double-stranded, and composed of heavy (H) and light (L) chains or strands.
  • Contains 16,569 bp.
  • Encodes 13 protein subunits of the respiratory chain (of a total of about 67) –
  1. Seven subunits of NADH dehydrogenase (complex I) and Cytochrome b of complex III
  2. Three subunits of cytochrome oxidase (complex IV)
  3. Two subunits of ATP synthase
  • Encodes large (16S) and (12S) mt ribosomal RNAs
  • Encodes 22 mt tRNA molecules
  • Genetic code differs slightly from the standard code –
  1. UGA (standard stop codon) is read as Trp.
  2. AGP and AGG (standard codons for Arg) are read as stop codons,
  • Contains very few untranslated sequences.
  • Nemaline myopathy results due to mutations in mt- DNA
  • Heteroplasmy is the presence of mixture of more than one type of an organelle genome (mt- DNA) within a cell or individual.
  • High mutation rate (5 to 10 times that of nuclear DNA).
  • Comparisons of mtDNA sequences provide evidence about evolutionary origins of primates and other species.
  • High mutation rate occurs due to point mutation and large scale rearrangements.
  • mitochondrial DNA contains no (or very few) introns (i.e. untraslated sequences).

Mitochondrial DNA is always maternally inherited.

  1. Important mitochondrial diseases are mitochondrial encephalomyopathy with lactic aciilosis and stroke like episodes (MELAS),
  2. leber hereditary optic neuropathy, myoclonic epilepsy with ragged-red fibers, leigh syndrome, Pearson syndrome, kearns-sajre syndrome,
  3. chronic progressive external ophthalmoplegia and NARP (neurogenic weakness with ataxia & retinitis pigmentosa).
  • All children from affected mother will inherit the disease but it will not be transmitted from an afiected father to his children

Exam Important

  • Is closede circular, double-stranded, and composed of heavy (H) and light (L) chains or strands.
  • Contains 16,569 bp.
  • Encodes 13 protein subunits of the respiratory chain (of a total of about 67)
  • Nemaline myopathy results due to mutations in mt- DNA
  • Heteroplasmy is the presence of mixture of more than one type of an organelle genome (mt- DNA) within a cell or individual.
  • High mutation rate (5 to 10 times that of nuclear DNA).
  • Comparisons of mtDNA sequences provide evidence about evolutionary origins of primates and other species.
  • High mutation rate occurs due to point mutation and large scale rearrangements.
  • mitochondrial DNA contains no (or very few) introns (i.e. untraslated sequences).
  • Mitochondrial DNA is always maternally inherited.
  • All children from affected mother will inherit the disease but it will not be transmitted from an afiected father to his children
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External Ear- Pinna / Auricle

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EXTERNAL EAR- Pinna / Auricle

AURICLE OR PINNA

  • The entire pinna (except its lobule and outer part of external acoustic canal) is made up of a framework of a single piece of yellow elastic cartilage
  • There is no cartilage between the tragus and crus of the helix – incisura terminalis
  • An incision made in this area will not cut through the cartilage – used for endaural approach in surgery of external auditory canal and mastoid.
  • Skin over the pinna is closely adherent to the perichondrium on the lateral surface while it is loosely attached on the medial surface.
  • Incisura terminalis is the area between the tragus and crus of helix

NERVE SUPPLY OF PINNA

Greater auricular nerve(C2C3)

  • Major part of the skin of Pinna is supplied by Greater Auricular nerve.
  • The great auricular supplies the whole of the cranial (medial /back) surface of auricle  and the posterior part of lateral (front) surface (helix, anthelix, and lobule).

Lesser occipital nerve(C2)

  • Auriculotemporal nerve (mandibular branch of 5th nerve)
  • Auricular branch of Vagus (Arnold’s N)
  • Facial nerve

DEVELOPMENT OF PINNA

  • Ear pinna develops from Ecdoderm.
  • Pinna is formed at birth.
  • The auricle starts to develop when 6 hillocks appear around the first pharyngeal groove(cleft), which lies between the first and the second branchial arches.
  • First branchial cleft is the precursor of external auditory canal.
  • Around the sixth week of embryonic life, a series of six tubercles appear around the first branchial cleft.
  • They progressively coalesce to form the auricle/Pinna. Branchial clefts are ectodermal in origin.

LYMPHATIC DRAINAGE OF PINNA

  • Concha, Tragus, Fossa triangularis-  Pre auricular and parotid nodes
  • Lobule and antitragus  –  Infra-auricular nodes
  • Helix and anti-helix   – Post auricular nodes, deep jugular and spinal accessory nodes

CLINICAL SIGNIFICANCE

  • Keratocanthoma-Flesh-colored, dome-shaped, on the  ear lobe with  central keratin-filled crater and surrounded by  proliferating squamous epithelium. This  lesion  regresses over/  the  next month   and   then   disappears.
  • Malignant Otitis externa-Ear pain and drainage in an elderly diabetic patient must raise concern about malignant external otitis.It is associated with tenderness in the pinna and  swelling and inflammation of the external auditory meatus.This infection is almost always caused by P. aeruginosa.
  • Ramsay Hunt Syndrome-A clinical condition characterised by a facial palsy and often associated with facial pain and the appearance of vesicles on the canal and pinna.Vertigo and sensor neural hearing loss (VIIIth nerve) may occur.
  • Boil can occur on Pinna.
  • Acute mastoiditis is characterized by Clouding of Mastoid Air cells,Deafness and Outward and downward deviation of the pinna.
  • Darwin’s tubercle (or auricular tubercle) is a congenital earcondition which often presents as a thickening on the helix at the junction of the upper and middle thirds.
  • Boxer’s ear is Hematoma of Auricle
    • It is the collection of blood between the auricular cartilage and its perichondrium.
    • It is often the result of blunt trauma seen in boxers, wrestlers and rugby players, so called Boxer’s ear.
    • Extravasated blood may clot and then organize resulting in typical deformity of cauliflower ear.

Exam Important

  • The entire pinna (except its lobule and outer part of external acoustic canal) is made up of a framework of a single piece of yellow elastic cartilage
  • Pinna develops from the cleft of  1st and 2nd pharyngeal arch
  • Ear pinna develops from Ectoderm
  • Skin over the pinna is closely adherent to the perichondrium on the lateral surface while it is loosely attached on the medial surface.
  • Greater auricular nerve(C2C3)-Supplies Major Part of Pinna
  • Sensory nerve supply of pinna is Mandibular nerve

Cauliflower ear (boxer’s ear, wrestler’s ear)

  1. Is an acquired deformity of the outer ear.
  2. In this injury, the ear can shrivel up and fold in on itself and appear pale, giving it a cauliflower-like appearance, hence the term cauliflower ear.
  3. Wrestlers, boxers and martial artists in particular are susceptible to this type of injury.
  4. When the ear is struck and a blood clot develops under the skin, or the skin is sheared from the cartilage, the connection of the skin to the cartilage is disrupted.

 

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Von Recklinghausen’s Disneurofibromatosisease

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(VON RECKLINGHAUSEN’S DISNEUROFIBROMATOSISEASE)

NEUROFIBROMATOSIS (VON RECKLINGHAUSEN’S DISEASE)

  • Neurofibromatosis type 1 (NF1) and type 2 (NF2) are neurocutaneous disorders inherited as autosomal dominant genetic syndromes..

Neurofibromatosis type 1

  • The clinical criteria used to diagnose NF1 are as follows, in the absence of alternative diagnoses:
  • Six or more café-au-lait spots or hyperpigmented macules =5 mm in diameter in prepubertal children and 15 mm postpubertal
  • Axillary or inguinal freckles (>2 freckles)
  • Two or more typical neurofibromas or one plexiform neurofibroma
  • Optic nerve glioma
  • Two or more iris hamartomas (Lisch nodules), often identified only through slit-lamp examination by an ophthalmologist
  • Sphenoid dysplasia or typical long-bone abnormalities such as pseudarthrosis
  • First-degree relative (eg, mother, father, sister, brother) with NF1.

Neurofibromatosis type 2 

  • It is a genetic disorder marked by the predisposition to develop a variety of tumors of the central and peripheral nervous systems. In contrast to neurofibromatosis type 1 (NF1), NF2 produces a paucity of cutaneous manifestations.
  • Clinical diagnosis of NF2 requires that an individual present with at least 1 of the following clinical scenarios :
  • Bilateral vestibular schwannomas
  • A first degree relative with NF2 and Unilateral vestibular schwannoma or Any two of: meningioma, schwannoma, glioma, neurofibroma, posterior subcapsular lenticular opacities
  • Unilateral vestibular schwannoma and Any two of: meningioma, schwannoma, glioma, neurofibroma, posterior subcapsular lenticular opacities
  • Multiple meningiomas and Unilateral vestibular schwannoma or Any two of: schwannoma, glioma, neurofibroma, cataract.

Difference b/w Schwannoma & Neurofibroma

Schwannoma (or Neurilemmoma)

  • are true encapsulated neoplasm composed of schwann cells.
  • It compresses the nerve of origin.
  • There is a plane of cleavage separating the nerve from the mass.

Neurofibroma

  • are unencapsulated benign neoplasm of schwann cells and fibroblasts.
  • The tumor involves the nerve. Grossly it appears as expanded nerve.
  • It is composed of mixture of schwann cell and fibroblast and contains axons within it.
  • It can not be demarcated from the nerve therefore can not be removed without sacrificing the nerve.

Difference between NF-1 and NF-2:

Feature

NF1

NF2

Mutation

NFl gene on chromosome 17 causes

NF2 gene on chromosome 22q.

von Recklinghausen’s disease. The NFl

NF2 encodes a protein called

gene is a tumor-suppressor gene; it encodes a protein, neurofibromin

neurofibromin 2, schwannomin,or merlin

Cutaneous feat

cutaneous neurofibromas, pigmented

lesions of the skin called café au lait

spots, freckling in non-sun-exposed

areas such as the axilla, hamartomas

of the iris termed Lisch nodules, and

pseudoarthrosis of the tibia

Multiple café au lait spots and

peripheral neurofibromas occur

rarely                                                   

Complications

Aqueductal stenosis with

hydrocephalus, scoliosis, short stature,

hypertension, epilepsy, and mental

retardation may also occur.

A characteristic type of cataract,

juvenile posterior subcapsular

lenticular opacity, occurs in NF2

Neurological features

 Patients with NF1 are at increased

risk of developing nervous

system neoplasms, including plexiform

neurofibromas, optic pathway gliomas

ependymomas, meningiomas

astrocytomas, and

pheochromocytomas. Neurofibromas

may undergo secondary malignant

degeneration and become

sarcomatous.

 NF2 is characterized by the

development of bilateral vestibular

schwannomas in >90% of

individuals who inherit the gene

Patients with NF2 also have a

predisposition for the development

of meningiomas, gliomas, and

schwannomas of cranial and spinal

nerves

Exam Important

  • Neurofibromatosis shows which of the Autosomal Dominant type of inheritance.
  • Neurofibromatosis may be associated with Cataract, Scoliosis, Hypertrophy of limb and Neurofibroma.
  •  Neurofibromatosis-1 is asociated with family history, Optic Glioma and Axillary Freckles.
  • Optic Gliomas are the most common intracranial tumors of Neurofibromatosis 1.
  • Neurofibromatosis type 2 is associated with Bilateral Acoustic Neuroma, Cafe-au-lait spots, Axillary Freckling, Lisch Nodule, Meningioma
  • Gene for NF-2 is located on chromosome 22.
  • Neurofibroma are unencapsulated and needs to be resected along the nerve fibres.
  • Neurofibromatosis presents as Elephantiasis neuromatodes, Plexiform neuroma,Von Recklinghausen’s disease.
  • Plexiform neurofibromatosis commonly affects Trigeminal Nerve.
  • Neurofibromatosis may be associated with Pheochromocytoma.
  • The pathognomic sign of Neurofibromatosis is Axillary Freckling.
  • Scoliosisis is the MOST common skeletal manifestation in Type-1 Neurofibromatosis.
  • Juveile Myelomonocytic Leukemia  is the most common tumour associated with Neurofibromatosis -1 (NF-I) in a child.
  • Rib notching,Pseudarthrosis may be seen in Neurofibromatosis.
  • Wide neural foramina is associated with Neurofibromatosis.-I.
  • Ependymomas are commonly associated with Neurofibromatosis-II.
  • A 22-year-old patient, Sreeraj presents with multiple neural tumors, pigmented iris hamartomas, and numerous tan macules on his skin. He informs the physician that his father, as well as one uncle and his paternal grandfather, had a similar condition. This patient likely suffers from Neurofibromatosis.-I.
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Bioterrorism Agent

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Bioterrorism Agent

DEFINIITION:

  • Bioterrorism is terrorism involving the intentional release or dissemination of biological agents. 
  • These agents are bacteria, viruses, fungi, or toxins, and may be in a naturally occurring or a human-modified form, in much the same way in biological warfare.
  • Sentinel laboratories are mainly involved in Control of Bioterrorism

Category A

Definition

The U.S. public health system and primary healthcare providers must be prepared to address various biological agents, including pathogens that are rarely seen in the United States. High-priority agents include organisms that pose a risk to national security because they

  • Can be easily disseminated or transmitted from person to person;
  • Result in high mortality rates and have the potential for major public health impact;
  • Might cause public panic and social disruption; and
  • Require special action for public health preparedness.

Agents/Diseases

  • Anthrax (Bacillus anthracis)
  • Botulism (Clostridium botulinum toxin)
  • Plague (Yersinia pestis)(highest potential)
  • pox (variola major)
  • Tularemia (Francisella tularensis)
  • Viral hemorrhagic fevers, including
    • Filoviruses (Ebola, Marburg)
    • Arenaviruses (Lassa, Machupo)

Category B

Definition

Second highest priority agents include those that

  • Are moderately easy to disseminate;
  • Result in moderate morbidity rates and low mortality rates; and
  • Require specific enhancements of CDC’s diagnostic capacity and enhanced disease surveillance.

Agents/Diseases

  • Brucellosis (Brucella species)
  • Epsilon toxin of Clostridium perfringens
  • Food safety threats (Salmonella species, Escherichia coli O157:H7, Shigella)
  • Glanders (Burkholderia mallei)
  • Melioidosis (Burkholderia pseudomallei)
  • Psittacosis (Chlamydia psittaci)
  • Q fever (Coxiella burnetii)
  • Ricin toxin from Ricinus communis (castor beans)
  • Staphylococcal enterotoxin B
  • Typhus fever (Rickettsia prowazekii)
  • Viral encephalitis (alphaviruses, such as eastern equine encephalitis, Venezuelan equine encephalitis, and western equine encephalitis])
  • Water safety threats (Vibrio cholerae, Cryptosporidium parvum)

Category C

Definition

Third highest priority agents include emerging pathogens that could be engineered for mass dissemination in the future because of

  • Availability;
  • Ease of production and dissemination; and
  • Potential for high morbidity and mortality rates and major health impact.

Agents

  • Emerging infectious diseases such as Nipah virus and hantavirus

Exam Important

Sentinel laboratories are mainly involved in Control of Bioterrorism

Category A bioterrorism agents are Ebola, Small pox, Botulism, Hemorrhagic fever, Yersinia & Clostridium botulinum

Cholera belongs to category-B of bioterrorism 

Plague carries the highest potential for use as biological weapons for microbial bioterrorism

B. anthracis is an Agent for bioterrorism

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Salvage Pathway Of Purine Nucleotides

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Salvage pathway of purine nucleotide synthesis

Q. 1 The purines salvage pathway is for:
 A Hypoxanthine and Xanthine
 B Hypoxanthine andAdenine
 C Adenine and Guanine
 D Xanthine and Guanine
Q. 1 The purines salvage pathway is for:
 A Hypoxanthine and Xanthine
 B Hypoxanthine andAdenine
 C Adenine and Guanine
 D Xanthine and Guanine
Ans. B
Explanation:Hypoxanthine andAdenine

Q. 2

Which among the following are the substrates needed for purine salvage pathway?

 A

Hypoxanthine and Xanthine
 B

Hypoxanthine and Adenine
 C

Adenine and Guanine
 D

Xanthine and Guanine
Q. 2

Which among the following are the substrates needed for purine salvage pathway?

 A

Hypoxanthine and Xanthine
 B

Hypoxanthine and Adenine
 C

Adenine and Guanine
 D

Xanthine and Guanine
Ans. B
Explanation:

Conversion of purines, their ribonucleosides, and their deoxyribonucleosides to mononucleotides involves “salvage reactions”.
The more important mechanism involves phosphoribosylation by PRPP of a free purine (Pu) to form a purine 5′-mononucleotide (Pu-RP). Phosphoryl transfer from ATP, catalyzed by adenosine- and hypoxanthine-phosphoribosyl transferases, converts adenine, hypoxanthine, and guanine to their mononucleotides. 
 
A second salvage mechanism involves phosphoryl transfer from ATP to a purine ribonucleoside. Phosphorylation of the purine nucleotides, catalyzed by adenosine kinase, converts adenosine and deoxyadenosine to AMP and dAMP. Similarly, deoxycytidine kinase phosphorylates deoxycytidine and 2′-deoxyguanosine, forming dCMP and dGMP.
 
Ref: Rodwell V.W. (2011). Chapter 33. Metabolism of Purine & Pyrimidine Nucleotides. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.

 

Q. 3

Salvage pathway of purine biosynthesis is important for ‑

 A

Liver
 B

RBCs
 C

Kidney
 D

Lung
Q. 3

Salvage pathway of purine biosynthesis is important for ‑

 A

Liver
 B

RBCs
 C

Kidney
 D

Lung
Ans. B
Explanation:

 

Purine nucleotide synthesis occurs by two pathways :

1.De novo synthesis

2.Salvage pathway

Liver is the major site of purine nucleotide biosynthesis (de novo).

Certain tissues cannot synthesize purine nucleotides by de novo patyway, e g. brain, erythrocytes and polymor­phonuclear leukocytes.

These are dependent on salvage pathway for synthesis of purine nucleotides by using exogenous purines, which are formed by degradation of purine nucleotides synthesized in liver.

Quiz In Between

Q. 4 Salvage pathway of purine nucleotide synthesis are used by all except ‑

 A

Brain
 B

Liver
 C

RBC
 D

Leukocytes
Q. 4

Salvage pathway of purine nucleotide synthesis are used by all except ‑

 A

Brain
 B

Liver
 C

RBC
 D

Leukocytes
Ans. B
Explanation:

 

Purine nucleotide synthesis occurs by two pathways :-

1.De novo synthesis

2.Salvage pathway

Liver is the major site of purine nucleotide biosynthesis (de novo).

Certain tissues cannot synthesize purine nucleotides by de novo patyway, e g. brain, erythrocytes and polymorphonuclear leukocytes.

These are dependent on salvage pathway for synthesis of purine nucleotides by using exogenous purines, which are formed by degradation of purine nucleotides synthesized in liver.

Q. 5 Salvage pathway of purine nucleotide synthesis are used by all except ‑

 A

Brain
 B

Liver
 C

RBC
 D

Leukocytes
Q. 5

Salvage pathway of purine nucleotide synthesis are used by all except ‑

 A

Brain
 B

Liver
 C

RBC
 D

Leukocytes
Ans. B
Explanation:

Ans. is ‘b’ i.e., Liver

  • Purine nucleotide synthesis occurs by two pathways :
  • De novo synthesis
  • Salvage pathway
  • Liver is the major site of purine nucleotide biosynthesis (de novo).
  • Certain tissues cannot synthesize purine nucleotides by de novo patyway, e g. brain, erythrocytes and polymorphonuclear leukocytes.
  • These are dependent on salvage pathway for synthesis of purine nucleotides by using exogenous purines, which are formed by degradation of purine nucleotides synthesized in liver.

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Factors affecting enzyme activity

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Factors affecting enzyme activity

Factors affecting enzyme activity

Introduction: 

  • Enzyme activity can be affected by a variety of factors, such as temperature, pH, and concentration.
  • Decrease in activation  energy leads to an increase in enzyme activity.
  • Enzymes work best within specific temperature and pH ranges, and sub-optimal conditions can cause an enzyme to lose its ability to bind to a substrate.
  • One  unit enzyme  activity  is  defined  as the  amount  causing  transformation  of 1.0  micro  mole  of  substrate  per  minute(Micromole / minute)  at  25o  C
  • Temperature: Raising temperature generally speeds up a reaction, and lowering temperature slows down a reaction. However, extreme high temperatures can cause an enzyme to lose its shape (denature) and stop working.
  1. Bell  shaped  curve  is  obtained  by  plotting temperature against  velocity  of reaction
  2. The optimum  temperature  for  most  human  enzymes is  between  35  and  400C.
  3. The  temperature  coefiicient  (Q10)  is  the  factor  by which  the  rate  of  a biologic process increases  for  a 10’C increase  in  temperature.
  • pH: Each enzyme has an optimum pH range. Changing the pH outside of this range will slow enzyme activity. Extreme pH values can cause enzymes to denature.
  • Enzyme concentration: Increasing enzyme concentration will speed up the reaction, as long as there is substrate available to bind to. Once all of the substrate is bound, the reaction will no longer speed up, since there will be nothing for additional enzymes to bind to.      
  • Substrate concentration: Increasing substrate concentration also increases the rate of reaction to a certain point. Once all of the enzymes have bound, any substrate increase will have no effect on the rate of reaction, as the available enzymes will be saturated and working at their maximum rate

Exam Important

  • One  unit enzyme  activity  is  defined  as the  amount  causing  transformation  of 1.0  micro  mole  of  substrate  per  minute  at  25o  C.\
  • Decrease in activation  energy leads to an increase in enzyme activity
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