Summar Of Staphylococcus Bacteria

SPECIES	MODE OF TRANSMISSION	CULTURE MEDIA	DISEASES	IDENTIFYING POINTS	CLINICAL FEATURES	PREVENTION	TREATMENT	Lab. TEST
Staphylococcus Aureus	nose is the main site of colonization, The skin, Hand contact is an important mode of transmission, S. aureus is also found in the vagina, shedding from human lesions and fomites such as towels and clothing contaminated by these lesions.	Blood agar, Mannitol salt agar	pyogenic infections (e.g., endocarditis, septic arthritis, and osteomyelitis), food poisoning, scalded skin syndrome,  and toxic shock syndrome	Gram+ cocci arrange in cluster (Grapelike), Catalase+, Coagulase+, Ferments Mannitol, B- hemolysis & Goleden colour colony on blood agar	Food poisoning (gastroenteritis) short incubation period (1–8 hours). vomiting more prominent than diarrhea. Toxic shock syndrome fever; Hypotension, sunburn-like rash. Scalded-skin syndrome fever, large bullae, and an erythematous macular rash	Cleanliness, frequent handwashing, and aseptic management of lesions. intranasal mupirocin or by oral antibiotics, such as ciprofloxacin	nafcillin or cloxacillin  cephalosporins, or vancomycin     Mupirocin in skin infections caused by S. aureus	Smears from staphylococcal lesions. Cultures of S. aureus typically yield golden-yellow colonies that are usually β-hemolytic
Staphylococcus epidermidis	found on skin and enter the bloodstream at the site of IV catheters that penetrate through the skin	Blood agar	prosthetic valve endocarditis and prosthetic joint infections	Gram+ cocci arrange in cluster (Grapelike), Catalase+, Coagulase-, no hemolysis & white colour colony on blood agar Sensitive to novobiocin	·         Flu-like symptoms, such as fever and chills, Fatigue. ·         Aching joints and muscles, Night sweats.		Nafcillin, vancomycin	Cultures of coagulase-negative staphylococci typically yield white colonies that are nonhemolytic
Staphylococcus Saprophyticus	Transmitted through sexual contact	Blood agar	Urinary Tract infection (especially cervicitis)	Gram+ cocci arrange in cluster (Grapelike), Catalase+, Coagulase-, no hemolysis & white colour colony on blood agar Resistant  to novobiocin	·         Large amounts of unusual vaginal discharge, ·         Frequent, painful urination.		trimethoprim-sulfamethoxazole or ciprofloxacin	Cultures of coagulase-negative staphylococci typically yield white colonies that are nonhemolytic

 

Inflammation

INFLAMMATION: It is a protective response by a vascularized tissue against any pathogen (bacteria, viruses, parasites) and cell injury to provide healing/ repair to that injured or infected tissue by destroying them.

TYPES OF INFLAMMATION:

1) ACUTE INFLAMMATION

2) CHRONIC INFLAMMATION

ACUTE INFLAMMATION:

·     An immediate and early response to injury

·     Relatively short duration (from few minutes upto few days)

·     Form inflammatory exudate

·     Mainly delivers neutrophil leukocytes (WBC) to the site of injury.

VASCULAR EVENTS  OF ACUTE INFLAMMATION:

1) Changes in Blood Vessel Diameter:  Initial vasoconstriction followed by vasodilation

2) Changes in Blood Flow: Initial increase in blood velocity due vasodilation but soon blood flow becomes slow due to increase in blood vessel permeability (loss of fluid from blood increases blood viscosity).

3) Increase in Vessel Permeability: Walls of blood vessels contain intercellular junctions (pores) which normally allows the passage of small molecules (water & ions). But in acute inflammation, endothelilal cells lining the blood vessels contracts causes the widening of these pores, therefore allows large molecules protein & plasma fluid to pass through the vessel walls. This process is known as exudation. Swelling caused by exudation is called inflammatory edema.

MECHANISM OF INC. PERMEABILITY OF VESSELS:

·     Immediate transient response:  

Ø      It occurs in response to mild injury

Ø      Permeability begins 1-2 minutes after the onset of injury and remains about 15-30 minutes

Ø      Mediated by histamine, bradykinin & leukotrines which causes contration of endothelial cells resulting in widening of pores

·     Delayed-prolonged response:

Ø      It occurs in response to moderate injury

Ø      Permeability begins 30minutes to 10 hours after the the onset of injury & reaches its peak in about 4-12 hours

Ø      Permeability increases due to direct injury of endothelial cells

·     Immediate-prolomged response

Ø   It occurs in response to severe injury

Ø   Permeability begins immediately after the injury and last for one to several days

Ø   Permeability increases due to necrosis of endothelial cells.

FACTORS WHICH REGULATES TRANSPORT OF EXUDATE:

·     Capillary Hydrostatic Pressure: It tends to escape the fluid out of the vessel.

·     Osmotic Pressure Of Protein In Intersitial Space: It tends to pull the fluid from vessels to interstitial space.

DURING INFLAMMATION EXUDATE FORMATION OCCURS DUE TO:

Increased capillary hydrostatic pressure due to enhance blood flow

Increased vascular permeability allowing plama protein to enter in intersitial space where they exert osmotic pressure & draws more fluid from the vessels

CELLULAR ( LEUKOCYTES) EVENTS:

SEQUENCE OF CELLULAR EVENTS:

1) MARGINATION:  Normally RBC & WBC flows in the central axis of blood vessel. During acute infalmmation, Due to increase in permeability, the flow of blood is slow inside vessel & therefore RBC stick together forming clumps or roulaex which is larger than WBC. These clumps forces WBCs to the periphery towards vessel walls (endothelial cells).

2) ADHESION: WBC becomes attach (adhere) to the endothelial cells of vessel wall. This adhesion is because of adhesion molecules present on the surfaces of both WBC & endothelial cells.

3) EMIGIRATION: Adherent leukocytes leaves the blood vessels and enters into interstitial space through intercellular junctions (pores).

It takes place in 2-10 minuts.

4) CHEMOTAXIS:  Process by which leukocytes are attracted towards and move towards an attractants usually a chemical substance at the site of injury.

5) PHAGOCYTOSIS: Process by which micro-organism and other forein body are engulfed and destroyed by neutrophils & macrophages.

This process is divided in three steps:

    I.            Recognition & Attachment: White Blood Cells indentify the object which they have to phagocytize. Recognition and attachment of most of the microorganism is facillitated by coating them with serum protein called  “Opsonin” which inturn binds to specific receptors on the leukocytes.

Opsonins are (i) C3b (ii) IgG

Engulfment:  Process occurs by pseudopodial extensions of leukocytes cytoplasm which completely encloses the foreign particles forming phagosome. Membranes of lysosomal granules fuse with it and form phagolysosomes. Lysosomes discharge their content into phagolysosomes causing killing & degradation of microorganis

Posterior Spinocerebellar Tract Short notes / flowchart (Neuroanatomy & Physiology)

POSTERIOR SPINOCEREBELLAR TRACT

• 1ST ORDER NEURON LIES IN POSTERIOR ROOT GANGLION, PASSES ITS AXONS TOWARDS POSTERIOR GRAY COLUMN AND SYNAPSE THERE WITH CELLS (2nd ORDER NEURONS). THESE NEURONS COLLECTIVELY CALLED AS NUCLEUS DORSALIS (CLARKE'S COLUMN). 

• THE AXONS OF 2nd ORDER NEURON ENTERS THE POSTERIOLATERAL PART OF LATERAL WHITE COLUMN & ASCENDS TO THE MEDULLA.

• HERE, THE AXONS (TRACT) JOINS THE INFERIOR CEREBELLAR PEDUNCLES AND TERMINATES IN CEREBELLUM.

Types Of Stretching Therapeutic Exercise

TYPES OF STRETCHING ACCORDING TO DURATION OF STRETCH:

1) STATIC STRETCHING: Soft tissues are elongated just past the point of its resistance & then held in the lengthen position with a sustained stretch force over a period of time.

2) CYCLIC (INTERMITTENT) STRETCHING: Short duration stretch stretch force repeatedly but gradually applied then released and then reapplied.

“In cyclic stretcing low intensity stretching is used & In ballistic stretching high intensity stretching is used hence both are different from eachother”.

TYPES OF STRETCHING ACCORDING TO SPEED OF STRETCH:

3) BALLISTIC STRETCHING: A rapid high speed and high intensity forceful intermittent stretch.

TYPES OF STRETCHING ACCORDING TO MODE OF STRETCH:

4 ) MANUAL STRETCHING: A therapist applies force externally to move the involve body segment slightly to the point beyond the point of tissue resistance and available ROM.

5) SELF STRETCHING: Stretching procedures carried out by patient independently after careful instruction & supervison practice.

6) MECHANICAL STRETCHING: Stretch force applied by devices with low intensity over a prolonged period of time to create permanent lengthening of soft tissue

CLINICAL ANATOMY OF KNEE JOINT

DESCRIPTION:

Knee Joint, also termed as tibiofibular joint is one of the most important joint in human body which helps in movement and weight bearing. Knee Joint is encased by a capsule filled with fluid called synovial fluid. It is a complex joint contains great clinical significance.

TYPE:

Synovial Hinge Joint

LIGAMENTS AND THEIR FUNCTIONS:

The Ligaments Of Knee Joint are divided under two categories:

      1) Extracapsular Ligaments

      2) Intracapsular Ligaments

EXTRACAPSULAR LIGAMENTS:

LIGAMENTS	FUNCTIONS
Patellar Ligament	Connects Patella with Tibia
Medial Collateral Ligament	Prevents lateral displacement of knee joint
Lateral Collateral Ligament	Prevents medial displacement of knee joint

INTRACAPSULAR LIGAMENTS:

LIGAMENTS	FUNCTIONS
Medial & Lateral Menisci	Act as a shock absorber
Anterior Cruciate Ligament	Prevents the knee from Hyperextension
Posterior Cruciate Ligament	Supports the posterior side of the knee

CLINICAL CASES:

    ·      During sports or any strenous activities, If a blow (any       hard objects) hits the medial side of the knee joint,             Lateral Collateral Ligament will most likely to be           injured.

    ·      During sports or any strenous activities, If a blow              (any hard objects) hits the lateral side of the knee joint,      Medial Collateral Ligament will most likely to be          injured.

    ·      In an accident, in which knee becomes hyperextended      above its normal range of motion, Anterior Cruciate          Ligament will most likely to be teared. (Anterior                Cruciate Ligament injury is common as compared to        Posterior Cruciate Ligament)

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ANTERIOR COMPARTMENT OF THIGH 

Posted 

OBJECTIVES:

Identify the muscles of the anterior compartment of thigh in terms of their origin, insertion, nerve supply and actions.

CONTENTS

• Muscles Of The Anterior Compartment Of Thigh
• Their Nerve Supply
• Actions
• Origin Insertion
• Summary

INTRODUCTION:

In order to make study easier, The Anatomy of thigh is studied in three compartments, namely Anterior, Posterior and Medial Compartmant Of Thigh. The discussion topic of this article is the Anterior Compartment Of Thigh.

MUSCLES:

• QUADRICEPS: The major muscle group present in the Anterior compartment of the thigh. Rectus Femoris, Vastus Lateralis, Vastus Medialis and Vastus Intermedius are the muscles forming this group.
• ILIOPSOAS: A small group muscle in the Anterior compartment of the thigh formed by muscles Iliacus, Psoas Major and Psoas Minor. They are termed as one because they share common tendon.
• PECTINEUS
• SARTORIUS

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NERVE SUPPLY

All the muscles of the Anterior compartment of thigh is innervated by Femoral Nerve (L2,L3 and L4) except Psoas Major & Minor, which are innervated by L1, l2 & L3 anterior rami. Femoral nerve the main nerve of lumbar plexuses formed by anterior rami of lumbar 2nd,3rd and 4th nerves.

MUSCLE ACTIONS:

• QUADRICEPS: Extension of leg at knee joint
• ILIOPSOAS: Flexes thigh at hip joint
• PECTINEUS: Flexion, Adduction & assist in medial rotation
• SARTORIUS: At Hip Joint – Flexion, Abduction & Lateral Rotation At Knee Joint – Flexion

ORIGIN AND INSERTION:

• QUADRICEPS: Rectus Femoris Originate from Anterior Inferior Iliac Spine, Vastus Lateralis Originate from greater trochanter & Lateral lip of Linea Aspera, Vastus Medialis Originate from intertrochanteric line & Medial lip of Linea Aspera, Vastus Intermedius Originate from Anterolateral surface of Femur shaft. All the four muscles insert in patella bone by sharing common tendon “Quadriceps Tendon”.
• ILIOPSOAS: Iliacus Muscle Originate from Iliac Crest & Iliac Fossa of Ilium Bone & Insert in Lesser Trochanter of femur. Psoas Major & Minor Orginate from Each side of Thoracic 12th till Lumbar 5 vertebrae & Insert in Lesser Trochanter Of Femur
• PECTINEUS: Originate from Pubis ( Superior Ramus) & Insert in Pectineal Line of Femur bone
• SARTORIUS: Originate from Anterior Superior Iliac Spine & Insert in Superior medial surface of Tibia bone

SUMMARY:

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