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NEET MDS Synopsis

COENZYMES
Biochemistry

COENZYMES

 Enzymes may be simple proteins, or complex enzymes.

A complex enzyme contains a non-protein part, called as prosthetic group (co-enzymes).

Coenzymes are heat stable low molecular weight organic compound. The combined form of protein and the co-enzyme are called as holo-enzyme. The heat labile or unstable part of the holo-enzyme is called as apo-enzyme. The apo-enzyme gives necessary three dimensional structures required for the enzymatic chemical reaction.

Co-enzymes are very essential for the biological activities of the enzyme.

Co-enzymes combine loosely with apo-enzyme and are released easily by dialysis. Most of the co-enzymes are derivatives of vitamin B complex

First Generation Cephalosporins
Pharmacology

First Generation Cephalosporins

Prototype Drugs are CEFAZOLIN (for IV use) and CEPHALEXIN (oral use).

1. Staph. aureus - excellent activity against b-lactamase-producing strains
Not effective against methicillin-resistant Staph. aureus & epidermidis

2. Streptococci - excellent activity versus Streptococcus sp.
Not effective against penicillin-resistant Strep. pneumoniae

3. Other Gm + bacteria - excellent activity except for Enterococcus sp.

4. Moderate activity against gram negative bacteria.

Caution: resistance may occur in all cases.
Susceptible organisms include:

E. coli
Proteus mirabilis
Indole + Proteus sp. (many strains resistant)
Haemophilus influenzae (some strains resistant)
Neisseria sp. (some gonococci resistant)


Uses
1. Upper respiratory tract infections due to Staph. and Strep.
2. Lower respiratory tract infections due to susceptible bacteria e.g. Strep.pneumoniae in penicillin-allergic patient (previous rash)
3. Uncomplicated urinary tract infections (Cephalexin)
4. Surgical prophylaxis for orthopedic and cardiovascular operations (cefazolin preferred because of longer half-life)
5. Staphylococcal infections of skin and skin structure

Sliding Osseous Genioplasty
Oral and Maxillofacial Surgery

Sliding Osseous Genioplasty
Sliding osseous genioplasty is a surgical technique designed
to enhance the projection of the chin, thereby improving facial aesthetics. This
procedure is particularly advantageous for patients with retrogathia,
where the chin is positioned further back than normal, and who typically present
with Class I occlusion (normal bite relationship) without
significant dentofacial deformities.
Indications for Sliding Osseous Genioplasty


Aesthetic Chin Surgery:

Most patients seeking this procedure do not have severe dentofacial
deformities. They desire increased chin projection to achieve better
facial balance and aesthetics.



Retrogathia:

Patients with a receding chin can significantly benefit from sliding
osseous genioplasty, as it allows for the forward repositioning of the
chin.



Procedure Overview
Sliding Osseous Genioplasty involves several key steps:


Surgical Technique:

Incision: The procedure can be performed through an
intraoral incision (inside the mouth) or an extraoral incision (under
the chin) to access the chin bone (mandibular symphysis).
Bone Mobilization: A horizontal osteotomy (cut) is
made in the chin bone to create a movable segment. This allows the
surgeon to slide the bone segment forward to increase chin projection.
Fixation: Once the desired position is achieved,
the bone segment is secured in place using plates and screws or other
fixation methods to maintain stability during the healing process.



Versatility:

Shorter and Longer Advancements: The technique can
be tailored to achieve both shorter and longer advancements of the chin,
depending on the patient's aesthetic goals.
Vertical Height Alterations: Sliding osseous
genioplasty is particularly effective for making vertical height
adjustments to the chin, allowing for a customized approach to facial
contouring.



Recovery


Postoperative Care:

Patients may experience swelling, bruising, and discomfort following
the procedure. Pain relief medications are typically prescribed to
manage discomfort.
A soft diet is often recommended during the initial recovery phase
to minimize strain on the surgical site.



Follow-Up Appointments:

Regular follow-up visits are necessary to monitor healing, assess
the alignment of the chin, and ensure that there are no complications.
The surgeon will evaluate the aesthetic outcome and make any
necessary adjustments to the postoperative care plan.



Macrolide
Pharmacology

Macrolide

The macrolides are a group of  drugs (typically antibiotics) whose activity stems from the presence of a macrolide ring, a large  lactone ring to which one or more deoxy sugars, usually cladinose and desosamine, are attached. The lactone ring can be either 14, 15 or 16-membered. Macrolides belong to the polyketide class of natural products.

The most commonly-prescribed macrolide antibiotics are:  

Erythromycin,  Clarithromycin, Azithromycin, roxithromycin,

Others are: spiramycin (used for treating  toxoplasmosis), ansamycin, oleandomycin, carbomycin and tylocine.

There is also a new class of antibiotics called ketolides that is structurally related to the macrolides. Ketolides such as telithromycin are used to fight respiratory tract infections caused by macrolide-resistant bacteria.

Non-antibiotic macrolides :The drug Tacrolimus, which is used as an

immunosuppressant, is also a macrolide. It has similar activity to  cyclosporine.

Uses : respiratory tract infections and soft tissue infections.

Beta-hemolytic  streptococci,  pneumococci, staphylococci and enterococci are usually susceptible to macrolides. Unlike penicillin, macrolides have shown effective against mycoplasma, mycobacteria, some rickettsia and chlamydia.

Mechanism of action: Inhibition of bacterial protein synthesis by binding reversibly to the subunit 50S of the bacterial ribosome, thereby inhibiting translocation of peptidyl-tRNA. This action is mainly bacteriostatic, but can also be bactericidal in high concentrations

Resistance : Bacterial resistance to macrolides occurs by alteration of the structure of the bacterial ribosome.

Hemorrhage
Oral and Maxillofacial Surgery

Types of Hemorrhage
Hemorrhage, or excessive bleeding, can occur during and after surgical
procedures. Understanding the different types of hemorrhage is crucial for
effective management and prevention of complications. The three main types of
hemorrhage are primary, reactionary, and secondary hemorrhage.
1. Primary Hemorrhage

Definition: Primary hemorrhage refers to bleeding that
occurs at the time of surgery.
Causes:
Injury to blood vessels during the surgical procedure.
Inadequate hemostasis (control of bleeding) during the operation.


Management:
Immediate control of bleeding through direct pressure,
cauterization, or ligation of blood vessels.
Use of hemostatic agents or sutures to secure bleeding vessels.


Clinical Significance: Prompt recognition and
management of primary hemorrhage are essential to prevent significant blood
loss and ensure patient safety during surgery.

2. Reactionary Hemorrhage

Definition: Reactionary hemorrhage occurs within a few
hours after surgery, typically when the initial vasoconstriction of damaged
blood vessels subsides.
Causes:
The natural response of blood vessels to constrict after injury may
initially control bleeding. However, as the vasoconstriction diminishes,
previously damaged vessels may begin to bleed again.
Movement or changes in position of the patient can also contribute
to the reopening of previously clamped vessels.


Management:
Monitoring the patient closely in the immediate postoperative period
for signs of bleeding.
If reactionary hemorrhage occurs, surgical intervention may be
necessary to identify and control the source of bleeding.


Clinical Significance: Awareness of the potential for
reactionary hemorrhage is important for postoperative care, as it can lead
to complications if not addressed promptly.

3. Secondary Hemorrhage

Definition: Secondary hemorrhage refers to bleeding
that occurs up to 14 days postoperatively, often as a result of infection or
necrosis of tissue.
Causes:
Infection at the surgical site can lead to tissue breakdown and
erosion of blood vessels, resulting in bleeding.
Sloughing of necrotic tissue may also expose blood vessels that were
previously protected.


Management:
Careful monitoring for signs of infection, such as increased pain,
swelling, or discharge from the surgical site.
Surgical intervention may be required to control bleeding and
address the underlying infection.
Antibiotic therapy may be necessary to treat the infection and
prevent further complications.


Clinical Significance: Secondary hemorrhage can be a
serious complication, as it may indicate underlying issues such as infection
or inadequate healing. Early recognition and management are crucial to
prevent significant blood loss and promote recovery.

HERPES SIMPLEX
General Pathology

HERPES SIMPLEX

An infection with herpes simplex virus characterized by one or many clusters of small vesicles filled with clear fluid on slightly raised inflammatory bases.

The two types of herpes simplex virus (HSV) are HSV-1 and HSV-2. HSV-1 commonly causes herpes labialis, herpetic stomatitis, and keratitis; HSV-2 usually causes genital herpes, is transmitted primarily by direct (usually sexual) contact with lesions, and results in skin lesions

Primary infection of HSV-1 typically causes a gingivostomatitis, which is most common in infants and young children. Symptoms include irritability, anorexia, fever, gingival inflammation, and painful ulcers of the mouth.

Primary infection of HSV-2 typically occurs on the vulva and vagina or penis in young adults

Herpetic whitlow, a swollen, painful, and erythematous lesion of the distal phalanx, results from inoculation of HSV through a cutaneous break or abrasion and is most common in health care workers.

RESPIRATORY DISORDERS - Emphysema
Physiology

4.    Emphysema
1. Permanent enlargement of airways with distension of alveolar walls
 
    Thickened Bronchial Submucosa, Edema & Cellular Infiltration (loss of elasticity), Dilation of Air spaces, due to destruction of alveolar walls (Air trapped by obstruction)

2.    Lower Respiratory tree destruction

    Respiratory Bronchioles, Alveolar ducts, & Alveolar sacs

Types of Emphysema:
    
    1.    Centrilobular (Centriacinar) = Respiratory Bronchioles
    Rarely seen in non Smokers, More in Men than Women, Found in Smokers with Bronchitis

    2.    Panlobular (Panacinar) 

    Hereditary, Single autosomal recessive gene. Deficient in 1-globulin (1-antitrypsin), Protects respiratory tract from neutrophil elastase (Enzyme that distroys lung connective tissue) , Aged persons, Results from Bronchi or Bronchiolar constriction

    NOTE: Smoking = Leading cause of Bronchitis, Emphysema
 

HEART DISORDERS
Physiology

HEART DISORDERS


Pump failure => Alters pressure (flow) =>alters oxygen carrying capacity.

Renin release (Juxtaglomerular cells) Kidney
Converts Angiotensinogen => Angiotensin I
In lungs Angiotensin I Converted => Angiotensin II
Angiotensin II = powerful vasoconstrictor (raises pressure, increases afterload)

stimulates thirst
stimulates adrenal cortex to release Aldosterone
(Sodium retention, potassium loss)
stimulates kidney directly to reabsorb Sodium
releases ADH from Posterior Pituitary




Myocardial Infarction
 


Myocardial Cells die from lack of Oxygen
Adjacent vessels (collateral) dilate to compensate
Intracellular Enzymes leak from dying cells (Necrosis)

Creatine Kinase CK (Creatine Phosphokinase) 3 forms

One isoenzyme = exclusively Heart (MB)
CK-MB blood levels found 2-5 hrs, peak in 24 hrs
Lactic Dehydrogenase found 6-10 hours after. points less clearly to infarction


Serum glutamic oxaloacetic transaminase (SGOT)

Found 6 hrs after infarction, peaks 24-48 hrs at 2 to 15 times normal,
SGOT returns to normal after 3-4 days




Myocardium weakens = Decreased CO & SV (severe - death)
Infarct heal by fibrous repair
Hypertrophy of undamaged myocardial cells

Increased contractility to restore normal CO
Improved by exercise program


Prognosis

10% uncomplicated recovery
20% Suddenly fatal
Rest MI not fatal immediately, 15% will die from related causes




Congenital heart disease (Affect oxygenation of blood)

Septal defects
Ductus arteriosus
Valvular heart disease

Stenosis = cusps, fibrotic & thickened, Sometimes fused, can not open
Regurgitation = cusps, retracted, Do not close, blood moves backwards





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