Rabu, 22 Juni 2011

Old Surgical Instruments Pictures Collection

Lithotome (1740s-1830s)

Knife in 1900s

Hysterotome 1860-90

Mouth Gag 1880s-1910

Hernia Tool 1850's

Hemorrhoid Forcep 1800s

Ecraseur 1870's

Circumcition Knife 1770's

Hirtz compass 1915

Bullet Extractor 1500s

Artificial Leech 1800's

Arrow Remover 1500's

Amputation Saw 1600's

Cervical Dilator 1800's

Selasa, 14 Juni 2011

Removable Appliences-Principles of Applience Therapy Powerpoint Presentation Free Download

This Presentation Includes,
  • Orthodontic movement of teeth
  • Active components
  • Springs
  • bows
  • Screws
  • Retentive components
  • Base Plate
Removable Appliences-Principles of Applience Therapy
Powerpoint Presentation Free Download

Development of Dentition Related to Orthodontics PowerPoint Presentation Free Download

This Presentation Includes,
  • Deciduous Dentition
  • Over jet
  • Over bite
  • Arch Relationship
  • Sequence of Eruption
  • Development of Dentition
  • Physiological Diastema
  • Jaw size Relationship
  • Occlusal Features
Development of Dentition Related to Orthodontics
PowerPoint Presentation Free Download

Key Words : pediatric dentist children's dentist kids dentist pediatric dentistry childrens dentist dentist children dentist for kids pediatric dental dental care pediatric dental office pediatric dentistry children dentist for child pediatric dental office kid's dentist pedodontist dental sealants

Class 2 Division 1 Malocclusion Powerpoint Presentation Free Download

This Presentation Includes,
  • Problems in Class 2 Division 1 Malocclusion
  • Timing of Treatment
  • Features of Case suitable for Early Correction
  • Treatment Objectives
  • Treatments with Removable Appliances
  • Precautions
  • Clinical Guidelines
  • Assessment with progression
  • Mandibular growth with removable appliences
Class 2 Division 1 Malocclusion
PowerPoint Presentation Free Download

Class 2 Division 1 Malocclusion PowerPoint Presentation Free Download

Jumat, 10 Juni 2011

Cellular Adaptations PowerPoint Presentation Free Download

Cellular Adaptations PowerPoint Presentation includes
  • Hyperplasia
  • Hypertrophy
  • Atrophy
  • Cellular adaptation to abnormal stimuli
  • Metaplasia
Cellular Adaptations
PowerPoint Presentation Free Download

Skin Pigmentations and Calcifications PowerPoint Presentation free Download

This "Skin Pigmentations and Calcifications" PowerPoint Presentation Includes
  • Skin Pigments
  • Hyper pigmentation
  • Hypo pigmentation
  • Addison’s disease
  • CafĂ© Au Leit Pigmentation
  • Neurofibromatosis
  • Hyper-pigmented skin nodules
  • Lack of pigmentation
  • Vitiligo
  • Ochronosis
  • Haemosiderosis
  • Haemachromatosis/Bronze diabetes
  • Wilson’s disease
  • Lipofuscins
  • Exogenous pigments
  • Heterotrophic calcification
  • Dystrophic calcification
  • Metastatic calcification
  • Mechanism of calcification
  • Chondrocalcinosis
Skin Pigmentations and Calcifications
PowerPoint Presentation Free Download

Kamis, 09 Juni 2011

Management of Dental Patient on antiplatelet & anticoagulant treatment

Anti platelet drugs and anticoagulants are prescribed more than in the past
·       Increased prevalence of ischaemic heart disease, strokes and thrombophilia
·       More aging population due to increased life expectancy

Anti Platelet Medication is indicated for
·       Ischaemia heart disease
·       Peripheral vascular disease
·       Strokes due to thromboembolic disease

How do anti platelet drugs affect clotting ?
·       Platelets provide the initial haemostatic plug at the site of a vascular injury.
·       They are also involved in pathological processes and are an important contributor to arterial thrombosis leading to myocardial infarction and ischaemic stroke.

Antiplatelet medications include

Low dose aspirin (75mg-300mg daily).
·        Secondary prevention of thrombotic cardiovascular
·        or cerebrovascular disease
·        and following coronary artery bypass

·        Prevention of atherothrombotic events in patients suffering myocardial infarction
·        Ischaemic stroke or peripheral arterial disease
·        unstable angina or non-Q-wave myocardial infarction in acute coronary syndrome

Dipyridamole (Persantin, Persantin Retard).
·        Used as an adjunct to oral anticoagulation for the prophylaxis of thromboembolism associated with prosthetic heart valves,
·        For secondary prevention of ischaemic stroke and transient ischaemic attacks.

Asasantin Retard
·        Contains both aspirin and dipyridamole and is used for the secondary prevention of stroke and transient ischaemic attacks.
All antiplatelet medications affect clotting by inhibiting platelet aggregation
Aspirin and clopidogrel irreversibly inhibit platelet aggregation within one hour of ingestion and this lasts for the life of the platelets (7-10 days). The effect is only overcome by the manufacture of new platelets.
The action of dipyridamole is reversible.
Non-steroidal anti-inflammatory drugs (NSAIDs) other than aspirin (e.g. ibuprofen, diclofenac) have a reversible effect on platelet aggregation and platelet function is restored once the drug is cleared from the circulation.

What are the thromboembolic risks associated with stopping antiplatelet medications in the perioperative period?
Stopping aspirin prior to surgical procedures may increase the risk of thromboembolic events by 0.005%.
What are the risks of bleeding associated with continuing antiplatelet
medications in the perioperative period?
Patients taking antiplatelet medications will have a prolonged bleeding time but this may not be clinically relevant.
Postoperative bleeding after dental procedures can be controlled using local haemostatic measures.

Clinically significant postoperative bleeding
·       Continues beyond 12 hours
·       Causes the patient to call or return to the dental practice or accident and emergency department
·       Results in the development of a large haematoma or ecchymosis within the oral soft tissues
·       Requires a blood transfusion
·       Patients with underlying hepatic, renal or bone marrow disorders often have disease related Bleeding disorders.
·       Bleeding risk also increases with age and with heavy alcohol consumption.

How do the risks of thromboembolic events and postoperative bleeding balance?
·       Bleeding complications, while inconvenient, do not carry the same risks as thromboembolic complications.Patients are more at risk of permanent disability or death if they stop antiplatelet medications prior to a surgical procedure than if they continue it.
·       Published reviews of the available literature advise that aspirin should not be stopped prior to dental surgical procedures.
·       Thromboembolic events, including fatalities, have been reported after antiplatelet withdrawal.
·       Although the risk is low, the outcome is serious. This must be balanced against the fact that there is no single report of uncontrollable bleeding when dental procedures have been carried out without stopping antiplatelet medications
·       Antiplatelet medications should only be discontinued in the perioperative period when the haemorrhagic risk of continuing them is definitely greater than the cardiovascular risk associated with their discontinuation.
·       Consensus is that for minor surgical procedures, including procedures, antiplatelet medications should not be stopped or doses altered but that local haemostatic measures are used to control bleeding.

Which patients taking antiplatelet medication should not undergo surgical procedures in primary care?
·       Liver impairment and/or alcoholism renal failure
·       Thrombocytopenia, haemophilia or other disorder of haemostasis
·       Those currently receiving a course of cytotoxic medication.
·       Patients requiring major surgery are unlikely to be treated in the primary care setting.

For what procedures can antiplatelet medications be safely continued?
·       Minor surgical procedures can be safely carried out without altering the antiplatelet medication dose. Those likely to be carried out in primary care will be
·        Simple extraction of up to three teeth, gingival surgery, crown and bridge procedures, dental scaling and the surgical removal of teeth.
·        When more than 3 teeth need to be extracted then multiple visits will be required. The extractions may be planned to remove 2-3 teeth at a time, by quadrants, or singly at separate visits.
·       Scaling and gingival surgery should initially be restricted to a limited area to assess if bleeding is problematic.
Patients on Warfarin
INR range
·       Prophylaxis of deep vein thrombosis 2-3
·       Prophylaxis of pulmonary embolism 2-3
·       Atrial fibrillation 2-3
·       Recurrence of embolism (not on warfarin) 2-3
·       Recurrence of embolism (on warfarin) 3-4
·       Mechanical prosthetic heart valves 3-4
·       Antiphospholipid antibody syndrome 3-4
*** In theory all patients on Warfarin should have INR <4
Are patients at risk of thromboembolic effects if Warfarin discontineud
Stopping Warfarin for two days increases thrombolic effects
Stopping Warfarin can lead to a rebound hypercoagulable state ?
Are patients at risk of bleeding if Warfarin continues? Yes
Treatment with Warfarin impairs clotting and the patients have increased risk of bleeding during surgical procedures and post operatively.
Bleeding in mouth can be excessive even in non anticoagulated patients as the tooth support structures are highly vascular and due to the fibrinolytic effect of saliva.
Most cases of bleeding can be managed by pressure or repacking and resuturing the socket
The incidence of post operative bleeding not controlled by local measures varies from 0-3.5%

How do the thromboembolic effects and bleeding risk balance?
Bleeding complications, while inconvenient, do not carry the same risk as thrombo-embolic complications.
Patients whose INR are within the therapeutic range are more at risk of permanent disability or death if they have Warfarin stopped prior to surgical procedure than continuing it.

Which patients taking Warfarin should not undergo surgery in primary care
Patients who have INR over 4 should not undergo surgery without consulting the haematologist. Their Warfarin dose needs to be adjusted before surgery.
Patients who are maintained with an INR over 4 needs to be referred to a dental hospital for surgery.

When should the INR be measured before a dental procedure?
INR must be measured prior to dental procedures, ideally this should be done 24 hours before the procedure.
For patients who have stable INR values, the INR should be measured at least 72 hours before the procedure.

Up to what INR value can dental procedures be carried out?
Minor surgical procedures can be safely carried out in patients with INR <4
Minor procedures can be carried out without altering the Warfarin therapy if the INR is within therapeutic range.

How should the risk of bleeding due to either antiplatelet or anticoagulants be managed?
Think about the timing of the surgery. Planned surgery should ideally be:
At the beginning of the day - this allows more time to deal with immediate re-bleeding problems.
Early in the week - this allows for delayed re-bleeding episodes occurring after 24–48 hours to be dealt with during the working week.
Local anaesthetic
A local anaesthetic containing a vasoconstrictor should be administered by infiltration or by intraligamentary injection wherever practical.
Regional nerve blocks should be avoided when possible. However, if there is no alternative, local anaesthetic should be administered cautiously using an aspirating syringe.
Local vasoconstriction may be encouraged by infiltrating a small amount of local anaesthetic containing adrenaline (epinephrine) close to the site of surgery.
Local haemostasis
Sockets should be gently packed with an absorbable haemostatic dressing e.g.
oxidised cellulose, collagen sponge, resorbable gelatin, sponge
Then carefully sutured. Resorbable sutures.
If non-resorbable sutures are used, remove after 4-7 days.
Following closure, pressure should be applied to the socket(s) by using a gauze pad that the patient bites down on for 15 to 30 minutes.
Efforts should be made to make the procedure as atraumatic as possible and any bleeding should be managed using local measures.
Tranexemic mouth washes are useful.
Patients should be given clear instructions on the management of the clot in the postoperative period and advised
To look after the initial clot by resting while the local anaesthetic wears off and the clot fully forms (2-3 hours)
To avoid rinsing the mouth for 24 hours
Not to suck hard or disturb the socket with the tongue or any foreign object
To avoid hot liquids and hard foods for the rest of the day
To avoid chewing on the affected side until it is clear that a stable clot has formed.
Care should then be taken to avoid dislodging the clot if bleeding continues or restarts, to apply pressure over the socket using a folded clean handkerchief or gauze pad. Place the pad over the socket and bite down firmly for 20 minutes. If bleeding does not stop, the dentist should be contacted; repacking and re suturing of the socket may be required
whom to contact if they have excessive or prolonged postoperative bleeding.

How should postoperative pain control be managed?
Generally paracetamol is considered a safe over the counter analgesic for patients taking antiplatelet medications and it may be taken in normal doses if pain control is needed and no contraindication exists.
Patients should be advised to not to take Aspirin at analgesic doses and non-steroidal anti-inflammatory drugs (NSAIDs) e.g. ibuprofen are considered less safe and should be avoided if possible
Are there any drug interactions that are relevant to patients on antiplatelet drugs undergoing dental surgical procedures
NSAIDs in combination with aspirin or clopidogrel should be used with caution. NSAIDs can damage the lining of the gastro-intestinal tract leading to bleeding that may be worsened by aspirin or clopidogrel.
There is no evidence of an interaction between dipyridamole and NSAIDs.
The concomitant use of dipyridamole plus aspirin does not increase the risk of bleeding.

Drug interactions with Warfarin
Amoxycillin: Increases INR and may cause bleeding
Metranidazole: Caution! Interacts with Warfarin and should be avoided. If unavoidable, use 1/3-1/2 dose of Warfarin.
Erythromycin: unpredictable interaction
Aspirin & NSAID: Avoid! There is increased risk of gastro intestinal haemorrhage
Antiplatelet and anticoagulant therapy does not need to be stopped before minor dental surgical procedures
Discontinuing antiplatelet /anticoagulation therapy for surgery was associated with an increased risk of thromboembolism
Good local haemostasis & better planning will decrease the excessive bleeding and minimize complications

Chronic Inflammation,Granulomatous Dieases,Tuberculosis Pathology Lecture Note

Chronic inflammation

Chronic Suppurative on acute:

Chronic granulomatus: (Initiates without an acute phase)

Suppurative in type:


Inadequate or delayed drain leads to thick fibrous wall formation.

The residual bacteria get reactivated

Pus formation.

Presence of foreign material or indigestible dead tissue.

Eg: Osteomyelitis, damaged Collagen

Chronic inflammation

Follow acute inflammation

Persistence of the stimulus

Disturbance to the healing process

Repeated bouts of acute inflammation and healing in between.

Low grade persistent infection.


Prolong process in which destruction and acute inflammation proceeds together with the healing process.


Sequelae of an acute inflammation

Foreign bodies

Microorganisms where body can mount limited immune reactions

Impaired body defense

Immune reactions

Chronic inflammation without an acute phase

Infection: TB, Leprosy, Syphilis

Immunological: Rheumatiod arthritis Ulcerative colitis Crohn’s disease

Poor bloodsupply (leg ulcer)

Chronic inflammatory lesions

May vary histologically according to causative agent

However there is a set of morphological features in common.


Infiltration by mononuclear cells



plasma cells

Proliferation of blood vessels/fibrosis (angiogenesis)


Tissue destruction (induce by inflammatory cells)

Mononuclear phagocytic system

Blood monocyte:

Macrophages (at extra vascular tissue)

Tissue macrophages (Scattered in connective tissue or concentrated in organs)

Eg: Kupffer cells in Liver

Sinus histiocytes in lymph nodes

Alveolar macrophages in lung

Osteoclasts in bones

Microglia (CNS)



Morphological transformation (macrophages and giant cells)


Secretion of biologically active products

Cells types present




Mast cells

Existence of CI, AI and repair

Macrophages persist at the site (Due to the influence of chemical mediators)

Destruction of invading microorganisms /normal tissues

Secretion of chemical mediators by macrophages

Functions of them,

Proliferation of fibroblasts, Laying down of collagen

Angiogenesis, Activation of lympho macrophages

· Dead and dieing leukocytes/necrotic tissues helps in developing acute inflammation

Granulomas /Granulomatus infection

Chronic inflammatory lesion in the form of mass.

Collection of macrophages or modified macrophages (epitheliod / giant cells)

Granulomas /Granulomatus infection

A granuloma is a focal area of granulomatus inflammation.

Consist of macrophage aggregation

Epithelial cell transformation

Collar of lymphocytes

Appearance giant cells and of fibrosis can see with the time




Cat scratch disease



Mycotic infections

Two types of granulomas: Base on pathogenesis

Foreign body type:

Form around foreign bodies

Immune type: When the foreign practical are capable of induce cell mediate immune responses

(but not always granulomas will develop)


Granulomas is a result of chronic inflammatory reaction containing a collection of cells of monocytic series arrange in a compact mass.



Epithelioid cells

Giant cells: Langhans giant cells

Foreign body type giant cells

Accumulation of macrophages

· Under the influence of chemotaxis

C5a, fibrinopeptides, cationic proteins

Lymphokines :

PDGF, TGF(beta)

products of collagen brake down

· By mitotic division

· Immobilization and prolong survival (if the irritants are low virulent )


· Chronic disease common worldwide.

· Causes a characteristic granulomatous inflammation

· Inability of the neutrophils to kill the micro organisms due to lipoprotein coating.

· Mycobacterium tuberculosis.

Hominis (lungs)

Bovis (Tonsils, Intestine)


Droplet from patients (weeks or months)



However need sustain contact than casual contact.

Tissue damage

MT has no Endotoxins


Histiolitic enzymes

Development of immune response against outer coat of the organism.

Tuberculin test

2 to 4 weeks after infection : + Tuberculin test

PPD (purified protein derivative)

(Culture in which TB is grown)

Induration More that 5.mm within 48 hours.

Positivity indicates infection but not the disease.

Primary Tuberculosis

Occurs in individuals who have never previously been infected with M. tuberculosis (childhood infection if TB is common, adult life if uncommon)

Usually caused by inhalation of the organisms or rarely by ingestion of the organism.

Primary infection

Lungs Hilum

Tonsils neck nodes

Intestine mesentery

Primary Tuberculosis

In respiratory system, inhalation of the organisms cause a subpleural lesion usually in the lower part of the upper lobe or upper part of the lower lobe. This is called Ghon focus.

Location is in these sites is because bacterium is a strict aerobe and prefers these well oxygenated regions

Ghon’s focus

· When the tissue is invaded by the mycobacteria there is no hypersensitivity reaction. Instead there is acute, non specific inflammatory response with predominant neutrophils.

· This is followed by macrophages which ingest the bacilli and present Ags to to T lymphocytes leading to proliferation of a clone of T cells .

· The emergence of specific hypersensitivity lead to release of lymphokines,that attract more macrophages.

· These accumulate to form the characteristic granuloma.

Ghon focus

Usually single

1 to 2 cm

Location –Beneath pleura- mid zone of the lung

Primary complex

Tubercle bacilli, either free or contained in macrophages, may drain to the regional lymph nodes and set up granulomatous inflammation, causing massive lymph node enlargement.

The combination of the Ghon focus, draining lymphatics and the regional lymph nodes is called the primary complex.

Calcification of the lymph nodes

Microscopic appearance

Sequelae of primary complex

Healing with small fibrous scar replacing caseous necrosis. Lesion will be walled off.


Reactivation of infection later when host defences become lowered.

plural effusion

Enlarged caseous nodes can obstruct bronchi, leading to collapse, retention of secretion and inflammatory consolidation

Caseous node erodes into a bronchi with satellite lesions in lungs (TB bronchopneumonia).

Eroding into a pulmonary vein causing generalised milliary TB.

Erosion into pulmonary artery leads to miliary TB of lungs

TB bronchopneumonia

· Opening of the caseous node to a bronchus.

· Air bone infection

· TB bronchopneumonia

· (Multiple pneumonic patches arrangeed in and around terminal bronchi)

· The lesions spread rapidly and accumulate macrophages and lymphocytes followed by necrosis

TB bronchopneumonia

Necrotic patches get enlarged and discharged which will lead to dissemination and cavitations. (no fibrous walls)


TB bronchopneumonia can happen after both 1ry and 2ry TB.

Rapidly spreading tuberculous bronchopneumonia: debilitated by intercurrent disease, diabetes, malnutrition etc.

Acute miliary tuberculosis of the lungs due to blood stream spread to lungs. Grey tubercles visible to naked eye 3mm in diameter. More numerous and larger in upper lobes than lower lobes. Microscopically these are ill formed and often giant cells are absent. Usually these lesions do not cavitate

Effects on the other organs of the body

Miliary tuberculosis due to systemic spread to kineys, spleen, brain, liver etc.

Tuberculous ulcers in the intestine due swallowed sputum.

Tuberculosis of larynx due to direct spread from sputum.

Secondary amyloidosis.

Miliary TB

Common with 1ry TB

Due to involvement of veins

Multiple scatted tubercles

Not well developed/uniform in size

1-2 mm

Some times without giant cells (necrosis)

Secondary Tuberculosis (Post primary)

Infection may me exogenous or endogenous

After active primary infection

Reactivation asymptomatic primary lesions:


Severe illness,

Intercurrent lung infection,

Systemic immunosuppression

Exogenous: caused by inhaled organisms


During primary tuberculosis or during BCG immunisation, the patient develops cell mediated immunity to antigens of tubercle bacillus.

This is demonstrated by skin test (Mantoux) test

Immunity is associated with increased resistance to subsequent infection.

Re infected lesions:

Apex of the lungs

Endogenous infections (swallowing sputum)

Metastatic lesions are similar to re-infected


Large in size (spread locally) no lymph node involvement

Cavity formation

Caseous material discharge gradually leaving a small cavity.

Cavities can become very large with overgrowth of fibrous tissue.

Cavity walls are irregular with raised bands representing obliterated blood vessels.

The surface is lined by caseous material or by pus and debris mixed with blood.

If the disease is inactive the wall becomes very smooth

· In early cases the lesions are often in the apices of the lungs

· In advanced cases there may be more than one cavitatory lesion.

· All the lesions are distributed in the upper part of the lungs

· Caseation may involve the wall of a bronchus leading to obstruction of the lumen.

Sequelae of tuberculous cavities
Local effects

· Due to fibrosis lung tissue shrinks causing bronchiectasis (upper lobe bronchiectasis)

· Blood vessels can become weaken and rupture leading to haemoptysis

· Aneurysm formation- called Rasmoussen’s aneurism leading to fatal haemorhage.

· Fungal infections can be localized in these cavities.