Talk to us?

NEETMDS- courses, NBDE, ADC, NDEB, ORE, SDLE-Eduinfy.com

NEET MDS Synopsis

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





EMBOLISM
General Pathology

EMBOLISM

Definition: transportation of an abnormal mass of an abnormal mass of undissolved material from one part of circulation to another. The mass transported is called embolus.

Types
I .Thrombi and clots.
2. Gas or air.
3. Fat
4.Amniotic fluid.
5.Tumour

Thromboembolism 
This is the commonest type of embolus and may be formed of the primary thrombus  or more often of propagated clot region which is loosely attached.

Emboli from venous thrombi can result In impaction in the pulmonary  arteries and result in sudden death.
Embolism from cardiac or arterial thrombi results in systemic embolism causing infraction and gangrene.

Gaseous
This occurs when gas is introduced into the circulation:
•    Accidental opening of large veins during surgery.
•    Mismanaged transfusion. .
As air is  readily absorbed into blood only  sudden introduction or large quantities of air produces effects
Caisson’s Disease  bubbling of nitrogen from the blood during sudden decompression as seen during deep sea diving.

Fat Embolism
Causes
•    Fractures especially of long bones and multiple
•    Crush injuries.

Sites of impaction:

o    Lungs.
o    Systemic: causing -
    →    petechial skin haemorrhages.
    →    Embolism to brain leading to coma and death.
    →     Conjunctival and retinal haemorrhages
    
Tumor Embolism.

Invasion of vascular channe1.s is a feature of malignant neoplasms and this leads to:
•    Metastatic deposits,
•    DlC
 

Investment Materials
Dental Materials

Investment Materials

Investment is mold-making material

Applications

a. Mold-making materials for casting alloys
b. Mold-making materials for denture production

Classification

a. Gypsum-bonded investments (based on gypsum products for matrix)

b. Phosphate-bonded investments

c. Silicate-bonded investments

Components

a. Liquid-water or other reactant starts formation of matrix binder by reacting with reactant powder
b. Powder-reactant powder, filler, or modifiers

Manipulation

a. P/L mixed and placed in container around wax pattern
b. After setting, the investment is heated to eliminate the wax pattern in preparation for casting
 

Endodontic Microbiology
Endodontics

Bacterial portals to pulp: caries (most common source), exposed dentinal tubules (tubule permeability ↓ by dentinal fluid, live odontoblastic processes, tertiary and peritubular dentin)

1.        Vital pulp is very resistant to microbial invasion but necrotic pulps are rapidly colonized

2.        Rarely does periodontal disease → pulp necrosis

3.        Anachoresis: microbes carried in blood to area of inflammation where they establish infection

Caries → pulp disease: infecting bacteria are immobile, carried to pulp by binary fission, dentinal fluid movement

1.        Smooth surface and pit and fissure caries: S. mutans (important in early caries) and S. sobrinus

2.        Root caries: Actinomyces spp.

3.        Mostly anaerobes in deep caries. 

4.        Once pulp exposed by caries, many opportunists enter (e.g., yeast, viruses) → polymicrobial infection

Pulp reaction to bacteria: non-specific inflammation and specific immunologic reactions

1.        Initially inflammation is a chronic cellular response (lymphocytes, plasma cells, macrophages) → formation of peritubular dentin (↓ permeability of tubules) and often tertiary dentin (irregular, less tubular, barrier)

2.        Carious pulp exposure → acute inflammation (PMN infiltration → abscess formation).  Pulp may remain inflamed for a long time or become necrotic (depends on virulence, host response, circulation, drainage, etc.)

Endodontic infections: most commonly Prevotella nigrescens; also many Prevotella & Porphyromonas sp.

1.        Actinomyces and Propionibacterium species can persist in periradicular tissues in presence of chronic inflammation; they respond to RCT but need surgery or abx to resolve infection

2.        Streptococcus faecalis is commonly found in root canals requiring retreatment due to persistent inflammation

Root canal ecosystem: lack of circulation in pulp → compromised host defense

1.        Favors growth of anaerobes that metabolize peptides and amino acids rather than carbohydrates

2.        Bacteriocins: antibiotic-like proteins made by one species of bacteria that inhibit growth of another species

Virulence factors: fimbriae, capsules, enzymes (neutralize Ig and complement), polyamines (↑ # in infected canals)

1.        LPS: G(-), → periradicular pathosis; when released from cell wall = endotoxin (can diffuse across dentin)

2.        Extracellular vesicles: may → hemagglutination, hemolysis, bacterial adhesion, proteolysis

3.        Short-chain fatty acids: affect PMN chemotaxis, degranulation, etc.; butyric acid → IL-1 production (→ bone resorption and periradicular pathosis)

Pathosis and treatment:

1.        Acute apical periodontitis (AAP): pulpal inflammation extends to periradicular tissues; initial response

2.        Chronic apical periodontitis (CAP): can be asymptomatic (controversial whether bacteria can colonize)

3.        Acute apical abscess (AAA), phoenix abscesses (acute exacerbation of CAP), and suppurative apical periodontitis: all characterized by many PMNs, necrotic tissue, and bacteria

Treatment of endodontic infections: must remove reservoir of infection by thorough debridement

1.        Debridement: removal of substrates that support microorganisms; use sodium hypochlorite (NaOCl) to irrigate canals (dissolves some organic debris in areas that can’t be reached by instruments); creates smear layer

2.        Intracanal medication: recommend calcium hydroxide (greatest antimicrobial effect between appointments) inserted into pulp chamber then driven into canals (lentulo spiral, plugger, or counterclockwise rotation of files) and covered with sterile cotton pellet and temporary restoration (at least 3mm thick)

3.        Drainage: for severe infections to ↓ pressure (improve circulation), release bacteria and products; consider abx

4.        Culturing: rarely needed but if so, sterilize tissue with chlorhexidine and obtain submucosal sample via aspiration with a 16- to 20-gauge needle

Blastomycosis (North American Blastomycosis; Gilchrist's Disease)
General Pathology

Blastomycosis (North American Blastomycosis; Gilchrist's Disease)

A disease caused by inhalation of mold conidia (spores) of Blastomyces dermatitidis, which convert to yeasts and invade the lungs, occasionally spreading hematogenously to the skin or focal sites in other tissues.

Pulmonary blastomycosis tends to occur as individual cases of progressive infection

Symptoms are nonspecific and may include a productive or dry hacking cough, chest pain, dyspnea, fever, chills, and drenching sweats. Pleural effusion occurs occasionally. Some patients have rapidly progressive infections, and adult respiratory distress syndrome may develop.

Management and Treatment of Le Fort Fractures
Oral and Maxillofacial Surgery

Management and Treatment of Le Fort Fractures
Le Fort fractures require careful assessment and management to restore facial
anatomy, function, and aesthetics. The treatment approach may vary depending on
the type and severity of the fracture.

Le Fort I Fracture
Initial Assessment:

Airway Management: Ensure the airway is patent,
especially if there is significant swelling or potential for airway
compromise.
Neurological Assessment: Evaluate for any signs of
neurological injury.

Treatment:


Non-Surgical Management:

Observation: In cases of non-displaced fractures,
close monitoring may be sufficient.
Pain Management: Analgesics to manage pain.



Surgical Management:

Open Reduction and Internal Fixation (ORIF):
Indicated for displaced fractures to restore occlusion and facial
symmetry.
Maxillomandibular Fixation (MMF): May be used
temporarily to stabilize the fracture during healing.



Postoperative Care:

Follow-Up: Regular follow-up to monitor healing and
occlusion.
Oral Hygiene: Emphasize the importance of
maintaining oral hygiene to prevent infection.




Le Fort II Fracture
Initial Assessment:

Airway Management: Critical due to potential airway
compromise.
Neurological Assessment: Evaluate for any signs of
neurological injury.

Treatment:


Non-Surgical Management:

Observation: For non-displaced fractures, close
monitoring may be sufficient.
Pain Management: Analgesics to manage pain.



Surgical Management:

Open Reduction and Internal Fixation (ORIF):
Required for displaced fractures to restore occlusion and facial
symmetry.
Maxillomandibular Fixation (MMF): May be used to
stabilize the fracture during healing.



Postoperative Care:

Follow-Up: Regular follow-up to monitor healing and
occlusion.
Oral Hygiene: Emphasize the importance of
maintaining oral hygiene to prevent infection.




Le Fort III Fracture
Initial Assessment:

Airway Management: Critical due to potential airway
compromise and significant facial swelling.
Neurological Assessment: Evaluate for any signs of
neurological injury.

Treatment:


Non-Surgical Management:

Observation: In cases of non-displaced fractures,
close monitoring may be sufficient.
Pain Management: Analgesics to manage pain.



Surgical Management:

Open Reduction and Internal Fixation (ORIF):
Essential for restoring facial anatomy and occlusion. This may involve
complex reconstruction of the midface.
Maxillomandibular Fixation (MMF): Often used to
stabilize the fracture during healing.
Craniofacial Reconstruction: In cases of severe
displacement or associated injuries, additional reconstructive
procedures may be necessary.



Postoperative Care:

Follow-Up: Regular follow-up to monitor healing,
occlusion, and any complications.
Oral Hygiene: Emphasize the importance of
maintaining oral hygiene to prevent infection.
Physical Therapy: May be necessary to restore
function and mobility.




General Considerations for All Le Fort Fractures

Antibiotic Prophylaxis: Consideration for prophylactic
antibiotics to prevent infection, especially in open fractures.
Nutritional Support: Ensure adequate nutrition,
especially if oral intake is compromised.
Psychological Support: Address any psychological impact
of facial injuries, especially in pediatric patients.

Drugs used in Parasitology Treatment
Pharmacology

Amphotericin B: Naegleria fowleri, Leishmania donovani

Metronidazole: Giardia lamblia, Trichomona vaginalis, Entamoeba hystolytica

Nitazoxanide: Cryptosporidium

Bendazoles or Pyrantel Pamoate: Enterobius vermicularis, Ascaris lumbricoides, Ancylostoma duodenale, Necator americanus (ne M atodes)

Mebendazole: Toxocara canis

Albendazole: Strongyloides stercolaris, Toxocara canis, neurocysticercosis, Echinococcus granulosus.

Paziquantel: Taenia solium, Schistosoma, Diphylobotrium latum, Clonorchis (P latyhelminthes)

Pyrimethamine + Sulfadiazine: Toxoplasma gondii

Suramin: Trypanosma bruceii (blood borne)

Melarsoprol: Trypanosoma bruceii (CNS)

Nifurtimox or Benznidazole: Trypanosoma cruzi

Quinidine (IV): severe Plasmodium infx

Mefloquine or Atovaquone/Proguanil: Plasmodium resistant

Atovaquone + Azythromycin: Babesia

Diethylcarbamazine (DEC): Loa loa, Wucheria bancrofti

Ivermectin: Onchocerca volvulus, Strongyloides stercolaris

Sodium stibogluconate (Pentavalent Antimony): Leishmania donovani

Cloroquine: Plasmodium falciparum, Plasmodium malariae

Cloroquine + Primaquine: Plasmodium ovale, Plasmodium vivax

Antianginal Drugs
Pharmacology

Antianginal Drugs

Organic Nitrates :
Short acting: Glyceryl trinitrate (Nitroglycerine, GTN), Amyl Nitrate
Long Acting: Isosrbide dinitrate (Short acting by sublingual route), Erythrityl tetranitrate, penta erythrityl tetranitrate

Beta-adrenergic blocking agents : Propanolol, Metoprolol
Calcium channel blockers Verapamil, Nifedipine, Dipyridamole
 
Mechanism of action 
– Decrease myocardial demand 
– increase blood supply to the myocardium

Explore by Exams