Infectious Diseases Long Essays

Infectious Diseases Long Essays

Question 1. What is the differential diagnosis of ulcers over the penis? How do you treat syphilis?

Answer:

Differential Diagnosis of Ulcers Over Penis:

  • Chancre
  • Chancroid
  • lymphogranuloma venereum
  • Genital herpes
  • Neoplasm

Syphilis:

  • It is a sexually transmitted disease

Syphilis Clinical Features:

  1. Primary syphilis
    • Incubation period- about 21 days
    • Chancre develops
    • It is a solitary, painless, indurated, non-tendered, ulcerated, or eroded lesion
    • Initial,ly it was a dull red macule
    • Later it becomes ulcerated
    • Regional lymphadenopathy
  2. Secondary syphilis
    • Appears about 6-8 weeks
    • Skin lesions appear as macules, papules, fol-locules, or, papulosquamous patches
    • Circinate lesions develop on the face
    • Headache
    • Fever, anorexia
    • Joint and muscle pain
    • Laryngitis, pharyngitis
    • Generalised lymphadenopathy
    • Lesions develop over the mucocutaneous junction
  3. Tertiary syphilis
    • Develops about 5-10 years after primary infection
    • Affects the skin, central nervous system, CVS, mucous membrane
    • Lesions are called gumma
    • It is localized, chronic granulomatous lesion with a nodular or ulcerated surface
    • Causes generalized paresis, dementia, and strokes
    • Bone lesions cause osteomyelitis and destruction of joints

Syphilis Treatment:

Infectious Diseases Differntial Diagnosis Of Ulcers Over Penis Treatment

Question 2. Describe clinical features, diagnosis, complications, and management of typhoid fever.
(or)
Discuss the etiology, clinical features, complications, and management of enteric fever.

Answer:

Typhoid Or Enteric Fever:

  • It is an acute systemic illness

Etiology:

  • Salmonella typhi
  • Salmonella paratyphi

Enteric Fever Clinical Features:

  • Incubation period- 10-14 days
  1. First 5-7 days
    • High-grade, remittent fever with chills
    • Headache
    • Aches
    • Malaise
    • Constipation
    • Leucopenia
    • Dry cough
    • Epistaxis
    • Relative bradycardia
  2. Between 1st and 2nd week
    • Rose spots develop over the trunk as small macules, red in color, and blanch on pressure
    • Splenomegaly
    • Bronchitis
    • Abdominal pain
    • Abdominal distension
    • Diarrhea
  3. After 2nd week
    • Confusion
    • Delirium
    • Toxaemia
    • Coma

Read And Learn More: General Medicine Question and Answers

Enteric Fever Diagnosis:

Infectious Diseases Typhoid Fever Diagnosis

Enteric Fever Complications:

  1. Intestinal complications
    • Hemorrhage
    • Paralytic ileus
    • Perforation
    • Peritonitis
  2. Extraintestinal complication
    • Meningitis
    • Cholecystitis
    • Pneumonia
    • Myocarditis
    • Bone and joint infection
    • Encephalopathy
    • Granulomatous hepatitis
    • Nephritis

Enteric Fever Management

Infectious Diseases Thyroid Fever Management

Question 3. Describe the etiology, pathology, clinical features, and management of cervical TB lymphadenitis.

Answer:

Tuberculous Lymphadenitis:

  • It is defined as achronic specific granulomatous inflammation with caseation necrosis of the lymph node

Etiology:

  • Mycobacterium tuberculosis complex which includes M. tuberculosis, M. bovis, M. africanum, M. canetti, and M.caprae

Pathology:

  • Pathological stages of the disease are:
  1. Stage 1- lymphoid hyperplasia
    • Formation of tubercles and granulomas occurs without cassation necrosis
  2. Stages 2 and 3
    • Caseation necrosis in the affected lymph nodes occurs
    • It is followed by the destruction of capsules of lymph nodes
    • Periadenitis
  3. Stage 4
    • There is a rupture of caseous material into the surrounding soft tissue
    • Formation of abscess cavity

Tuberculous Lymphadenitis Clinical Features:

  • Persistent, painless swelling of the lymph nodes
  • Release of discharge of fluid
  • Fever
  • Weight loss
  • Fatigue
  • Night sweats

tuberculous LymphadenitisManagement:

  1. Anti-tubercular therapy
    • Isoniazid, Rifampicin, Pyrazinamide, and Ethambutol are given for 2 months
    • Followed by Isoniazid and Rifampicin for the next 4 months
  2. DOTS therapy
  3. Surgery- indicated in
    • Persistent fluctuant lesions
    • Failure with chemotherapy
    • Symptomatic relief

Question 4. Describe the etiology, clinical features, and management of intestinal amoebiasis.

Answer:

Intestinal amoebiasis

Caused by entamoeba histolytic

  • E. histolytica can cause two types of pathological lesions as follows

1. Primary (or) Intestinal Amoebiasis:

Infectious Diseases Primary or intestinal amoebiasis

  • This condition is called amoebic dysentery.
  • These ulcers may be generalized (or) may be localized to the ileocaecal (or) sigmoidorectal region.
  • Occasionally ulcers may involve deeper tissues and cause perforation (or) peritonitis.
  • Erosion of blood vessels may lead to bleeding.
  • The superficial lesions generally heal without scarring.
  • Deep ulcers form scars leading to strictures, partial obstruction, and thickening of the gut wall.

2. Extra-intestinal amoebiasis (or) secondary (or) metastatic lesions.

  • Amoebic liver abscess:

Infectious Diseases Primary or intestinal amoebiasis

Question 5. Diphtheria-etiology, Clinical FeatuManagementtntA

Answer:

Etiology:

  • It is caused by Corynebacterium diphtheria

Diphtheria-etiology Clinical Features:

  • It is insidious at the onset
  • Moderate grade fever
  • Tachycardia
  • Sore throat
  • Formation of greyish-greenish pseudomembrane on the tonsils
  • Swollen neck- Bull neck
  • Tender lymphadenopathy
  • Nasal infection
  • Hoarseness of voice
  • Cough
  • Respiratory obstruction
  • Acute circulatory failure
  • Myocarditis
  • Nerve palsies
  • Dysphagia
  • Dysphonia
  • Paraesthesia in the limbs

Diphtheria-Etiology Management:

  1. Antitoxin diphtheric serum (ADS)
    • The dose varies from 20,000 to 1,00,000 units depending on the duration and severity of the disease
    • In mild cases, a lesser dose may be used
  2. Antibiotics
    • Penicillin G-6,00,000 units every 12 hourly intravenously or
    • Amoxycillin 500 mg 8 hourly for 7-10 days
    • Patient allergic to penicillin
      • Erythromycin- 500 mg 6 hoourly or
      • Azithromycin 500 mg daily or
      • Rifampicin 600 mg daily
  3. Tracheostomy

Infectious Diseases Short Essays

Question 1. Oral manifestations of diphtheria

Answer:

Oral manifestations of diphtheria

  • Diphtheria is an infectious disease caused by Corynebacterium Diphtheriae
  • It is characterized by local exudative inflammation of the upper respiratory tract and usually with the formation of pseudomembrane at the level of the nasopharynx
  • Oral manifestations
      • Sore throat
        • Formation of thick, fibrinous, greyish-green pseudomembrane on tonsils, larynx, pharynx
          • Exudation in tonsillar area
          • Hoarseness of voice
          • Paralysis of the soft palate
          • Dysphagia
          • Dysphonia
          • Cervical Lymphadenopathy

Question 2. NSAIDs

Answer:

NSAIDs Classification

Infectious Diseases NSAIDs Classification

Question 3. Oral manifestations of AIDS

Answer:

Oral manifestations of AIDS

  1. Bacterial infections
    • Tuberculosis
    • M. avium complex
    • Salmonellosis
  2. Viral infection
    • Herpes simplex
    • Varicella zoster
    • Epstein Barr virus
  3. Mycotic infections
    • Pneumocystis pneumonia
    • Candidiasis
    • Aspergillosis
    • Cryptococcosis
  4. Parasitic infection
    • Toxoplasmosis
    • Cryptosporidiosis
  5. Malignancies
    • Kaposi’s sarcoma
    • B cell lymphoma

Read And Learn More: General Medicine Question and Answers

Question 4. Human immunodeficiency virus (HIV)- post-exposure prophylaxis

Answer:

Human immunodeficiency virus (HIV)- post-exposure prophylaxis

  • Following exposure, postexposure prophylaxis may be required depending upon the category of exposure and HIV status of the exposure source
  • Drugs used are:
  1. Zidovudine 300 mg BD
  2. Lamivudine 150 mg BD
  3. Protease inhibitors
    • Lopinavir 400 mg BD or 800 md OD
    • Ritonovir 100 mg BD or 200 mg OD
      • Drugs are started within the first 72 hours
      • It should be continued for 4 weeks
      • The injured site on the wound should be thoroughly washed with soap and water
      • Antiseptics are also used

Question 5. Gonorrhoea

Answer:

Gonorrhoea Definition:

  • It is a communicable sexually transmitted disease of humans

Etiology:

  • It is caused by Neisseria gonorrhoea

Gonorrhoea Clinical Features:

  1. In males
    • Dysuria
    • Increased frequency of micturition
    • Purulent discharge per urethra
    • Oedema of penis
    • Erythema of urethral meatus with purulent discharge
  2. In females
    • Dysuria
    • Vaginal discharge
    • Abnormal menstrual bleeding
    • Rectal discomfort
  3. In homosexuals
    • Asymptomatic
  4. In children
    • Conjunctivae
    • Involvement of pharynx or respiratory tract

Gonorrhoea Complications:

  • Acute epididymitis
  • Prostatitis
  • Periuretheral abscess or fistula
  • Salpingitis
  • Barthorlin’s abscess
  • Premature birth
  • Arthritis
  • Bacteraemia
  • Perihepatitis

Gonorrhoea Treatment:

  1. For uncomplicated gonorrhea
    • 2.4 g of procaine penicillin IM + 1 g of oral probenecid or
    • Oral amoxicillin 2-3 g + Oral probenecid 1 g or
    • Cotrimoxazole (400+80 mg) 8 tablets orally
  2. In penicillin-resistant gonorrhea
    • Ciprofloxacin-250-500 mg orally single dose or
    • Cefotaxime- 0.5-1 g IM as single dose or
    • Cefixime- 400 mg orally as a single dose or
    • Ceftriaxone-250 mg IM as single dose
  3. In gonorrhea with complications
    • Aqueous crystalline penicillin G-10 million units 4 daily for 5 days
    • Ciprofloxacin 500 mg twice daily for 5 days
    • Ceftriaxone 1 g 4 daily for 5 days

Question 6. Chickenpox

Answer:

Chickenpox

  • Chickenpox is caused by Varicella zoster virus
  • It rarely occurs a second time
  • The virus enters the mucosa of the upper respiratory tract and spreads by droplets from the throat

Chickenpox Clinical Features:

  • It involves young children and adults
  • The incubation period is 14-21 days
  • Malaise
  • Low-grade fever followed by a rash
  • Rash is macula papular
  • Heals by scabs formation

Chickenpox Sites Involved:

  • Skin lesions- over trunk and face then spread to peripheral parts of the body
  • Mucosal lesions- affects the mucosa of the pharynx and vagina

Chickenpox Complications:

  • Superinfection of skin due to frequent scratching
  • Encephalitis
  • Cerebellar ataxia
  • Myocarditis
  • Osteomyelitis
  • Septic arthritis
  • Septicaemia
  • Hepatitis
  • Pneumonia

Question 7. Herpes simplex

Answer:

Herpes simplex

  • It is a DNA virus o It belongs to the herpesviridae family.
  • Man is the only natural host.
  • Herpes simplex virus has two types as follows.
  1. Herpes simplex type 1 – is usually associated with oral and ocular lesions.
  2. Herpes simplex type 2 – is usually associated with genital infections.
    • Lesions caused by herpes simplex depend on the site of infection, age, and immune status of the individual as follows:
    • Cutaneous infections: These include:
      • Fever
      • Blisters on the cheeks, chins around the mouth, (or) on the forehand
      • Napkin rash on the buttocks of children, – Herpetic with low in medical professionals.
    • Eczema herpeticum:
      • The generalized herpetic eruption is seen in children suffering from eczema.
    • Mucosal lesions:
      • Acute gingivostomatitis
      • Recurrent herpes labialis.
    • Ophthalmic lesions:
      • Keratoconjunctivitis
      • Follicular conjunctivitis.
    • Visceral lesions:
    • Nervous system:
      • HSV meningitis,
      • Sacral autonomic dysfunction.
    • Genital lesions:
      • Infection of cervix, vagina, vulva (females)
  3. Congenital lesions:
    • Subclinical or localized infection of skin mouth or eyes.
    • Besides primary infections, herpes viruses may present as latent infection, reactivation, and recrudescence.

Question 8. Herpes labialis

Answer:

Herpes labialis

  • It occurs in patients with no prior infection with Herpes Simplex Virus-1

Herpes labialis Clinical Features:

  • Age- children and young adults
  • Incubation period-5-7 days
  1. Prodromal generalized symptoms
    • Fever
    • Malaise
    • Headache
    • Nausea, vomiting
    • Painful mouth
    • Sore throat
    • Irritability
    • Excessive drooling of saliva
    • Lack of tactile sensation
    • Cervical lymphadenopathy
  2. Later symptoms
    • Numerous vesicle formations over keratinized mucosa
    • Vesicles are thin-walled
    • They contain clear fluid
    • They rupture leaving multiple, small, punctuate shallow painful ulcers of 2-6 mm
    • Ulcers are surrounded by a red ring of inflammation
    • Ulcers may become secondarily infected
    • Healing starts in about 3 days and is completed within 7-14 days

Herpes labialis Treatment:

  • To prevent secondary infection- antibiotics are used
  • To control fever- Antipyretics are given

Question 9. Mumps

Answer:

Mumps

  • Mumps is an acute viral infectious disease characterized by unilateral (or) bilateral nonsuppurative enlargement of the salivary glands usually the parotid gland.
  • Submandibular and sublingual glands are occasionally involved.
  • Usually, children are affected. May also occur in adults.
  • Also known as epidemic parotitis

Mumps Causative organism:

  • Organisms involved in paramyxovirus.

Mumps Route of infection:

  • Infection is acquired by inhalation (or) direct contact or through the conjunctiva.
  • The incubation period is 12 – 18 days.

Mumps Clinical Features:

  • Unilateral (or) bilateral swelling of parotid glands.
  • Fever, malaise
  • Local pain and tender
  • Involvement of extra parotid sites can cause more serious problems as follows.
    • CNS involvement may lead to
      • Meningitis,
      • Meningoencephalitis
      • Orchitis

Mumps Complications:

  • Orchitis
  • Oophoritis
  • Arthritis
  • Nephritis
  • Pancreatitis
  • Thyroiditis and myocarditis

Mumps Laboratory Diagnosis:

  • Isolation of viruses from CSF, saline (or) urine.
  • Serological tests with paired serum samples tested for the rise in the titer of antibodies by complement fixation test, ELISA, and haemagglutination tests.
  • Serum amylase levare els elevated in both parotitis and acute pancreatitis.

Mumps Treatment:

  • Treatment is conservative maintaining hydration. Prevention is using MMR vaccine

Question 10. Diphtheria

Answer:

Diphtheria Clinical Features:

  • It is insidious at the onset
  • Moderate grade fever
  • Tachycardia
  • Sore throat
  • Formation of greyish-greenish pseudomembrane on the tonsils
  • Swollen neck- Bull neck
  • Tender lymphadenopathy
  • Nasal infection
  • Hoarseness of voice
  • Cough
  • Respiratory obstruction
  • Acute circulatory failure
  • Myocarditis
  • Nerve palsies
  • Dysphagia
  • Dysphonia
  • Paraesthesia in the limbs

Diphtheria Management:

1. Antitoxin diphtheric serum (ADS)

  • The dose varies from 20,000 to 1,00,000 units depending on {ho duration and severity of the disease
  • In mild cases, a lesser dose may be used

2. Antibiotics

  • Penicillin G-o.00,000 units every 12 hourly intravenously or
  • Amoxycillin 500 mg S hourly for 7-10 days
  • Patient allergic to penicillin
    • Erythromycin- 500 mg 6 hourly or
    • Azithromycin 500 mg daily or
    • Riftamoicin 600 mg daily

3. Tradieostomy

Question 11. Three malarial parasites

Answer:

Three malarial parasites

  • Malaria is a disease caused by four plasmodium speeds which are as follows:
  1. P. vivax
  2. P. Falciparum
  3. P. Malaria
  4. P. Ovale.

Infectious Diseases Employee student

Question 12. Widal test

Answer:

Widal test

  • It is an agglutination test for detection of agglutinin H and O in patients with enteric fever

Widal test Procedure:

  • Mix equal volumes of serial dilutions of the serum and H and O antigens
  • Incubate in a water bath at 37 degrees C for 4 hours
  • Read after overnight refrigeration at 4 degrees C

Widal test Result:

  • A Titre upto 160 indicates enteric fever

Question 13. Chancre

Answer:

Chancre

  • Chancre is a typical lesion of primary syphilis that appears on genitals/at extragenital sites in 2-4 weeks after exposure to infection.
  • Initially, the lesion is a painless papule that ulcerates in the center so that the fully developed chancre is an indurated lesion with central ulceration accompanied by regional lymphadenitis.
  • Chancre heals without scarring, even in the absence of treatment.

Question 14. Two spirochaetal diseases

Answer:

Two spirochaetal diseases

Infectious Diseases Two Spirochaetal Diseases

Question 15. Oral manifestations of syphilis

Answer:

Oral manifestations of syphilis

  • Syphilis is a sexually transmitted disease caused by spirochaetes, treponema pallidum.
  • Syphilis is divided into 3 stages depending upon the period after which the lesions appear and the type of lesions.
  • They are primary, secondary, and tertiary.
  • Oral lesions occur in secondary syphilis known as mucous patches, on the tongue, gingiva, etc., or as a split papule on the lips, which are highly infectious.
  • Tertiary/late syphilis/gumma is a granuloma with central necrosis, noninfectious, and is most common on the tongue and palate.
  • Palatal perforation by ulcer after vigorous antibiotic use is known as the Herxheimer reaction.
  • In congenital/prenatal syphilis, the most constant finding is relatively short roots of mandibular permanent 1st molars, short maxilla, Hutchinson triad (teeth, eye/ear involved), hypoplasia of incisors and molars i.e., notched incisors and mulberry molars.
  • Treatment: Penicillin is the drug of choice.

Question 16. Congenital syphilis

Answer:

Congenital syphilis Major features are:

  • Hutchinson’s triad includes.
  • Hutchinson’s teeth-small, widely spaced, peg-shaped permanent teeth.
  • Notched central incisors
  • Intestinal keratitis with blindness and deafness from Stir cranial nerve injury.
  • Saddle shaped nose
  • Bony lesions like epiphysis and periostitis
  • Mucocutaneous lesions of acquired secondary syphilis
  • Diffuse fibrosis in the liver.

Question 17. VDRL test

Answer:

VDRL test

  • It is an abbreviated form of the Venereal Disease Research Laboratory test
  • It is the most widely used test for syphilis
  • It is a simple arid rapid test
  • It is a slide flocculation test

VDRL test Procedure:

  • Cardiolipin antigen is freshly prepared
  • A drop of this is added to a drop of inactivated patient’s serum on a slide
  • Mix it by shaking

VDRL test Result:

  • If floccules appear it indicates a positive test

Question 18. Prednisolone

Answer:

Prednisolone

  • Prednisolone has potent glucocorticoid and mild mineralocorticoid activity
  • It is the most commonly used glucocorticoid

Prednisolone Uses:

  • Replacement therapy
  • Rheumatoid arthritis
  • Osteoarthritis
  • Acute gout
  • Allergic diseases
  • Bronchial asthma
  • Collagen diseases
  • Eye diseases
  • Renal diseases
  • Skin diseases
  • GIT diseases
  • Liver diseases
  • Malignancies
  • Organ transplantation

Prednisolone Adverse Effects:

  • HPA axis suppression
  • Cushing’s syndrome
  • Hyperglycemia
  • Susceptibility to infection is increased
  • Osteoporosis
  • Avascular necrosis
  • Peptic ulceration
  • Mental disturbances
  • Cataract and glaucoma
  • Delayed wound healing

Question 19. Metronidazole

Answer:

Metronidazole

  • Metronidazole is a nitroimidazole

Metronidazole Mechanism of Action:

  • It is prodrug
  • Susceptible micro-organisms reduce the nitro group of metronidazole by nitroreductase
  • Convert it into a cytotoxic derivative
  • It binds to DNA
  • Inhibits protein synthesis

Metronidazole Uses:

  • Anaerobic infection
  • Amoebiasis
  • Trichomonas vaginitis
  • Giardiasis
  • H.pylori infection
  • Pseudomembranous colitis
  • Draetmcwlosis
  • Topical application

Metronidazole Adverse Reactions:

  • Nausea, anorexia, abdominal pain, metallic taste in mouth
  • Headache, dizziness
  • Stomatitis, glossitis
  • Furry tongue
  • Insomnia, ataxia, vertigo
  • Peripheral neuropathy
  • Pruritis, urticaria, skin rashes

Question 20. Aminoglycosides

Answer:

Aminoglycosides

  • Aminoglycosides are antibiotics with amino sugars in glycosidic linkages

Aminoglycosides Mechanism of Action:

  • Penetrate bacterial cell membrane
  • Bind to 30S ribosomes
  • Inhibits bacterial protein synthesis

Aminoglycosides Uses:

  • Tuberculosis
  • Subacute bacterial endocarditis
  • Plaque
  • Tularemia
  • Brucellosis

Aminoglycosides Adverse Effects:

  • Ototoxicity
  • Nephrotoxicity
  • Neuromuscular blockade

Aminoglycosides Examples:

  • Streptomycin
  • Kanamycin
  • Tobramycin
  • Neomycin
  • Gentamicin
  • Netilmicin

Question 21. Chloramphenicol

Answer:

Chloramphenicol

  • Chloramphenicol Is a broad spectrum and loll.

Chloramphenicol Mechanism of Action:

  • It binds to 50S ribosome
  • Inhibits transpeptidation reaction
  • Inhibits protein synthesis

Chloramphenicol Uses:

  • Typhoid lever
  • Bacterial meningitis
  • Anaerobic infections
  • Rickettsial infection
  • Kyo infections

Chloramphenicol Adverse Reactions:

  • Gastrointestinal disturbances- nausea, vomiting, diarrhea
  • Bone marrow depression
  • Gray baby syndrome
  • Hypersensitivity reactions
  • Superinfection

Question 22. Malaria

Answer:

Malaria is a disease caused by four plasmodium species which are as follows:

  1. P. vivax
  2. P. Falciparum
  3. Malaria
  4. P. Ovale.

Malaria Life Cycle:

The malarial parasites pass their life cycle in two hosts.

  1. Man intermediate host [a sexual development
  2. Femalanopheles mosquito delinitive host [sexual development].

Malaria Clinical Features:

  • Intermittent fever which is named malaria is caused by plasmodium
  • It consists of
    • Febrile paroxysm
      • It comprises of three stages
    • Anaemia
      • Microcytic or normocytic hypochromic anemia develops
    • Splenomegaly.
      • The spleen becomes enlarged and palpable
      • Black water fever and pernicious malaria are the most commonly seen complications in falciparum malaria.

Infectious Diseases Malaria Clinical Features

Question 23. Ludwig’s angina

Answer:

Ludwig’s angina

  • Ludwig’s angina was described by Wilhelm Fredrich Von Ludwig in 1836
  • It is rapidly spreading cellulitis involving simultaneously all three spaces i.e. Submandibular, sublingual, and submental spaces

Etiology:

  • Odontogenic infection
  • Traumatic injuries
  • Infective condition
  • Pathologic conditions

Ludwig’s angina Clinical Features:

  1. Generalised symptoms
    • Dehydration
    • Fever
    • Dysphagia
    • Dyspnoea
    • Hoarseness of voice
    • Stridor
  2. Extraoral features
    • Brawny hard swelling
    • Erythematous skin
    • Local rise in temperature
    • Drooling of saliva
    • Respiratory distress
  3. Intraoral features
    • Trismus
    • Raised floor of mouth
    • Airway obstruction
    • Increased salivation

Ludwig’s angina Management:

  • Airway maintenance
  • Removal of the causative factor
  • Administration of 4 fluids
  • Antibiotics
    • Penicillin G-2-4 million units TV 4-6 hourly
    • Gentamycin-80 mg IM BD
    • Metronidazole-400 mg 8 hourly
    • Erythromycin-600 mg 6-8 hourly
    • Amoxicillin-500 mg 6-8 hourly orally
      • Surgical management

Infectious Diseases Short Question And Answers

Infectious Diseases Short Question And Answers

Question 1. Four complications of viral hepatitis

Answer:

Four complications of viral hepatitis

  • Hepatic necrosis
  • Chronic hepatitis
  • Cirrhosis of liver
  • Hepatic failure
  • Hepatocellular carcinoma

Question 2. Infectious Mononucleosis

Answer:

Infectious Mononucleosis

  • It is an acute febrile illness associated with lymph node enlargement caused by Epstein Barr virus
  • Features
    • Affects adolescents and adults
    • The incubation period is 7-10 days
  • Clinical features
    • Fever, malaise
    • Conjunctival haemorrhage
    • Maculopapular rash
    • Sore throat
    • Lymphadenopathy
    • Splenomegaly

Infectious Mononucleosis Complications

  • Chronic fatigue
  • Hepatitis
  • Hemolytic anemia
  • Thrombocytopenia pleurisy
  • Myocarditis
  • Meningoencephalitis
  • Rupture of an enlarged spleen

Question 3. Rubella

Answer:

Rubella

  • Rubella is a mild childhood disease
  • It may be acquired congenital or postnatally

Rubella Features:

  • Infection is acquired by inhalation
  • Incutwbon synod-2-3 weeks
  • Fever, malaise
  • Headache
  • Mild conjunctivitis
  • Lymphadenopathy
  • Rasa develops on the forehead and face
  • It spreads downward to the trunk and extremities
  • It lasts for 1-5 days

Read And Learn More: General Medicine Question and Answers

Rubella Prevention:

  • It is prevented by MMR vaccine

Question 4. Mumps

Answer:

Mumps

  • The incubation period is 12 – 18 days.

Mumps Clinical Features:

  • Unilateral (or) bilateral swelling of parotid glands,
  • Fever, malaise
  • Local pain and tender
  • The involvement of extra parotid sites can cause more serious problems as follows.
    • CNS involvement may lead to
      • Meningitis,
      • Meningoencephalitis
      • Orchitis

Question 5. Measles

Answer:

Measles Clinical Features:

  • Insidious in onset
  • Moderate fever
  • Tachycardia
  • Sore throat
  • Formation of greyish-greenish pseudomembrane on tonsils
  • Associated nausea and vomiting
  • Bull neck- swollen neck
  • Tender lymphadenopathy
  • Xasal infection
  • Hoarseness of voice
  • Cough
  • Respiratory obstruction
  • Toxaemi
  • Acute peripheral circulatory failure
  • Nerve paralysis
  • Dysphagia
  • Dysphonia
  • Paraesthesia

Question 6. Prevention of measles

Answer:

Prevention of measles

  1. Active immunization
    • One injection of live attenuated measles vaccine along -with mumps and rubella vaccines, MMR vaccine to children over 1 year
  2. Passive immunization
    • Human normal immunoglobulin is used

Dose:

Infectious Diseases Prevention Of Measles

Question 7. Diphtheria

Answer:

Diphtheria Clinical Features:

  • It is insidious at the onset
  • Moderate grade fever
  • Tachycardia
  • Sore throat
  • Formation of greyish-greenish pseudomembrane on the tonsils
  • Swollen neck- Bull neck
  • Tender lymphadenopathy
  • Nasal infection
  • Hoarseness of voice
  • Cough
  • Respiratory obstruction
  • Acute circulatory failure
  • Myocarditis
  • Nerve palsies
  • Dysphagia
  • Dysphonia
  • Paraesthesia in the limbs

Question 8. Ascariasis

Answer:

Ascariasis

  • Infection caused by Ascaris lumbricoides is known as ascariasis

Ascariasis Features:

  • Migrating larvae in the lungs cause dyspnoea, wheezing, cough, and signs of pneumonia
  • Loss of appetite
  • Malnutrition
  • Fever
  • Eosinophilic leukocytosis
  • Appendicitis
  • Liver abscess

Ascariasis Diagnosis:

  1. Stool examination- demonstrates adult worms or eggs
  2. Barium meal- Demonstrate adult worms
  3. Serodiagnosis- detects antibodies

Ascariasis Treatment:

  • Pyrantel pamoate-11 mg/kg given orally
  • Mebendazole-100 mg twice daily for three days

Question 9. Hookworm Disease
(or)
Ankylostomiasis

Answer:

Hookworm Disease

  • Hookworm disease is a symptomatic infection caused by Ankylostoma duodenal and Necatar Ameri- can
  • Occurs in all tropical and subtropical countries

Hookworm Disease Clinical Features:

  • Dermatitis
  • Lesions in the lungs- bronchitis and bronchopneumonia
  • Microcytic, hypochromic anemia
  • Epigastric pain
  • Dyspepsia
  • Vomiting
  • Diarrhea

Hookworm Disease Diagnosis:

  1. Blood examination
    • Eosinophilia
    • Microcytic, hypochromic anemia
  2. Stool examination
    • Shows occult blood

Hookworm Disease Treatment:

  • High protein diet
  • Oral iron preparations
  • Blood transfusion
  • Drugs used are- mabendazole, albendazole, pyrantelpamoate

Question 10. Amoebic dysentery

Answer:

Amoebic dysentery

  • Amoebic dysentery is also known as intestinal amoebiasis
  • It is a condition in which the infection is confined to the intestine and is characterized by the passage of blood and mucus in the stool

Amoebic dyssentery Types:

  1. Acute amoebic dyssentery
    • Multiple ulcers occur
    • These ulcers are deep and extensive
    • Its complications are
      • Pericaecal and pericolic abscess
      • Amoebic appendicitis
      • Perforation
      • Generalized peritonitis
      • Gangrene of guts
      • Fistula
  2. Chronic amoebic dyssentery
    • A single latent ulcer is present in the caecum while multiple small superficial ulcers are scattered throughout the large intestine
    • Stricture formation occurs
    • Amoeboma in the caecum and large intestine develops

Question 11. Treatment of malaria

Answer:

Treatment of malaria

  1. General management
    • Use of analgesics and antipyretics to treat fever
    • Administration of intravenous fluids
  2. Treatment of acute attack
    • Chloroquine-600 mg followed by 300 mg in 6 hours and then 150 mg twice a day for 3 days
    • Chloroquine-resistant cases- Dihydrochloride 600 mg salt three times a day by mouth for 5 days
    • Followed by a single dose of sulphadoxine 1.5 g combined with pyrimethamine 75 mg

Question 12. Complication of malaria

Answer:

Complication of malaria

  1. Pernicious malaria
  2. Black water fever.

1. Pernicious malaria:

  • It is a life-threatening condition

Pernicious malaria Cause:

  • It is due to heavy parasitization.

Pernicious Malaria Clinical Features:

  • It is grouped into the following:

Infectious Diseases Complication Of malaria

2. Blackwater fever:

  • This occurs in persons who are previously infected and had inadequate doses of quinine

Blackwater Fever Clinical Features:

  • Intravascular hemolysis,
  • Fever,
  • Haemoglobinuria
  • Vomiting and prostration with the passage of dark red (or) blackish urine hence called backwater fever.

Blackwater Fever Mechanism:

  • An autoimmune mechanism may be involved in hemolysis
  • Parasitized erythrocytes during previous infection act as antigen
  • Antibodies are formed against it
  • Due to this antigen-antibody reaction, massive destruction of erythrocytes occurs
  • There is excessive deposition of haemosiderin pigment in the liver, spleen, and kidneys.
  • Sequel of black water fever include
    • Circulatory failure
    • Renal failure,
    • Liver failure,
    • Anaemia.

Question 13. Complication of mumps

Answer:

Complication of mumps

  • Orchitis
  • Oophoritis
  • Arthritis
  • Nephritis
  • Pancreatitis
  • Thyroiditis and myocarditis.

Question 14. Diagnosis of typhoid fever

Answer:

Diagnosis of typhoid fever

Infectious Diseases Typhoid Fever Diagnosis

Question 15. Complications of typhoid fever

Answer:

Complications of typhoid fever

  1. Intestinal complications
    • Hemorrhage
    • Paralytic ileus
    • Perforation
    • Peritonitis
  2. Extraintestinal complication
    • Meningitis
    • Cholecystitis
    • Pneumonia
    • Myocarditis
    • Bone and joint infection
    • Encephalopathy
    • Granulomatous hepatitis
    • Nephritis

Question 16. Clinical features of typhoid fever

Answer:

Clinical features of typhoid fever

  • Incubation period- 10-14 days
  1. First 5-7 days
    • High-grade, remittent fever with chills
    • Headache
    • Aches
    • Malaise
    • Constipation
    • Leucopenia
    • Dry cough
    • Epistaxis
    • Relative bradycardia
  2. Between 1st and 2nd week
    • Rose spots develop over the trunk as small macules, red in color, and blanch on pressure
    • Splenomegaly
    • Bronchitis
    • Abdominal pain
    • Abdominal distension
    • Diarrhea
  3. After 2nd week
    • Confusion
    • Delirium
    • Toxaemia
    • Coma

Infectious Diseases Types Of Diseases Transmission

Question 17. Lepromatous leprosy

Answer:

Lepromatous leprosy

  • Leprosy caused by mycobacterium leprae is of 2 types wepromatous leprosy represents low resistance and tuberculoid leprosy represents high resistance.
  • Lepromatous leprosy is characterized by multiple symmetrical skin lesions that are hypopigmented and erythematous maculopapular/nodular.
  • Nerve involvement is present with less severe sensory distribution.
  • Histopathology involves the collection of foamy macrophages/lepra cells in the dermis separated from the epidermis by a clear zone.

Question 18. Lepra reaction

Answer:

Lepra reaction

  • Lepra reaction/reactional leprosy:
  • There may be two types:
  1. Type 1 (Reversal reactions),
  2. Type 2 (Erythema, nodosum leprosum)

1. Type 1: the polar forms of leprosy donor undergo any change in clinical ami histopathological picture.

  • Borderline groups are unstable and may move across the spectrum in either direction with upgrading/downgrading of patients’ immune stale.
  1. Upgrading read ion: Characterized by increased cell-mediated immunity and occurs in patients of borderline Icpromalous (BL) type on treatment who upgrade/shift towards tuberculoid type.
  2. Downgrading reaction: Characterized by lowering of cellular immunity and is seen in borderline tuberculoid (BT) type who downgrade/shift towards Icpromalous type.

2. Type 2: Occurs in Icpromalous patients after treatment. It is characterized by tender cutaneous nodules, fever, iridocyclitis, synovitis, and lymph node involvement.

Question 19. Diagnosis of AIDS

Answer:

Tests for AIDS:

  1. ELISA( Enzyme-Linked Immunosorbent Assay)
    • It is a color reaction test
    • Method:
      • A serum containing antibodies is developed from the patient’s blood sample
      • It is added to the ELISA plate
      • Wash off the inactive antibodies
      • A second layer of antibodies called conjugate is added
      • Excess antibodies are again washed off
      • A substrate is added to it
    • Result:
      • Color becomes darker- positive test
      • No color change- negative test
  2. Western blot
    • Method
      • Viral proteins from the patient’s blood sample are passed through a gel
      • The separated proteins are then passed through an electric current
      • Human serum is added
      • A chromogen is added to it
  3. Result:
    • A specific band of viral protein is detected

Question 20. Quinolones

Answer:

Quinolones

  • Quinolones are a group of synthetic antimicrobial agents

Quinolones Uses:

  • Uncomplicated UTI
  • Diarrhea

Quinolones Adverse Effects:

  • Hemolytic anemia
  • Allergic reactions
  • Headache
  • Myalgia
  • Drowsiness

Examples:

  • Nalidixic acid
  • Oxalinic acid
  • Cinoxacin

Question 21. Cephalosporins

Answer:

Cephalosporins

  • Cephalosporins are semi-synthetic antibiotics with a beta-lactam ring

Cephalosporins Uses:

  • Gram-negative infections
  • Surgical prophylaxis
  • Gonorrhea
  • Meningitis
  • Mixed aerobic and anaerobic infection
  • Typhoid
  • Nosocomial infection
  • Orodental infection

Cephalosporins Adverse Reactions:

  • Hypersensitivity reactions
  • Nephrotoxicity
  • Diarrhea
  • Bleeding
  • Low WBC count
  • Pain at the injection site
  • Disulfiram like reaction

Question 22. Triple vaccine, Dan PT

Answer:

Triple vaccine, DPT

  • DPT is used as an active immunization
  • It is combination of Diphtheria toxoid, pertusis vaccine and tetanus toxoid

DPT Route of Administration:

  • Intramuscular

DPT Dose:

  • Initial dose- 6 weeks
  • Three doses are completed at intervals of 4-6 weeks
  • Booster doses-18 months and 5 years

DPT Adverse Reactions:

  • Transient local inflammation
  • Fever
  • Occthe asional convulsions

DPT Advantages:

  • Minimizes the number of injections
  • Improves immune response

Question 23. Anti-amoebic drugs

Answer:

Anti-amoebic drugs

  • Anti-amoebic drugs are drugs used in amoebiasis

Anti-amoebic drugs Classification:

  1. Drugs effective in both intestinal and extra-intestinal amoebiasis
    • Metronidazole
    • Tinidazole
    • Secnidazole
    • Omid azole
    • Satranidazole
    • Emetine
  2. Drugs effective in intestinal amoebiasis
    • Diloxanide furoate
    • Quiniodochlo
    • Iodoquinol
    • Tetracyclines
  3. Drugs effective in extraintestinal amoebiasis
    • Chloroquine

Question 24. Quinsy

Answer:

Quinsy

  • It is an infection in connective tissue between the tonsil and the superior constrictor
  • It is also called peritonitis sellar abscess

Quinsy Fethe features:

  • Acute pain in the throat
  • Pain radiates to the ear
  • Dysphagia
  • Nausea
  • Constipation
  • Poor oral hygiene
  • Body ache
  • Headache
  • Enlarged lymph nodes
  • Dyspnoea
  • Trismus
  • Deviation of uvula
  • Hoarseness of voice
  • Foul breath

Quinsy Management:

  • Antibiotics
  • Incision over the most prominent part
  • Analgesics
  • Warm saline gargles 4 fluids
  • Tonsillectomy

Question 25. Rabies prevention

Answer:

Rabies prevention

  • Rabies vaccines are two types
  1. Neural
  2. Non-neural

1. Neural Vaccines:

  1. Semple vaccine:
    • The most widely used vaccine
    • Developed by Semple at Central Research Institute, Kasauli.
    • It is a 5% suspension of infected sheep brain and inactivated by 5% phenol at 37°C leaving no residual live virus.
  2. Beta Propiolactone (BPL) Vacine:
    • Modified sample vaccine
    • Instead of phenol, BPL is used as an activating agent.
  3. Infant brain vaccine:
    • Used widely in America to Reduce neurological complications.
      • Vaccination Schedules:
        • Nowadays it’s not used.
        • In the past, they were given subcutaneously on the anterior abdominal wall.
        • 7 – 14 injections depend on the degree of risk.

2.  Non-Neural Vaccines:

  1. Duck Egg Vaccine:
    • BPL is used as an inactivating agent
    • It has poor immunogenicity so not used now.
  2. Tissue culture vaccines:
    • Following cell culture vaccines are available in India.
      • Human diploid cell strain vaccine [HDCS]
        • The HDCS vaccine is prepared by growing rabies virus on human diploid cells and is inactivated with BPL.
        • This vaccine is highly antigenic and free of side effects
    • Purified chick embryo cell vaccine [PCEC]
      • PCEC is now widely used.
      • It is cheaper
      • It contains BPL inactivated flurry LEP strain
    • Purified Vero cell vaccine [PVC]
      • This vaccine is under study

Question 26. Antiviral drugs

Answer:

Antiviral drugs

Infectious Diseases Antiviral Drugs

Question 27. BCG

Answer:

BCG

  • The Bacille Calmette Guerin (BCG) vaccine was prepared by Calmette and Guerin in 1921
  • Used for protection against tuberculosis infections

BCG Forms:

  • Liquid form
  • Freeze-dried form- commonly used

Dose and Administration:

  • 0.1 ml is administered intradermally soon after birth

BCG Result:

  • A small nodule develops at the injection site in about 2-3 weeks
  • it gradually increases in size upto 441 mm in diameter
  • It breaks into a shallow ulcer leaving 4-8 mm diameter round scar

BCG Contraindications:

  • AIDS patients
  • Eczema
  • Pertussis
  • Measles
  • Patients on steroids

Question 28. Complications of Hepatitis B

Answer:

Complications of hepatitis B are:

  1. Cirrhosis of liver
  2. Liver failure
  3. Hepatocellular carcinoma

Question 29. Chloroquine

Answer:

Chloroquine

  • Chloroquine is antimalarial drug
  • It is a synthetic 4-arninoquinolone

Chloroquine Uses:

  • Malaria
  • Extra-intestinal amoebiasis
  • Photogenic reactions
  • Lepra reactions

Chloroquine Adverse Reactions:

  • Severe nausea and vomiting
  • Pruritis
  • Headache
  • Visual disturbances
  • Insomnia
  • Skin rashes
  • Cardiomyopathy
  • Peripheral neuropathy
  • Psychiatric problems
  • Blurring of vision
  • Confusion
  • Bleaching of hair

Question 30. Human insulins

Answer:

Human insulins

  • Human insulin is produced by recombinant DMA technology
  • They are expensive
  • Absorbed rapidly

Human insulins Forms:

  • Regular B Lente
  • Isophane insulin
  • Lente
  • Ultralente preparations

Human insulins Advantages:

  • Less antigenic
  • More stable
  • Fewer chances of resistance
  • Less chances of lipodystrophy

Human insulins indications:

  • Allergy to conventional preparations
  • Insulin resistance
  • Lipodystrophy at the injection site
  • Pregnancy

Question 31. Four causes of lymphadenopathy

Answer:

Lymphadenopathy Causes:

  1. Inflammatory
    • Acute lymphadenitis
    • Chronic lymphadenitis
    • Granulomatous lymphaleukemiaeoplastic
    • Benign
    • Malignant
  2. Lymphatic leukaemia
    • Autoimmune disorders
    • Juvenile rheumatoid arthritis
    • Collagen diseases like systemic lupus erythematosus, polyarteritis nodosa
  3. Generalised lymphadenopathy
    1. Tuberculosis
    2. Syphilis- secondary stage
    3. Infectious mononucleosis
    4. Sarcoidosis
    5. Toxoplasmosis
    6. Hodgkin’s disease
    7. Lymphosarcoma

Endocrine And Metabolic Diseases Short Essays

Question 1. Hypercalcemia

Answer:

Hypercalcemia Causes:

  • Conditions associated with hypercalcemia and increased PTH levels
    • Hyperparathyroidism
    • Chronic renal failure
  • Conditions associated with hypercalcemia and low PTH levels
    • Multiple myeloma
    • Sarcoidosis
    • Hyperthyroidism
    • Thiazide diuretics
    • Milk alkali syndrome
    • Familial

Hypercalcemia Clinical features

  • Nausea, vomiting
  • Pain in abdomen
  • Dehydration
  • Hypotension

Hypercalcemia Treatment:

  • Avoid calcium-containing antacids
  • Replacement of fluid and electrolytes by 4-6 l of normal saline
    • To correct dehydration, hypotension, and calcium levels
  • Forced diuresis by saline and diuretic frusemide given 4 to depress tubular reabsorption of calcium
  • Drugs given include a generation bis- phosphonate ex: pamidronate given as a single 4 dose of 15-60 mg in normal saline
  • Calcitonin is used in emergency state
  • Cinacalcet is used orally in hypercalcemia crisis

Question 2. Thyrotoxicosis

Answer:

Thyrotoxicosis

  • It is a clinically toxic manifestation due to excess thyroid hormones

Thyrotoxicosis Causes:

  • Common causes
  • Grave’s disease
  • Toxic nodular goitre
    • Multinodular
    • Solitary nodule
  • Less common causes
    • Thyroiditis Drug-induced
    • Factitious
    • Iodine induced
  • Rarely
    • Pituitary or ectopic TSH
    • Thyroid carcinoma

Thyrotoxicosis Clinical features:

  • Goitre
  • Weight loss, vomiting, diarrhea
  • Increased pulse rate, dyspnea, arrhythmia
  • Nervousness, restlessness, tremors, muscular weakness
  • Perspiration, clubbing, loss of hair, pre-tibial myxoedema
  • Amenorrhea, abortions, infertility, loss of libido
  • Lid lag, exophthalmos, diplopia, watering of eyes
  • Fatigue, heat intolerance, polydipsia

Question 3. Calcium homeostasis

Answer:

Regulation of Calcium/ Hemostasis:

  • Calcium level is regulated by

Calcitriol

  • It is the active form of vitamin D

Calcium homeostasis Mechanism:

Diseases Of The Gastrointestinal System Gingival Induces Synthesis Of Calcium Binding Protein

  • It also promotes calcification and remodeling of bone.

2. Parathyroid hormones

  • Secreted by Parathyroid glands

Read And Learn More: General Medicine Question and Answers

Calcium Homeostasis Mechanism:

Endocrine And Metabolic Diseases Calcium Homeostasis Mechanism

Question 4. Hypoglycemia-clinical features and management

Answer:

Hypoglycaemia

  • It is defined as a fall in blood glucose concentration below 3.1 mmol/1

Hypoglycaemia Clinical Features:

  1. CVS symptoms
    • Palpitation
    • Tachycardia
    • Anxiety
    • Cardiac arrhythmias
  2. CNS symptoms
    • Tremors
    • Confusion
    • Headache
    • Tiredness
    • Difficulty in concentration
    • Slurred speech
    • Drowsiness
    • Convulsion
    • Coma
  3. GIT symptoms
    • Nausea
    • Vomiting
  4. Dermatological symptoms
    • Sweating
    • Hypothermia

Hypoglycaemia Management:

  1. In unconscious patients
    • Stop anti-diabetic medication
    • Administer 50 ml of 50% intravenous glucose
    • Intramuscular injection of 1 ml of glucagon
  2. Unconscious patients
    • Oral glucose intake
  3. In severe cases
    • 1 mg glucagon subcutaneously or intramuscularly and repeated if necessary after 10 minutes

Question 5. Neurological complications of diabetes mellitus

Answer:

Neurological complications of diabetes mellitus

  • Diabetes can involve any part of the nervous system except the brain
  • Precipitating factors
  1. Poor glycaemic control
  2. Long control of diabetes

Pathological Changes:

  • Axonal degeneration of myelinated and nonmyelinated fibers
  • Patchy, segmental demyelination
  • Vasculopathy

Endocrine And Metabolic Diseases Neurological Complications Of Diabetes Mellitus

Question 6. Grave’s disease

Answer:

Grave’s disease

  • Grave’s disease is a diffuse goiter affecting the whole functioning thyroid tissue causing hypertrophy and hyperplasia due to abnormal thyroid stimulants

Grave’s Disease Clinical Features

  • It is a classical triad composed of
  1. Goitre
    • Diffuse and symmetric enlargement of thyroid
    • The gland surface is smooth
    • Bruit is heard
  2. Thyrotoxicosis
    • Excitability
    • Restlessness
    • Emotionally unstable
    • Insomnia
    • Muscle weakness
    • Fatigue
    • Myopathy
    • Heat intolerance
    • Increased sweating
    • Weight loss
    • Tachycardia
    • Palpitation
    • Increased cardiac output
    • Gynaecomastia
    • Increased libido
    • Pretibial myxoedema
  3. Exophthalmos
    • Protrusion of eyeballs

Grave’s Disease Treatment:

  1. Anti-thyroid drugs
    • To restore the patient to the euthyroid state
  2. Radioactive iodine
    • It destroys thyroid cells and reduces the mass of thyroid-functioning tissue
  3. Surgery
    • Reduce active thyroid mass

Question 7. Acromegaly- clinical features and complications

Answer:

Acromegaly:

  • Acromegaly occurs due to excess secretion of GH later in life after epiphyseal closure

Acromegaly Clinical Features:

  • Thick bones-larger hands and feet
  • Enlarged skull
  • Increased intracranial pressure
  • Headache
  • Photophobia
  • Visual disturbances
  • Hepatomegaly
  • Cardiomegaly
  • Osteoporosis
  • Arthralgia
  • Excessive sweating
  • Myalgia
  • Bowing of legs
  • Barrel shaped chest

Acromegaly Oral Manifestations:

  • Enlarged mandible
  • Class 3 malocclusion
  • Macroglossia D Thick lips
  • Proclination of teeth
  • Hypercementosis
  • Large nose, ears, and prominent eyebrows
  • Periodontitis
  • Enlargement of maxillary air sinuses

Acromegaly Complications:

  • High blood pressure (hypertension)
  • Cardiovascular disease, particularly enlargement of the heart (Cardiomyopathy)
  • Osteoarthritis
  • Diabetes mellitus
  • Precancerous growths (polyps) on the lining of your colon
  • Sleep apnea is a condition in which breathing repeatedly stops and starts during sleep
  • Carpal tunnel syndrome
  • Reduced secretion of other pituitary hormones (hypopituitarism)
  • Uterine fibroids, benign tumors in the uterus
  • Spinal cord compression
  • Vision loss

Question 8. Addison’s disease

Answer:

Addison’s disease

  • It is due to progressive destruction of the three zones of the adrenal cortex and medulla with lymphatic infiltration

Addison’s Disease Clinical Features:

  1. Glucocorticoid insufficiency
    • Weight loss
    • Nausea and vomiting
    • Malaise
    • Weakness
    • Anorexia
    • Diarrhea
    • Constipation
    • Postural hypotension
    • Hypoglycaemia
  2. Mineralocorticoid deficiency
    • Hypotension
  3. Loss of androgens
    • Reduction of pubic and axillary hair in females
  4. Increased ACTH secretion
    • Pigmentation of exposed areas, pressure areas, mucous membranes, conjunctivae, and recently acquired scars

Question 9. Diabetes and surgery

Answer:

Diabetes and surgery

  • Patients with diabetes need to maintain very good oral hygiene as they are prone to odontogenic, periodontal, and other infections
  • In well-controlled diabetics, dental procedures generally do not require any special precautions
  • Antibiotic coverage may be required
  • In uncontrolled diabetics, infections and wound healing may be a problem even after minor procedures
  • If major dental procedures or surgery is to be undertaken, prior control of diabetes by the physician is needed
  • If the patient is on only oral antihyperglycemic drugs, he should start insulin
  • Dental procedures may often reduce food intake and diabetics may go to hypoglycemia
  • Dose adjustments may be required

Question 10. Gestational diabetes mellitus

Answer:

Gestational diabetes mellitus

  • It is defined as glucose intolerance that develops during pregnancy and usually cures after delivery
  • Persons affected are
  1. Older women
  2. Obese/overweight women
  3. Women with a history of delivering large babies
  4. Women with a history of gestational diabetes

Gestational Diabetes Mellitus Diagnosis:

  • All women during pregnane}7 should be screened based on random blood sugar tests in each trimester
  • 50 mg oral glucose is administered and serum glucose is measured at 60 min
  • If the glucose level is less than 140 mg, it is normal if not then the following step is taken
  • 100 mg of glucose is administered and glucose in the fasting state is measured at 1,2 and 3 hours
  • Deviation from normal levels indicates gestational diabetes

Normal Values:

Endocrine And Metabolic Diseases Diabetes And Surgery Normal Values

Question 11. Cushing’s syndrome

Answer:

Cushing’s syndrome

  • Cushing’s syndrome is caused by increased plasma glucocorticoid levels due to enhanced production of cortisol

Cushing’s Syndrome Clinical Features:

  • Age- common in 3rd and 4th decades of life
  • Females are more affected
  • Obesity
  • Truncal fullness
  • Moon facies
  • Buffalo hump
  • Purple striae are seen on the abdomen
  • Oligomenorrhoea and amenorrhoea
  • Impotence in males
  • Elevated blood pressure
  • Muscle weakness
  • Bone pain
  • Decreased glucose tolerance

Cushing’s Syndrome Investigations:

  • Screening test
  • Determine free cortisol in urine
  • Plasma ACTH measurement
  • Plasma ACTH levels of more than 200-500 Pg per ml indicate Cushing’s syndrome
  • Dexamethasone suppression test
  • Plasma values above 5 microgram/100 ml suggest Cushing’s syndrome

Cushing’s Syndrome Treatment:

  • Medical treatment
  • Metyrapone- dose- 2-6 g per day in divided dose
  • Aminoglutethimide-1-2 g per day
  • Surgical treatment
  • Pituitary irradiation
  • Adrenalectomy

Question 12. Eye signs on thyrotoxicosis

Answer:

Eye signs on thyrotoxicosis

  1. Exophthalmos
    • It means protrusion of the eyeball
  2. Spasm of the upper eyelid with lid retraction
  3. Proptosis with widening of the palpebral fissure
  4. Supraorbital and infraorbital swelling
  5. Congestion, edema, and chemosis of the conjunctiva
  6. Papilloedema
  7. Corneal ulceration
  8. External ophthalmoplegia
  9. Weakness of the extrinsic ocular muscles
  10. Other signs
    • Von Giraffe’s sign
      • When the patient is asked to look down, his upper eyelid fails to follow the rotation of the eyeball and thus lags behind
    • Joffroy’s sign
      • When the patient is asked to look upwards with the head fixed, there will be the absence of wrinkling on the forehead
    • Moebius sign
      • Failure of convergence of eyeballs
    • Dalrymple’s sign
      • Upper sclera is seen due to retraction of the upper eyelid
    • Stellwag’s sign
      • Absence of normal blinking

Endocrine And Metabolic Diseases Long Essays

Question 1. Describe the etiology, clinical features, and management of tetanus.

Answer:

Tetanus:

  • It is a disorder of neuromuscular excitability

Etiology:

  • It is caused by exotoxin, tetanospasmin liberated by clostridium tetani

Etiology Clinical Features:

  • Trismus
  • Dysphagia
  • Risussardonicus- in it eyebrows and corners of the mouth are drawn up due to spasms of the muscles of the face and jaw
  • Opisthotonus- rigidity of the muscles of the neck and trunk
  • Elevation of temperature
  • Rapid pulse
  • Cyanosis

Etiology Types:

  1. Acute tetanus
    • The incubation period is less than 10 days
  2. Chronic tetanus
    • The incubation period is about a month
  3. Delayed tetanus or latent tetanus
    • In it organism remains latent for many years
  4. Local tetanus
    • There is the presence of local contraction of muscles
  5. Cephalic tetanus
    • There is irritation or paralysis of the cranial nerves
  6. Bulbar tetanus
    • There is an extensive spasm of the muscles of deglutition and respiration
  7. Late tetanus
    • The inoculation period is prolonged
  8. Tetanus neonatorum
    • Recurrent tetanus

Etiology Management:

  1. Passive immunization
    • 1 Lac units of Anti-tetanus serum is given half intravenously and half intramuscularly
  2. Antibiotics
    • Penicillin injection of 10 lac units every 4 hours
    • Metronidazole
    • Tetracycline
  3. Wound care
    • Thorough cleansing and debridement
    • Removal of all necrotic tissues and foreign bodies
    • All stitches are removed
    • Blood clots, foreign bodies, and pus are cleared
    • The wound should be left open
  4. The patient is isolated to a quiet, dark, and well-ventilated room
  5. Further treatment depends on the severity of the cases
    • In mild cases
      • Prozac in -200 mg IM
      • Barbiturate, amylobarbitone, or injection diazepam-5-40 mg 4 times in a day
    • In moderate cases
      • Passage of nasogastric tube for feeding
      • Passage of self-retaining catheter to drain the bladder
      • Administration of intravenous fluid
      • Maintenance of intake and output chart
      • Tracheostomy
    • In very severe cases
      • Use of muscle relaxant, 40 mg turbo- marine initially 4 and then IM injections
      • Tracheostomy
      • Sedation with pentothal sodium
      • Nasogastric feeding
      • Elimination of visceral stimuli
      • Intravenous administration of fluid and electrolytes
      • Constant nursing

Question 2. Describe the etiology and clinical features of acromegaly with special experience in dental problems.

Answer:

Acromegaly:

  • Acromegaly occurs due to excess secretion of GH later in life after epiphyseal closure

Etiology:

  • Pituitary adenoma
  • Pancreatic islet cell tumors
  • Hypothalamic tumors
  • Bronchial carcinoid
  • Small cell carcinoma of Hung

Acromegaly Clinical Features:

  • Thick bones-larger hands and feet
  • Enlarged skull
  • Increased intracranial pressure
  • Headache
  • Photophobia
  • Visual disturbances
  • Hepatomegaly

Read And Learn More: General Medicine Question and Answers

  • Cardiomegaly
  • Osteoporosis
  • Arthralgia
  • Excessive sweating
  • Myalgia
  • Bowing of legs
  • Barrel shaped chest

Acromegaly Oral Manifestations:

  • Enlarged mandible
  • Class 3 malocclusion
  • Macroglossia
  • Thick lips
  • Proclination of teeth
  • Hypercementosis
  • Large nose, ears, and prominent eyebrows
  • Periodontitis
  • Enlargement of maxillary air sinuses

Endocrine And Metabolic Diseases Diagnosis

Question 3. Enumerate the proliferating factors, pathogenesis, investigations, and management of diabetic ketoacidosis.

Answer:

Diabetic Ketoacidosis:

  • It is a complication of diabetes mellitus

Diabetic Ketoacidosis Proliferating Factors:

  • Undetected or undiagnosed type 1 diabetes
  • Stress
  • Infection

Diabetic Ketoacidosis Pathogenesis:

Endocrine And Metabolic Diseases Diabetic Ketoacidosis Pathogenesis

Diabetic Ketoacidosis Investigations:

  • Diabetic ketoacidosis is confirmed by
    1. Hyperglycaemia
    2. Ketonaemia
    3. 1 leavy ketonuria
    4. Acidosis

Diabetic Ketoacidosis Management:

  1. Correction of hyperglycemia
    • Administration of regular insulin 0.1 U/k bolus followed by 0.1 U/kg/ hour by ccontnousIV infusion till the patient recovers
  2. Correction of dehydration
    • Normal saline infusion of 1 liter in the first hour
    • Then 1 litre over the next 4 hours
    • Then quantity is titrated
  3. Correction of acidosis
    • Use of sodium bicarbonate
  4. Potassium
    • 10-20 mEq/hour potassium chloride is added to the drip for rapid correction of hyperglycemia

Question 4. Classify diabetes mellitus. Discuss the complications and management of diabetes mellitus

Answer:

Diabetes mellitus

  • Diabetes mellitus is defined as a heterogeneous metabolic disorder characterized by the common feature of chronic hyperglycemia with disturbance of carbohydrate, fat, and protein metabolism

Diabetes Mellitus Classification:

  1. Primary diabetes
    • Type 1- IInsulin-dependentdiabete mellitus
      • IImmunemediated
      • Nonimmune mediated
    • Type 2- NNoninsulin-dependentdiabetes mellitus
      • Obese
      • Non-obese
  2. Secondary diabetes
    • Pancreatic diabetes
    • Hormonal or endocrinal abnormalities
    • DDrug-inducedInsulin receptors antibodies
    • Genetic syndromes

Diabetes Mellitus Complications:

  1. Acute metabolic complications
    • Diabetic ketoacidosis
      • Develop in patients with severe insulin deficiency
      • Clinical Features:
        • Nausea, vomiting, anorexia
        • Deep and fast breathing
        • Mental confusion
        • Coma
    • Hyperosmolar hyperglycaemia nonketotic coma
      • It is a complication of type 2 diabetes mellitus
      • Caused by severe dehydration which leads to sustained hyperglycemia diuresis
      • Clinical Features:
        • High blood sugar
        • High plasma osmolality
        • Thrombotic and bleeding complications
    • Hypoglycaemia
      • Develop in type 1 diabetes mellitus
      • Clinical Features:
        • Permanent brain damage
        • Worsening of diabetic control
        • Rebound hyperglycaemia
  2. Late systemic complications
    • Atherosclerosis
      • Common in both type 1 and type 2 diabetes mellitus
      • Atherosclerosis may lead to
        • Myocardial infarction
        • Cerebral stroke
        • Gangrene of toes and feet
    • Diabetic microangiopathy
      • It is the abasementmembrane thickening of small blood vessels and capillaries of different organs and tissues
      • Occurs due to increased glycosylation of hemoglobin and other proteins
    • Diabetic nephropathy
      • It is a severe complication of diabetes mellitus
      • Occurs in both types
      • Features:
        • Asymptomatic proteinuria
        • Nephrotic syndrome
        • Progressive
        • Renal failure
        • Hypertension
    • Diabetic neuropathy
      • Effects all parts of the nervous system
    • Diabetic retinopathy
      • It is the cause of blindness
      • Other retinal complications include
        • Glaucoma
        • Cataract
        • Corneal disease
    • Infections
      • Diabetic patients are more susceptible to infections like tuberculosis, pyelonephritis, otitis, carbuncles and diabetic ulcers

Diabetes Mellitus Management:

  1. Diet management
    • The daily energy requirement for an individual is calculated according to age, weight, height, and activity
    • Calorie requirement:
      • For men- 36 kcal/kg
      • For women-34 kcal/kg
  2. Lifestyle modification
    • Physical exercise
    • Reduction of weight
    • Avoid alcohol and smoking
    • Behavioural exercises
  3. Oral hypoglycaemic drugs
    • Sulphonylureas
    • Meglitinides
    • Biguanides
    • Thiazolidinedione derivatives
    • Alpha-glucosidase inhibitors
  4. Insulin

Question 5. Discuss the complication of systemic ccorticosteroidtherapy with special reference to dental practice

Answer:

Complications of Systemic Corticosteroids:

  1. Metabolic effects
    • Mood changes from euphoria to depression
    • Fluid retention and edema
    • Hypertension
    • Glucose intolerance
    • Osteoporosis
    • Increased susceptibility to infection
    • Reactivation of latent tuberculosis
    • Impaired wound healing
    • Gastric erosions
    • Masked perforation
    • HHemorrhagefrom stomach and duodenum
  2. Suppression of hypothalamic-pituitary-adrenal axis
    • It occurs with high-dose therapy
    • This makes it difficult to withdraw steroids

Measures to Reduce Side Effects:

  • Use of the lowest possible dose
  • Administer on alternate days rather than daily
  • Use of morning dose rather than any other time
  • Use of steroids for established cases
  • Monitor caloric intake to prevent weight gain and reduce sodium intake
  • Use of H2 receptor blockers or proton pump inhibitors
  • Provide high calcium intake and vitamin D

Question 6. Outline the conditions wthatproduce pigmentation of oral mucosa. Discuss the clinical features of Addison’s disease.

Answer:

Causes of Oral Pigmentation:

  • Autoimmune adrenalitis
  • Tubcrculousadrenalitis
  • Bilateral adrenalectomy
  • Drugs-ketoconazole
  • Metastases in the adrenal
  • Haemochromatosis
  • Amyloidosis
  • Histoplasmosis

Addison’s Disease:

  • It is due to progressive destruction of the three zones of the adrenal cortex and medulla with lymphatic infiltration

Oral Pigmentation Clinical Features:

  1. Glucocorticoid insufficiency
    • Weight loss
    • Nausea and vomiting
    • Malaise
    • Weakness
    • Anorexia
    • Diarrhea
    • Constipation
    • Postural hypotension
    • Hypoglycaemia
  2. Mineralocorticoid deficiency
    • Hypotension
  3. Loss of aandrogensReduction of pubic and axillary hair in females
  4. Increased ACTH secretion
    • Pigmentation of exposed areas, pressure areas, mucous membranes, conjunctivae, and recently acquired scars

Question 7. Define hypo- and hyperthyroidism. Discuss clinical features, investigations, and treatment of hypothyroidism.

Answer:

Hyperthyroidism Definition:

  1. Hypothyroidism
    • It is a clinical condition caused by low levels of circulating thyroid hormones
  2. Hyperthyroidism
    • It is a clinical syndrome that results from exposure of the body tissues to excess circulating free thyroid hormones

Hypothyroidism Clinical Features:

  1. In new bom
    • Cretinism
    • Mental retardation
    • Poor growth
    • Difficult to nurse a baby
    • Dwarfism
  2. During childhood or adolescence
    • Juvenile hypothyroidism
    • Child appears young
    • Mental deficiency
    • Abdominal distension
    • Umbilical hernia
    • Prolapse of rectum
  3. In adults
    • Fatigue
    • Weight gain
    • Skin becomes thickened and puffy
    • Muscle cramps
    • Paraesthesia
    • Impaired speech
    • Reduced cardiac output
    • Elevation of blood pressure
    • Shortness of breath
    • Abdominal distension
    • Aches and pains
    • Anaemia
    • Alopecia
    • Menorrhagia, infertility
    • Constipation

Hypothyroidism Investigations:

  • Serum T3 and T4 levels- low
  • Serum TSH- high
  • Thyroid peroxidase antibodies- present
  • Serum cholesterol triglyceride- high
  • ECG- shows bradycardia, low amplitude of QRS, and ST-T changes
  • Blood- macrocytic anemia
  • X-ray chest- shows cardiomegaly
  • Photomtogram- delayed ankle jerk

Hypothyroidism Treatment:

  • Replacement of thyroid hormones by L-thyroxine
  • Initial starting dose-50-100 micrograms daily as a single dose empty stomach in the morning for the first 3-4 weeks
  • The dose is increased to 150 micrograms daily
  • The maximum dose is 300 micrograms in a day
  • In older persons or persons with ischaemic heart disease, a low dose of L-thyroxine 25 microgram/day is started and gradually increased

Question 8. Discuss the etiology, clinical features, and management of thyrotoxicosis. Mention a note on thyroid function tests

Answer:

Thyrotoxicosis is a syndrome resulting from an increased level of free thyroxin

Thyrotoxicosis Clinical Features

  • Hyperactivity
  • Irritability
  • Heat intolerance
  • Palpitations
  • Fatigue
  • Weakness
  • Weight loss
  • Increased appetite
  • Tachycardia
  • Systolic hypertension
  • Presence of tremors
  • Cardiac arrhythmias
  • Excessive sweating
  • Exophthalmos

Thyrotoxicosis Management:

  1. General management
    • Rest
    • Nutritious diet
  2. Drug therapy
    • Carbimazole
    • Initial dose of 30 nag/ day, maintenance dose of 10-20 mg/day is given
    • Potassium perchlorate – 800 nag/day in divided doses
    • Sodium or potassium iodide 6-10 nag/day
  3. Surgical treatment
    • Subtotal thyroidectomy
  4. Radioiodine treatment
    • Iodine is given in ddosesof 8-10 millicuries

Thyroid Function Tests:

  1. Measurement of radioactive iodine uptake
    • The normal value is 30%
    • Higher values indicate thyrotoxicosis
    • It is no longer used because of
      • Lack of sensitivity
      • Lack of specificity
      • Time-consuming
      • Complicated procedures
  2. Measurement of total T3 and T4 in blood by radioimmunoassay
    • Widely used
    • Normal Values:
      • Serum T3 total- 70-200 ng/1
      • Serum T4 total- 5.5-13.5 microgram/1
    • Drawbacks:
      • Measure the total amount of hormone
      • Gets changed with the fluctuations in their binding protein
  3. Measurement of free T3 and T4 in blood
    • NORMAL VALUES
    • Serum free T3-1-2.6 nmol/1
    • Serum free T4-10-27 nmol/1
  4. Estimation of TSH
    • Normal value- 0.15-3.5 mIU/1
    • High levels of ooccurin primary hypothyroidism
    • Low levels ooccurin hyperthyroidism and hypopituitarism
  5. Ultrasound of thyroid
    • Measure the size and mass of the thyroid
    • Detects shape and nodularity of thyroid
  6. Thyroid scan
    • It is used to detect functioning and nonfunctioning nodules in the thyroid
    • I131 or 99mTc is used for
  7. Antithyroid antibodies
    • Detects autoimmune thyroid disorders
    • Stimulating antibodies and TSH receptor-blocking antibodies are raised in Grave’s disease
  8. Needle biopsy of thyroid
    • Detects malignancy

Question 9. Discuss ethe tiology, clinical features, and management of myxoedema

Answer:

Myxoedema:

  • Myxoedema indicates severe hypothyroidism

Etiology:

  1. Primary causes
    • Spontaneous atrophic hypothyroidism
    • Iodine deficiency
    • Following 1131 therapy
    • Post thyroidectomy
    • Hashimoto’s thyroiditis
    • Radiation
  2. Secondary causes
    • Destruction of the pituitary gland
    • Post-surgery
    • Post radiation
    • Tumour
    • Disorders of hypothalamus

Myxoedema Clinical Features:

  1. General symptoms
    • Age and sex- Middle-aged males are frequently affected
    • Weakness
    • Fatigue
    • Lethargy
    • Low blood pressure
    • Mental retardation
    • Dry coarse skin
    • Swelling of the face and extremities
    • Cold intolerance
    • Husky voice
    • Decreased sweating
    • Anorexia
    • Loss of memory
    • Hearing impairment
    • Arthralgia
    • Muscle cramps
    • Paraesthesia
  2. Oral manifestations
    • Peri-orbital puffiness
    • Loss of facial hair
    • Swollen tongue, lips, and eyelids
    • Difficulty in speech
    • Underdevelopment of maxilla and mandible

Myxoedema Management:

  • Replacement of thyroid hormones by L-thyroxine
  • Initial starting dose-50-100 micrograms daily as a single dose empty stomach in the morning for the first 3-4 weeks
  • The dose is increased to 150 micrograms daily the maximum dose is 300 micrograms every day
  • In older persons or persons with ischaemic heart disease, a low dose of L-thyroxine 25 microgram/day is started and gradually increased

Question 10. Describe etiology, clinical features, diagnosis, and treatment of hyperthyroidism.

Answer:

Hyperthyroidism:

  • It is a clinical syndrome that results from exposure of the body tissues to excess of circulating free thyroid hormones

Etiology:

  1. Common
    • Grave’s disease
    • Toxic nodular goitre
      • Multinodular
      • Solitary nodule
  2. Less common
    • Thyroiditis
    • Drug-induced
    • Self-induced
    • Iodine excess
  3. Rare causes
    • Pituitary or ectopic TSH
    • Thyroid carcinoma

Hyperthyroidism Clinical Features:

  1. Goitre
  2. Gastrointestinal symptoms
    • Weight loss
    • Diarrhea
    • Vomiting
  3. Cardiovascular symptoms
    • Sinus tachycardia
    • Exertional dyspnoea
    • Arrhythmias
    • Precipitation of angina
  4. Neuromuscular symptoms
    • Nervousness, irritability
    • Restlessness
    • Tremors of hands
    • Muscular weakness
    • Exaggerated tendon reflexes
  5. Dermatological symptoms
    • Increased sweating
    • Clubbing of fingers
    • Loss of hairs
    • Redness of palms
  6. Reproductive symptoms
    • Menstrual irregularity
    • Abortions
    • Infertility
    • Loss of libido
  7. Ophthalmological
    • Lid retraction
    • Wide palpebral fissures
    • Exophthalmos
    • Diplopia
    • Excessive watering of eyes
  8. Miscellaneous
    • Heat intolerance
    • Excessive thirst
    • Fatigue
  9. Oral manifestations
    • Early exfoliation of deciduous teeth
    • Premature eruption of permanent teeth
    • Alveolar bone atrophy
    • Increased susceptibility to oral infections

Hyperthyroidism Diagnosis:

  • T3 and T4 levels- elevated
  • TSH levels- low
  • 131I uptake is increased
  • Serum cholesterol level- low
  • ECG changes- shows tachycardia, arrhythmias, ST- T changes
  • USG- shows diffuse goitre
  • Increased BMR
  • Decreased urinary excretion of iodine

Hyperthyroidism Treatment:

  1. Drug therapy
    • Anti-thyroid drugs
      • Carbimazole
      • Propylthiouracil -100-150 mg
    • Beta-blockers
      • Propanolol-80-160 mg daily
      • Metoprolol-50 mg/ day
  2. Radioactive ablation of thyroid
  3. Subtotal thyroidectomy
  4. Treatment of relapse
    • Long-term drug therapy is used
    • Radioactive iodine therapy
  5. Management of ophthalmopathy
    • Use of 60 mg of prednisolone daily
  6. Management of dermopathy
    • Local betamethasone ointment or triamcinolone injection may be used

Question 11. What are the causes of hypocalcemia? Describe clinical features and outline the treatment of tetany

Answer:

Hypocalcaemia:

  • It is a condition of low levels of calcium

Causes Of Hypocalcaemia:

  • Sepsis
  • Burns
  • Acute pancreatitis
  • Acute renal failure
  • Alkalosis
  • Drugs like diuretics, protamine, heparin, and glucagon
  • Toxic shock syndrome
  • Hypomagnesaemia
  • Plasmapheresis
  • Extensive transfusion
  • Malignancy

Tetany:

  • It is a clinical condition characterized by low levels of ionized calcium leading to increased neuromuscular excitability

Tetany Clinical Features:

  1. In children
    • Characteristic triad- carpopedal spasm, stridor and convulsion
    • Carpopedal spasm- flexion at metacarpophalangeal joints and extension at interphase- large joints wwithotherposition of the thumb
    • Stridor- closure of the glottis
  2. In adults
    • Tingling sensation in peripheral parts of limbs or around the mouth
    • Painful carpopedal spasm
    • Rarely stridor and convulsions
  3. Signs
    • Trousseau’s sign
      • Raising the blood pressure above systolic level by inflation of the sphygmomanometer cuff produces carpal spasm within 3-5 minutes
    • Chvostek’s sign
      • A tap at the facial nerve at an angle of the aw produces twitching of facial muscles

Tetany Treatment:

  1. Treatment of hypocalcemia
    • Injection of 20 ml of 10% calcium gluconate
  2. Treatment of alkalosis
    • Intravenous administration of isotonic saline
    • Withdrawal of alkalies
    • Inhalation of 5% CO2in oxygen- to treat hyperventilation
    • Psychotherapy

 

Haemorrhage Shock And Blood Transfusion Short Question and Answer

Question 1. Types of shock.

Answer:

Various types of shock are as follows:

Haemorrhage Shock And Blood Transfusion Types Of Shock

Question 2. Septic shock.

Answer:

Aetiology:

  • Release of endotoxin by gram-negative organisms.
  • Severe septicaemia.
  • Peritonitis.
  • Meningitis

Question 3. Neurogenic shock.

Answer:

Neurogenic Shock Causes:

  • Paraplegia, quadriplegia.
  • Trauma to the spinal cord.
  • Spinal anaesthesia.

Neurogenic Shock Clinical Features:

  • Skin remains warm, pink and well-perfused.
  • Urinary output – normal.
  • Heart rate-rapid.
  • Blood pressure is decreased.

Question 4. Cardiogenic shock.

Answer:

Cardiogenic Shock Causes:

  • Injury to heart
  • Myocardial infarction.
  • Cardiac arrhythmia.
  • Congestive cardiac failure.

Cardiogenic Shock Clinical Features:

  • Initially
    • Skin is pale and cool.
    • Urine output reduced.
  • Later
    • Rapid pulse.
    • Hypotension
    • Distended neck veins.
    • The liver is enlarged.
    • The heart becomes enlarged.

Question 5. Hypovolaemic shock.

Answer:

Hypovolaemic Shock Causes:

  • Blood and plasma loss
  • Electrolyte loss.

Question 6. Crush Syndrome.

Answer:

Crush Syndrome

It is a symptom complex in which a portion of the body becomes crushed due to a heavy weight falling on that portion and is kept there for some time to crush all the tissues in that portion.

Crush Syndrome Causes:

  • Earthquakes
  • Mine injuries
  • Air raids
  • Collapse of building.
  • Use of tourniquet for a longer period.

Crush Syndrome Clinical Features:

  • Extravasaion of blood into muscles.
  • Muscles are crushed and swollen.
  • Acute renal tubular necrosis.
  • Reduced urinary output.
  • Tense and painful extremities.

Crush Syndrome Treatment:

  • Application of tourniquet.
  • Parallel incisions are made to relieve tension.
  • Administration of intravenous fluid.
  • Catheterization of bladder.
  • Hemodialysis is a severe condition.

Read And Learn More: General Surgery Question and Answers

Question 7. Hypokalaemia.

Answer:

Hypokalaemia

Potassium deficiency in diet is called hypokalemia.

Hypokalaemia Causes:

  • Following trauma.
    • Starvation
    • Loss of gastrointestinal secretion.

Hypokalaemia Clinical features:

  • Gradual onset of drowsiness.
  • Slow and slurred speech.
  • Irritability.
  • Muscular hypotonia and weakness.
  • Absence of deep reflexes.
  • Slow pulse rate.
  • Diminished intestinal motility.
  • Low BP.
  • Skin remains warm and dry.

Hypokalaemia Treatment:

  • Replacement of potassium deficit.

Question 8. Acidosis.

Answer:

Acidosis

An increase in pH leads to acidosis.

Acidosis Types:

  1. Metabolic acidosis.
    • In it, there is a gain or retention of fixed acids or loss of base.
    • Cause:
      • Diabetic acidosis.
      • Lactic acidosis.
      • Renal insufficiency.
      • Rapid transfusion of bank blood.
      • Diarrhoea.
    • Clinical Features:
      • Increase in rate and depth of breathing.
      • Rapid and noisy respiration.
      • Raised pulse rate and blood pressure.
      • Urine becomes strongly acidic.
    • Treatment:
      • Administration of ringer’s lactate solution.
  2. Respiratory acidosis.
    • Causes:
      • Lung disorders.
      • Peritonitis
      • Crush injury.
      • Depressed respiratory centre.
      • Airway obstruction.

Acidosis Clinical Features:

  • Slow rise in BP.
  • Abnormal respiration.
  • Restlessness.
  • Hypertension
  • Tachycardia.

Acidosis Treatment:

  • Mechanical ventilation
  • Endotracheal intubation.
  • Avoid over-sedation and over-use of muscle relaxants.

Question 9. Haemorrhage.

Answer:

Haemorrhage

Haemorrhage is defined as the escape of blood from blood vessels.

Haemorrhage Classification:

  1. Based on the bleeding haemorrhage.
    • External and internal.
    • Arterial, venous or capillary.
  2. Based on the time of appearance.
    • Primary – Secondary – Reactionary.

Question 10. Secondary Haemorrhage.

Answer:

Secondary Haemorrhage

It is a bleeding that occurs usually after 7-14 days of injury.

Secondary Haemorrhage Causes:

  • Infection.
  • Sloughing part of the arterial wall.

Secondary Haemorrhage Clinical features:

  • Preceded by warning haemorrhage staining the dressings.
  • Followed by moderate to severe haemorrhages.

Secondary Haemorrhage Types:

  • Externally – example: at operation site of haemorrhoids- tomy.
  • Internally Example: haematemesis following peptic ulcer operation.

Question 11. Hemophilia.

Answer:

Hemophilia

Hemophilia is an X-linked recessive disorder of coagulation factors.

Hemophilia Types:

  1. Hemophilia A-classic haemophilia – due to factor 8 deficiency.
  2. Hemophilia B-Christmas disease -due to factor 9 deficiency.
  3. Von Willebrand’s disease due to deficiency of von Willebrand factor.

Hemophilia Clinical features:

  • Easy bruising
  • Prolonged bleeding.
  • Spontaneous bleeding into subcutaneous tissue.
  • GIT bleeding.
  • Hpitaxis.
  • Recurrent haemarthrosis.
  • Hematuria.
  • Intracranial haemorrhage.

Question 12. Disseminated intravascular coagulation (DTC)

Answer:

Disseminated intravascular coagulation (DTC)

Disseminated intravascular coagulation is a complex thrombo-hemorrhagic disorder occurring as a secondary complication in some systemic diseases.

Pathogenesis:

  • Includes
  1. Activation of coagulation
  2. Thrombotic phase
  3. Consumption phase.
  4. Secondary fibrinolysis.

Question 13. Blood groups.

Answer:

Blood groups

Blood groups are classified based on the presence or absence of specific agglutinogen or antigen on the surface of RBC.

Major blood groups are:

1. ABO system

Haemorrhage Shock And Blood Transfusion Blood Groups

2. Rh blood group.

    • Rh factor is an antigen present in RBC.
    • Persons having D antigen are called Rh-positive.

Question 14. Rh factor.

Answer:

Rh factor

  • Rh factor is an antigen present in RBC.
  • It was first discovered by Landsteiner and Weiner in rhesus monkey.
  • It is detected only in RBCs
  • It is inherited from both parents as homozygous positive DD, heterozygous negative Dd or homozygous negative dd.
  • Rh Antibody is absent in plasma.
  • But its production can be evoked by.
    • Transfusion with Rh-positive blood.
    • Entrance of Rh-positive blood from foetus into circulation of Rh-negative mother.

Question 15. Blood Transfusion.

Answer:

Blood Transfusion

It is a process of transferring blood or blood-based products from one person into the circulatory system of another.

Blood Transfusion Types:

  1. Typical stored CPD blood from the blood bank.
  2. Filtered blood-filtered through a membrane with 40 |im pores.
  3. Warm blood is used in cardiopulmonary operations.
  4. Autotransfusion – preserving and then transfusing one’s blood.
  5. Replacement transfusion – used in newborns.

Haemorrhage Shock And Blood Transfusion

Question 16. Indications of blood transfusion.

Answer:

Acute haemorrhage.

  • During operations, preoperatively and postoperatively.
  • Anaemia.
  • Malnutrition.
  • In severe burns.
  • In coagulation disorders.
  • In erythroblastosis fetalis.
  • During chemotherapy.

Question 17. Complications of blood transfusion.

Answer:

Complications of blood transfusion

  1. Transfusion reactions
    • Incompatibility
    • Pyrexia reactions
    • Allergic reactions
    • Sensitisation to leucocytes and platelets
  2. Transmission of diseases
    • Serum hepatitis
    • AIDS
  3. Reactions caused by massive transfusion.
    • Acid-base imbalance.
    • Hyperkalaemia.
    • Citrate toxicity.
    • Hypothermia.
    • Failure of coagulation.
  4. Complication of over-transfusion.
    • Congestive cardiac failure.
  5. Other complications.
    • Thrombophlebitis
    • Air embolism.

Question 18. Types of haemorrhage

Answer:

Types of haemorrhage

  1. According to the source
    • External haemorrhage – seen externally
    • Internal haemorrhage – not seen externally
  2. According to the vessels involved
    • Arterial haemorrhage – haemorrhage coming out of the artery
    • Venous haemorrhage – haemorrhage coming out of vein
    • Capillary haemorrhage – haemorrhage coming out of the capillary
  3. According to the time of appearance
    • Primary haemorrhage – at the time of injury
    • Reactionary haemorrhage – within 24 hours of injury
    • Secondary haemorrhage – after 7-14 days of injury

Question 19. Reactions to blood transfusion

Answer:

Reactions to blood transfusion

Haemorrhage Shock And Blood Transfusion Reactions To Bllod Transfusion

Haemorrhage Shock And Blood Transfusion Long Essays

Haemorrhage Shock And Blood Transfusion Long Essays

Question 1. Classify shock. Describe the pathophysiology, clinical features and management of shocks.

Answer:

Shock:

  • Shock is a condition in which circulation fails to meet the nutritional needs of the cells and fails to remove the metabolic waste products.
  • It is characterized by hypoperfusion and severe dysfunction of vital organs.

Shock Classification:

  1. Haematogenic or hypovolaemic shock.
    • Occurs due to loss of blood, plasma or body water and electrolytes.
    • Caused by haemorrhage, vomiting, diarrhoea, dehydration, etc.
  2. Traumatic shock.
    • Caused by major fractures, crush injuries, bums, extensive soft tissue injuries and intraabdominal injuries.
  3. Neurogenic shock.
    • Caused by paraplegia, quadriplegia, trauma to the spinal cord and spinal anaesthesia.
  4. Cardiogenic shock.
    • Caused by injury to heart, myocardial infarction or congestive cardiac failure.
  5. Septic shock.
    • Occurs due to gram-negative septicaemia.
  6. Miscellaneous types – includes:
    • Anaphylactic shock.

Physiology: It can be described as 2 processes.

  1. Reduced effective circulating volume.
    • May result either.
      • By actual loss of blood volume or
      • By decreased cardiac output.
  2. Tissue anoxia.

Haemorrhage Shock And Blood Transfusion Reduction In effective Circulating Blood Volume

Shock Clinical features:

Haemorrhage Shock And Blood Transfusion Shock Clinical Features

Management: AIMS:

  • To increase cardiac output.
  • To improve tissue perfusion to vital organs.

Shock Treatment:

  1. Maintenance.
    • Maintain patent airway and oxygen.
    • Head position – At low position with face turned to one side
  2. Control of haemorrhage.
    • Done by elevation, compression bandages or by ligation of blood vessels.
  3. Extracellular fluid replacement.
    • Nonsugar, nonprotein crystalloid is preferred.
    • Normal saline or ringer’s lactate should be started first.
  4. Correct acid-base disturbance.
  5. Drugs.

Haemorrhage Shock And Blood Transfusion Shock Treatment

Question 2. Describe the pathophysiology, clinical features and treatment of septic shock.

Answer:

Septic Shock:

  • Septic shock is caused due to release of endotoxin in blood mostly by Gram-negative organisms.
  • Occurs in cases of severe septicaemia, peritonitis or meningitis.
  • Pathophysiology.

Presence of gram-positive and gram-negative organism

Local inflammation occurs

Release of endotoxins from organism

Activation of neutrophils, monocytes & macrophages.

Release of inflammatory mediators.

Cellular chemotaxis.

Endothelial injury

Activation of the coagulation cascade

Massive fluid loss

Septic shock

Septic Shock Clinical Features:

  • Initially, chills and fever above 100oC occurs.

Septic Shock Types:

  1. Early warm shock.
    • There is cutaneous vasodilation.
    • Body temperature increases
    • Cutaneous vasodilatation occurs.
    • Arterial blood pressure falls.
    • Cardiac output increases.
    • Skin remains warm, pink and well-perfused.
    • Pulse rate increases
  2. Late cold shock.
    • There is increased vascular permeability
    • Cardiac output decreasing.
    • Hypovolemia occurs.

Read And Learn More: General Surgery Question and Answers

Septic Shock Treatment:

  • Removal of septic focus.
    • Drainage of pus under anaesthesia.
    • Closure of perforation.
    • Resection of gangrene.
  • Antibiotis.
    • Administered after antibiotic sensitivity tests.
    • Initial antibiotics are
      • Cephalothin – 6 – 8 gm/day IV in 4 – 6 divided doses.
      • Gentamicin – 5 mg/kg/day.
      • Clindamycin
  • Fluid replacement.
    • Crystalloids such as isotonic saline as Ringer’s lactate may be used.
    • Blood transfusion – to maintain haemoglobin level to 10 mg%.
  • Supportive care.
    • Oxygenation.
    • Mechanical ventilation.
    • Endotracheal intubation.
  • Steroids.
    • Short-term, high-dose steroid therapy is used.
    • Initial dose of 15 – 30 mg/ kg body weight of methylprednisolone is given.
    • Same dose repeated within 4 hours.
    • Vasoactive drugs.
  • Vasodilators such as phenoxybenzamine is used along with fluid replacement.
    • Inotropic agents such as isoproterenol is used to restore adequate circulation.
    • It produces mild peripheral vasodilation.
    • There is slight fall in BP.

Question 3. Describe the pathophysiology, clinical features and management of haemorrhage or hypovolaemic shock.

Answer:

Haemorrhage shock/Hypovolaemic shock: Such shock occurs due to sudden loss of blood volume or loss of fluid from the vascular space.

Pathophysiology:

Haemorrhage

Loss of blood

Decreased filling of right heart.

Decreased filling of the pulmonary vasculature

Decreased filling of left atrium and ventricle

Decrease in stroke volume.

Drop in arterial blood pressure

Hypovolaemic Shock Clinical Features:

  • Depending on the degree of blood loss it can be described into three types.

Haemorrhage Shock And Blood Transfusion Haemorrhage Or Hypovolaemic Shock

Hypovolaemic Shock Management:

  1. Resuscitation.
    • Maintain airway with adequate ventilation and oxygenation.
    • Lower the head with jaw support.
  2. Immediate control of bleeding.
    • Raise the footend of the bed.
    • Use of compression bandages.
  3. Extracellular fluid replacement.
    • Ringer’s lactate, Ringer’s acetate or normal saline supplemented with 1-2 ampules of sodium bicarbonate is used.
    • 1000 – 2000 ml solution is given within 45 min intravenously.
    • Blood transfusion done if required.

Question 4. Describe neurogenic shock and its management.

Answer:

Neurogenic Shock Causes:

  • Paraplegia.
  • Quadriplegia.
  • Trauma to spinal cord
  • Spinal anaesthesia.

Pathophysiology:

Blockade of sympathetic nervous system

Loss of arterial and venous tone

Peripheral pooling of blood.

Decrease in cardiac filling
i
Decrease in stroke volume.

Decrease in pulmonary blood volume.

Decrease in cardiac output.

Shock

Neurogenic Shock Clinical Features:

  • Skin remains warm, pink and well-perfused.
  • Urinary output – normal.
  • Heart rate-rapid.
  • Blood pressure – decreased

Neurogenic Shock Management:

  1. Elevation of the legs to correct peripheral pooling of blood.
  2. Fluid administration to increase cardiac output.
  3. Use of vasoconstrictor drug.
    • It increases BP and myocardial activity.

Question 5. Classify haemorrhage and its management and Describe the causes, clinical features, How will you manage a case of primary haemorrhage after a dental extraction?.

Answer:

Haemorrhage: Haemorrhage is defined as escape of blood from blood vessels.

Haemorrhage Classification:

  1. According to the source:
    • External haemorrhage.
      • Seen externally.
    • Internal haemorrhage.
      • Not seen externally, it is hidden,
      • Example: GIT bleeding.
    • Arterial haemorrhage.
      • It is haemorrhage coming out of artery.
      • It is bright red in colour.
    • Venous haemorrhage.
      • It is haemorrhage coming out of vein.
      • It is dark red in colour.
    • Capillary haemorrhage.
      • It is haemorrhage coming out of capillary
      • It is bright red in color and it oozes out
  2. According to the time of appearance:
    • Primary haemorrhage.
      • Occurs at the time of injury.
    • Reactionary haemorrhage.
      • Occurs within 24 hours of injury.
      • Secondary haemorrhage.
    • Occurs after 7-14 days of injury.

Haemorrhage  Management:

  • To stop blood loss.
  1. Rest.
    • Use of sedative and analgesics.
    • Morphine is administered IM/IV.
    • Inj. Pethidine is better than morphine.
  2. Position of patient.
    • Head end of bed is raised in haemorrhage oc- curing after thyroidectomy.
    • Foot end of bed raised in case of haemorrhage from varicose veins.
  3. Pressure and packing.
    • Use of sterile gauze pieces and pressure bondage.
    • At home, it can be done by clean linen cloth.
  4. Operative methods.
    • Haemorrhage can be controlled by.
      • Use of artery forceps.
      • Ligation of blood vessels.
      • Smaller vessels are coagulated with diathermy.
      • Bigger vessels are sutured
      • In case of oozing blood-following is used
        • Oxycel or gelatine sponge.
        • Gauze soaked in adrenaline (1:1000)
        • Bone wax for bleeding occurring from the bone.

Haemorrhage  Causes:

  • Bleeding disorders.
  • Low platelet count
  • Anticoagulant medication.
  • Broken or ruptured blood vessels.
  • Severe trauma
  • After surgery.
  • After childbirth.

Haemorrhage  Clinical Features:

  • Blood loss
  • Increased pulse rate
  • Thready pulse
  • Low blood pressure
  • Pallor Restlessness
  • Deep respiration
  • Cold and calmmy extremities
  • Empty veins
  • Low urinary output.

Management of Primary Haemorrhage:

1. Post-extraction bleeding.

Removal of clots with gauze

Placement of gauze pad or tea bag over socket.

Patient is instructed to bite over it for 1 hour

Repeated 2-3 times.

Prevent disruption of clot

2. If bleeding continues.

Anaesthesize the area

Curette the socket

Remove existing clot and freshen the bone

Irrigate with normal saline
i
Place local haemostatic agent into socket

Suture under gentle tension

Question 6. Describe indications and complications of blood transfusion.

Answer:

Blood Transfusion: It is the process of transferring blood or blood-based products from one person into circulatory system of another.

Blood Transfusion Indications:

  • Acute haemorrhage – external or internal.
  • Certain major operations – like radical mastectomy.
  • In deep burns.
  • Preopera lively in anaemic patients.
  • Postoperatively in septicaemia.
  • In anaemia.
  • In severe malnutrition.
  • In coagulation disorders like hemophilia.
  • In treatment of erythroblastosis foetalis.
  • During chemotherapy of malignant diseases.

Blood Transfusion Complications:

  1. Transfusion reactions:
    • Incompatibility
      • Causes:
        • Incompatible transfusion.
        • Transfusion of hemcolyzed blood.
        • Transfusion of old blood.
      • Clinical features:
        • Fever, rigor.
        • Headache.
        • Nausea, vomiting.
        • Pain in the loins.
        • Tingling sensation in the extremities.
        • Feeling of tightness of chest
        • Dysponea.
        • Diminished urinary output.
        • Haemoglobunuria.
        • Jaundice
      • Treatment:
        • Stop the transfusion immediately.
        • Administration of 4 fluids.
        • Alkalization of blood with 10 ml of isotonic solution of sodium lactate and simultaneously 10 ml of saturated solution of sodium bicarbonate 4.
        • Use of 80 -120 mg frusemide IV to provoke diuresis.
        • Antihistamine and hydrocortisone may be prescribed.
    • Pyrexial reactions.
      • Causes:
        • Lack of sterilization
        • Infected donor’s apparatus
        • Iniected blood transfusion,
        • Rapid transfusion,
        • Presence of sulphur compounds in rubber tubing.
      • Clinical Features:
        • Pyrexia.
        • Rigor, chills.
        • Restlessness.
        • Headache.
        • Increased pulse rate.
        • Nausea and vomiting.
      • Treatment:
        • Stop transfusion immediately.
        • Cover the patient with blanket.
        • Antipyretic and antihistaminic drugs are injected.
    • Allergic reaction:
      • Cause:
        • Allergic reaction to plasma product
      • Features:
        • Mild tachycardia.
        • Urticarial rash.
        • Fever
        • Dysponea
        • Circulatory collapse.
      • Treatment:
        • Stop transfusion
        • Administer 10 mg chlorpheniramine.
    • Sensitization to leucocytes and platelets:
      • Use of antipyretics, antihistamines and steriods.
  2. Transmission of diseases:
    • Diseases transmitted ae.
      • Serum hepatitis
      • AIDS
      • Bacterial infections.
  3. Reactions caused by massive transfusion:
    • Acid base imabalance – alkalosis.
    • Hyperkalaemia.
    • Citrate toxicity.
    • Hypothermia.
    • Failure of cogulation.
  4. Complications of over-transfusion:
    • Congestive cardiac failure occurs.
  5. Other complications:
    • Thrombophlebitis
    • Air embolism.

Question 7. Define shock. Describe the pathophysiology and classification of shock. Discuss management of hypovolaemic shock

Answer:

Shock Definition: Shock is a condition in which circulation fails to meet the nutritional needs of the cells and fails to remove the metabolic waste products

Pathophysiology

  • Reduced effective volume
    • It may result either
      • By actual loss of blood volume or
      • By decreased cardiac output
  • Tissue anoxia
    • Reduction in effective circulating blood volume
    • Reduced venous return
    • Decreased cardiac output
    • Decreased oxygen supply
    • Tissue anoxia
    • Cellular injury
    • Release of inflammatory mediators
    • Results in shock

Shock Classification

  • Haematogenic or hypovolaemic shock
  • Traumatic shock
  • Neurogenic shock
  • Cardiogenic shock
  • Septic shock
  • Miscellaneous
    • Anaphylactic shock

Management of hypovolemic shock

  • Resuscitation
    • Maintain airway with adequate ventilation and oxygenation
    • Lower the head with jaw support
  • Immediate control of bleeding
    • Raise the foot end of the bed
    • Use of compression bandages
  • Extracellular fluid replacement
    • Ringer’s lactate, Ringer’s acetate or normal saline supplemented with 1-2 ampules of sodium bicarbonate is used
    • 1000-2000 ml solution is given within 45 min intravenously
    • Blood transfusion done if required

Question 8. What are blood components? Write in detail about the indications, contraindications and complications of blood transfusion.

Answer:

Blood components

  • There are four main components of blood
    • Plasma
    • Red blood cells or erythrocytes
    • White blood cells or leukocytes
    • Platelets

Blood transfusion

  • Indications
    • Acute haemorrhage
    • Major surgery
    • Deep burns
    • Pre-operative and post-operative in anaemia
    • In malnutrition
    • In coagulation disorders
    • In erythroblastosis fetalis
    • During chemotherapy in malignant diseases
  • Contraindications
    • Infections
    • Aortic stenosis
    • Angina
    • Significant cardiac or pulmonary disease
    • Coronary heart disease
    • Cyanotic heart disease
    • Uncontrolled hypertension
  • Complications
    • Transfusion reactions
      • Incompatibility
      • Pyrexial reactions
      • Allergic reactions.
    • Transmission of diseases
    • Reactions caused by massive transfusion
      • Acid base imbalance
      • Hyperkalaemia
      • Citrate toxicity
      • Hypothermia
      • Failure of coagulation
  • Complications of over transfusion
    • Congestive cardiac failure
  • Other complications
    • Thrombophlebitis
    • Air embolism

Normal Periodontium Short Essays

Question 1. Enzymes in the gingiva.
Answer:

Normal Periodontium Enzymes in gingiva.

Question 2. Cells of Periodontal Ligaments.
Answer:

1. Synthetic Cells:

Osteoblasts:

  • Covers the periodontal surface of the alveolar bone
  • It actively synthesizes ribosomes
  • Contains a largely open nucleus containing prominent nucleoli

2. Fibroblasts, spindle-shaped cells:

  • Most prominent cell
  • Synthesizes chondroitin sulfates, heparin sulfate, and hyaluronan sulfate
  • Synthesizes connective tissue matrix

Fibroblasts, spindle-shaped cells Produces:

  • Collagen fibers
  • Reticulin fibers
  • Oxytalan fibers
  • Elastin fibers

1. Cementoblast:

  • Seen lining cementum
  • Lay down cementum

2. Resorptive cells:

  • Osteoclast:
    • Multinucleated giant cell
    • Lies adjacent to the bone
    • Undergoes resorption of bone
    • Formed by monocytes
  • Fibroblast:
    • Contain fragments of collagen
    • These undergoes digestion
    • Results in resorption of bone
  • Cementoclast:
    • Located in Howships Lacunae
    • Causes resorption of cementum

3. Progenitor cells:

  • Formed in the basal cell layer
  • Basal cells have the ability to divide
  • One of the divided cells migrates to the superficial layer and the other remains as a progenitor cell

4. Epithelial cell rests of Malassez:

  • Remnants of Hertwig’s epithelial root sheath
  • Present near and parallel to root surfaces Attached to one another by desmosomes
  • During disease conditions, they undergo proliferation
  • Persists as a network strand, island, or tubule
  • Exhibits tonofilaments

5. Mast Cell:

  • Small, round, or oval cell
  • Contains cytoplasmic granules
  • Contains heparin and histamine
  • During an inflammatory response, these releases of histamine cause antigen-antibody formation

6. Macrophages:

  • Capable of phagocytosis

Question 3. Functions of Periodontal ligament.
Answer:

1. Physical Functions of Periodontal ligament:

  • Provide soft tissue casing
  • Protect nerves and vessels from injury
  • Transmit occlusal forces to the bone
    • By stretching of oblique fibers of PDL
    • Transmits tensional force to the bone
    • Results in bone formation
  • Attaches tooth to the bone
  • Maintains architecture of gingival tissue
  • Shock absorbent

2. Formative and Remodelling function:

  • Synthesis and resorption of cementum, PDL, and al-alveolar bone
  • Old cells and fibers are replaced by a new one

3. Nutritional and Sensory function:

  • Nutrition – Through blood supply
  • Sensory – Transmits sensation of touch, pressure and pain to CNS

Neural Transmission Functions of Periodontal ligament :

  • Apical area – Ruffini
  • Apex Pressure and vibration endings
  • Mid root – Meissners corpuscles

Question 5. Define alveolar bone and describe its composition.
Answer:

Alveolar Bone: H

  • It is that portion of the maxilla and mandible that forms and supports the tooth socket

Composition:

Cells:

1. Osteoblast: Cuboidal cells

Osteoblast Contains:

  • Rough endoplasmic reticulum
  • Large Golgi apparatus
  • Secretory vesicles

Osteoblast Functions:

  • Synthesize osteoid, collage
  • Regulate mineralization

Osteoblast Precursor: Progenitor cells

2. Osteoclasts: Multinucleated giant cells

Osteoclasts Precursor: blood-borne monocytes

Osteoclasts Functions: Resorptive cell, Secretes hydrolytic en-zymes

3. Osteocytes: These extend processes from lacunae to canaliculi

Osteocytes Function: Canaliculi bring oxygen and nutrients to osteocytes

4. Extracellular Matrix:

Extracellular Matrix Inorganic:

  • Calcium, Hydroxyl
  • Phosphate, Carbonate
  • Citrate, Sodium
  • Magnesium, Fluorine

Extracellular Matrix Organic:

  • Osteocalcin
  • Osteonectin
  • BMP
  • Proteoglycans
  • Glycoproteins

Question 6. Dentogingival junction.
Answer:

  • The junctional epithelium and the gingival fibers are together considered a dentogingival unit

Dentogingival Junction:

  • It represents a unique anatomic feature concerned with the attachment of gingiva to the tooth
  • It comprises an epithelial portion and a connective tissue portion

1. Epithelial portion:

  • It can be divided into
    • Gingival epithelium
    • Sulcular epithelium
    • Junctional epithelium

Normal Periodontium Portion and Features.

2. Connective tissue component:

  • It contains densely packed collagen fiber bundles.
  • It includes
  1. Dentogingival fibers
    • Extends from cementum into free and at-attached gingiva
  2. Alveologingival fibres
    • Extends from the alveolar crest into free and at-attached gingiva
  3. Circular fibers
    • Wrap around the tooth
  4. Dentoperiosteal fibres
    • Run from cementum, over the alveolar crest, and insert into the alveolar process
  5. Transseptal fibers
    • Runs interdentally from cementum to one tooth to the adjacent tooth

Question 7. Sulcular Epithelium.
Answer:

  • Sulcular epithelium is the epithelium lining the gingival sulcus
  • It is a thin,non-keratinized stratified squamous epithelium without recipes
  • It extends from the coronal limit of the junctional epithelium to the crest of the gingival margin
  • It usually shows many cells with hydropic degeneration
  • It lacks granulosum and corneum strata
  • Enzymes present have a lower degree of activity
  • It has the potential to keratinize if
    1. It is exposed to the oral cavity or
    2. The bacterial flora of the sulcus is totally eliminated

Sulcular Epithelium Importance:

  • It may act as a semipermeable membrane through which injurious bacterial products pass into the gingival and tissue fluid from the gingiva seeps into the sulcus

Question 8. Fenestrations and Dehiscences.
Answer:

Fenestration:

  • These are isolated areas in which the root surface is covered only by the periosteum and gingiva
  • Marginal bone is intact

Dehiscence:

  • Defect involving denudation of marginal bone

Etiology:

  • Root prominence
  • Malposition
  • Teeth in labial version

Common location:

  • Site – Facial bone
  • Teeth involve – Anterior

Importance:

  • Affect the outcome of surgical treatment

Question 9. Define and classify cementum. (or) Schroeder’s classification of cementum
Answer:

Cementum:

  • It is a calcified avascular mesenchymal tissue that forms the outer covering of the anatomic root

Cementum Classification:

1. Acellular fibrillar cementum:

  • Contains a mineralized ground substance
  • Does not contain fibres or cells

Acellular fibrillar cementum Site: On enamel near CEJ

2. Acellular extrinsic fiber cementum:

  • Contains Sharpey’s fibers
  • Does not contain cells

Acellular extrinsic fiber cementum Site: Coronal half of root surface

3. Cellular mixed stratified cementum:

  • Contains cells and fibres

Cellular mixed stratified cementum Site: Apical third of root, apices, and furcation areas

4. Cellular Intrinsic Fiber cementum:

  • Contains fibers but not cells

Cellular Intrinsic Fiber cementum Site: Resorption lacunae

5. Intermediate Cementum:

Intermediate Cementum Site: Apical 1/3rd of root

Intermediate Cementum Function: Attaches cementum to dentin

  • This is removed during root planning

Question 10. Junctional epithelium.
Answer:

  • It is the tissue that joins to the tooth on one side and the oral sulcular epithelium and connective tissue on the other
  • It forms the base of the sulcus

Junctional epithelium Attachment:

  • Attach to the tooth surface
    • By internal basal lamina
    • Reinforced by the gingival fibers
    • Consists of lamina dens and lamina lucida
  • Attach to gingival connective tissue
    • By external basal lamina

Junctional epithelium Features:

  • Consists of non-keratinizing epithelium
  • Thickness
    • Early life- 3-4 layers
    • Later- Increases
  • Length- 0.25-1.35 mm

Junctional epithelium Structure:

  • Consists of basal and suprabasal layer
  • Zones present are
    • Apical- germination
    • Middle- adhesion
    • Coronal-permeable
  • Cells present are
    • Basal cells- cuboidal/flattened
    • Suprabasal cells
    • Complex microvilli formation and interdigitation
    • Presence of leukocytes and lymphocytes
    • Desmosomes interconnect the cells

Question 11. Oxytalan fibers.
Answer:

  • The periodontal ligament contains two immature forms of fibers
  • They are xylan and cleaning fibers
  • The xylan fibers run parallel to the root surface in a vertical direction and bend to attach to the cementum. in the cervical third of the root
  • These fibers are associated with blood vessels and nerves of the periodontal ligament
  • They regulate the vascular flow
  • An elastic meshwork in the periodontal ligament is composed of many elastic lamellae with peripheral oxy- talan fibers and cleaning fibers
  • Oxytalan fibers develop de novo in the regenerated periodontal ligament

Question 12. Describe the mechanism by which ligament periodontal resists occlusal forces.
Answer:

1. Tensional theory:

  • It states that the principal fibers of the periodontal ligament are major factors in supporting the tooth and transmitting forces to the underlying bone
  • When a force is applied to the crown, the principal fibers first unfold and straighten and then transmit forces to the alveolar bone
  • When the alveolar bone has reached its limit, the load is transmitted to the basal bone

2. Viscoelastic theory:

  • It states that the displacement of the tooth is controlled by fluid movements with fibers having only a secondary role
  • When forces are transmitted to the tooth, the ex-intracellular fluid passes from the periodontal ligament into the marrow spaces of bone through fo- the lamina

3. Thixotropic theory:

  • According to this theory, the periodontal ligament has rheological behavior of thixotropic gel

Question 13. Significance of width of attached gingiva
Answer:

  • The width of the attached gingiva is the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or periodontal pocket

Normal Periodontium Significance of width of attached gingiva.

  • The width of the attached gingiva increases with age 4 and in supra-erupted teeth
  • On the lingual aspect of the mandible, the attached gingiva terminates at the junction of the lingual alveolar mucosa which is continuous with the mucous membrane lining the floor of the mouth

Normal Periodontium Long Essays

Periodontics Normal Periodontium Long Essays

Question 1. Define Gingiva. Describe the microscopic and macroscopic features of the gingiva. Add a note on the importance of GCF.
Answer:

Gingiva:

  • It is a part of oral mucosa that covers the alveolar process of the jaws and surrounds the neck of the teeth

Macroscopic:

  • Gingiva is divided into

1. Marginal Gingiva:

  • Border of the gingiva surrounding the teeth in the collar-like fashion
  • Demarcated apically by a shallow depression called “free gingival groove”

2. Attached Gingiva:

  • Part of the gingiva that is firm, resilient, and tightly bound to the underlying periosteum of the alveolar bone
  • The width of the attached gingiva is the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or periodontal pocket

3. Interdental Gingiva:

  • Occupies gingival embrasure

Parts: Facial papilla, lingual papilla and col

  • Lateral borders and tips of interdental papilla are formed by continuation of marginal gingiva.
  • In diastema, interdental papilla is absent

Normal Periodontium Anatomic land marks of gingiva.

Microscopic Features:

1. Oral/Outer Epithelium:

Outer Epithelium Layers:

  1. Outer Epithelium Basal layer:
    • Cells are cylindrical/cuboidal
    • Attach to the basement membrane
    • Cells have the ability to divide
    • Stratum Spinosum:
    • Large cells with short processes called spines
    • Cells have a prickled appearance
    • Cells are attached to one another with the help of desmosomes
    • Stratum Granulosum:
    • Keratohyalin granules are seen
    • Stratum Corneum:
    • The cytoplasm of cells in this layer is filled with keratin
    • It can be
    • Orthokeratinized – In this cells are devoid of a nucleus
    • Parakeratinized – In this cells contains the pinpoint nucleus
  2. Sulcular epithelium:
    • Extends from the gingival margin to the junctional epithelium
    • Made up of basal and prickle cell layer
  3.  Junctional epithelium:
    • It is the tissue that joins to the tooth on one side and to sul- color epithelium and connective tissue on the other
    • It is attached to the tooth surface by the internal basal lamina and to the gingival connective tissue by an external basal lamina

Outer Epithelium Connective tissue:

  • Termed as lamina propria
  • Superficial papillary layer:
  • Contains epithelial ridges
  • Deeper Reticular layer:
  • Contains collagen fibers

Outer Epithelium Cells:

  • Fibroblast
  • Mast cells
  • Macrophages
  • Inflammatory cells

Outer Epithelium Fibers present:

  • Collagen fibers
  • Reticulin fibers
  • Oxytalan fibers
  • Elastin fibers

Normal Periodontium Non-keratinized epithelium

Normal Periodontium The principal group of fibers.

Importance Of Gingival Crevicular Fluid:

1. Cicardian periodicity:

  • There is a gradual increase in a gingival fluid amount from 6:00 am to 10:00 pm and decreases afterward
  • This is called Cicardian periodicity

2. Sex hormones:

  • Female sex hormones increase flow
  • Pregnancy, ovulation, and hormonal contraceptives increase gingival fluid

3. Smoking:

  • Causes an immediate transient increase in flow

4. Periodontal therapy:

  • An increase in gingival fluid occurs during the healing period

Question 2. Define gingiva. Describe morphological, histo- logical, and functional features of normal gin- give.
Answer:

Gingiva:

  • It is a part of oral mucosa that covers the alveolar process of the jaws and surrounds the neck of the teeth.

Morphological Features:

  • Gingiva is divided into
  1. Marginal gingiva:
    • It is border of the gingiva surrounding the teeth in col- lar like fashion
    • It is demarcated apically by a shallow depression called a “free gingival groove”
  2. Attached gingiva:
    • It is part of the gingiva that is firm, resilient, and tightly bound to the underlying periosteum of the alveolar hone
    • The width of the attached gingiva is the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or periodontal pocket
  3. Interdental gingiva:
    • It occupies gingival embrasure
    • Its parts are facial papilla, lingual papilla, and col
    • Lateral borders and tips of interdental papilla are formed by the continuation of the marginal gingiva
    • In diastema, interdental papilla is absent

Normal Periodontium Anatomic land marks of gingiva.

Histological Features:

1. Epithelium:

Epithelium Layers:

  1. Basal layer:
    • Cells are cylindrical/cuboidal
    • Attach to the basement membrane
    • Cells have the ability to divide
    • One of the divided cells migrates to the superficial layer
    • Basal cells are separated from connective tissue by a basement membrane
    • Beneath the basal cell, the electro-lucent zone can be seen called lamina lucida
    • Beneath it, there is electron dense zone called lamina densa
    • Hemidesmosomes attach epithelium to the connective tissue.
  2. Stratum Spinosum:
    • Large cells with short processes called spines
    • Cells have a prickled appearance
    • Cells are attached to one another with the help of desmosomes
  3. Stratum Granulosum:
    • Keratohyalin granules are seen
  4. Stratum Corneum:
    • The cytoplasm of cells in this layer are filled with keratin
    • It can be
    • Orthokeratinized – In this cells are devoid of a nucleus
    • Parakeratinized – In this cells contains pinpoint nucleus

2. Sulcular epithelium:

  • Extends from the gingival margin to the junctional epithelium
  • Made up of basal and prickle cell layer

3. Junctional epithelium:

  • It is the tissue that joins to the tooth on one side and to sul- color epithelium and connective tissue on the other
  • It is attached to the tooth surface by an internal basal lamina and to the gingival connective tissue by an external basal lamina

Connective tissue:

  • Termed as lamina propria
  • Superficial papillary layer:
    • Contains epithelial ridges
  • Deeper Reticular layer:

Cells:

  • Contains collagen fibers
  • Fibroblast
  • Mast cells
  • Macrophages
  • Inflammatory cells

Fibers present:

  • Collagen fibers
  • Reticulin fibers
  • Oxytalan fibers
  • Elastin fibers

Importance Of Gingival Crevicular Fluid:

1. Cicardian periodicity:

  • There is a gradual increase in gingival fluid amount from 6:00 am to 10:00 pm and decreases afterward
  • This is called Cicardian periodicity

2. Sex hormones:

  • Female sex hormones increase flow
  • Pregnancy, ovulation, and hormonal contraceptives increase gingival fluid

3. Smoking:

  • Causes an immediate transient increase in flow

4. Periodontal therapy:

  • An increase in gingival fluid occurs during the healing period

Gingival Crevicular Fluid Functions:

1. Attached gingival:

  • It braces marginal gingiva
  • It allows for proper deflection of food
  • It provides room for proper placement of toothbrush
  • It is important for the overall maintenance of gingival health

2. Gingival crevicular fluid:

  • It cleanses material from the sulcus
  • It improves the adhesion of the epithelium to the tooth by plasma proteins
  • It possesses antimicrobial properties
  • It exerts antibody activity to defend gingiva
  • It transports a variety of molecules

3. Gingival fibers:

  • Provides support to the gingiva and attaches it to the bone
  • It anchors the tooth to the bone
  • Maintains relationship of adjacent teeth
  • Secures alignment of teeth in the arch

Question 3. Define PDL. Write in detail about its structure and function. (or) Enumerate principal groups of periodontal ligament fibers. Add a note on the cellular elements and functions of PDL. Principal Fibres of PDL. (Extra cellular components)
Answer:

Periodontal Ligaments:

  • It is the connective tissue that surrounds the root and connects it with the bone

Periodontal Ligaments Structure:

Cells:

1. Synthetic Cells:

  • Osteoblasts:
    • Covers the periodontal surface of alveolar bone
    • It actively synthesizes ribosomes
    • Contains a largely open nucleus containing prominent nucleoli
  • Fibroblasts, spindle-shaped cells:
    • Most prominent cell
    • Synthesizes chondroitin sulfates, heparin sulfate and hyaluronan sulfate
    • Synthesizes connective tissue matrix
  • Produces:
    • Collagen fibers
    • Reticulin fibers
    • Oxytalan fibers
    • Elastin fibers
  • Cementoblast:
    • Seen lining cementum
    • Lay down cementum

2. Resorptive cells:

  • Osteoclast:
    • Multinucleated giant cell
    • Lies adjacent to the bone
    • Undergoes resorption of bone – Formed by monocytes
  • Fibroblast:
    • Contain fragments of collagen – These undergo digestion
    • Results in resorption of bone
  • Cementoclast:
    • Located in Howships Lacunae
    • Causes resorption of cementum

3. Progenitor cells:

  • Formed in the basal cell layer
  • Basal cells have the ability to divide
  • One of the divided cells migrates to the superficial layer and the other remains as a progenitor cell

4. Epithelial cell rests of Malassez:

  • Remnants of Hertwig’s epithelial root sheath are Present near and parallel to root surfaces
  • Attached to one another by desmosomes
  • During disease condition, they undergo proliferation
  • Persists as a network strand, island, or tubule
  • Exhibits tonofilaments

5. Mast Cell:

  • Small, round, or oval cell
  • Contains cytoplasmic granules
  • Contains heparin and histamine
  • During an inflammatory response, these releases- time causes antigen- antibody formation

6. Macrophages:

  • Capable of phagocytosis

Extracellular Components

1. Fibres:

  • Collagen:
    • Synthesized by fibroblasts, chondroblasts, os
    • neoblasts, odontoblast, and other cells
    • Type 1,3 and 4 are common
  • Oxytalin:
    • Provide elastic properties to PDL

Principal Fibres:

  1. Trans-septal group:
    • Connects cementum of one tooth with that of other
  2. Alveolar crest:
    • Extends from cementum to alveolar crest Function: Retains tooth in the socket, Retains lateral tooth movement
  3. Horizontal group:
    • Extends from cementum to alveolar bone
  4. Oblique group:
    • Extends coronally from the cementum to bone Function: Resist axially directed forces
  5. Apical group:
    • From cementum to the bone of alveolar fundus Function: Prevents tipping movement, Resists luxation
  6. Inter-radicular fibers:
    • Presents between cementum of a multi-rooted tooth.
    • Function: Resists luxation, Resists tipping and torquing

Normal Periodontium Functions of periodontal ligament.

2. Ground substance:

  • Glycosaminoglycan – hyaluronic acid, proteoglycan- cane
  • Glycoproteins – fibronectin and laminin

Principal Fibres Functions:

1. Physical:

  • Provide soft tissue casing
  • Protect nerves and vessels from injury
  • Transmit occlusal forces to the bone
    • By stretching of oblique fibers of PDL
    • Transmits tensional force to the bone
  • Results in bone formation Attach tooth to the bone
  • Maintains architecture of gingival tissue
  • Shock absorbent

2. Formative and Remodelling function:

  • Synthesis and resorption of cementum, PDL, and al- alveolar bone
  • Old cells and fibers are replaced by a new one

3. Nutritional and Sensory function:

  • Nutrition – Through blood supply
  • Sensory Transmits sensation of touch, pressure, and pain to CNS

Neural Transmission

  • Apical area – Ruffini
  • Apex Pressure and vibration endings
  • Mid root – Meissners corpuscles

Question 4. Discuss the role of alveolar bone in health and periodontal diseases.
Answer:

Alveolar Bone In Health:

  • It is that portion of the maxilla and mandible that forms and supports the tooth socket
  • The alveolar process is thickened ridge of bone that contains tooth sockets that bear teeth
  • The alveolar bone proper is the thin layer that provides attachment to principal fibers of the periodontal ligament Alveolar bone is perforated with numerous openings for intra-alveolar nerves and blood vessels
  • It consists of:

1. Cells:

  1. Osteoblast:
    • Cuboidal cell
    • Contains
    • Rough endoplasmic reticulum
    • Large Golgi apparatus
    • Secretory vesicles
    • Functions:
    • Synthesizes osteoid and collagen
    • Regulates mineralization
    • Precursor:
    • Progenitor cell
  2. Osteoclasts:
    • Multinucleated giant cells
    • Precursor- Blood-borne monocytes
    • Functions:
    • Resorption of bone
    • Secretes hydrolytic enzymes
  3. Osteocytes:
    • These extend processes from lacunae to ca- canaliculi
    • Functions:
    • Canaliculi bring oxygen and nutrients to os- osteocytes

2. Extracellular matrix:

  • Inorganic:
    • Calcium
    • Hydroxyl
    • Phosphate
    • Carbonate
    • Citrate
    • Sodium
    • Magnesium
    • Fluorine
  • Organic:
    • Osteocalcin
    • Osteonectin
    • BMP
    • Proteoglycans
    • Glycoproteins
    • Parathyroid hormone regulates bone removed- selling by both bone formation and bone re- sorption

Alveolar Bone In Disease:

  • Fenestration and dehiscence are seen during disease in relation to alveolar bone

Bone In Disease Fenestration:

  • These are isolated areas in which the root surface is covered only by the periosteum and the gingiva Marginal bone is intact

Dehiscence:

  • It is a defect involving the denudation of marginal bone

Bone In Disease Etiology:

  • Root prominence
  • Malposition
  • Teeth in labial version

Bone In Disease Common Location:

  • Site- Facial bone
  • Teeth commonly involved- Anterior

Bone In Disease Importance:

  • Affects the outcome of surgical treatment

Intraoral Radiographic Techniques Short Essays

Intraoral Radiographic Techniques Short Essays

Question 1. Paralleling technique/Long cone technique.
Answer.

Paralleling technique

  • In this technique the X-ray film is placed parallel to the long axis of the tooth and the central ray of the X-ray beam is directed at right angles to the tooth and film
  • The film must be placed away from the tooth and towards the middle of the oral cavity
  • The object film distance must be increased
  • It is also referred to as the long-cone technique

Long Cone Technique Target Film Distance:

  • The target film distance is large
  • This results in less image magnification and better definition

Long Cone Technique  Film Holders:

  • This technique requires filmholders

Long Cone Technique  Film:

  • Ideally, the size of the film used will depend upon the teeth being radiographed
    • Size 1: used for interiors
    • Size 2: used for posteriors

Long Cone Technique  Film Placement:

  • The white side of the film always faces the teeth
  • For interiors, the film is placed vertically
  • For posteriors, the film is placed horizontally
  • The identification dot on the film is always placed toward the occlusal surface
  • Always place the film away from the teeth and towards the middle of the oral cavity
  • The film must be positioned to cover the prescribed area of the teeth to be examined

Long Cone Technique  Patient Position:

  • Explain the procedure to the patient
  • Position the patient comfortably on the chair
  • Adjust the patient’s head such that the occlusal place of the upper arch is parallel to the floor
  • Mid sagittal plane is perpendicular to the floor
  • Secure lead apron and thyroid collar
  • Remove all objects from the mouth that may interfere with the film exposure

Long Cone Technique  Basic Rules:

  • Film placement film must cover the prescribed area of the teeth to be examined
  • Film position the film must be placed parallel to the long axis of the tooth
  • The holder is rotated so that the teeth to be examined are touching the block
  • The correct focal spot to film distance is determined
    • In vertical angulation, the central ray of the X-ray beam is directed perpendicular to the film, and the long axis of the tooth
    • In horizontal angulation, the central ray of the X-ray beam is directed through the contact areas of the film are exposed
    • Film exposure the X-ray beam must be centered on the film to ensure that all areas of the film are exposed
  • Exposure is made

Oral Radiology Intraoral Radiographic Techniques Positions of the film tooth and the central ray of the x ray beam

Oral Radiology Intraoral Radiographic Techniques The film is placed closed to the tooth and is not parallel to the long axis of the tooth

Read And Learn More: Oral Radiology Question and Answers

Oral Radiology Intraoral Radiographic Techniques Increased object film distance the film is placed

Oral Radiology Intraoral Radiographic Techniques In this diagram the x rays pass through the contact areas

Long Cone Technique  Advantages:

  • This technique produces an image that has dimensional accuracy
  • It is simple and easy to learn and use
  • It is easy to standardize and can be accurately duplicated or repeated
  • Facial screens can be used
  • There is decreased secondary radiation
  • The shadow of the Zygomatic bone appears above the apices of the molar teeth
  • The periodontal levels are well represented
  • There is minimal foreshortening or elongation
  • Good detection of interproximal caries
  • Useful in handicapped and compromised patients as the relative position of the film packet, teeth, and X-ray beam are always maintained

Long Cone Technique  Disadvantages:

  • The film-holding device is difficult to place in children and patients with shallow palate
  • The film-holding device causes discomfort to the patient
  • Object film distance is increased
  • There is an increase in the exposure time
  • It is more space-consuming
  • Sometimes the apices of the teeth are very close to the edge of the film and so not well appreciated
  • The holders need to be autoclaved

Question 2. Principles of projection geometry.
Answer.

Principles of projection geometry

  • The basic principles of projection geometry are as follows:
    • The focal spot should be as small as possible
    • The focal spot object distance should be as long as possible
    • The object film distance should be as small as possible
    • The long axis of the object and the film planes should be paralleling
    • The X-ray beam should strike the object and the film planes at tight angles
    • There should be no movement of the tube, film, or patient during exposure

Oral Radiology Intraoral Radiographic Techniques The smaller the focal spot area

Oral Radiology Intraoral Radiographic Techniques A longer PID and target film

Oral Radiology Intraoral Radiographic Techniques To limit distortion the central ray

Oral Radiology Intraoral Radiographic Techniques Illustrating the influence of motion

Question 3. Bitewing radiograph
Answer.

Bitewing radiograph

  • It is also called Short Cone Technique
  • It is based on the principle known as “Ciesenzky’s rule of isometry”
  • It states that the two triangles at equal if they have two equal angles and share a common side
  • The X-ray beam should bisect the imaginary bisector that bisects the angle formed by the film and the long axis of the tooth
  • When the rule is strictly followed, the resultant image obtained is accurate

Oral Radiology Intraoral Radiographic Techniques Angle A is bisected by line AC

Oral Radiology Intraoral Radiographic Techniques The image on the film is equal to the length of the tooth

Bitewing Radiograph Guidelines:

  • The white side of the film always faces the teeth
  • Anterior films are always placed vertically
  • Posterior films are always placed horizontally
  • The incisal or occlusal edge of the film must extend approximately 1/8th inch beyond the incisal or occlusal surface of the tooth
  • Always center the film over the area to be examined
  • If the patient’s finger is used for stabilization, instruct the patient to gently push the film against the lingual/palatal surface of the tooth

Bitewing Radiograph Basic Rules:

  • Film placement film must cover the prescribed area of the teeth to be examined
  • Film position the film must be placed parallel to the long axis of the tooth
  • In vertical angulation, the central ray of the X-ray beam is directed perpendicular to the film and the long axis of the tooth
  • In horizontal angulation, the central ray of the X-ray beam is directed through the contact areas of the film are exposed
  • Film exposure the X-ray beam must be centered on the film to ensure that all areas of the film are exposed

Bitewing Radiograph Advantages:

  • It can be used in patients with shallow palate, bony growth
  • It is quick and comfortable
  • Decreased exposure time required
  • Short PID is used
  • If angulations are correct, the image obtained is of the same size
  • No sterilization of holders is required as they are not used

Bitewing Radiograph Disadvantages:

  • Image distortion may occur due to the use of short PID
  • By using a film holder it becomes difficult to visualize the imaginary bisector
  • Incorrect horizontal angulation results in overlapping
  • Incorrect vertical angulation leads to elongation or foreshortening
  • If the patient’s finger is used for stabilization, the patient may shift the film before or during exposure
  • The patient’s hand is exposed unnecessarily
  • The periodontal tissues are poorly represented
  • Overlapping of shadows of Zygomatic bone occurs
  • The Buccal roots of premolars and molars are foreshortened
  • The crowns of the teeth are often distorted.

Intraoral Radiographic Techniques.