Tag: HYT Module

Corynebacterium Diphtheria: Clinical manifestation, Complications, Diagnosis and Treatment

Corynebacterium Diphtheria: Clinical manifestation, Complications, Diagnosis and Treatment


Introduction

  • Most common in children of 2-5 years.

Incubation period

  • 2-5days

Mode of transmission

  • Droplet spread

Types

  • Faucial(commonest )
  • Laryngeal
  • Nasal
  • Conjunctival
  • Otitic
  • Vulvovaginal
  • Cutaneous mainly around mouth and nose

Respiratory Diphtheria

  • MC type Tonsillopharyngeal (Faucial)
  • Symptoms
    • Fever
    • sore throat
    • Weakness
    • Malignant or hypertoxic or bull neck appearance
  • Complications
  • Mechanical complication
    • Pseudomembrane may extend to the larynx
    • Lead to laryngeal obstruction, asphyxia and death.
  • Systemic effects
    • Myocarditis:Cardiac damage permanent
    • peripheral polyneuropathy of descending type.
  • Risk
    • Involvement larynx or tracheobronchial tree 
    • Children(because of small airway size).
  • First muscle involve in paralysis – palatopharynges.
  • Ciliary paralysis occur but not pupillary paralysis
  • Most common ophthalmic effect of diphtheria is Isolated ocular palsies 
  • Blurred vision with preserved light reflex.
  • Degenerative changes in adrenal, kidney and liver may occur.
  • Cause of death
    • circulatory failure.

Cutaneous Diphtheria

  • Punched out ulcers
  • Caused by non-toxigenic strains.

 Invasive infection

  • Rare
  • Risk factors are 
    • preexisting cardiac abnormalities
    • IV drug abusers
    • alcoholic cirrhosi

Prevention

  • Active immunization by Toxoid
  • Immunization cannot prevent carrier stage.
  • Active immunization –
    • Combined DPT.
  • Perfussis component in DPT increase potency of diphtheria toxoid.
  • Toxoid of diphtheria shows Danysz phenomenon and Ehrlich phenomenon
  • contact isolation is must.

DIAGNOSIS:

Culture:

  • Respiratory diphtheria diagnosis clinical
  • Cutaneous diphtheria requires lab confirmation.

The throat swabs are inoculated on the following culture media:

  • Loefflers serum slope
  • Tellurite blood agar
  • Blood agar

Virulence tests:

  • These tests demonstrate the production of exotoxin by bacteria isolated on culture.

Virulence testing may be done by:                        

  • In vivo: Guinea pigs and rabbits- by subcutaneous or intracutaneous.
  • In vitro: Eleks gel precipitation test ( test for toxigenicity)and tissue culture tests
  • Schick test:
  • Done to demonstrate circulating diptheria antitoxin.
  • Skin test based on neutralization reaction 
CONTROL ARM TEST ARM INFERENCE
No Reaction No Reaction  Immune
No Reaction Positive

Red flush of 1-5 cms diameter,

generally appears within 24-36 hr

reaching its maximum develop-

ment by 4-7 day. 

This fades slowly

Susceptible to

infection

Red flush but less circumscribed

than positive fades by 4th day

Pseudo positive

Red flush equally in both arms

less circumscribed

Allergic type

interpreted as

Schick type

Pseudo positive reaction  Show positive reaction

Combined reaction

 Susceptible

TREATMENT:

  • Erythromycin (orally or by injection) for 14 days (40 mg/kg per day with a maximum of 2 g/d), or
  • Procaine penicillin G given intramuscularly for 14 days (300,000 U/d for patients weighing10 kg).
  • Patients with allergies to penicillin G or erythromycin can use rifampin or clindamycin.
  • Diphtheria antitoxin is given intradermal
  • Post exposure prophylaxis in health care professionals is not  indicated in infections with diphtheria

Exam Important

Introduction

  • Most common in children of 2-5 years.

Incubation period

  • 2-5days

Mode of transmission

  • Droplet spread

Types

  • Faucial(commonest )
  • Laryngeal
  • Nasal
  • Conjunctival
  • Otitic
  • Vulvovaginal
  • Cutaneous mainly around mouth and nose

Respiratory Diphtheria

  • MC type Tonsillopharyngeal (Faucial)
  • Complications
  • Mechanical complication
    • Pseudomembrane may extend to the larynx
    • Lead to laryngeal obstruction, asphyxia and death.
  • Systemic effects
    • Myocarditis
    • Peripheral polyneuropathy of descending type.
  • First muscle involve in paralysis – palatopharynges.
  • Ciliary paralysis occur but not pupillary paralysis
  • Most common ophthalmic effect of diphtheria is Isolated ocular palsies 

Cutaneous Diphtheria

  • Punched out ulcers
  • Caused by non-toxigenic strains.

 Invasive infection

  • Rare

DIAGNOSIS:

Culture:

  • Respiratory diphtheria diagnosis clinical
  • Cutaneous diphtheria requires lab confirmation.
  • The throat swabs are inoculated.
Virulence tests:

Virulence testing may be done by:                        

  • In vivo: Guinea pigs and rabbits- by subcutaneous or intracutaneous.
  • In vitro: Eleks gel precipitation test ( test for toxigenicity)and tissue culture tests

Schick test:

  • Done to demonstrate circulating diptheria antitoxin.
  • Skin test based on neutralization reaction 
CONTROL ARM TEST ARM INFERENCE
No Reaction No Reaction  Immune
No Reaction Positive

Red flush of 1-5 cms diameter,

generally appears within 24-36 hr

reaching its maximum develop-

ment by 4-7 day. 

This fadesslowly

Susceptible to

infection

Red flush but less circumscribed

than positive fades by 4th day

 Pseudo positive

Red flush equally in both arms

less circumscribed

Allergic type

interpreted as

Schick type

Pseudo positive reaction  Show positive reaction

Combined reaction

 Susceptible

TREATMENT:

  • Erythromycin DOC
  • Procaine penicillin G .
  • Patients with allergies to penicillin G or erythromycin can use rifampin or clindamycin.
  • Diphtheria antitoxin is given intradermal
  • Post exposure prophylaxis in health care professionals is not  indicated in infections with diphtheria
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Shigella : Clinical Findings, Pathogenesis, Lab Diagnosis and Treatment

Shigella : Clinical Findings, Pathogenesis, Lab Diagnosis and Treatment


 Introduction:

SOURCE:

  • MAN: CASE OR CARRIER

MODE OF SPREAD:

  • CONTAMINATED FINGERS, FOOD, FLIES, FOMITES
  • PERSON TO PERSON TRANSMISSION
  • Gut pathology is due to toxin

INFECTIVE DOSE:

  • 10-100 VIABLE BACILLI
  • HIGHEST CONCENTRATION IN STOOL DURING EARLY/ACUTE INFECTION:
  • 103 TO 109 VIABLE BACILLI PER GRAM OF STOOL
PATHOGENESIS

Invasiveness (main):

  • Bacteria invade basolateral surface of colon epithelium
  • Intracellular replication
  • Cell to cell spread with the help of microbial protein
    •  ICS A (ATP-ase)
    •  Host protein cadherin L – CAM.
  • Responsible for late dysentery.
  • Nontoxic mutants can cause dysentery but non-inttasive can’t produce dysentery.

Toxins:

  • Endotoxin 
    • LPS
    • Cause irritation of bowel.

Shigella Dysenteriae-

  • Produces heat labile exotoxin (Shigabacillus exotoxin)

Affect gut and CNS:

  • Show  neurotoxicity on blood vessel of CNS
  • Can lead to miningsmus and coma.
  • Cytotoxicity = Verotoxin I or Shiga like toxin
  • Toxin has two peptide subunit.Toxins produce early, non bloody voluminous diarrhea.
    • A unit (N-glycosidase) of cytotoxin hydrolyzes adenine from specific sites of 60s RNA
    • Inhibits protein synthesis.
    • Contributes to fatal nature.

CLINICAL SYMPTOMS:

  • Shigella  Associated with hemolytic uremic Syndrome
  • Ranges from asymptomatic infection to severe bacillary dysentery
  • Two-stage disease: watery diarrhea changing to dysentery with frequent small stools with blood and mucus, tenesmus, cramps, fever

Early stage:

  • Watery diarrhoea attributed to the enterotoxic activity of Shiga toxin
  • Fever attributed to neurotoxic activity of toxin  
  • Majority of lesion are in distal colon.

COMPLICATIONS

  • Toxic dilatation
  • Colonic perforation
  • Thrombotic thrombocytopenic purpura
  • Reactive arthritis
  • Reiter’s syndrome.
  • HUS
    • Schistocytes are suggestive of hemolytic-uremic syndrome (HUS)

DIAGNOSIS

  • Sampling: fresh stool, mucus flakes and rectal swabs
  • Selenite F broth(0.4%) is used as enrichment and transport media (for 9-12hours)
  • Total blood count reveals anemia and thrombocytopenia, and schistocytes
  • Increase blood urea nitrogen(BUN)
  • Invasive test for shigella is Rabbit ileal loop

TREATMENT:

  • Oral rehydration therapy (No antibiotics) for mild to moderate dehydration.
  • Ciprofloxacin, Fluoroquinol,  Azithromycin, Pivmecillinam, Ceftriaxone
  • Preventing infected individuals from handling food
  • DOC for multiresistant Nalidixic acid.

Exam Important

 Introduction:

  • PERSON TO PERSON TRANSMISSION
  • Gut pathology is due to toxin

INFECTIVE DOSE:

  •  10-100 VIABLE BACILLI

Toxins:

  • Endotoxin 
    • LPS
    • Cause irritation of bowel.

Shigella Dysenteriae-

  • Produces heat labile exotoxin (Shiga bacillus exotoxin)

Affect gut and CNS:

  • Show  neurotoxicity on blood vessel of CNS
  • Cytotoxicity = Verotoxin I or Shiga like toxin
  • Toxins produce early, non bloody voluminous diarrhea.

CLINICAL SYMPTOMS:

  • Shigella  Associated with hemolytic uremic Syndrome
  • Ranges from asymptomatic infection to severe bacillary dysentery
  • Two-stage disease: watery diarrhea changing to dysentery with frequent small stools with blood and mucus, tenesmus, cramps, fever

Early stage:

  • Watery diarrhoea attributed to the enterotoxic activity of Shiga toxin
  • Fever attributed to neurotoxic activity of toxin  
  • Majority of lesion are in distal colon.

COMPLICATIONS

  • HUS
    • Schistocytes are suggestive of hemolytic-uremic syndrome (HUS)

DIAGNOSIS

  • Sampling: fresh stool, mucus flakes and rectal swabs
  • Selenite F broth(0.4%) is used as enrichment and transport media (for 9-12hours)
  • Total blood count reveals anemia and thrombocytopenia, and schistocytes
  • Increase blood urea nitrogen(BUN)
  • Invasive test for shigella is Rabbit ileal loop

TREATMENT:

  • Oral rehydration therapy (No antibiotics) for mild to moderate dehydration.
  • Ciprofloxacin, Fluoroquinol,  Azithromycin, Pivmecillinam, Ceftriaxone
  • DOC for multiresistant Nalidixic acid.

 

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Clostridium tetani : Diagnosis, treatment and Prevention

Clostridium tetani : Diagnosis, treatment and Prevention


Diagnosis of tetanus

Based entirely on clinical findings: 

  • History of an injury
  • Particularly one in which either soil or fecal material has been introduced
  • 6-12 days before the onset of typical clinical findings.
  • Wound should be cultured in suspected cases.

Other laboratory findings may be –

  1. Leukocytosis
  2. Muscle enzyme levels may be raised
  3.  Electromyogram 
  • Show continuous discharge of motor units a
  • Shortening or absence of the silent interval.

Treatment of tetanus

  • Treatment of tetanus includes :

1. Antimicrobial therapy :- 

  • Eradicate vegetative cells
  • Penicillin and metronidazole are first line drugs. 
  • Clindamycin and erythromycin are alternatives for penicillin – allergic patients.
  • Tetracycline is not used.

2. Antitoxin :-

  • Neutralize circulating toxin. 
  • All wounds must be thoroughly cleaned soon after injury
  • Human tetanus immune globuline (TIG) is the preparation of choice.
  • Administered within time it neutralizes tetanus toxin and significantly lowers the mortality
  • Serious wound + uncertain about  immunization should receive both
  1. Tetanus toxoid (active immunity)
  2. Tetanus immune globulin (Passive immunity)

Control of muscle spasms :-

  • Muscle spasms cause laryngospasm or sustained contraction of ventilatory muscles. 
  • Therefore painful and life threatening.
  • Benzodiazepines (Diazepam, lorazepam, midazolam) are used most commonly.
  •  Alternatives are Barbiturates and chlorpromazine. 
  • Mechanical ventilation used for spasms unresponsive to medications. 
  • Other agents include propofol, dantrolene, intrathecal baclofen, succinylcholine and magnesium sulfate.

Respiratory care :-

  •  Intubation or tracheostomy, with or without mechanical ventilation may be required.

Autonomic dysfunction :- 

  • For sympathetic overactivity labetalol, esmolol or clonidine may be used.

Vaccine :- 

  • Patient recovering from tetanus should be actively immunized.

Prevention

Active immunization

  • Protective level of antitoxin > 0.01 IU/ml serum
  • Active immunity offered by tetanus toxoid is effective in 100% of the patients 
  • Adsorbed toxoid are more beneficial
  • Should never freeze

Monovalent Vaccine:

  • 2 dose of purified tetanus toxoid (IT) should be given at interval of 1-2 month
  • Ist booster after 1 year of 2nd dose.
  • 2nd booster after 5 years of 3rd dose.

Combined Vaccine :

  • DPT .

Passive immunization :

  • Human tetanus hyper immunoglobulin (TIG) is best prophylactic to use.
  • Toxin already bound to neural tissue is not affected.

Combined active and passive immunization:

  • Patient is given TIG in one arm
  • TT in other arm
  • Followed by another dose of TT 6 weeks later and third dose 1 year later.
  • TIG contraindicated during pregnancy.
  • The purpose of antitoxin is for immediate temporary protection
  • The purpose of tetanus toxoid is for long lasting protection
  • TT is useful even after 12 hours have elapsed following injury.

Pregnancy

Primigravida

  • Tetanus toxoids appear safe during pregnancy
  • Administered intramuscularly.
  • 0.5 ml tetanus toxoid is given at 6 weeks interval for 2 times
  • The first one to be given between 16-24 weeks.

Multigravida (completely immunized in last 5 years): 

  • 1 booster dose is sufficient

Multigravida (partially immunized in previous pregnancy in last 5 years):

  •  2 doses, 1 month apart, after I trimester.

Multigravida (unimmunized in previous pregnancy in last 5 years):

  •  2 doses, I month apart, after I trimester

 Multigravida (completely immunized in previous pregnancy earlier than 5 years): 

  • 2 doses, I month apart, after I trimester.

Exam Important

Diagnosis of tetanus

  • Muscle enzyme levels may be raised

Treatment of tetanus

  1. Antimicrobial therapy 
  2. Antitoxin :-
  • Human tetanus immune globuline (TIG) is the preparation of choice.
  • Administered within time it neutralizes tetanus toxin and significantly lowers the mortality
  • Serious wound + uncertain about  immunization should receive both
  1. Tetanus toxoid (active immunity)
  2. Tetanus immune globulin (Passive immunity)

Prevention
Active immunization

  • Protective level of antitoxin > 0.01 IU/ml serum
  • Active immunity offered by tetanus toxoid is effective in 100% of the patients 
  • Adsorbed toxoid are more beneficial
  • Should never freeze

Monovalent Vaccine:

  • 2 dose of purified tetanus toxoid (IT) should be given at interval of 1-2 month
  • Ist booster after 1 year of 2nd dose.
  • 2nd booster after 5 years of 3rd dose.

Combined Vaccine :

  • DPT .

Passive immunization :

  • Human tetanus hyperimmunoglobulin (TIG) is best prophylactic to use.
  • Toxin already bound to neural tissue is not affected.

Combined active and passive immunization:

  • Patient is given TIG in one arm
  • TT in other arm
  • Followed by another dose of TT 6 weeks later and third dose 1 year later.
  • TIG contraindicated during pregnancy.
  • The purpose of antitoxin is for immediate temporary protection
  • The purpose of tetanus toxoid is for long lasting protection
  • TT is useful even after 12 hours have elapsed following injury.

Pregnancy

Primigravida

  • Tetanus toxoids appear safe during pregnancy
  • 0.5 ml tetanus toxoid is given at 6 weeks interval for 2 times
  • The first one to be given between 16-24 weeks.

Multigravida (completely immunized in last 5 years): 

  • 1 booster dose is sufficient

Multigravida (partially immunized in previous pregnancy in last 5 years):

  •  2 doses, 1 month apart, after I trimester.

Multigravida (unimmunized in previous pregnancy in last 5 years):

  •  2 doses, I month apart, after I trimester

 Multigravida (completely immunized in previous pregnancy earlier than 5 years): 

  • 2 doses, I month apart, after I trimester.

 

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Treponema Pallidum: Diagnosis and Treatment

Treponema Pallidum: Diagnosis and Treatment


Diagnosis:

1.Demonstration of Organism

  • Darkfield microscopic examination of lesion exudate such as chancre of primary syphilis 
  • Immunofluorescence or immunohistochemical method more reliable.

2. Serological tests for Syphilis:

  • Serologic testing is considered the standard method of detection for all stages of syphilis. 

(a) Non-treponemal tests 

  1. RPR (Rapid plasma reagin)
  2. VDRL

VDRL principle:

  • Heat-inactivated (to destroy complement) serum of patient is reacted with freshly prepared non-treponemal antigen
  • Flocculation reaction (antigen and antibody complex are suspended) occurs.
  • The flocculation can be observed by using microscope.

The sensitivity of the Non-treponemal tests like VDRL and RPR tests :

  • 78-86% for detecting primary syphilis
  • 100% for detecting secondary syphilis
  •  95-98% for detecting tertiary syphilis.
  • Specificity ranges from 85-99% .

Possibility of false-positive results in: 

  • Viral Hepatitis, SLE, and Leprosy.

 (b)Treponemal test

  • Confirmation of any positive or equivocal nontreponemal test result should follow with a treponemal test
  1. Fluorescent treponemal antibody-absorption (FTA-ABS)
  2. Microhemagglutination assay T pallidum (MHA-TP)
  3. T pallidum hemagglutination (TPHA)
  4. FTA-ABS-Confirmatory test
  5. TPI (Treponemal pallidum immobilization) test(most specific)
  • Sensitivity of 84% for detecting primary syphilis infection
  • 100% sensitivity for detecting syphilis infection in other stages
  • Its specificity is 96%.
  • Congenital syphilis can be best diagnosed by IgM FTA- ABS
    • Ig M does not cross the placenta
    • Its presence in neonatal serum confirms congenital syphilis.
    • Capita M test and the 19S Ig M FTA-ABS test are available

Treatment of syphilis

  • Primary or secondary syphilis –
    •  Benzathine penicillin G 2.4 million units intramuscularly (IM) in a single dose
  • Early latent syphilis – 
    • Benzathine penicillin G 2.4 million units IM in a single dose
  • Late latent syphilis or latent syphilis of unknown duration –
    •  Benzathine penicillin G 7.2 million units total, administered as 3 doses of 2.4 million units IM each at 1-week intervals
  • Pregnancy – In patients with a history of penicillin allergy, skin testing is recommended.
    • Treatment appropriate to the stage of syphilis is recommended.

Exam Important

  • Treponema pallidum isolation from CSF is maximum in the secondary stage of syphilis.
  •  Infection leads to lifelong immunity.
  • Penicillin is the only recommended agent for treatment of syphilis in pregnancy.
  •  If the patient has a documented penicillin allergy, desensitization and penicillin therapy should be given.
  • Seropositive infant not treated at birth if mother received penicillin in 3rd trimester
  • Biological False positive/ BFP serological test for syphilis may be encountered in:  Primary or secondary syphilis – Benzathine penicillin G 2.4 million units intramuscularly (IM) in a single dose
    • Viral Hepatitis, SLE, and Leprosy.
  • Congenital syphilis can be best diagnosed by IgM FTA- ABS
  • Most sensitive diagnosis during secondary stage of syphilis is VDRL.

Treponemal Test-

  • Fluorescent treponemal antibody-absorption (FTA-ABS)
  • Microhemagglutination assay T pallidum (MHA-TP)
  • T pallidum hemagglutination (TPHA)
  • FTA-ABS-Confirmatory test
  • TPI (Treponemal pallidum immobilization) test(most specific)
  • Non-treponemal tests 
    • RPR (Rapid plasma reagin)
    • VDRL
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Dementia

DEMENTIA


DEMENTIA

Introduction:

  • Defined as a progressive impairment of cognitive functions in absence of any disturbances of consciousness.

Prevalence:

  • Increases with age.
  • 5% in population older than 65 years; 20-40% in older than 85 years. 

Symptoms:

1. Cognitive impairment:

  • Characterized by 4 A’s: amnesia, aphasia, apraxia & agnosia.

Amnesia: 

  • Memory impairment.
  • Can be episodic (memory for events) & semantic (memory for facts rules, words and language) & visuospatial deficits.

Aphasia: 

  • Disturbances of language function.

Apraxia: 

  • Inability to perform learned motor functions.
  • Eg: Difficulties in functions like buttoning the shirt or combing the hair.

Agnosia:

  • Inability to interpret sensory stimulus.
  • Most common disturbance -‘prosopagnosia” – Inability identifing face.

Other cognitive impairments:

  • Disturbances in executive functioning (i.e. planning, organizing, sequencing & abstracting).

2. Behavioral & psychological symptoms:

  • Personality changes, hallucinations & delusions, depression, manic & anxiety symptoms, apathy, agitation, aggression, wandering circadian rhythm disturbances, catastrophic reaction.
    • Catastrophic reaction – Subjective awareness of intellectual deficits in stressful situation result in emotional outburst in dementia patient.

3. Focal neurological signs & symptoms:

  • Seen in vascular dementia (multi-infarct dementia) corresponding to site of vascular insults.

Types:

1. Depending on reversibility – Reversible dementia (15% patients) & Irreversible dementia.

Causes of reversible dementia:

  • Neurosurgical conditions (subdural hematoma, normal pressure hydrocephalus, intracranial tumors, intracranial abscess).
  • Infectious causes (meningitis, encephalitis, neurosyphilis, lyme disease).
  • Metabolic causes (vitamin B12 or folate deficiency, niacin deficiency, hypo and hyperthyroidism, hypo & hyperparathyroidism).
  • Others (drugs and toxins, alcohol abuse, autoimmune encephalitis).

2. Depending on involvement of area of brain:

  • Cortical & Sub-cortical (As to area affetced by dementing process first).

Cortical dementias: 

Clinical features: 

  • Characterized by early involvement of cortical structures & hence, early appearance of cortical dysfunction.
  • Amnesia, apraxia, aphasia, agnosia & acalculia (impaired mathematical skills) indicating cortical involvement.

Subcortical dementia: 

Clinical features

  • Early involvement of subcortical structures (basal ganglia, brain stem nuclei & cerebellum).
  • Characterized by early presentation of motor symptoms (abnormal movements like tics, chorea, dysarthria).
  • Significant disturbances of executive functioning.
  • Prominent behavioral & psychological symptoms (apathy, depression, bradyphrenia (slowness of thinking).

Conditions associated: 

  • Parkinson’s disease, Wilson’s disease, Huntington’s disease, multiple sclerosis, progressive supranuclear palsy, normal pressure hydrocephalus.

Other types of dementia:

  • Vascular dementia (multi-infarct dementia), lewy body disease (dementia with lewy body), HIV related Dementia, frontotemporol dementia (FTD) & pseudodementia

1. Vascular dementia (multi-infarct dementia):

  • 2nd most common type of dementia.
  • History of stroke.

Causes:

  • Occurrence of multiple cerebral infarction (due to occlusion of cerebral vessels by arteriosclerotic plaques or thromboemboli) → progressive deterioration of brain functions →  dementia.
  • Acute exacerbations corresponding to new infarcts → Stepwise deterioration of symptoms (step-ladder pattern).

Treatment: 

  • Management of risk factors & cholinesterase inhibitors.

2. Binswanger’s disease:

  • Also referred as “subcortical arteriosclerotic encephalopathy”.
  • Characterized by multiple small white matter infarctions —> Result in subcortical dementia symptoms.

3. Lewy Body Disease (Dementia with Lewy Body):

  • Clinical features similar to Alzheimer’s disease.

Pick’s dlsease: 

  • One pathological variant of FTD. 
  • Characterized by presence of pick’s bodies.
  • Earlier onset (45-65 years).
  • Presents with behavioral symptoms & change in personality with relative memory preservation.

7. Pseudodementia:

  • Depression in elderly patients mimicing dementia symptoms.

Management for dementia:

  • mini mental status examination (MMSE):
    • Screening test.
    • Evaluation of cognitive functions.
    • Score of less than 24 (out of a maximum 30) – Suggestive of dementia.

Medications:

  • Cholinesterase inhibitors  – Donepezil, rivastigmine, galantamine & tacrine.
  • NMDA receptor antagonist – Memantine.
  • Symptomatic treatment – For behavioral & psychological symptoms of dementia.
    • Includes antidepressants, antipsychotics & benzodiazepines.

Exam Important

  • Cognitive impairment in dementia is characterized by 4 A’s: amnesia, aphasia, apraxia & agnosia.
  • Catastrophic reaction is subjective awareness of intellectual deficits in stressful situation result in emotional outburst in dementia patient.
  • Reverslble causes of dementia includes subdural hematoma, normal pressure hydrocephalus, intracranial tumors, intracranial abscess.
  • Alzheimer’s disease is the prototype of cortical dementia.
  • Binswanger’s disease is also known as subcortical arteriosclerotic encephalopathy.
  • Pick’s dlsease is one pathological variant of FTD characterized by earlier onset & presence of pick’s bodies.
  • Depression in elderly patients may mimic symptoms of dementia and hence is known as pseudodementia.
  • The evaluation of cognitive tunctions in dementia is done using screening test of mini mental status examination (MMSE).
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Amnestic Disorders

AMNESTIC DISORDERS


AMNESTIC DISORDERS

  • Broad category including variety of conditions presenting amnestic syndrome.

Features:

  • Characterized by inability to form new memories (anterograde amnesia) & inability to recall previously remembered knowledge (retrograde amnesia).
  • Short-term & recent memory – Impaired with preservation of remote & immediate memory.

Causes:

Major causes:

  • Thiamine deficiency (Korsakoff syndrome).
  • Hypoglycemia.
  • Primary brain conditions (head trauma, seizures, cerebral tumors, cerebrovascular disease, hypoxia, electroconvulsive therapy, multiple sclerosis).
  • Substance related disorders (alcohol, benzodiazepines).

Exam Important

  • Major causes of amnestic disorders are thiamine deficiency (Korsakoff syndrome), hypoglycemia, primary brain conditions (head trauma, seizures, cerebral tumors, cerebrovascular disease, hypoxia, electroconvulsive therapy, multiple sclerosis).
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Dyssomnia & Parasomnia

DYSSOMNIA & PARASOMNIA


DYSSOMNIA & PARASOMNIA

I) Dysomnia

Introduction:

  • Characterized by abnormality in duration or quality of sleep.

Subtypes:

  • Insomnia.
  • Hypersomnia.

1. Insomnia:

Features:

  • Decreased sleep.
  • Difficulty in initiation of sleep.
  • Difficulty in maintenance of sleep.
  • Frequent awakening during night.
  • Early morning awakening.
  • Nonrestorative sleep.
  • Not feeling refreshed in morning due to poor quality of sleep.

Syndromes associated:

Periodic limb movement disorder: 

  • Non-restorative sleep and day time sleepiness.

Restless leg syndrome (Ekbom syndrome):

  • Difficulty in initiation of sleep due to moving legs. Treated with ropinirole (dopamine agonist).

Treatment:

  • Benzodiazepines, zolpidem & hypnotics.

2. Hypersomnia:

Features: 

  • Excessive sleepiness.
  • Prolonged sleep episodes.
  • Excessive day time sleep episodes.

Syndromes associated:

Narcolepsy:

  • Reduced latency of REM sleep (reaching REM sleep earlier).
  • Sleep attacks (irresistible urge for sleep at anytime of day) & sleep paralysis (Occurs in morning. patient awake but unable to move body).

Kleine-Levin syndrome:

  • Characterized by episodes of hypersomnia, hyperphagia & hypersexuality (increased sexual activity).

II). PARASOMNIA:

Introduction:

  • Disorders characterized by dysfunctional events associated with sleep.

Subtypes:

Stage 4, NREM sleep disorders:

  • Occur during stage 4, NREM.

Events:

  • Night terror or sleep terror (pavor nocturnus).
  • Sleepwalking (somnambulism).

Sleep-related enuresis – 

  • Most common cause of bed wetting – Due to psychosocial (sibling rivalry).
  • Treated by bed alarms, imipramine & intranasal desmopressin.
    • Bruxism (teeth grinding).
    • Sleep talking (somniloquy).

Other sleep disorders:

Nightmare:

  • Occurs during REM sleep.
  • Patient able to recall dream (contrast to night terror).

Exam Important

  • Restless leg syndrome (Ekbom syndrome) is associated with sleep disturbances treated with ropinirole.
  • Narcolepsy exhibits reduced latency of REM sleep.
  • Kleine-Levin syndrome is characterized by episodes of hypersomnia, hyperphagia & hypersexuality.
  • Night terror or sleep terror (pavor nocturnus), Sleepwalking (somnambulism), Sleep-related enuresis & Bruxism (teeth grinding) are all features of Stage 4, NREM sleep disorders.
  • Sleep-related enuresis is most common cause of bed wetting.
  • Nightmare occurs during REM sleep.
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Compilation Of Psychiatric Disorders In Pediatric Patients

COMPILATION OF PSYCHIATRIC DISORDERS IN PEDIATRIC PATIENTS


COMPILATION OF PSYCHIATRIC DISORDERS IN PEDIATRIC PATIENTS

  • Important psychiatric disorders in pediatric patients include,
    • Conduct disorder.
    • Oppositional defiant disorder.
    • Specific disorders of scholastic skills – Learning disorders.

Conduct disorder:

  • Associated with unsatisfactory family relationships & failure at school.
  • Later stages lead to antisocial personality disorder (dissocial personality disorder).

Features:

Characterized by –

  • Repetitive & persistent pattern of disregard for rights of others.
  • Aggressiveness & dissocial behavior (excessive fighting or bullying).
  • Cruelty to animals/people.
  • Severe destruction of property (fire setting).
  • Stealing.
  • Truancy from school.
  • Repeated lying.
  • Frequent running from school & home.
  • Defiance of authority figures.
  • Disobedience pattern.

Oppositional defiant disorder:

  • Less severe than conduct disorder.

Features: 

  • Characterized by persistently negativistic & defiant behavior (frequent arguing with adults, refusal to comply with adults).
  • Frequent loss of temper (deliberately annoying adults).
  • Note: No serious violations (theft, fire setting, destruction, etc.) – Unlike conduct disorder.

Management:

  • Conduct & oppositional defiant disorder –
    • Family intervention & behavioral therapy.
    • Low dose antipsychotics effective in some.

Learning disorders:

  • Also referred as Specific developmental disorders of cholastic skills”.

Features: 

  • Characterized by significant impairment in one or more of scholastic skills which are out of proportion to intellectual functioning of child.
  • Eg: Significant difficulty in reading while having normal writing & arithmetic skills with normal IQ.

Subtypes: 

  • Specific reading disorder (Dyslexia).
  • Disorder of written expression (specific spelling disorder).
  • Specific disorder of arithmetic skills.
  • Mixed disorders of scholastic skills (reading, writing & arithmetics).

Other features:

  • Inattention.
  • Hyperactivity.
  • Emotional disturbances.

Exam Important

  • Repetitive & persistent pattern of disregard for rights of others is seen in conduct disorder.
  • Aggressiveness & dissocial behavior (excessive fighting or bullying) and repeated lying is feature of conduct disorder.
  • Dyslexia is specific reading disorder.
  • Learning disorders are developmental disorders are characterized by significant impairment in one or more of the scholastic skills which are out of proportion to intellectual functioning of child.
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Mental Retardation

MENTAL RETARDATION


MENTAL RETARDATION

Introduction:

  • Condition characterized by incomplete development of intellectual functions & adaptive skills (skills for successful Iife).
  • Intelligence is measured by Intelligence Quotient (IQ).

Calculation method:

  • IQ = Mental age/Chronological age x 100 
    • Maximum denominator – 15 (even for elderly assessment).
  • IQ less than 70 – Considered as “mental retardation”.

Category & their IQ:

  • Normal – 90-109
  • Borderline – 70-89
  • Mild mental retardation – 50-69
  • Moderate mental retardation – 35-49
  • Severe mental retardation – 20-34
  • Profound mental retardation – <20.
  • Level of functioning varies with severity of mental retardation.

Causes: 

  • Down syndrome & fragile-X syndrome – Most common chromosomal cause.

Features:

  • Behavioral problems in mental retardation – Have maladaptive behavior (aggression, self injurious behaviors, hyperactivity, etc).

Management:

  • Modified by behavioral therapy techniques – Contingency management.
    • Desired behaviors rewarded & undesired behaviors punished.

Exam Important

  • Calculation for IQ = Mental age/Chronological age x 100.
  • IQ less than 70 is considered as “mental retardation”.
  • Down syndrome & fragile-X syndrome are the most common chromosomal cause of mental retardation.
  • Behavioral problems in mental retardation are managed by behavioral therapy techniques like contingency management.
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Electroconvulsive Therapy (Ect)

ELECTROCONVULSIVE THERAPY (ECT)


ELECTROCONVULSIVE THERAPY (ECT)

Introduction:

  • A type of convulsive therapies used for psychiatric disorders treatment.
  • Usage of electricity as an agent inducing convulsions – Referred as “electroconvulsive therapy.”

Types:

A. Direct ECT:

  • Anesthetic agents & muscle relaxants not used.
  • Generalized convulsions produced result in fractures or teeth dislocations.
  • Higher incidence of side effects – Rarely used now.

B. Modified ECT (Indirect ECT):

  • Anesthetic agents & muscle relaxants are administered before ECT.
  • Muscles relaxed → risk of bone fractures &other injures from motor activity during seizures minimized.

Technique:

  • Based on electrode placement – Bilateral ECT & Unilteral ECT.

Bilateral ECT: 

  • Most commonly used.
  • Involves electrodes placed on both sides of skull (bifronto-temporal electrode placement).

MOA:

  • Induction of bilateral generalized seizure via ECTs.
  • By down regulation of postslnaptic beta-adrenergic receptors.
  • Changes in growth factors & molecular mechanisms (increased brain derived neurotrophic factor, BDNF)
  • Neurogenesis (hippocampus).

Indications:

Depression (Major depressiue disorder): 

  • Both major depressive disorder & bipolar disorder.
  • Mainly for depression with suicide risk (Acute suicidal patients).
  • Depression with stupor.
  • Depression with psychotic symptoms (psychotic depression or delusional depression).

Manic episode:

  • Acute mania – Not 1st line treatment.
  • Only for intolerant/unresponsive to pharmacotherapy.
  • Severe maniac patients with suicide risk.

Schizophrenia:

  • Catatonic schizophrenia – 1st line treatment.
  • Note: Not effective in chronic schizophrenia.

Other indications:

  • Intractable seizures.
  • Neuroleptic malignant syndrome.
  • Delirium.
  • On-off phenomenon of Parkinson’s disease

Adverse effects:

Memory disturbances:

  • Most common side effect.
  • Retrograde amnesia more common.
  • Mild & recovery within 1-6 months after treatment.

Other side effects:

  • Delirium
  • Headache
  • Muscle aches
  • Fractures (very rare with modified ECT)
  • Nausea
  • Vomiting.

Contraindications:

  • No absolute contraindications.

Relative contraindication:

  • Raised intracranial tension (space occupying lesion in CNS).
  • Recent myocardial infarction
  • Severe hypertension
  • Cerebrovascular disease
  • Severe pulmonary disease
  • Retinal detachment

Note: Pregnancy not a contraindication.

Exam Important

  • Generalized convulsions produced during direct ECT result in fractures or teeth dislocations.
  • ECT is used for major depressiue disorder, catatonic schizophrenia, intractable seizures, neuroleptic malignant syndrome, delirium & on-off phenomenon of Parkinson’s disease.
  • ECT not effective in chronic schizophrenia.
  • Memory disturbances most commonly retrograde amnesia occur as side effect to ECT.
  • There are no absolute contraindications to ECT.
  • Raised intracranial tension (space occupying lesion in CNS) is a relative contraindication to ECT.
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