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Mr ASHOK BISHNOI
Lecturer JINR
• First described by German psychiatrist
◦ Alois Alzheimer (1906)
Introduction:-
“is a slowly progressive disease of the brain
that is characterized by impairment of
memory and eventually by disturbances in
reasoning, planning, language, & perception”
Definition:-
• Generally diagnosed in people over 65 years of
age
 -Early-onset (before 65); only 5-10% of patients
• 4.5+ million Americans suffer from it
• 1 in 6 women over 55
• 1 in 10 men over 55
Incidence:-
 Idiopathic
 Cholinergic hypothesis
◦ -Caused by reduced synthesis of acetylcholine
◦ -Destruction of these neurons causes disruptions in distant
neuronal networks (perception, memory, judgment)
 Amyloid hypothesis
◦ -Abnormal breakdown; buildup of amyloid beta deposits
◦ -Damaged amyloid proteins build to toxic levels, causing call
damage and death
Genetics
Etiology:-
• Obesity
• High blood pressure
• Head trauma
• High cholesterol
• Depression
• Lower rates in highly educated
• Family history
Risk factors:-
Due to etiological factor
Amyloidosis ( Amyloid Decreased production
of acetylcholine
preserved protein
deposition in neurone)
Memory loss, Forgetfulness, Depression, Loss their
familiar Phases, Place, Object & Environment
Pathophysiology:-
1.Mild AD:-
Memory disturbance
Poor judgement
Irritability
Agitation
Suspicious
Apathy
Cognitive impairment
Clinical Manifestations according to types:-
2.Moderate A D:-
 Language disturbance
 Impaired word finding
 Spontaneous speech
 Paraphrasis (word used in the wrong context)
 Motor disturbance
 Hyper orality (the desire to take everything in to
the mouth to suck, chew, taste)
 Swallowing difficulty
 Depression
 Delusion
3.Severe A D:-
Communication disturbance
Urinary, faecal incontinence
Pneumonia
 Memory loss that disrupts daily life.
 Challenges in planning or solving problems.
Some people may
experience changes in their ability to develop and follow a plan or work with
numbers. They may have trouble following a familiar recipe or keeping track
of monthly bills. They may have difficulty concentrating and take much
longer to do things than they did before.
 Difficulty completing familiar tasks at home,
at work.
 Confusion with time or place.
 Trouble understanding visual images and
spatial relationships.
 New problems with words in speaking
or writing.
 Misplacing things and losing the
ability to retrace steps.
 Decreased or poor judgment.
 Withdrawal from work or social
activities.
 Changes in mood and personality.
 History
 Physical examination
 (MSE) Mental State Examination (used to
evaluate the cognitive impairments)
 C.T Scan
 MRI
 PET
Diagnostic evaluation:-
.
PET scan of the brain of a person with AD showing a loss of
function in the temporal lobe.
 Aricept Used to delay or slow the symptoms of AD
Donepezil • Loses its effect over time
• Used for mild, moderate and severe AD
• Does not prevent or cure AD
 Celexa
Citalopram Used to reduce depression and anxiety
• May take 4 to 6 weeks to work
• Sometimes used to help people get to sleep
 Depakote Used to treat severe aggression
Sodium Valproate • Also used to treat depression and anxiety
 Exelon Used to delay or slow the symptoms of AD
Rivastigmine • Loses its effect over time
• Used for mild to moderate AD
• Can get in pill form or as a skin patch
• Does not prevent or cure AD
Management of AD:-
Nursing management:-

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ppt on Alzheimer’s disease

  • 2.
  • 3. • First described by German psychiatrist ◦ Alois Alzheimer (1906) Introduction:-
  • 4. “is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, & perception” Definition:-
  • 5. • Generally diagnosed in people over 65 years of age  -Early-onset (before 65); only 5-10% of patients • 4.5+ million Americans suffer from it • 1 in 6 women over 55 • 1 in 10 men over 55 Incidence:-
  • 6.
  • 7.  Idiopathic  Cholinergic hypothesis ◦ -Caused by reduced synthesis of acetylcholine ◦ -Destruction of these neurons causes disruptions in distant neuronal networks (perception, memory, judgment)  Amyloid hypothesis ◦ -Abnormal breakdown; buildup of amyloid beta deposits ◦ -Damaged amyloid proteins build to toxic levels, causing call damage and death Genetics Etiology:-
  • 8. • Obesity • High blood pressure • Head trauma • High cholesterol • Depression • Lower rates in highly educated • Family history Risk factors:-
  • 9. Due to etiological factor Amyloidosis ( Amyloid Decreased production of acetylcholine preserved protein deposition in neurone) Memory loss, Forgetfulness, Depression, Loss their familiar Phases, Place, Object & Environment Pathophysiology:-
  • 10. 1.Mild AD:- Memory disturbance Poor judgement Irritability Agitation Suspicious Apathy Cognitive impairment Clinical Manifestations according to types:-
  • 11. 2.Moderate A D:-  Language disturbance  Impaired word finding  Spontaneous speech  Paraphrasis (word used in the wrong context)  Motor disturbance  Hyper orality (the desire to take everything in to the mouth to suck, chew, taste)  Swallowing difficulty  Depression  Delusion
  • 12. 3.Severe A D:- Communication disturbance Urinary, faecal incontinence Pneumonia
  • 13.  Memory loss that disrupts daily life.  Challenges in planning or solving problems. Some people may experience changes in their ability to develop and follow a plan or work with numbers. They may have trouble following a familiar recipe or keeping track of monthly bills. They may have difficulty concentrating and take much longer to do things than they did before.  Difficulty completing familiar tasks at home, at work.  Confusion with time or place.  Trouble understanding visual images and spatial relationships.
  • 14.  New problems with words in speaking or writing.  Misplacing things and losing the ability to retrace steps.  Decreased or poor judgment.  Withdrawal from work or social activities.  Changes in mood and personality.
  • 15.  History  Physical examination  (MSE) Mental State Examination (used to evaluate the cognitive impairments)  C.T Scan  MRI  PET Diagnostic evaluation:-
  • 16. . PET scan of the brain of a person with AD showing a loss of function in the temporal lobe.
  • 17.  Aricept Used to delay or slow the symptoms of AD Donepezil • Loses its effect over time • Used for mild, moderate and severe AD • Does not prevent or cure AD  Celexa Citalopram Used to reduce depression and anxiety • May take 4 to 6 weeks to work • Sometimes used to help people get to sleep  Depakote Used to treat severe aggression Sodium Valproate • Also used to treat depression and anxiety  Exelon Used to delay or slow the symptoms of AD Rivastigmine • Loses its effect over time • Used for mild to moderate AD • Can get in pill form or as a skin patch • Does not prevent or cure AD Management of AD:-