Where Am I?

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Where Am I? by Mind Map: Where Am I?

1. dozapine dosage

2. shcu as revastagmin,

3. AD

4. Trigger Text

4.1. 1

4.1.1. Mrs Um Mohammed, age 80, has been brought to your by her daughter who informs you that her mother has become increasingly forgetful over the last approximately 12 months: at times unaware of the day and date, and she often forgets prayer times and there is a gradual and progressive decline in her memory. She is becoming concerned with her mother’s ability to cope at home, particularly given the declining health of her father. Mrs Um Mohammed acknowledges that she occasionally has problems remembering people’s names, but feels that she has a good memory for her age. Her daughter agrees that her memory is at times very good, and better than her own for remembering items from their shared past

4.2. 2

4.2.1. Two years later, you receive a call from Mrs Um Mohammed neighbour of five years, who has found Mrs. Mohammed wandering the street, uncertain of where she is. The neighbour tells you that initially Mrs Mohammed ran away, claiming that the she was trying to kill her. She also tells you that Mrs Mohammed is usually independent and friendly, but over the last few days has seemed increasingly confused, and has been calling out during the night. While sharing lunch the day before, Mrs Mohammed had been drowsy, and had coughed a number of times. The neighbour has taken her back into the house, and has found your number by the telephone

5. Step1: Identify cues

5.1. Difficult words

5.1.1. no words

5.2. Cues

5.2.1. 1- 80 years old female

5.2.2. 2- brought by her daughter

5.2.3. 3- forgetfulness over the last year At time not aware of day and date long term memory is intact the loss of the memory is gradual and progressive

5.2.4. 4- her husband health is deteriorating

6. Sep2: problem Formulation

6.1. An 80 years old female brought by her daughter complaining of increasing forgetfulness and memory deterioration. However, her long term memory is intact.

7. Step3: Hypothesis Generation

7.1. 1- learning and memory

7.1.1. memory it is located in the temporal and pre-frontal area

7.1.2. when there is a lesion, patient will develop the aggressive reaction

7.1.3. bapis circuit of the memory

7.1.4. mamilary body

7.1.5. amegdula

7.1.6. hypocampus

7.2. 2-the medical term for forgetfulness is amnesia

7.2.1. the definition of the memory memory is defined as the encoding of the information within the brain the second componant in the storing of the information the third is the retreaval the information

7.2.2. memory is defined as the encoding of the information within the brain

7.2.3. memory is defined as the encoding of the information within the brain

7.3. 3- one of the causes is the accumulation of protein within the brain cytoplasm

7.3.1. so it would interfere with the transportation and leading to the memory loss

7.4. 4-infection by herpis simplex in the temporal lobe

7.5. 5- as aging process occur, their will be a neuropalstisity

7.6. 6- new memory build up

7.6.1. an increase between the wiring and connection of the neurons the AMDA and NAMD receptors are involved in this process

7.7. 7- the problem might be specifically within the storage part of memory process.

7.7.1. the reason of that could be trumatic, HIV , krestfild- jacop disease and enciphalitis

7.8. 8- vascular injury to the brain such as multi infarct dementia

7.9. 9- Huntington disease would develop dementia later in the disease

7.10. 10- iatrogenic caused by using drug,like the benzodiazpin, B-blocker, atropin derivatives and IV drud abuse

7.11. 11- alcohol consumption leading to worcis korsicoof syndrome

7.12. 12- frontotemporal dementia

7.13. 13- depression might lead to psudodementia

7.14. 14- mass occupying lesion (Tumor) near to the temporal lobe. However it is unlikely

7.15. 15- Multiple sclerosis

7.16. 16- hypothyroidism associated dementia

7.17. vitamin B 12

8. Step4: Hypothesis Organization

8.1. alzahimar disease

8.2. dementai with lowy body

9. Step5: Learning Objectives

9.1. 1- to know the definition of demintia pathophysiology and sign and symptoms

9.2. 2-To describe the normal anatomy and physiology of memory

9.3. 3- to know the definition of alzahimar pathophysiology and sign and symptoms

10. Step6: Review of learning obejectives

10.1. anatomy and physiology

10.1.1. declirative memory stored in the medial temporal lobe

10.1.2. nondeclirative is stored in the neocortex,etc.

10.1.3. the hippocampus structures it is started by the entorine gyrus then the dentate gureus followed by the sending some axons to the CA1 a prat of the hippocumpus then to the CA1 and eventually to the sabiculum

10.1.4. physiology the conseladation is the process by which we can store the information the long term memory

10.2. dementai

10.2.1. defined as progressive deteroratioon of cognetive function it has a lot of sign and symptoms which gathered in the word MEALS

10.2.2. reversaible depprestion alcholoism vit B1 hydrocephalus vit B12

10.2.3. the causes of dementai irreversible AD 60-70% vascular frontotemporal dementai with lowy body

10.2.4. the dementai is not a nortmal aging process of losing the memory it has a behavioral and mood problem

10.3. AD

10.3.1. rick factors Age female family history

10.3.2. protective factor smoking and high level of education

10.3.3. defined as progressive loss on the memory independent of the attention state

10.3.4. sign and symptoms loss of memory followed by the disability and imobility

10.3.5. patholophysiology mainly the deposition of the AB in the cytoplasm of the nerve cell through the nonamyiolginc pathway which invole the B and G secretase

11. step7 : inquiry plan

11.1. history

11.1.1. HPI SOCRATES she feels her old memory is better than her daughter she has some dificality in the rememabring the name of less familior people there is some gradual progression in the memory loss there is an interference with Daily actives

11.1.2. Family history um moammed parents die at a young ages

11.1.3. social history um mohammed is a retired house wife she has life in the same house with her husband for 45 her husband has a prostate cancer

11.1.4. past medical history nothing important

11.2. vital signs of the second visit

11.2.1. remarkable decrease in the standing BP

11.2.2. there is a inquiry about if she has a pnemonia

11.2.3. the remaining physical examination can not be performed because of the low level of cooperation

11.3. physical examination

11.3.1. vital signs appeared well T37 PR 90 BP 130/70 laying BP 115/65 standing

11.3.2. Neuro examination cognetive state not oriented in place and time she coulg copying a bentagon less than 22 the rest is normal

11.3.3. other physical examination is normal

11.4. investigation

11.4.1. CBC

11.4.2. electolites

11.4.3. imaging

11.4.4. thyroid function test

11.4.5. vitamins

12. step 8 : diagnosis

13. Step 9 : Review

14. Step 10 : Management

14.1. goal of management

14.1.1. there is no cureble treatment of AD

14.1.2. so only symptomatic treatmet

14.2. mamintine if the oatient has modrate to sever symptoms.

14.2.1. is a NMDA inhibitor

14.3. some patient wiould develop depression

14.3.1. so we will givw them a anti-depressive treatment

14.4. estrogen replacement therapy

14.4.1. is might increase the incedance of AD

14.4.2. it mignt increase the chance of developing cancer

14.5. non pharmacological management

14.5.1. observaing the patient

14.5.2. the environment especially in the kitchen and other part of the home

14.5.3. familly support

14.5.4. nursing house

14.5.5. rotien physical activities cardiopulmonary fittness

14.5.6. give them a rotien ,so they could be focus in their lifestyle

14.5.7. eveloation of their sycological staus

14.5.8. well educated person will have less incedance to have this disease so solving the pazzl will help to decrease the progression

14.5.9. patient education

14.5.10. discussion of the problem that those patient they can not judge things approprittly

14.6. in general the ACH is an important nerotransmittors in the brain,so the main treatment of AD is anticholanstraize inhebitor

14.6.1. when you start take one of theim and start solw and go slow

14.6.2. tacrine , revastagmine, dozpine, glantamine

14.6.3. it is effective in the decrease the progression of the disease , but without any curable effect

14.6.4. it might leed to fractures ,so they need a close monitor

14.7. for the behavior changes we give valoraic acid

14.8. the compination of both is better in the treatment of the modrate to sever form of the AD

14.9. diatery measure

14.9.1. medatrainan diet

14.10. preventive measure

14.10.1. such as alcohol and smoking

15. Step 11 : Feedback and resurces

15.1. devidson

15.2. kumar

15.3. medscape