Where Am I?

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Where Am I? por Mind Map: Where Am I?

1. dozapine dosage

2. shcu as revastagmin,

3. AD

4. Step6: Review of learning obejectives

4.1. anatomy and physiology

4.1.1. declirative memory stored in the medial temporal lobe

4.1.2. nondeclirative is stored in the neocortex,etc.

4.1.3. the hippocampus structures

4.1.3.1. 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

4.1.4. physiology

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

4.2. dementai

4.2.1. defined as progressive deteroratioon of cognetive function

4.2.1.1. it has a lot of sign and symptoms which gathered in the word MEALS

4.2.2. reversaible

4.2.2.1. depprestion

4.2.2.2. alcholoism

4.2.2.3. vit B1

4.2.2.4. hydrocephalus

4.2.2.5. vit B12

4.2.3. the causes of dementai

4.2.3.1. irreversible

4.2.3.1.1. AD 60-70%

4.2.3.1.2. vascular

4.2.3.1.3. frontotemporal

4.2.3.1.4. dementai with lowy body

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

4.3. AD

4.3.1. rick factors

4.3.1.1. Age

4.3.1.2. female

4.3.1.3. family history

4.3.2. protective factor

4.3.2.1. smoking

4.3.2.2. and high level of education

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

4.3.4. sign and symptoms

4.3.4.1. loss of memory followed by the disability and imobility

4.3.5. patholophysiology

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

5. step7 : inquiry plan

5.1. history

5.1.1. HPI

5.1.1.1. SOCRATES

5.1.1.1.1. she feels her old memory is better than her daughter

5.1.1.1.2. she has some dificality in the rememabring the name of less familior people

5.1.1.1.3. there is some gradual progression in the memory loss

5.1.1.1.4. there is an interference with Daily actives

5.1.2. Family history

5.1.2.1. um moammed parents die at a young ages

5.1.3. social history

5.1.3.1. um mohammed is a retired house wife

5.1.3.2. she has life in the same house with her husband for 45

5.1.3.3. her husband has a prostate cancer

5.1.4. past medical history

5.1.4.1. nothing important

5.2. vital signs of the second visit

5.2.1. remarkable decrease in the standing BP

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

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

5.3. physical examination

5.3.1. vital signs

5.3.1.1. appeared well

5.3.1.2. T37

5.3.1.3. PR 90

5.3.1.4. BP 130/70 laying

5.3.1.5. BP 115/65 standing

5.3.2. Neuro examination

5.3.2.1. cognetive state

5.3.2.1.1. not oriented in place and time

5.3.2.1.2. she coulg copying a bentagon

5.3.2.1.3. less than 22

5.3.2.2. the rest is normal

5.3.3. other physical examination is normal

5.4. investigation

5.4.1. CBC

5.4.2. electolites

5.4.3. imaging

5.4.4. thyroid function test

5.4.5. vitamins

6. step 8 : diagnosis

7. Step 9 : Review

8. Step 10 : Management

8.1. goal of management

8.1.1. there is no cureble treatment of AD

8.1.2. so only symptomatic treatmet

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

8.2.1. is a NMDA inhibitor

8.3. some patient wiould develop depression

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

8.4. estrogen replacement therapy

8.4.1. is might increase the incedance of AD

8.4.2. it mignt increase the chance of developing cancer

8.5. non pharmacological management

8.5.1. observaing the patient

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

8.5.3. familly support

8.5.4. nursing house

8.5.5. rotien physical activities

8.5.5.1. cardiopulmonary fittness

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

8.5.7. eveloation of their sycological staus

8.5.8. well educated person will have less incedance to have this disease

8.5.8.1. so solving the pazzl will help to decrease the progression

8.5.9. patient education

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

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

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

8.6.2. tacrine , revastagmine, dozpine, glantamine

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

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

8.7. for the behavior changes we give valoraic acid

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

8.9. diatery measure

8.9.1. medatrainan diet

8.10. preventive measure

8.10.1. such as alcohol and smoking

9. Step 11 : Feedback and resurces

9.1. devidson

9.2. kumar

9.3. medscape

10. Trigger Text

10.1. 1

10.1.1. 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

10.2. 2

10.2.1. 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

11. Step1: Identify cues

11.1. Difficult words

11.1.1. no words

11.2. Cues

11.2.1. 1- 80 years old female

11.2.2. 2- brought by her daughter

11.2.3. 3- forgetfulness over the last year

11.2.3.1. At time not aware of day and date

11.2.3.2. long term memory is intact

11.2.3.3. the loss of the memory is gradual and progressive

11.2.4. 4- her husband health is deteriorating

12. Sep2: problem Formulation

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

13. Step3: Hypothesis Generation

13.1. 1- learning and memory

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

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

13.1.3. bapis circuit of the memory

13.1.4. mamilary body

13.1.5. amegdula

13.1.6. hypocampus

13.2. 2-the medical term for forgetfulness is amnesia

13.2.1. the definition of the memory

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

13.2.1.2. the second componant in the storing of the information

13.2.1.3. the third is the retreaval the information

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

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

13.3. 3- one of the causes is the accumulation of protein within the brain cytoplasm

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

13.4. 4-infection by herpis simplex in the temporal lobe

13.5. 5- as aging process occur, their will be a neuropalstisity

13.6. 6- new memory build up

13.6.1. an increase between the wiring and connection of the neurons

13.6.1.1. the AMDA and NAMD receptors are involved in this process

13.7. 7- the problem might be specifically within the storage part of memory process.

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

13.8. 8- vascular injury to the brain such as multi infarct dementia

13.9. 9- Huntington disease would develop dementia later in the disease

13.10. 10- iatrogenic caused by using drug,like the benzodiazpin, B-blocker, atropin derivatives and IV drud abuse

13.11. 11- alcohol consumption leading to worcis korsicoof syndrome

13.12. 12- frontotemporal dementia

13.13. 13- depression might lead to psudodementia

13.14. 14- mass occupying lesion (Tumor) near to the temporal lobe. However it is unlikely

13.15. 15- Multiple sclerosis

13.16. 16- hypothyroidism associated dementia

13.17. vitamin B 12

14. Step4: Hypothesis Organization

14.1. alzahimar disease

14.2. dementai with lowy body

15. Step5: Learning Objectives

15.1. 1- to know the definition of demintia pathophysiology and sign and symptoms

15.2. 2-To describe the normal anatomy and physiology of memory

15.3. 3- to know the definition of alzahimar pathophysiology and sign and symptoms