GOing down hill

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GOing down hill by Mind Map: GOing down hill

1. step one

1.1. difficult words

1.1.1. plump: obese

1.1.2. flustered: confused

1.1.3. dappled: spotted

1.2. cues

1.2.1. male; 4th decade

1.2.2. fat

1.2.3. closed eyes and ehauxted

1.2.4. exahusted

1.2.5. flustered

1.2.6. discolerd dappled ankles

1.2.7. pitting edema

1.2.8. 2 year onset

1.2.9. breathlessness on exertion for few monthes

1.2.10. medical attention not sought inintially

1.2.11. dyspnea worsened

1.2.12. gain weight

1.2.13. swollen ankle

1.2.14. sleep troubled

1.2.15. orhtopnea

2. step2

2.1. problem formulation: an obese man in his forties presented with breathlessness for the last two years which has been worsened recently; associated with ankle swelling and weight gain. he can't sleep flat.

3. step3

3.1. hypothesis generation:

3.1.1. edema is due to undermined hydrostatic pressure or oncotic one

3.1.2. heart problem or failure

3.1.3. renal problem

3.1.4. infection

3.1.5. breathlessness is due to heart failure oe weakness; v\q mismatch

3.1.6. hyperlipedimia: precipitate in heart failure

3.1.7. gaining weight could be the cause. or just a symptom

3.1.8. lung problem

3.1.9. bilatiral edema: kidney, lung, or heart disease.

3.1.10. heart is overwhelmed

3.1.11. dyspnea: obsteructive, distructive or hemoblobin problem.

3.1.12. left sided problem cause pulmunary edema.

3.1.13. CHF causing pulmonary or generalised edema

3.1.14. DVT as underlying cause

3.1.15. OSA as underlying cause

3.1.16. AI good pasture syndrome

3.1.17. Anemia

3.1.18. CHF causing pulmonary or generalised edema

3.2. hypothesis generation:

3.3. hypothesis generation:

4. step4

4.1. hypothesis organisation

4.1.1. Primary problems

4.1.1.1. hypertention

4.1.1.2. Kidney faailure

4.1.1.3. hyperlipidemia

4.1.1.4. lung problems

4.1.1.4.1. COPD

4.1.1.5. OSA

4.1.1.6. Anemia

4.1.1.7. Good Pasture

4.1.2. Secondary manifestations

4.1.2.1. CHF

4.1.2.2. edema

5. step5

5.1. OBJECTIVES

5.1.1. to describe the pathophysiology of developing edema (consider the causes).

5.1.2. to learn about CHF(causes -pathophysiology manifestations- risk factors- infestgations)

6. step6

6.1. revision

6.1.1. EDEMA

6.1.1.1. edema develop from hydrostatic pressure

6.1.1.1.1. volume increase

6.1.1.1.2. venous obstruction

6.1.1.2. types

6.1.1.2.1. transudate

6.1.1.2.2. exudate

6.1.1.3. other cassification

6.1.1.3.1. inflammtory

6.1.1.3.2. non-inflammatory

6.1.2. CHF

6.1.2.1. CAUSES

6.1.2.1.1. left venticular dysfunction

6.1.2.1.2. incresed afterload

6.1.2.1.3. valvular disease

6.1.2.1.4. COPD

6.1.2.1.5. OSA

6.1.2.1.6. IHD

6.1.2.1.7. CARDIOMYOPATHY

6.1.2.1.8. thyroid diseas

6.1.2.1.9. main causees

6.1.2.2. PATHOPHYSIOLOGY

6.1.2.2.1. low stroke volume

6.1.2.2.2. less ejection volume

6.1.2.2.3. franksarling mechanism to compensate

6.1.2.2.4. RAAS to compansate

6.1.2.3. manifestaions

6.1.2.3.1. pulmonary edema

6.1.2.3.2. DYSPNEA

6.1.2.3.3. orthpnea

6.1.2.3.4. fatique

6.1.2.3.5. cardiomegaly

6.1.2.4. risk factors

6.1.2.4.1. hyperlipidemia

6.1.2.4.2. diabetes

6.1.2.4.3. hypertension

6.1.2.4.4. smoking

6.1.2.4.5. family history

6.1.2.5. infestigations

6.1.2.5.1. cbc

6.1.2.5.2. BNP

6.1.2.5.3. CXR

6.1.2.6. definition

6.1.2.6.1. inabilily to pump suffeceint amount of blood

7. step7

7.1. inquiry plan

7.1.1. HISTORY

7.1.1.1. SMOKER 20C\D

7.1.1.2. alchohol 5 cups

7.1.1.3. appendectomy - tosillectomy

7.1.1.4. married

7.1.1.5. chronic cough with grey sputum

7.1.1.6. seasonal infections

7.1.2. examination

7.1.2.1. height 173

7.1.2.2. w: 100 kg

7.1.2.3. 36.7 c

7.1.2.4. 120\70 mmgh laying

7.1.2.5. RR: 30\m

7.1.2.6. can't lay flat

7.1.2.7. JVP=6

7.1.2.8. 100 beats\m

7.1.2.9. 3cm liver below CM

7.1.2.10. 3rd HS

7.1.2.11. systolic murmer

7.1.2.12. basal carackles

7.1.3. D

8. step8

8.1. diagnostic dicision

8.1.1. CHF

8.2. objectives

8.2.1. management of CHF

9. step9

9.1. revision

10. step10

10.1. managmement

10.1.1. pharma

10.1.1.1. diureteics

10.1.1.1.1. furosomide

10.1.1.1.2. metolazone

10.1.1.1.3. SE

10.1.1.1.4. no effect on survival

10.1.1.2. ACEI

10.1.1.2.1. IMPROVE SURVIVAL

10.1.1.2.2. NOT BEFORE DIURETICS

10.1.1.2.3. SMALL DOSES

10.1.1.2.4. SE

10.1.1.3. beta-blocker

10.1.1.3.1. inhibit remodeling

10.1.1.3.2. relive heart mouscle

10.1.1.3.3. beta 1 selective

10.1.1.3.4. improve mortaltity

10.1.1.4. spirolactone

10.1.1.4.1. improve mortality

10.1.1.5. angiotensin II receptor antagonist

10.1.1.5.1. candesartan

10.1.1.5.2. no cough

10.1.1.6. acute setting

10.1.1.6.1. morphin

10.1.1.7. digoxin

10.1.1.7.1. not primary considered

10.1.1.8. evapridin

10.1.1.8.1. block calcium channel

10.1.1.9. nitrates

10.1.2. non pharma

10.1.2.1. dietary restriction

10.1.2.1.1. low salt

10.1.2.2. weight reduction

10.1.2.2.1. our pt

10.1.2.3. alchohol abstenence

10.1.2.3.1. our pt

10.1.2.4. smoking cessation

10.1.2.4.1. our pt

10.1.2.5. education

10.1.2.5.1. weight and dose and diet

10.1.2.6. devises

10.1.2.6.1. AICD

10.1.2.6.2. pacemaker

10.1.2.6.3. remodeling devises

10.1.2.7. heart transplant

10.1.2.7.1. NOT gold standard

10.1.2.7.2. comlication

10.1.2.7.3. usually ypunger pt

10.1.2.7.4. not for our pt

10.1.2.8. valvular repair

10.1.2.9. exercise

10.1.3. classification of severity

10.1.3.1. NYHA

10.1.3.1.1. class 1

10.1.3.1.2. class 2

10.1.3.1.3. class 3

10.1.3.1.4. class4

10.1.4. goals

10.1.4.1. control symptoms

10.1.4.2. prevent complication

10.1.4.3. increase survival

11. resourecses and feddback

11.1. cumar

11.2. sherwede

11.3. myoclininc

11.4. e.medicine

11.5. robbin

11.6. uptodate

11.7. abo ossa's lecture