Dec 23, 2007
Nov 29, 2007
Nov 28, 2007
면역반응
면역반응은 임파구에 의해 이루어집니다.
임파구에는 세가지의 종류가 있습니다.
1. B임파구 2. T임파구 3. Null cell
우선 첫째 Null cell 에 대한 설명입니다.
Null cell은 Nutural Killer cell(=NK cell=자연살해세포)와
Antibody Dependent Cytotoxic Cell(ADCC, K-cell)로 나뉘며 5%의 비율로 존재합니다.
Nutural Killer cell(=NK cell=자연살해세포)는
항원에 감작(노출되었다는 뜻으로 보면 됩니다) 된 적이 없는데도
(보통 항원과 만난 후 다음에 또 만나면 그 항원을 알아보고 파괴할려고 덤비죠?)
종양세포, 감염세포, 기타 이물질을 파괴하는 기능을 합니다.
(자연살해세포는 주로 여자들에게 더 많습니다. 그래서 기본적인 저항력이 여자가 더 강하다고 할 수 있습니다.)
Antibody Dependent Cytotoxic Cell(ADCC, K-cell) 는 항체와 결합되어 있는
이물질을 제거하는 역할을 합니다.
(항원에 노출되면 항체가 결합하게 되는데 그것을 제거하는 것을 말합니다.)
둘째 B임파구 에 대한 설명입니다.
B임파구는 순환하지 않고 25% 임파계에 존재하면서 체액면역을 담당합니다.
B임파구는 골수의 간세포에서 만들어져서 Bursa상동기관에서 성숙 (임파선, 편도선,
장, 골수, 간과 같은 기관에서 어른이 되기 위해 성장한다는 말입니다.) 하고 항원과
결합하여, 감작 B임파구가 됩니다. 여기서 혈장세포와 기억세포로 분화하게 됩니다.
혈장세포는 T임파구의 도움 (밑에서 나오겠지만 T4=TH세포, 즉 보조T임파구를 말합니다.)
을 받아 많은 항체를 생산하여 항원에 대한 항체를 생산하여 항원을 무력하게 하는
반응, 즉 체액면역을 담당합니다.
(여기서 주의해야 할 점은 직접! 항체가 면역을 담당하는 것이 아니란겁니다)
그리고 기억세포 는 임파절에 저장되어 있으면서 조상이 만난 항원을 기억하고 있다가
똑같은 항원이 들어오면 빠르게 혈장세포로 전환합니다.( 임파절에 숨어있다가 전에
만났던 항원녀석을 기억하고 있다가 다시 똑같은 놈이 들어오면 재빠르게 혈장세포로
변신하는거죠^^;)
B임파구의 종류는 다음과 같습니다.
1) IgG : 80% 세포외액에 다량 존재하며, 면역반응 후기에 생산됩니다(2차반응), 보체
활성, 태반통과 (태반을 통과하므로 엄마로부터 유전이 되는 임파구라 할 수 있습니
다.)
2) IgM : 6% 혈관내 존재하며 면역반응 초기에 생산됩니다 .(1차반응)(이것은 유일하
게 T임파구의 도움없이 생산 가능한 임파구로 신생아가 가지고 있습니다.)
3) IgA : 13% 인체의 분비물에 존재하여 점막표면을 보호합니다 .(눈물, 침, 장액, 기
관지액 등에 존재합니다. 그래서 아마 상처가 나면 침묻혀라~라는 소리가 나왔는지도
모르겠군요.)
4) IgD : 1% 임파구 표면에 소량 위치하며 정확한 기능은 모릅니다.. 아동의 우유에 대한 과민반응시 나타난다고 합니다.
5) IgE : 0.002% 혈청내 존재하며 알러지 반응을 유발합니다.
셋째 T임파구에 대한 설명입니다.
T임파구는 70%로 혈중에 순환하며 직접면역(세포면역) 을 담당합니다.
골수의 간세포에서 생산되어 흉선에서 성숙하고 항원과 결합하여 감작T임파구에서 주
효세포로 분화되어 직접 면역반응에 관여하게 됩니다 .(B임파구와 자라는 기관만 틀리
고 비슷합니다.)
주효세포는 다음과 같습니다.
1) Memory T cell = Delayed T cell(T1= TD) < /STRONG> : 임파절에 남아있다가 똑같은 항원이 들
어오면 즉시 반응력 있는 다른 세포로 전환합니다 .(꼭 B임파구에서 기억세포와 비슷하
죠?)
2) Killer T cell = Cytotoxic T cell(T2= TC) < /STRONG> : 직접 항원을 죽일 수 있는 독성물질
을 방출하여 항원을 죽입니다.
3) Suppressor Tcell(T3=TS=억제T임파구)
세포성, 체액성 면역을 적절한 시기에 종식시키는 일 (목적달성을 했는데도 계속 면역
반응이 일어나면 곤란하겠지요? 그것을 중단시키는 역할을 합니다.) 을 하며 Helper T
cell(보조T임파구=TH)에 의해 활성화됨
4) Helper Tcell(T4=TH=보조T임파구=>CD4양성T림프구)
다른 T cell, B cell에 작용하여 면역을 촉진합니다 . 그리고 MIF, MAF를 분비하여 대
식세포 활동을 조절하고 InterleukinⅡ를 방출합니다.
그 이외에도 항원표현세포(항체가 항원을 알아보도록 표시한다고 할 수 있죠), 세포성
면역반응매개물질 로 여러 가지가 있습니다.
임파구에는 세가지의 종류가 있습니다.
1. B임파구 2. T임파구 3. Null cell
우선 첫째 Null cell 에 대한 설명입니다.
Null cell은 Nutural Killer cell(=NK cell=자연살해세포)와
Antibody Dependent Cytotoxic Cell(ADCC, K-cell)로 나뉘며 5%의 비율로 존재합니다.
Nutural Killer cell(=NK cell=자연살해세포)는
항원에 감작(노출되었다는 뜻으로 보면 됩니다) 된 적이 없는데도
(보통 항원과 만난 후 다음에 또 만나면 그 항원을 알아보고 파괴할려고 덤비죠?)
종양세포, 감염세포, 기타 이물질을 파괴하는 기능을 합니다.
(자연살해세포는 주로 여자들에게 더 많습니다. 그래서 기본적인 저항력이 여자가 더 강하다고 할 수 있습니다.)
Antibody Dependent Cytotoxic Cell(ADCC, K-cell) 는 항체와 결합되어 있는
이물질을 제거하는 역할을 합니다.
(항원에 노출되면 항체가 결합하게 되는데 그것을 제거하는 것을 말합니다.)
둘째 B임파구 에 대한 설명입니다.
B임파구는 순환하지 않고 25% 임파계에 존재하면서 체액면역을 담당합니다.
B임파구는 골수의 간세포에서 만들어져서 Bursa상동기관에서 성숙 (임파선, 편도선,
장, 골수, 간과 같은 기관에서 어른이 되기 위해 성장한다는 말입니다.) 하고 항원과
결합하여, 감작 B임파구가 됩니다. 여기서 혈장세포와 기억세포로 분화하게 됩니다.
혈장세포는 T임파구의 도움 (밑에서 나오겠지만 T4=TH세포, 즉 보조T임파구를 말합니다.)
을 받아 많은 항체를 생산하여 항원에 대한 항체를 생산하여 항원을 무력하게 하는
반응, 즉 체액면역을 담당합니다.
(여기서 주의해야 할 점은 직접! 항체가 면역을 담당하는 것이 아니란겁니다)
그리고 기억세포 는 임파절에 저장되어 있으면서 조상이 만난 항원을 기억하고 있다가
똑같은 항원이 들어오면 빠르게 혈장세포로 전환합니다.( 임파절에 숨어있다가 전에
만났던 항원녀석을 기억하고 있다가 다시 똑같은 놈이 들어오면 재빠르게 혈장세포로
변신하는거죠^^;)
B임파구의 종류는 다음과 같습니다.
1) IgG : 80% 세포외액에 다량 존재하며, 면역반응 후기에 생산됩니다(2차반응), 보체
활성, 태반통과 (태반을 통과하므로 엄마로부터 유전이 되는 임파구라 할 수 있습니
다.)
2) IgM : 6% 혈관내 존재하며 면역반응 초기에 생산됩니다 .(1차반응)(이것은 유일하
게 T임파구의 도움없이 생산 가능한 임파구로 신생아가 가지고 있습니다.)
3) IgA : 13% 인체의 분비물에 존재하여 점막표면을 보호합니다 .(눈물, 침, 장액, 기
관지액 등에 존재합니다. 그래서 아마 상처가 나면 침묻혀라~라는 소리가 나왔는지도
모르겠군요.)
4) IgD : 1% 임파구 표면에 소량 위치하며 정확한 기능은 모릅니다.. 아동의 우유에 대한 과민반응시 나타난다고 합니다.
5) IgE : 0.002% 혈청내 존재하며 알러지 반응을 유발합니다.
셋째 T임파구에 대한 설명입니다.
T임파구는 70%로 혈중에 순환하며 직접면역(세포면역) 을 담당합니다.
골수의 간세포에서 생산되어 흉선에서 성숙하고 항원과 결합하여 감작T임파구에서 주
효세포로 분화되어 직접 면역반응에 관여하게 됩니다 .(B임파구와 자라는 기관만 틀리
고 비슷합니다.)
주효세포는 다음과 같습니다.
1) Memory T cell = Delayed T cell(T1= TD) < /STRONG> : 임파절에 남아있다가 똑같은 항원이 들
어오면 즉시 반응력 있는 다른 세포로 전환합니다 .(꼭 B임파구에서 기억세포와 비슷하
죠?)
2) Killer T cell = Cytotoxic T cell(T2= TC) < /STRONG> : 직접 항원을 죽일 수 있는 독성물질
을 방출하여 항원을 죽입니다.
3) Suppressor Tcell(T3=TS=억제T임파구)
세포성, 체액성 면역을 적절한 시기에 종식시키는 일 (목적달성을 했는데도 계속 면역
반응이 일어나면 곤란하겠지요? 그것을 중단시키는 역할을 합니다.) 을 하며 Helper T
cell(보조T임파구=TH)에 의해 활성화됨
4) Helper Tcell(T4=TH=보조T임파구=>CD4양성T림프구)
다른 T cell, B cell에 작용하여 면역을 촉진합니다 . 그리고 MIF, MAF를 분비하여 대
식세포 활동을 조절하고 InterleukinⅡ를 방출합니다.
그 이외에도 항원표현세포(항체가 항원을 알아보도록 표시한다고 할 수 있죠), 세포성
면역반응매개물질 로 여러 가지가 있습니다.
Jun 6, 2007
bone tumor
age dependent tumor
;osteosarcoma, euing sarcoma, metastatic tumor
FCD(4-8세), NOF(older) 는 같은 pathology, age에 따라 나눔
site dependent
;epi : chondroblastoma, eosinophilic granuloma
dia : Ewing sarcoma, NOF, enchondroma, fibrous dysplasia
meta : 대부분
central : enchondroma, SBC, fibrous dysplasia
cortical : osteoid osteoma(nidus), NOF
giant cell tumor와 chondroblastoma는 epiphyseal plate로 구분
Ewing vs. osteomyelitis
chondrosarcoma vs. simple bone cyst
osteochondroma : exophytic
;osteosarcoma, euing sarcoma, metastatic tumor
FCD(4-8세), NOF(older) 는 같은 pathology, age에 따라 나눔
site dependent
;epi : chondroblastoma, eosinophilic granuloma
dia : Ewing sarcoma, NOF, enchondroma, fibrous dysplasia
meta : 대부분
central : enchondroma, SBC, fibrous dysplasia
cortical : osteoid osteoma(nidus), NOF
giant cell tumor와 chondroblastoma는 epiphyseal plate로 구분
Ewing vs. osteomyelitis
chondrosarcoma vs. simple bone cyst
osteochondroma : exophytic
May 28, 2007
Acute appendicitis
Pathophysiology
Luminal obstruction
(viral infection -> inflammatory ulceration of mucosa -> enlarged lymphoid follicles or fecalith)
-> Secretion of mucus
-> Distends the organ
-> Venous engorgement & arterial compromise
-> Gangrene and perforation
Luminal obstruction
(viral infection -> inflammatory ulceration of mucosa -> enlarged lymphoid follicles or fecalith)
-> Secretion of mucus
-> Distends the organ
-> Venous engorgement & arterial compromise
-> Gangrene and perforation
Positive effect of smoking
Sarcoidosis
Ulcerative colitis
Diabetes melitus
Gestational hypertension
Osteoporosis
Ulcerative colitis
Diabetes melitus
Gestational hypertension
Osteoporosis
Apr 29, 2007
Apr 18, 2007
lung segment
RIGHT LUNGSuperior lobe
apical
posterior
anterior
Middle love
lateral
medial
Lower lobe
superior
anterior
medial
lateral
posterior
LEFT LUNG
Superior lobe
apical
posterior
anterior
superior
inferior
Inferior lobe
superoir
anterior basal
medial basal
lateral basal
posterior basal
Apr 16, 2007
HF, MI treatment
HF
+ACEi
-ARB
+diuretics(spironolactone)
+B-blockers
-digitalis
-dopamine
+vasodilators(hydralazine)
-anticoagulant
Stable angina
-nitrate
-B-blockers
-calcium channel blocker
-antiplatelet agents
-ACEi
Unstable angina
-nitrate
-B-blocker
-calcium channel blocker
-ACEi
-statins
-morphine
-aspirin, heparin
Variant angina
-calcium channel blocker
-nitrate
-prazocin
MI
-nitroglycerin
-morphine
+B-blocker
+ACEi
+aspirin
*NSTEMI 에서는 thrombolytics 쓰지 않음
+ACEi
-ARB
+diuretics(spironolactone)
+B-blockers
-digitalis
-dopamine
+vasodilators(hydralazine)
-anticoagulant
Stable angina
-nitrate
-B-blockers
-calcium channel blocker
-antiplatelet agents
-ACEi
Unstable angina
-nitrate
-B-blocker
-calcium channel blocker
-ACEi
-statins
-morphine
-aspirin, heparin
Variant angina
-calcium channel blocker
-nitrate
-prazocin
MI
-nitroglycerin
-morphine
+B-blocker
+ACEi
+aspirin
*NSTEMI 에서는 thrombolytics 쓰지 않음
ARDS diagnostic criteria
1. Acute onset
2. Pulmonary artery wedge pressure
3. Bilateral infiltrates on chest radiography
4. Acute respiratory distress syndrome is present if Pao2/Fio2 ratio
*Acute lung injury (ALI) is present if Pao2/Fio2 ratio is
2. Pulmonary artery wedge pressure
3. Bilateral infiltrates on chest radiography
4. Acute respiratory distress syndrome is present if Pao2/Fio2 ratio
*Acute lung injury (ALI) is present if Pao2/Fio2 ratio is
Apr 9, 2007
Hemiplegia와 Hemiparesis
* Define hemiplegia and distinguish it from hemiparesis.
* Differentiate between spastic hemiparesis and flacid hemiparesis.
Hemiplegia is total paralysis of the arm, leg, and trunk on the same side of the body, whereas hemiparesis is weakness on one side of the body. The most common cause is stroke. The paralysis presents as weakness which may be present with abnormal tone (e.g. rigidity or spasticity). In the stance phase, leg instability (i.e. knee buckling or hyperextension) may make walking unsafe, energy inefficient, and/or painful. During swing phase inadequate limb clearance, sensory deficits, impaired balance, and/or pain may contribute to loss of balance, falls, and increased anxiety associated with walking. There is a loss of motor control that prevents the patient from precisely controlling the timing and intensity of muscle action. The ability to compensate for this lack of control is best in hemiplegia compared to other central neurological lesions because one side of the body is entirely intact (Perry, 181).
The phases of the gait cycle are altered dramatically in hemiplegia. Spasticity and/or weakness are the main causes of limb deformity that interfere with walking in hemiparesis, and the degree of impairment depends on the magnitude of the neurological deficit.
In spastic hemiparesis the leg is swung in a semi-circle from the hip with the pelvis tilted upward and the hip abducted. The knee may hyperextend due to inappropriate quadriceps activity. This stiff knee gait inhibits limb advancement and deprives the patient of shock-absorbing knee flexion during weight acceptance. The ankle excessively plantar flexes and may invert (equinovarus). The arm may be held flexed and adducted with minimal swing. In milder cases, some patients may only lose the arm swing and the foot may scrape the floor.
Equinovarus (inversion) is the most common pathologic lower limb posture in hemiparetic patients. Contact with the ground occurs with the forefoot first and weight is placed mostly on the lateral border of the foot, often with toe flexion. During the swing phase, the plantarflexion and inversion of the foot is continued resulting in problematic toe clearance (Craik, 414).
If spasticity is not present, there is excess hip and knee flexion during mid swing in order to ensure foot clearance. The terminal swing and loading response phases are lost because the flexor activity during limb advancement changes to excess extensor activity during weight acceptance. There is premature relaxation of tibialis anterior as well as premature activation of soleus. The result is a gait that is similar to marching on tip-toes on the effected side.
The overall results of the compensatory movements generated by the hemiparetic patient include a decrease in walking velocity with a shorter duration of stance phase, decreased weight bearing, and increased swing time for the affected leg. The unaffected leg has an increased stance time and decreased step length.
Dropfoot may be the only indication of a mildly hemiplegic stroke patient. The cause is impaired selective control of ankle dorsiflexors which results in excessive plantar flexion with an otherwise normal gait. Mid swing is the phase where the abnormality is most apparent. The excessively plantar flexed ankle causes a toe drag or the patient compensates by increasing flexion at the hip and knee (Perry, 314).
Compensatory movements used by hemiplegic patients during walking produce abnormal displacement of the center of gravity, resulting in increased energy expenditure. The oxygen consumption of hemiplegic patients at various walking speeds was found to be 64% higher than in normal elderly at the same speed. The unassisted comfortable walking speeds of hemiplegic patients were on average 46% slower than normals. Because of the significant decrease in walking speed of hemiplegic patients, the oxygen consumption rate at comfortable walking speeds is lower than normal despite the inefficiency of the hemiplegic gait pattern. When the hemiplegic patients used metal short leg braces their oxygen consumption dropped to 54% above normal and their walking speed increased to 39% below normal (Spivek, 319).
* Differentiate between spastic hemiparesis and flacid hemiparesis.
Hemiplegia is total paralysis of the arm, leg, and trunk on the same side of the body, whereas hemiparesis is weakness on one side of the body. The most common cause is stroke. The paralysis presents as weakness which may be present with abnormal tone (e.g. rigidity or spasticity). In the stance phase, leg instability (i.e. knee buckling or hyperextension) may make walking unsafe, energy inefficient, and/or painful. During swing phase inadequate limb clearance, sensory deficits, impaired balance, and/or pain may contribute to loss of balance, falls, and increased anxiety associated with walking. There is a loss of motor control that prevents the patient from precisely controlling the timing and intensity of muscle action. The ability to compensate for this lack of control is best in hemiplegia compared to other central neurological lesions because one side of the body is entirely intact (Perry, 181).
The phases of the gait cycle are altered dramatically in hemiplegia. Spasticity and/or weakness are the main causes of limb deformity that interfere with walking in hemiparesis, and the degree of impairment depends on the magnitude of the neurological deficit.
In spastic hemiparesis the leg is swung in a semi-circle from the hip with the pelvis tilted upward and the hip abducted. The knee may hyperextend due to inappropriate quadriceps activity. This stiff knee gait inhibits limb advancement and deprives the patient of shock-absorbing knee flexion during weight acceptance. The ankle excessively plantar flexes and may invert (equinovarus). The arm may be held flexed and adducted with minimal swing. In milder cases, some patients may only lose the arm swing and the foot may scrape the floor.
Equinovarus (inversion) is the most common pathologic lower limb posture in hemiparetic patients. Contact with the ground occurs with the forefoot first and weight is placed mostly on the lateral border of the foot, often with toe flexion. During the swing phase, the plantarflexion and inversion of the foot is continued resulting in problematic toe clearance (Craik, 414).
If spasticity is not present, there is excess hip and knee flexion during mid swing in order to ensure foot clearance. The terminal swing and loading response phases are lost because the flexor activity during limb advancement changes to excess extensor activity during weight acceptance. There is premature relaxation of tibialis anterior as well as premature activation of soleus. The result is a gait that is similar to marching on tip-toes on the effected side.
The overall results of the compensatory movements generated by the hemiparetic patient include a decrease in walking velocity with a shorter duration of stance phase, decreased weight bearing, and increased swing time for the affected leg. The unaffected leg has an increased stance time and decreased step length.
Dropfoot may be the only indication of a mildly hemiplegic stroke patient. The cause is impaired selective control of ankle dorsiflexors which results in excessive plantar flexion with an otherwise normal gait. Mid swing is the phase where the abnormality is most apparent. The excessively plantar flexed ankle causes a toe drag or the patient compensates by increasing flexion at the hip and knee (Perry, 314).
Compensatory movements used by hemiplegic patients during walking produce abnormal displacement of the center of gravity, resulting in increased energy expenditure. The oxygen consumption of hemiplegic patients at various walking speeds was found to be 64% higher than in normal elderly at the same speed. The unassisted comfortable walking speeds of hemiplegic patients were on average 46% slower than normals. Because of the significant decrease in walking speed of hemiplegic patients, the oxygen consumption rate at comfortable walking speeds is lower than normal despite the inefficiency of the hemiplegic gait pattern. When the hemiplegic patients used metal short leg braces their oxygen consumption dropped to 54% above normal and their walking speed increased to 39% below normal (Spivek, 319).
Apr 6, 2007
Where The Wild Roses Grow
Nick Cave & Kylie Minogue
[Murder ballads - Where the wild roses grow]
[Murder ballads - Where the wild roses grow]
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
From the first day I saw her I knew she was the one
As she stared in my eyes and smiled
For her lips were the colour of the roses
They grew down the river, all bloody and wild
When he knocked on my door and entered the room
My trembling subsided in his sure embrace
He would be my first man, and with a careful hand
He wiped the tears that ran down my face
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
On the second day I brought her a flower
She was more beautiful than any woman I'd seen
I said, "Do you know where the wild roses grow
So sweet and scarlet and free?"
On the second day he came with a single rose
Said, "Will you give me your loss and your sorrow?"
I nodded my head, as I lied on the bed
He said, "If I show you the roses will you follow?"
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
On the third day he took me to the river
He showed me the roses and we kissed
And the last thing I heard was a muttered word
As he stood smiling above me with a rock in his fist
On the last day I took her where the wild roses grow
And she lay on the bank, the wind light as a thief
As I kissed her goodbye, I said, "All beauty must die"
And lent down and planted a rose between her teeth
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
For my name was Elisa Day
For my name was Elisa Day
카일리 미노그의 보이스가 정말 인상적인 중독성 강한 곡.
첫남자에게 돌로 맞아 죽은 여자 이야기를 이렇게 아름답게 풀어낼 수 있을까.
들어보라고 하고 싶은 노랜데..
마릴린 맨슨 불타는 사진 올리고 분신 자살한 친구 얘기에
말이 나오다 쏙 들어가버렸다.
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
From the first day I saw her I knew she was the one
As she stared in my eyes and smiled
For her lips were the colour of the roses
They grew down the river, all bloody and wild
When he knocked on my door and entered the room
My trembling subsided in his sure embrace
He would be my first man, and with a careful hand
He wiped the tears that ran down my face
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
On the second day I brought her a flower
She was more beautiful than any woman I'd seen
I said, "Do you know where the wild roses grow
So sweet and scarlet and free?"
On the second day he came with a single rose
Said, "Will you give me your loss and your sorrow?"
I nodded my head, as I lied on the bed
He said, "If I show you the roses will you follow?"
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
On the third day he took me to the river
He showed me the roses and we kissed
And the last thing I heard was a muttered word
As he stood smiling above me with a rock in his fist
On the last day I took her where the wild roses grow
And she lay on the bank, the wind light as a thief
As I kissed her goodbye, I said, "All beauty must die"
And lent down and planted a rose between her teeth
They call me the wild rose
But my name was Elisa Day
Why they call me it I do not know
For my name was Elisa Day
For my name was Elisa Day
For my name was Elisa Day
카일리 미노그의 보이스가 정말 인상적인 중독성 강한 곡.
첫남자에게 돌로 맞아 죽은 여자 이야기를 이렇게 아름답게 풀어낼 수 있을까.
들어보라고 하고 싶은 노랜데..
마릴린 맨슨 불타는 사진 올리고 분신 자살한 친구 얘기에
말이 나오다 쏙 들어가버렸다.
Apr 5, 2007
Pulmonary function test
1. 폐활량 측정법(Spirometry)
-RV(residual volume): 잔기량
-IRV(inspiratory reserve volume): 흡기 예비기량
-ERV(expiratory reserve volume): 호기 예비기량
-VC(vital capacity): 폐활량
-IC(inspiratory capacity): 흡기용량
-FRC(functional residual capacity): 기능성 잔기용량, chest wall의 compliance와 lung elastic recoil이 같아서 평형을 이루는 lung volume
-TLC(total lung capacity): 총폐용량
-TLC=IC +FRC=VC +RV
-RV은 spirometry만으로는 측정 불가능
a. 노력성 폐활량(forced vital capacity, FVC)
-제한성폐질환의 지표
b. 1초간 노력성 호기(forced expiratory volume at 1sec, FEV₁)
-폐쇄성폐질환의 지표
c. FEV₁/FVC
d. 노력성 호기 중간유량(forced mid-expiratory flow, FEF25~75%)
-노력성 호기량의 중간부분 50%의 평균속도(maximal mid-expiratory flow rate)
-환자의 노력과 가장 관계없는 부분
-small airway dz의 조기 진단에 민감
-정상인에서도 많은 변이성을 보이므로 재현성은 떨어짐
e. 최대 호기유속(peak expiratory flow rate, PEFP)
-곡선에서 가장 경사가 가파른 부분
-central large airway 폐쇄시 이상소견을 보임
-운동능력 및 수술전후의 평가에 이용
-PaCO₂: arterial CO₂tension
-PeCO₂: mean expired CO₂tension
-정상인의 anatomical dead space 호흡량은 TV의 약 30%(1회 호흡량의 70%만 alveolar zone에 도달)
-physiologic dead space: 혈류가 흐르지 않는 폐포 공간(TV의 약 36%)
-제한성 환기장애: FEV₁/FVC 증가, FVC가 주로 감소
-restrictive(parenchymal): sarcoidosis, idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, pneumoconiosis, ARDS, ILD
-restrictive(extraparenchymal): neuromuscular dz(diaphragmatic weakness, MG, Guillain-Barre syndrome, cervical spine injury), chest wall dz(kyphoscoliosis, obesity, ankylosing spondylitis)
2. 유량기량 곡선(flow-volume curve)
-obstructive: 호기 시 곡선이 오목, 최대 호기유량 감소, FEF50% 크게 감소
-restrictive: 폐활량이 주로 감소하고, 유량은 별로 감소하지 않기 때문에 키가 크고 폭이 좁은 모양
-호기시 초반부 25%: 환자의 노력에 많은 영향을 받음
-호기시 후반부 75%: 환자의 노력과 관계없이 폐의 물리역학적 특성에 의해 결정(재현성 높고, 소기도의 초기 병변에 예민)
-fixed obstruction: 압력 차이에 영향을 받지 않으므로 호기와 흡기 시 모두 plateau 발생(예:tracheal stenosis, thyroid ca., bilateral vocal cord palsy)
-variable extrathoracic obstruction: 호기 시에는 내경이 확장되어 유량에 이상이 없으나, 흡기 시에는 대기압에 비해 상기도 압력이 낮아지기 때문에 상기도 내경이 좁아져서 plateau가 발생(예: croup, laryngitis, tracheal malacia, laryngeal or tracheal trauma)
-variable intrathoracic obstruction: 흡기 시에는 흉곽 내압이 음압이 되어 기도폐쇄 부위가 확장되어 유량에 이상이 없으나, 호기 시에는 반대로 plateau가 발생(예: COPD, bronchial asthma)
3. 폐용적의 측정
-RV 측정
-불활성 가스 방법
-체적변동 기록법(body plethysmography): 정확, compliance도 구할 수 있음
-면적 측정법
4. 기도저항
-생리학적인 실제 기도저항치를 측정하는 것(대개 체적변동기록법을 이용)
-R=∆P(대기압-alveolar pressure)/flow
-말초 소기도를 주로 침범하는 COPD의 초기진단에는 예민하지 못하고, 심한 만성기관지염이나 천식의 진단 및 경과 판단에 이용 가능
-임상에서 폐쇄성 폐질환의 진단 및 severity 판단은 보통 노력성 호기유량곡선을 이용
5. 폐탄성(lung compliance)
-폐의 distensibility(확장성)을 표시하는 지표로 elastic property의 기능
-정의: transpulmonary pressure 변화에 따른 폐용적의 변화
-transpulmonary pressure = alveolar pr.-pleural pr. = 구강압-식도내압
-폐용적의 차이에 의한 변동을 없애기 위해 compliance/FRC로써 나타냄
-정적 폐탄성=TV/inspiratory plateau pr.
-증가: emphysema
-감소: 폐부종, 무기폐, 폐렴, restrictive lung dz.
-흡기말과 호기말의 폐용적 차이를 transpulmonary pressure로 나눈 것
-frequency dependent lung compliance또는 effective respiratory system compliance라고도 부름
-정상인에서는 호흡횟수를 증가시켜도 동일하게 유지
-기도폐쇄가 있는 경우에는 호흡횟수를 증가시킬수록 감소
-폐쇄성 폐질환의 폐에서는 폐의 균질성이 변화하여, 호흡이 빨라지면 폐의 일부분에서는 공기의 출입이 늦어져 폐용적의 변화가 적어지고 따라서 동적폐탄성이 감소됨
6. 폐쇄용적(closing volume)
-single breath N₂washout curve: RV까지 숨을 내쉰 다음, 100% O₂를 총폐용량까지 1번 흡입한 후, 서서히 숨을 내쉬면서 구강에서 N₂농도를 측정하여 그래프를 그린 것
-1단계: 상기도 내의 100% O2만 나옴
-2단계: dead space +alveolar air(서서히 N2 농도가 증가)
-3단계: 상부/하부 alveolar air가 동시에 배출되어 일정한 농도 유지
-4단계: 하부의 기도가 폐쇄(하부의 흉막강압이 상부보다 높기 때문), 상부에서만 N2 배출(고농도의 N2)
-CV: 기도폐쇄가 일어나는 폐용적(4단계의 시적점), small airway obstruction 시 CV 증가
-CV이 증가하는 경우: 폐기종, 천식, 기관지염, 흡연, 노인, CHF(평상 호흡시에도 하부기도의 폐쇄가 일어나 V/Q mismatch 초래)
-폐포까지 신선한 공기를 적절히 공급하는 것(환기, ventilation)
-적절한 혈액의 순환(관류, perfusion)
-폐포와 모세혈관 사이에서 가스의 원활한 이동(확산, diffusion)
-폐포 가스와 모세혈관 혈액 사이의 적절한 접촉(ventilation-perfusion matching)
2. Oxyhemoglobin dissociation curve
-shift to right: 온도 증가, pH 감소, PaCO₂증가, 2,3-DPG 증가, 빈혈, 저혈압, 고지대
-shift to left: 온도 감소, pH 증가, PaCO2 감소, 2,3-DPG 감소, abnormal Hb, CO 중독
-2,3-DPG(diphosphoglycerate): O2보다 Hb에 대한 결합력이 커서 증가하면, Hb의 산소친화도를 감소시켜, O2는 Hb에서 해리되어 조직으로 공급
-Bohr's effect: PaCO₂가 증가하면 곡선이 오른쪽으로 이동
-Haldane effect: CO₂해리곡선은 HbO₂가 많이 형성될수록 오른쪽으로 이동
-혈액내에서의 O2 운반: Hb(97%), dissolved state(3%)
-혈액내에서의 CO2 운반: Hb(20~30%), HCO3(60~70%), dissolved state(7~10%)
3. Pulse oxymetry
-cutaneous arterial blood에서 산소 포화도(oxygen saturation, SaO₂)를 구함
-원리: oxygenated Hb과 total Hb를 측정하여 oxygenated Hb%을 계산
-60mmHg 이상의 PaO2에서는 PaO2의 변화를 정확히 반영하지 못함
-PaO2와 SaO2의 관계는 온도, pH, 2,3-DPG 등의 영향을 받음
-cutaneous perfusion 감소시 측정이 어렵거나 불가능할 수 있음(예: low CO, vasoconstriction)
-carboxyHb, metHb 등은 측정하지 못함
4. Alveolar ventilation
-PaCO₂가 가장 잘 반영
-PaCO₂=0.863*VCO₂/Va
-VCO₂: 분당 체내 CO₂생성량
-VA: 폐포 환기(alveolar ventilation)
5. Arterial hypoxemia의 evaluation
-폐포 환기 저하(hypoventilation)
-단락(shunt)
-환기-관류 불균형(V/Q mismatching)
-확산장애: 대부분 V/Q mismatching을 동반
-hypoventilation: respiratory drive 감소, NM dz
-다음 (A-a)DO₂확인
-Alveolar-arterial O₂difference=PAO₂-PaO
-PAO₂=150-1.25*PaCO₂(이상적 조건)
-(A-a)DO2=150-1.25*PaCO2-PaO2
-정상치 15mmHg 이하(30세 이하), 10년마다 3씩 증가, 노인에서는 30까지도 가능
-(A-a)DO₂증가: shunt, V/Q mismatching, diffusion 장애
-(A-a)DO₂정상: low inspired PO₂, hypoventilation(PaCO2는 증가)
-O₂supply로 교정 안 됨!
-예: atelectasis(ARDS), intraalveolar fluid filling(ARDS, CHF, 폐렴), 선천성 심장병, pulmonary arteriovenous shunt
-high V/Q area(high PaO₂)에서의 혈류와 low V/Q area(low PaO₂)에서의 혈류가 합쳐져서 arterial hypoxia를 일으킴
-O₂supply로 교정됨
-예: 천식, COPD, ILD, 폐렴, pul. embolism
-apex로 갈수록 V/Q ratio 증가(ventilation에 비해 perfusion이 더 많이 하강)
-apex로부터의 혈액이 base로부터의 것보다 PO₂높고, PCO₂낮다
-저산소증이 혈관에 미치는 영향: 전신혈관은 확장, 폐혈관은 수축
6. 폐확산능(Diffusing capacity, DLCO)
-확산: 높은 농도에서 낮은 농도로 분자의 수동적 이동
-주로 0.3% CO 가스를 이용하여 측정
-alveolar-capillary barrier thickness
-pul. capillary blood volume
-degree of V/Q, pulmonary edema
-hemoglobin level
-emphysema: alveolar wall의 파괴로 인한 surface area 감소에 의해
-pul. vascular bed의 volume 및 단면적 감소: primary pu. HTN, pul. embolism, pul. vascular dz
-membrane change: intraalveolar filling: 폐렴, 폐부종, ARDS 등
-폐절제술 후, 빈혈 등
-pul. capillary blood volume 증가하는 경우: CHF(초기), MS, ASD
-alveolar hemorrhage: alveolar lumen 내의 RBC에 CO가 결합(예: Goodpasture's syndrome)
-천식
-polycythemia
-운동, 비만, 임신, supine position
-원통형 가슴과 동반된 흉벽 강직성의 증가
-호흡근의 약화로 인한 근력 저하
-증가: FRC, RV, (A-a)DO₂
-감소: TLC, VC, 폐확산능, FEV₁
- 폐활량 및 정적 폐용적
-RV(residual volume): 잔기량
-IRV(inspiratory reserve volume): 흡기 예비기량
-ERV(expiratory reserve volume): 호기 예비기량
-VC(vital capacity): 폐활량
-IC(inspiratory capacity): 흡기용량
-FRC(functional residual capacity): 기능성 잔기용량, chest wall의 compliance와 lung elastic recoil이 같아서 평형을 이루는 lung volume
-TLC(total lung capacity): 총폐용량
-TLC=IC +FRC=VC +RV
-RV은 spirometry만으로는 측정 불가능
- 최대 노력성 호기곡선(maximal-effort expiratory spirogram)
a. 노력성 폐활량(forced vital capacity, FVC)
-제한성폐질환의 지표
b. 1초간 노력성 호기(forced expiratory volume at 1sec, FEV₁)
-폐쇄성폐질환의 지표
c. FEV₁/FVC
d. 노력성 호기 중간유량(forced mid-expiratory flow, FEF25~75%)
-노력성 호기량의 중간부분 50%의 평균속도(maximal mid-expiratory flow rate)
-환자의 노력과 가장 관계없는 부분
-small airway dz의 조기 진단에 민감
-정상인에서도 많은 변이성을 보이므로 재현성은 떨어짐
e. 최대 호기유속(peak expiratory flow rate, PEFP)
-곡선에서 가장 경사가 가파른 부분
-central large airway 폐쇄시 이상소견을 보임
- 최대 환기량(maximal voluntary ventilation, MVV)-환자가 자발적인 최대 노력으로 1분간 호흡할 수 있는 기량
-운동능력 및 수술전후의 평가에 이용
- 사강(dead space)
-PaCO₂: arterial CO₂tension
-PeCO₂: mean expired CO₂tension
-정상인의 anatomical dead space 호흡량은 TV의 약 30%(1회 호흡량의 70%만 alveolar zone에 도달)
-physiologic dead space: 혈류가 흐르지 않는 폐포 공간(TV의 약 36%)
- PFT에 의한 환기장애 분류
-제한성 환기장애: FEV₁/FVC 증가, FVC가 주로 감소
- 폐질환 분류
-restrictive(parenchymal): sarcoidosis, idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, pneumoconiosis, ARDS, ILD
-restrictive(extraparenchymal): neuromuscular dz(diaphragmatic weakness, MG, Guillain-Barre syndrome, cervical spine injury), chest wall dz(kyphoscoliosis, obesity, ankylosing spondylitis)
2. 유량기량 곡선(flow-volume curve)
-obstructive: 호기 시 곡선이 오목, 최대 호기유량 감소, FEF50% 크게 감소
-restrictive: 폐활량이 주로 감소하고, 유량은 별로 감소하지 않기 때문에 키가 크고 폭이 좁은 모양
-호기시 초반부 25%: 환자의 노력에 많은 영향을 받음
-호기시 후반부 75%: 환자의 노력과 관계없이 폐의 물리역학적 특성에 의해 결정(재현성 높고, 소기도의 초기 병변에 예민)
-fixed obstruction: 압력 차이에 영향을 받지 않으므로 호기와 흡기 시 모두 plateau 발생(예:tracheal stenosis, thyroid ca., bilateral vocal cord palsy)
-variable extrathoracic obstruction: 호기 시에는 내경이 확장되어 유량에 이상이 없으나, 흡기 시에는 대기압에 비해 상기도 압력이 낮아지기 때문에 상기도 내경이 좁아져서 plateau가 발생(예: croup, laryngitis, tracheal malacia, laryngeal or tracheal trauma)
-variable intrathoracic obstruction: 흡기 시에는 흉곽 내압이 음압이 되어 기도폐쇄 부위가 확장되어 유량에 이상이 없으나, 호기 시에는 반대로 plateau가 발생(예: COPD, bronchial asthma)
3. 폐용적의 측정
-RV 측정
-불활성 가스 방법
-체적변동 기록법(body plethysmography): 정확, compliance도 구할 수 있음
-면적 측정법
4. 기도저항
-생리학적인 실제 기도저항치를 측정하는 것(대개 체적변동기록법을 이용)
-R=∆P(대기압-alveolar pressure)/flow
-말초 소기도를 주로 침범하는 COPD의 초기진단에는 예민하지 못하고, 심한 만성기관지염이나 천식의 진단 및 경과 판단에 이용 가능
-임상에서 폐쇄성 폐질환의 진단 및 severity 판단은 보통 노력성 호기유량곡선을 이용
5. 폐탄성(lung compliance)
-폐의 distensibility(확장성)을 표시하는 지표로 elastic property의 기능
-정의: transpulmonary pressure 변화에 따른 폐용적의 변화
-transpulmonary pressure = alveolar pr.-pleural pr. = 구강압-식도내압
- 정적 폐탄성(static lung compliance)
-폐용적의 차이에 의한 변동을 없애기 위해 compliance/FRC로써 나타냄
-정적 폐탄성=TV/inspiratory plateau pr.
-증가: emphysema
-감소: 폐부종, 무기폐, 폐렴, restrictive lung dz.
- 동적 폐탄성(dynamic lung compliance)
-흡기말과 호기말의 폐용적 차이를 transpulmonary pressure로 나눈 것
-frequency dependent lung compliance또는 effective respiratory system compliance라고도 부름
-정상인에서는 호흡횟수를 증가시켜도 동일하게 유지
-기도폐쇄가 있는 경우에는 호흡횟수를 증가시킬수록 감소
-폐쇄성 폐질환의 폐에서는 폐의 균질성이 변화하여, 호흡이 빨라지면 폐의 일부분에서는 공기의 출입이 늦어져 폐용적의 변화가 적어지고 따라서 동적폐탄성이 감소됨
6. 폐쇄용적(closing volume)
-single breath N₂washout curve: RV까지 숨을 내쉰 다음, 100% O₂를 총폐용량까지 1번 흡입한 후, 서서히 숨을 내쉬면서 구강에서 N₂농도를 측정하여 그래프를 그린 것
-1단계: 상기도 내의 100% O2만 나옴
-2단계: dead space +alveolar air(서서히 N2 농도가 증가)
-3단계: 상부/하부 alveolar air가 동시에 배출되어 일정한 농도 유지
-4단계: 하부의 기도가 폐쇄(하부의 흉막강압이 상부보다 높기 때문), 상부에서만 N2 배출(고농도의 N2)
-CV: 기도폐쇄가 일어나는 폐용적(4단계의 시적점), small airway obstruction 시 CV 증가
-CV이 증가하는 경우: 폐기종, 천식, 기관지염, 흡연, 노인, CHF(평상 호흡시에도 하부기도의 폐쇄가 일어나 V/Q mismatch 초래)
- 가스 교환의 장애
-폐포까지 신선한 공기를 적절히 공급하는 것(환기, ventilation)
-적절한 혈액의 순환(관류, perfusion)
-폐포와 모세혈관 사이에서 가스의 원활한 이동(확산, diffusion)
-폐포 가스와 모세혈관 혈액 사이의 적절한 접촉(ventilation-perfusion matching)
2. Oxyhemoglobin dissociation curve
-shift to right: 온도 증가, pH 감소, PaCO₂증가, 2,3-DPG 증가, 빈혈, 저혈압, 고지대
-shift to left: 온도 감소, pH 증가, PaCO2 감소, 2,3-DPG 감소, abnormal Hb, CO 중독
-2,3-DPG(diphosphoglycerate): O2보다 Hb에 대한 결합력이 커서 증가하면, Hb의 산소친화도를 감소시켜, O2는 Hb에서 해리되어 조직으로 공급
-Bohr's effect: PaCO₂가 증가하면 곡선이 오른쪽으로 이동
-Haldane effect: CO₂해리곡선은 HbO₂가 많이 형성될수록 오른쪽으로 이동
-혈액내에서의 O2 운반: Hb(97%), dissolved state(3%)
-혈액내에서의 CO2 운반: Hb(20~30%), HCO3(60~70%), dissolved state(7~10%)
3. Pulse oxymetry
-cutaneous arterial blood에서 산소 포화도(oxygen saturation, SaO₂)를 구함
-원리: oxygenated Hb과 total Hb를 측정하여 oxygenated Hb%을 계산
-60mmHg 이상의 PaO2에서는 PaO2의 변화를 정확히 반영하지 못함
-PaO2와 SaO2의 관계는 온도, pH, 2,3-DPG 등의 영향을 받음
-cutaneous perfusion 감소시 측정이 어렵거나 불가능할 수 있음(예: low CO, vasoconstriction)
-carboxyHb, metHb 등은 측정하지 못함
4. Alveolar ventilation
-PaCO₂가 가장 잘 반영
-PaCO₂=0.863*VCO₂/Va
-VCO₂: 분당 체내 CO₂생성량
-VA: 폐포 환기(alveolar ventilation)
5. Arterial hypoxemia의 evaluation
- 저산소혈증의 기전
-폐포 환기 저하(hypoventilation)
-단락(shunt)
-환기-관류 불균형(V/Q mismatching)
-확산장애: 대부분 V/Q mismatching을 동반
- 감별진단
-hypoventilation: respiratory drive 감소, NM dz
-다음 (A-a)DO₂확인
-Alveolar-arterial O₂difference=PAO₂-PaO
-PAO₂=150-1.25*PaCO₂(이상적 조건)
-(A-a)DO2=150-1.25*PaCO2-PaO2
-정상치 15mmHg 이하(30세 이하), 10년마다 3씩 증가, 노인에서는 30까지도 가능
-(A-a)DO₂증가: shunt, V/Q mismatching, diffusion 장애
-(A-a)DO₂정상: low inspired PO₂, hypoventilation(PaCO2는 증가)
- shunt
-O₂supply로 교정 안 됨!
-예: atelectasis(ARDS), intraalveolar fluid filling(ARDS, CHF, 폐렴), 선천성 심장병, pulmonary arteriovenous shunt
- V/Q mismatch
-high V/Q area(high PaO₂)에서의 혈류와 low V/Q area(low PaO₂)에서의 혈류가 합쳐져서 arterial hypoxia를 일으킴
-O₂supply로 교정됨
-예: 천식, COPD, ILD, 폐렴, pul. embolism
-apex로 갈수록 V/Q ratio 증가(ventilation에 비해 perfusion이 더 많이 하강)
-apex로부터의 혈액이 base로부터의 것보다 PO₂높고, PCO₂낮다
-저산소증이 혈관에 미치는 영향: 전신혈관은 확장, 폐혈관은 수축
6. 폐확산능(Diffusing capacity, DLCO)
-확산: 높은 농도에서 낮은 농도로 분자의 수동적 이동
-주로 0.3% CO 가스를 이용하여 측정
- 영향을 미치는 인자
-alveolar-capillary barrier thickness
-pul. capillary blood volume
-degree of V/Q, pulmonary edema
-hemoglobin level
- 감소하는 경우
-emphysema: alveolar wall의 파괴로 인한 surface area 감소에 의해
-pul. vascular bed의 volume 및 단면적 감소: primary pu. HTN, pul. embolism, pul. vascular dz
-membrane change: intraalveolar filling: 폐렴, 폐부종, ARDS 등
-폐절제술 후, 빈혈 등
- 증가하는 경우
-pul. capillary blood volume 증가하는 경우: CHF(초기), MS, ASD
-alveolar hemorrhage: alveolar lumen 내의 RBC에 CO가 결합(예: Goodpasture's syndrome)
-천식
-polycythemia
-운동, 비만, 임신, supine position
- 노인에서의 폐기능 변화
-원통형 가슴과 동반된 흉벽 강직성의 증가
-호흡근의 약화로 인한 근력 저하
-증가: FRC, RV, (A-a)DO₂
-감소: TLC, VC, 폐확산능, FEV₁
Cor pulmonale
Clinical Manifestations
Acute RV failure causes pallor, sweating, hypotension, and a rapid pulse of small amplitude. The neck veins are distended and often exhibit prominent v waves secondary to tricuspid regurgitation. The liver may be pulsatile, distended, and tender. A systolic murmur of tricuspid regurgitation along the left sternal border may be accompanied by a presystolic (S4) gallop sound. Arterial blood gas frequently shows reduced PaO2 due to ventilation/perfusion mismatching and a low PaCO2 due to hyperventilation.
Acute RV failure causes pallor, sweating, hypotension, and a rapid pulse of small amplitude. The neck veins are distended and often exhibit prominent v waves secondary to tricuspid regurgitation. The liver may be pulsatile, distended, and tender. A systolic murmur of tricuspid regurgitation along the left sternal border may be accompanied by a presystolic (S4) gallop sound. Arterial blood gas frequently shows reduced PaO2 due to ventilation/perfusion mismatching and a low PaCO2 due to hyperventilation.
PEEP(Positive-end expiratory pressure)
PEEP is an adjuvunt to the mode ventilation used in cases where the FRC is reduced. At the end of expiration, the PEEP exerts pressure to oppose passive emptying of the lung and to keep the airway pressure above the atmospheric pressure. The presence of PEEP opens up collapse or unstable alveoli and increases the FRC and surface area for gas exchange, thus reducing the size of the shunt. Thus, if a large shunt is found to exist based on the estimation from 100% FiO2 (see above), then PEEP can be considered and the FiO2 can be lowered (<60%), to maintain adequate PaO2, thus reducing the risk of oxygen toxicity.
In addition to treating a shunt, PEEP is also therapeutic in decreasing the work of breathing. In pulmonary physiology, compliance is a measure of the "stiffness" of the lung and chest wall. The mathematical formula for compliance (C) = change in volume / change in pressure. Therefore, a higher compliance means that only small increases in pressure can lead to large increases in volume, which means the work of breathing is reduced. As the FRC increases with PEEP, the compliance also increases, since the partially inflated lung takes less energy to inflate further.
Indications
PEEP is a cardiodepressant and can cause severe hemodynamic consequences through decreasing venous return to the right heart and decreasing right ventricular. As such, it should be judiciously used and is indicated in two circumstances.
- If a PaO2 of 60 mmHg cannot be achieved with a FiO2 of 60%
- If the initial shunt estimation is greater than 25%
If used, PEEP is usually set with the minimal positive pressure to maintain an adequate PaO2 with a safe FiO2. As PEEP increase intrathoracic pressure, there can be a resulting decrease in venous return and decrease in cardiac output. A PEEP of less than 10 cmH2O is usually safe if intravascular volume depletion is absent. Older literature recommended routine placement of a Swan-Ganz catheter if the amount of PEEP used is > 10 cmH2 for hemodynamic monitoring. More recent literature has failed to find outcome benefits with routine PA catheterization when compaired to simple central venous pressure monitoring.[2] If cardiac output measurement is required, minimally invasive techniques, such as esophageal doppler monitoring or arterial waveform contour monitoring may be sufficient alternatives.[3][4] PEEP should be withdrawn from a patient until adequate PaO2 can be maintained with a FiO2 < 40%. When withdrawing, it is decreased through 1-2 cmH2O decrements while monitoring hemoglobin-oxygen saturations. Any unacceptable hemoglobin-oxygen saturation should prompt reinstitution of the last PEEP level that maintained good saturation.
Apr 4, 2007
Apr 3, 2007
Drug allergy
-adverse drug reaction (ADR)
common predictable ADR(typeA) 80%
less common unpredictable ADR(typeB) 20%
-type I hypersensitivity: IgE mediated, immediate reaction
allegen과 IgE 반응하고 mast cell과 결합해 histamine 분비
histamine은 주로 vasodilation 작용
ex) anaphylaxis, atopy, asthma, urticaria, angioedema
-type II hypersensitivity: antibody-dependent cytotoxic
ex) autoimmune hemolytic anemia, 수혈거부 반응, 중증근무력증, goodpasture's syndrome
-type III hypersensitivity: immune-complex mediated
ex) serum sickness, SLE, RA, 사구체신염, 혈관염
-type IV hypersensitivity: T-cell mediated, delayed type
ex) 접촉성 피부염, 결핵, 이식거부반응, hypersensitivity pneumonitis, 갑상선염, type1-DM
-delayed reaction: 72시간 이후
-진단: History taking이 가장 중요, skin test(skin test는 type I만 detection됨, 페니실린, 세팔로스포린, 펩타이드, 인슐린, 일부 전신 마취)
prick test/intradermal test(더 많은 양):대조군(식염수)보다 2*2mm 이상
-urticaria: 24hr 지속 안됨, migration, superficial dermis
-vascularitic urticaria: 24hr 지속
-angiodema: laryngeal edema, wheezing, deep dermis & subcutaneous tissue
-fixed drug eruption
-maculopapular erythematous eruption(m/c)
-bullous eruption: 가장 심한 경우 예) erythema multiform, Steven-Johnson syndrome, overlap SJS/TEM, toxic epidermal necrolysis
-Steven-Johnson syndrome: mucosal involve, 10% 이하 벗겨짐, Bactrim, NSAIDs, acetaminophen, 7~21일 후, 약물 중단, systemic early corticosteroid(가급적 빨리), IVIG
-toxic epidermal necrolysis: 30% 이상, ICU care, 원인 약물 중단, 필요없는 약물 중단, culture, 예방적 항생제는 사용하지 않음, systemic corticosteroid 금기!, IVIG 사용!
-Acute generalized exanthematous pustulosis
-drug fever: 7~10일 이후 발생, 끊은 후 72시간 내 감소, 열이 나도 well-being sense, CRP 상승, esosinophilia, relative bradycardia
-anaphylaxis: systemic, immediate hypersensitivity reaction, skin lesion을 잘 동반, biphasic, serum tryptase, vasovagal syncope DDx(HR 측정), epinephrine 1:1000 0.1ml/kg subcutaneous injection q 20 분
-anaphylactoid reaction: Non-IgE mediated, opioids, muscle relaxant, radiocontrast agents, NSAIDs, ACEi 관련
-penicillin allergy: type I~IV 모두 가능, I이 m/c, hapten hypothesis
-semisynthetic penicillin: maculopapular rash>>anaphylaxis, skin test의 효용성 떨어짐
-penicillin allergy 있는 환자 cepha 써도 괜찮음, cepha는 skin tset 안 함
-vancomycin: red-men syndrome
-aspirin &, NSAIDs: 진단 oral provocation test
common predictable ADR(typeA) 80%
less common unpredictable ADR(typeB) 20%
-type I hypersensitivity: IgE mediated, immediate reaction
allegen과 IgE 반응하고 mast cell과 결합해 histamine 분비
histamine은 주로 vasodilation 작용
ex) anaphylaxis, atopy, asthma, urticaria, angioedema
-type II hypersensitivity: antibody-dependent cytotoxic
ex) autoimmune hemolytic anemia, 수혈거부 반응, 중증근무력증, goodpasture's syndrome
-type III hypersensitivity: immune-complex mediated
ex) serum sickness, SLE, RA, 사구체신염, 혈관염
-type IV hypersensitivity: T-cell mediated, delayed type
ex) 접촉성 피부염, 결핵, 이식거부반응, hypersensitivity pneumonitis, 갑상선염, type1-DM
-delayed reaction: 72시간 이후
-진단: History taking이 가장 중요, skin test(skin test는 type I만 detection됨, 페니실린, 세팔로스포린, 펩타이드, 인슐린, 일부 전신 마취)
prick test/intradermal test(더 많은 양):대조군(식염수)보다 2*2mm 이상
-urticaria: 24hr 지속 안됨, migration, superficial dermis
-vascularitic urticaria: 24hr 지속
-angiodema: laryngeal edema, wheezing, deep dermis & subcutaneous tissue
-fixed drug eruption
-maculopapular erythematous eruption(m/c)
-bullous eruption: 가장 심한 경우 예) erythema multiform, Steven-Johnson syndrome, overlap SJS/TEM, toxic epidermal necrolysis
-Steven-Johnson syndrome: mucosal involve, 10% 이하 벗겨짐, Bactrim, NSAIDs, acetaminophen, 7~21일 후, 약물 중단, systemic early corticosteroid(가급적 빨리), IVIG
-toxic epidermal necrolysis: 30% 이상, ICU care, 원인 약물 중단, 필요없는 약물 중단, culture, 예방적 항생제는 사용하지 않음, systemic corticosteroid 금기!, IVIG 사용!
-Acute generalized exanthematous pustulosis
-drug fever: 7~10일 이후 발생, 끊은 후 72시간 내 감소, 열이 나도 well-being sense, CRP 상승, esosinophilia, relative bradycardia
-anaphylaxis: systemic, immediate hypersensitivity reaction, skin lesion을 잘 동반, biphasic, serum tryptase, vasovagal syncope DDx(HR 측정), epinephrine 1:1000 0.1ml/kg subcutaneous injection q 20 분
-anaphylactoid reaction: Non-IgE mediated, opioids, muscle relaxant, radiocontrast agents, NSAIDs, ACEi 관련
-penicillin allergy: type I~IV 모두 가능, I이 m/c, hapten hypothesis
-semisynthetic penicillin: maculopapular rash>>anaphylaxis, skin test의 효용성 떨어짐
-penicillin allergy 있는 환자 cepha 써도 괜찮음, cepha는 skin tset 안 함
-vancomycin: red-men syndrome
-aspirin &, NSAIDs: 진단 oral provocation test
Apr 2, 2007
Tuberculosis radiology
A posterior-anterior chest X-ray is the standard view used; other views (lateral or lordotic) or CT scans may be necessary. CDC guidelines for evaluation CXR
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In active pulmonary TB, infiltrates or consolidations and/or cavities are often seen in the upper lungs with or without mediastinal or hilar lymphadenopathy. However, lesions may appear anywhere in the lungs. In HIV and other immunosuppressed persons, any abnormality may indicate TB or the chest X-ray may even appear entirely normal.
Old healed tuberculosis usually presents as pulmonary nodules in the hilar area or upper lobes, with or without fibrotic scars and volume loss. Bronchiectasis and pleural scarring may be present.
Nodules and fibrotic scars may contain slowly multiplying tubercle bacilli with the potential for future progression to active tuberculosis. Persons with these findings, if they have a positive tuberculin skin test reaction, should be considered high-priority candidates for treatment of latent infection regardless of age. Conversely, calcified nodular lesions (calcified granuloma) pose a very low risk for future progression to active tuberculosis.
Abnormalities on chest radiographs may be suggestive of, but are never diagnostic of, TB. However, chest radiographs may be used to rule out the possibility of pulmonary TB in a person who has a positive reaction to the tuberculin skin test and no symptoms of disease.
CDC guidelines for evaluation CXR
A medical examination is mandatory for all refugees coming to the U.S. and all applicants outside the U.S. applying for an immigrant visa. The purpose of the medical examination is to identify applicants with inadmissible health-related conditions such as active tuberculosis. Outside the U.S., medical examinations are performed by approximately 400 physicians (panel physicians) selected by United States Department of State consular officials. In the U.S., medical examinations are performed by approximately 3,000 physicians (civil surgeons) designated by district directors of the U.S. Citizenship and Immigration Services. Guidelines were developed by the Centers for Disease Control and Prevention (CDC).
The chest X-ray and classification worksheet is designed to group findings into categories based on their likelihood of being related to TB or non-TB conditions needing medical follow-up (either at the time of the chest X-ray or after resettlement).
Normal findings:
These are films that are completely normal, with no identifiable cardiothoracic or musculoskeletal abnormality.aa
Abnormal findings:
Chest X-Ray Findings that Can Suggest ACTIVE TB:
This category comprises all findings typically associated with active pulmonary TB. An applicant with any of the following findings must submit sputum specimens for examination. Infiltrate or consolidation—Opacification of airspaces within the lung parenchyma. Consolidation or infiltrate can be dense or patchy and might have irregular, ill-defined, or hazy borders.
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- Any cavitary lesion—Lucency (darkened area) within the lung parenchyma, with or without irregular margins that might be surrounded by an area of airspace consolidation or infiltrates, or by nodular or fibrotic (reticular) densities, or both. The walls surrounding the lucent area can be thick or thin. Calcification can exist around a cavity.
- Nodule with poorly defined margins—Round density within the lung parenchyma, also called a tuberculoma. Nodules included in this category are those with margins that are indistinct or poorly defined. The surrounding haziness can be either subtle or readily apparent and suggests coexisting airspace consolidation.
- Pleural effusion—Presence of a significant amount of fluid within the pleural space. This finding must be distinguished from blunting of the costophrenic angle, which may or may not represent a small amount of fluid within the pleural space (except in children when even minor blunting must be considered a finding that can suggest active TB).
- Hilar or mediastinal lymphadenopathy (bihilar lymphadenopathy)—Enlargement of lymph nodes in one or both hila or within the mediastinum, with or without associated atelectasis or consolidation.
- Linear, interstitial disease (in children only)—Prominence of linear, interstitial (septal) markings.
- Other—Any other finding suggestive of active TB, such as miliary TB. Miliary findings are nodules of millet size (1 to 2 millimeters) distributed throughout the parenchyma.
Chest X-Ray Findings that Can Suggest INACTIVE TB:
This category includes findings that are suggestive of prior TB, that is inactive. It must be remembered that assessments of the activity of TB cannot be made accurately on the basis of a single radiograph alone. If there is any question of active TB, sputum smears must be obtained. Furthermore, if the applicant has any signs or symptoms of TB, sputum smears must be obtained. Obtaining sputum smears is necessary if there is any question of active TB. Therefore, any applicant might have findings grouped in this category, but still have active TB as suggested by
- The presence of signs or symptoms of TB (Class B1).
- Sputum smears positive for AFB (Class A).
- Discrete fibrotic scar or linear opacity—Discrete linear or reticular densities within the lung. The edges of these densities should be distinct and there should be no suggestion of airspace opacification or haziness between or surrounding these densities. Calcification can be present within the lesion and then the lesion is called a “fibrocalcific” scar.
- Discrete nodule(s) without calcification—One or more nodular densities with distinct borders and without any surrounding airspace opacification. Nodules are generally round or have rounded edges. These features allow them to be distinguished from infiltrates or airspace opacities. To be included here, these nodules must be noncalcified. Nodules that are calcified are included in the category “OTHER X-ray findings, No follow-up needed”.
- Discrete fibrotic scar with volume loss or retraction—Discrete linear densities with reduction in the space occupied by the upper lobe. Associated signs include upward deviation of the fissure or hilum on the corresponding side with asymmetry of the volumes of the two thoracic cavities.
- Discrete nodule(s) with volume loss or retraction—One or more nodular densities with distinct borders and no surrounding airspace opacification with reduction in the space occupied by the upper lobe. Nodules are generally round or have rounded edges.
- Other—Any other finding suggestive of prior TB, such as upper lobe bronchiectasis. Bronchiectasis is bronchial dilation with bronchial wall thickening.
OTHER Chest X-Ray Findings:
Follow-up needed:
This category includes findings that suggest the need for a follow-up evaluation for non-TB conditions either at the time of the chest X-ray or after resettlement of the applicant in the United States.
- Musculoskeletal abnormalities—New bony fractures or radiographically apparent bony abnormalities that need follow-up.
- Cardiac abnormalities—Cardiac enlargement or anomalies, vascular abnormalities, or any other radiographically apparent cardiovascular abnormality of significant nature to require follow-up.
- Pulmonary abnormalities—Pulmonary finding of a non-TB nature, such as a mass, that needs follow-up.
- Other—Any other finding that the panel physician believes needs follow-up, but is not one of the above.
No follow-up needed:
This category includes findings that are minor and not suggestive of TB disease. These findings require no follow-up evaluation after resettlement of the applicant.
- Pleural thickening—Irregularity or abnormal prominence of the pleural margin, including apical capping (thickening of the pleura in the apical region). Pleural thickening can be calcified.
- Diaphragmatic tenting—A localized accentuation of the normal convexity of the hemidiaphragm as if “pulled upwards by a string.”
- Blunting of costophrenic angle (in adults)—Loss of sharpness of one or both costophrenic angles. Blunting can be related to a small amount of fluid in the pleural space or to pleural thickening and, by itself, is a non-specific finding (except in children, when even minor blunting may suggest active TB). In contrast a large pleural effusion, or the presence of a significant amount of fluid in the pleural space, may be a sign of active TB at any age.
- Solitary calcified nodules or granuloma—Discrete calcified nodule or granuloma, or calcified lymph node. The calcified nodule can be within the lung, hila, or mediastinum. The borders must be sharp, distinct, and well defined. This was considered a Class B3 TB in the past; however, Class B3 has been omitted from the classification scheme because it has not been found to be associated with active TB.
- Minor musculoskeletal findings—Minor findings needing no follow-up.
- Minor cardiac findings—Minor findings needing no follow-up.
References
- Instructions to Panel Physicians for Completing CHEST X-RAY AND CLASSIFICATION WORKSHEET (DS-3024) from Centers for Disease Control and Prevention
External links
Additional X-ray images
These are links to pictures copyrighted by the websites...
- Chest X-ray Atlas - Select Diseases|Tuberculosis for TB CXR case studies (X-ray pictures showing cavities, infiltrates, scarring, pleural effusion, interstitial nodules of military TB, and TB spine) - from Loyola University Chicago Stritch School of Medicine ©
- eMedicine Radiology © - pictures of X-ray, CT scan, and MRI of various findings of TB disease:
- Lung, Primary Tuberculosis - focal opacity, consolidation, pleural effusion, lymphadenopathy, cavity, nodule.
- Lung, Postprimary Tuberculosis - bullous disease, cavity, opacity, nodule, adenopathy, miliary TB, pleural effusion, consolidation.
- Lung, Nontuberculous Mycobacterial Infections - cavity, volume loss, fibrosis, nodule, bronchiectasis, atelectasis, lymphadenopathy
- CNS Tuberculosis - vasculitis, tuberculoma, TB abscess, granuloma
- Gastrointestinal Tuberculosis - lymphadenopathy, stricture, dilation
- Genitourinary Tract Tuberculosis - calcification, granuloma, cavitation, edema, ulceration, abscess
Apr 1, 2007
Tremor
Essential Tremor: This tremor is rapid and fine. Essential tremor usually begins in early adulthood but can begin at any age. The tremor slowly becomes more obvious and becomes more noticeable among older age groups. It was once called senile tremor because it is more common among people older than 60. Some forms of essential tremor run in families and are sometimes called familial tremor. The cause is unknown.
Usually, essential tremor remains mild and does not indicate serious disease; however, it can be troublesome and embarrassing. It can affect handwriting and make using utensils difficult.
Essential tremor usually affects the arms and, rarely, the legs. The tremor usually stops when the arms or legs are at rest but becomes obvious when the limbs are outstretched and worsens when the limbs are held in uncomfortable positions. Essential tremor usually affects both sides of the body but may affect one side more than the other. Sometimes the tremor affects the head, causing it to tremble and bob, and the vocal cords, causing the voice to shake. In some people, the tremor gradually worsens over time, eventually resulting in disability.
Resting Tremor: This slow, coarse tremor occurs when the muscles are at rest, making an arm or a leg shake even when a person is completely relaxed. Resting tremor may develop when collections of nerve cells at the base of the cerebrum (including the basal ganglia) are disturbed. Such disturbances may result from Parkinson's disease, use of certain drugs (such as lithium Some Trade Names LITHANE, LITHONATE and antipsychotic drugs), or heavy metal poisoning (such as occurs in Wilson's disease, in which copper accumulates in body tissues).
Resting tremor, although sometimes embarrassing, usually interferes little with voluntary movements, such as drinking a glass of water.
Intention (Cerebellar) Tremor: This relatively slow, broad tremor occurs at the end of a purposeful movement, such as trying to press a button. Intention tremor may result from a damage to the cerebellum or its connections. Multiple sclerosis and stroke are common causes. Wilson's disease, alcoholism, and overuse of sedatives or anticonvulsants can cause the cerebellum to malfunction, resulting in intention tremor.
Intention tremor may increase during an activity, such as touching an object with the hand. The tremor may cause a person to miss the targeted object.
Flapping Tremor (Asterixis): This tremor is a coarse, slow, nonrhythmic movement that occurs when a person stretches out the arms and extends the hands. This tremor commonly results from liver failure and so has been called liver flap. However, it may also result from kidney failure and brain damage (encephalopathy) due to a metabolic disorder.
Muscle tone lapses suddenly and temporarily. As a result, the hand flaps; that is, it quickly drops, then returns to its original position. This tremor may be accompanied by other tremors and by myoclonus (see Movement Disorders: Myoclonus).
Diagnosis and Treatment
The development of a noticeable tremor should be evaluated by doctors. Doctors can usually identify the type of tremor by its characteristics. The type of tremor determines which procedures are performed. For essential tremor, doctors ask what drugs are being used and whether the person is experiencing anxiety or stress. Often, a blood test to detect an overactive thyroid gland is performed. For a resting tremor, a complete neurologic evaluation and other procedures to check for Parkinson's disease are performed. For intention tremor, an imaging procedure, such as computed tomography (CT) or magnetic resonance imaging (MRI), is often performed to look for damage to the brain. For flapping tremor, blood tests to evaluate liver and kidney function are performed.
Usually, treatment for a tremor is not needed. Avoiding uncomfortable positions can help. Objects should be grasped firmly but comfortably and held close to the body.
For people with essential tremor, drinking alcohol in moderation may reduce the tremor. However, heavy drinking or alcohol withdrawal can make the tremor worse. If people with essential tremor have difficulty using utensils or do work that requires steady hands, drugs may help. A beta-blocker, such as propranolol Some Trade Names INDERAL, is most commonly prescribed. If it does not help, primidone Some Trade Names MYSOLINE, an anticonvulsant, is often tried.
A resting tremor due to Parkinson's disease is treated as part of that disease. Intention tremors are difficult to treat, but if the condition affecting the cerebellum can be corrected, the tremor may resolve. For flapping tremor, the underlying liver or kidney disorder is treated. The tremor may resolve as liver or kidney function improves.
Brain surgery is performed only when an essential or a resting tremor is severe and disabling and drugs are ineffective. There are two types of surgery. In thalamotomy, parts of the thalamus (located at the base of the cerebrum, deep within the brain) are destroyed, and thus the pathways that produce the tremor are interrupted. In thalamic stimulation, an electrical probe is placed inside the thalamus. The probe delivers continuous high-frequency electrical stimulation to the thalamus, which generally reduces the tremor. Such procedures are available only at special centers.
Ref. The merk manuals online medical library
Mar 18, 2007
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