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לדפוס - חוברת מבחני גמר פנימית 2014 ללא תמונות 250283
לדפוס - חוברת מבחני גמר פנימית 2014 ללא תמונות 250283
2014
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Membranoproliferative
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. MRI
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.
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acute intestinal obstraction .
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Light Chain Deposition Disease
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46
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?
47
45
.
.
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Diffuse Large B-Cell Lymphoma .
Lymphoblastic Lymphoma .
.
.
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STAGE ?
I-A .
I-B .
B .II
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3
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80 . 37.8 2
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48
46
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68
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-
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,
. :
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,
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: . ,135/80 90 . ,
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.
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.
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.
.
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.
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. :
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. .
. .
. .
. .
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. .
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.
.
.
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.
?
.
, .
.
.
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50
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.
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.
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.
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.
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.
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. ,
53
51
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.
.
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.
.
.
.
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.
.
.
.
. .
. .
. .
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. .
?
..
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. .
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. .
. .
.
.
.
.
.
.
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. XI
Anti phospholipids syndrome
VII
. IX
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,
,
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.
.
.
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. .
.
.
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.
.
.
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.
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.
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.
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.
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.
. .
.
.
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,?
Posislreptococcal glomerulonephritis .
Good pasture syndrome .
IgA nephropathy .
Microscopic polyarteritis nodosa .
Scleredema crisis .
.31 ,55
60% TLC :,
RV 50% VC , , FEV1/VC
. ?
. .
. .
.
. .
54
52
,
.
. ?
..
Lymphangioleomyomatosis .
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drome ..Goodpasture's Syi
Hamman-Rich syndrome .
.32 ?
.
.
.
.
. .
.
.
.
.
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.
.
.
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.
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.
.
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.
.
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.
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. .
..
. .
. .
. .
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Streptococcal Toxic Shock Syndrome ?
. .
.
.
. .
. .
. . ARDS
.35 ?
..
..
.Reactive Arthritis .
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.42 ,30 15 .
2.5
. ?
. CT
.
.
.
.
. .
.
.36
?
Rich animal fat diet .
Inflammatory bowel disease .
Streptococc Bovis Bactermia .
Pneumococcal bacteremia .
Uterosigmoidostomy .
.43 ,22 .
.
, ,
Tenesmus 5 -.
.
, .
. 15,000
11.3 . 60
. ?
. .
Ulcerative C/otilis .
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.
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.
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.
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. .
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.
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.
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.
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.
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.
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,
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. .
. .
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.
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.
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. ?
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.
.
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.
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. 130/85.
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.63 56
.
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.
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.
?
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SIRS - systemic inflammatory response .
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.65 , 3 .
. PTT
, PT - .
?
. .
Fresh
. frosen plasma
,
.
. .
. .
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. TTE
.
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.
.
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.
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?
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. CT.
. .
. US .
.
.
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.
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.71 ,?
. .
.
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58
56
.
.
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.
.
.
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.
: ,,
PTT PT - ,
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.
.
.
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. + +
+.
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.
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. + +.
.78
?
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.Levofloxacin .
.Ceftriaxone .
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.Piperacillin .
.73 ,
?
.
20% .LDL
.
HDL .
. CPK
.
.
.
.
.
.79 71
.
.
TSH T4 T3 -
,
?
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. .Sick euthroide syndrome
. .
.
. .
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, 12.5"
5 132/83
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?
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. )(Ramipril
. )(Atenolol
. . .
. 24
.
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, ,
. :
TSH .T3 + FT4
?
.
.
. .
. 30%
.
.
.
.
.
.75 ,44 ,
.rapidly progressive glomerulonephritis
?
Diffuse proliferlative glomerulonephritis .
Mesangial proliferative .
glomerulonephritis
Minimal change glomerulonephritis .
glomerulonephritis Crescentie .
Merabrano proliterative .
glomerulonephritis
.76 55 ,
.
220/145 .
. 3.4",%
88" .%
?
.
.
.
.81 30
.
.
?
.
. 24
.
59
57
.
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. .
.86 22
4 .
, ,
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,
24 8.5 .
?
.
.
.
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. US
.
.
.
.
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.
. : 6.3
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?
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.
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.% ?
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.
HBA1C .
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?
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48 .
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.
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,
.
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.
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CT . MRI - ,
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.
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. .
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,
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.
,
. 5
2.2 .
?
Furosemide .
thiazide diuretic .
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. ACE
.
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.
.
.
110 , .110/80
.
?
. .D-DIMER
CT .
. .
US . .
. .
58
.
?
,
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. ,
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.
.91 24 ,15
, ,
.
.
?
.
. Phenoxybenzamine
.
.
.
. .
.96
?
Nephrotic range proteinuria .
nephritic syndrome .
Renal tubular acidosis .
Nephrogenic diabetes insipidus .
Fanconi syndrome .
.92 50
,
.PROPYLTHIOURACIL-
.
?
. -
PROPYLTHIOURACIL
.
50
.
50%
.
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.97 ,45
, ,
,
, .
.. .10
.
?
. 200'
.
.
.
.
. ,
.
. ,
.
.93
?
Nephrolithiasis .
Polycystic kidny Disease .
Distal renal tubular acidosis .
Amyloidosis .
Multifile myeloma .
.98 85
, , ,
.
?
.
.
.
. ,
.
. .
.
.
.94 60 ,
,
.
, ,
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,96 .3.9
?
.
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, .
,
. ?
Staph Aureus .
Salmonella .
Bacillus cere .
Clostridium perfingens .
Campiiobacier jejuni .
.100 ,35 .
.
.
. , . 3 -
. 18" .
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,
15 ,%
PTH
61
59
. ,
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HBSAG .2.3 -,
HBC IGM -ANTI . ?
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. .Peg-lnlerferon + Ribavinnc -
. .5%
. B
.
. .
.1
.2
.3
.4
.5
.6
.7
.8
.9
.10
.11
.12
.13
.14
.15
.16
.17
.18
.19
.20
.21
.22
.23
.24
.25
.26
.27
.28
.29
.30
.31
.32
.33
.34
.35
.36
.37
.38
.39+
.40
.41
.42
.43
.44
.45
.46
.47
.48
.49
.50
.51
.52
.53
.54
.55
.56
.57
.58
.59
.60
.61
.62
.63
.64
.65
.66
.67
.68
.69
.70
.71
.72
.73
.74
.75
.76
.77
.78
.79
.80
.81
.82
.83
.84
.85
.86
.87
.88
.89
.90
.91
.92
.93
.94
.95
.96
.97
.98
.99
.100
62
60
- 3009
63
61
64
62
65
63
.36
66
64
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67
65
68
66
.57 ,57
69
67
.95
70
68
.1
.2
.3
.4
.5
.6
.7
.8
.9
.10
.11
.12
.13
.14
.15
.16
.17
.18
.19
.20
.21
.22
.23
.24
.25
.26
.27
.28
.29
.30
.31?
.32
.33
.34
.35
.36
.37
.38
.39
.40
.41
.42
.43
.44
.45
.46
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.51
.52
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.56
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.58
.59
.60
.61
.62
.63
.64
.65
.66
.67
.68
.69
.70
.71
.72
.73
.74
.75
.76
.77
.78
.79
.80
.81
.82
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.85
.86
.87
.88
.89
.90
.91
.92
.93
.94
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.96
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.99
.100
71
69
- 3008
.1
.2
.
?
. .D-DIMERS
. .
. .
. -.
. .CT-ANGIO
?
Moraxella catarrahlis .
Yersinia pestis .
Borrelia recurrentis .
Bartonella henselae .
Toxoplasma gondii .
.3
!H.pylori
. 10
14 , .
. 1/3 3
.
. 4
, bismuth salicylate-
.PPI
. bismuth
salicylate .
.
.
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, .
.. 1
.. .2
. .
?
.
.
.
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.8
, 20 ,
,
. : 30,37 - ,
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PULSE , ."-
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?
. .
. .
. .
. D-DIMERS .
.
.
.9
,50 ,
. .
- ,
FEV1 : . FEV1/FVC
. , ?
. .
. .
. . COPD -
CT . .
. .
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16 .
,
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.
.
. preload
.
.
.
.
.
.
.
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Fever ?
.
.
.
.
.
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, 22 ,
.
.
?
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. .
. .
. .
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...
.
.
.
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, .
: ,
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72
70
)
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.
.
.
.
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. .
.
.
.
.
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?
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.
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.
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. .
. .
antidepressants
IB
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.
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.
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.
.
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- ,
. ,35 .
.
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. "
, HGB-9 gr/dl ,MCV -85 -
, . MG/DL 2.5 - .mg/dL12.5 -
BENCE JONES .
?
. .
. .PTH
CT . .
. .
. .
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. ,
, .
. ,
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?
..
.
.
.
. .
.20 ,89 .
948"/"
.
?
Rractional excretion of Sodium . .1
. .20
. .500
. .40
.
.20
.15
?
METFORMIN .
GLIBENCLAMIDE .
INSULIN .
ROSIGLITAZONE .
PIOGLITAZONE .
.21 ,50 .
180/98" ,
,2.1 ,67 ,354 2.2
105 .
.Membranous Nephropathy
?
. .
. .20%
. 60% "
.
.
.
. 60%
.
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, ,
- .
. BCR/ABL
?
.
.
IMATINIB MESYLATE (GLEEVEC) .
.
73
71
.27 64 , .
.
,
3 .
?
.
OPENING SNAP .
.
. parvus tardus
Bisferiens pulse .
.22 "
?EPO -
9-10% .
10-11% .
11-12% .
12-13% .
13-14% .
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) .(PIPS +DIPS
2
.
?
. .
. .RF
. .
. .
. PTH.
.28 24 .
IGM PARVOVIRUS B19 -
?
.
.
. .
. .
.
.
. -
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.
.
DIP) distal -
.(interphalangeal joints
.
.
.
2000 .
.
) (extensor .
.29 65 , , 38.5
, :
. 25% - .
?
. 8 gr/dl : , HGB -
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. .
. . 9/22
DRY TAP . .
. . M PROTEIN
.25 , 40 ) ,(SLE
.
,
, 85/55 - , 120 - ,
.
?
. ,
.
-.
. D-DIMERS
.
. -.
. .
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. : 2.5",%
78" .% US
10 .
?
. US
. 60 80%
. US
.
.
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.
: .MCV - 110 ,9
?
. .
.
.
. Antiparietal
.cell antibody
.
.
.
Schilling -
test .
.31 -
NON HODGKIN'S LYMPHOMA
?
. .
CT . , .
CT . .
. .
. .
74
72
.37 . 40
, .
,. -
.
?Primary pulmonary hypertension
..
. .
. .
. .
. .
.32 ,30 -
, .
, 38 ,
.
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) ALT 400, ALP /(.
3/ 1
/" .
7- ,
5 .
?
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. .
US . .
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.ANA
. .anti-mitochondria! AB -
.38 , 40 , ,
. .
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?
. .
. .90,000
Dry tap . .
. .
. .B12
.39
)"( ?
.
.MITRAL STENOSIS -
. "
.
.
.Primary pulmonary hypertension -
.
CHRONIC THROMBOEMBOLIC
.PULMONARY HYPERTENSION
.
.
.34 .
?
. .
. .
.
. .
. .
.40 ,50 ,
,
, .
.
30000 , .
-
. ,
?
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.
. .
. .
. .
.35 , 40
. -
, , 20000 -
.
?
. .
. .(ANA) antinuclear antibody
. .HIV
. IIBIIIA glycoprotein
).(Gp
. .15/17
.41 AMIODARONE
?
. TPO
.
.
.
.
.36 33
.
, C3ANCA ,
GBM .
?
IgA nephropathy .
Microscopic polyarteritis nodosa .
SLE .
Wegener's granulomatosis .
Good pasture's syndrome .
75
73
.46
22 ,
?
.
.
.
.
. 30
.42
?FMF
.
.
FMF
.
, .
. 90%
. ,
.
.47 ?
.
,
.
- ) dermatitis
.(herpetiformis
.
IgA anti-tissue transglutaminase (tTG) .
.
.
.
T.
.43 ,
?
. .
. ,
.
.
.
.
.
.
.
.48
?
.Streptococc viridans .
.Enterococci .
.HACEK group .
Staphylococcus aureus .
Staphylococcus epidermidis .
.44 50 ,
,METFORMIN ,GLIBENCLAMIDE
.NIFEDIPIN
,6.2 1.8 % 58 .%
110
,PH 7.29 ,% 140 %
.20
?
. METFORMIN
. -
.49
?
Familial adenomatous polyposis .
Gardner's syndrome .
Peutz Jeghers syndrome .
Inflammatory bowel disease .
Streptococcus bovis bacteremia .
MINERALCORTICOIDS
. FUROSAMIDE -
. SPIRINOLACTONE -
. PSEUDOHYPERKALEMIA -
.45 40 12
.
, .
?
. acetaminophen
5 .
.
. ,
, .
.
.
.
.
.
, nN-acetylcysteine
48.
.50 ,69 ,,
.
.
RCA
, ,
, , ,
, " .4
.
. , ?
.
.
. 20% ,
. ,
,
.
76
74
.56 82
, , .
2 ,
.
?
.
. ST ..
.
.
.
.51 45
.
12.7 ,% 2.8 .%
PTH .
?
.
.
-
.
.
.57 ,
?
. ,
.
. ,
.
. ,
.
. ,
.
. , .
.52 ,
?
.
.
.
.
.
.58 60 -
GLIBEMCLAMIDE ,
, 2.6
% 68 , %
?
.
. US
.
.
. CT
.53
ACARBOSE ?
.
.
SULFANYLUREAS
. IBD
. I
.59 pulsus
altemans
?
.
. 10
.
.
LSB .
.
.
pouch
, ,
,2.5
320 ,% 24
3.7 .
, ?
MINIMAL CHANGE DISEASE .
MEMBRANOUS NEPHROPATHY .
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Necrotizing Vasculitis
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120
118
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Focal and segmental glomerulosclerosis
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. LDL
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.).(Glucose
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(disease ?
.
.
.
.
.86 50 .
, ,.
- 48% , )Normal 60-100%
.(PT .
?
Ag . - Hbs HBV-surface
Anti-HCV . .HCV
IgM-HAV . .HAV
) Anti Smooth-Muscle Ab .
(
.
Diabetes Mellitus Type 1
.
.93 ,
?
..
. .
..
. .
.94 A
, ?
Ventricular Tachycardia .
125
123
.
.
.
.1
.2
.3
.4
.5
.6
.7
.8
.9
.10
.11
.12
.13
.14
.15
.16
.17
.18
.19
.20
.21
.22
.23
.24
.25
.95 70
.
?
. .
. 24.
. .
. .
.96 60
.
. .
.
?
. .
. CPK .
.
.
.
.
.97 ,40 , ,
.
?
. ).(GERD
. .
..
Post-Nasal Drip .
.98
?
NSAID. .
.Bisphosphonates .
Beta-Blocker. .
.Anti-Platelets .
126
124
.26
.27
.28
.29
.30
.31
.32
.33
.34
.35
.36
.37
.38
.39
.40
.41
.42
.43
.44
.45
.46
.47
.48
.49
.50
.51
.52
.53
.54
.55
.56
.57
.58
.59
.60
.61
.62
.63
.64
.65
.66
.67
.68
.69
.70
.71
.72
.73
.74
.75
.76
.77
.78
.79
.80
.81
.82
.83
.84
.85
.86
.87
.88
.89
.90
.91
.92
.93
.94
.95
.96
.97
.98
- 3000
?
.
.
. , ,
. ,
.1 ,20 " ,
.
.
20
" , .
.
?
. .
. FNA .
. US .
. .
.2
.7 "
" . -
Fludrocortisone
?Hydrocortisone
. .
. .
. nonfunctioning pituitary
macroadenoma.
. .
,30 ) Ulcerative
(Colitis 5- . -
.(Rafasal (Mesalamine
. .
, .
Alkaline Phosphatase 600
.8
?
. T .
. ST .up-sloping
. .
. .
.(IU/L (20-75
.
?
. -
.Rafasal
.Primary Biliary Cirrhosis (PBC) .
.Primary Sclerosing Cholangitis (PSC) .
. A ).(HAV
.9 35 ,
.
. " ,
. .
?
Insulinoma .
Glucagonoma .
Gastrinoma .
VIPoma .
.3
?Legionella pneumophila -
. .hypernatremia
. 90%.
. .
.
.
.10 40
3 . -
,
. - .50
. , 4 + -
1.5 24 . RF - -
ANA . ?
. .
. .Methotrexate-
. ).ACPA (anti CCP
. .Cyclophosphamide-
.4 ,30 ,
.
5"
4 .
?
. .
. .ASCA
..
CT ..
.5
:
,FVC= 82% predicted ,FEV1/FVC = 0.54
.11 75 )"(.
[ (Atenolol (Normiten --]
[ (Amlodipine (Norvasc - ].
Amitriptyline -
)[ (Elatrolet -] .
.
?
. Amitriptyline
.
. Atenolol
.
?
.
.
(Idiopathic Pulmonary Fibrosis (IPF/UIP .
rheumatoid arthritis associated ILD .
.6 60 , , ,
.pH: :
127
125
.
.
.
?
.
.
.
.
. .
. 5-7.
Amloipine
.
).Oxybutynin (Novitropan
.12 -
?Pancreatitis
Prednisone .
Metformin .
Simvastatin
.
Azathioprine .
.18 ,
,
.
.
.acute HIV syndrome -
?
.p24 antigen levels .
. .CD4
. HIV -.ELISA -
Western Blot ..HIV -
.13
ampicillin
?
. ,20 .
. 45
5.
. 45
.
. .30
.19 47
.
5-" ,
.
Polycythemia vera ?
. .MCV
. .JAK2
. .B12
. .
.14 30
.
.
, .
.
?
Staphylococcus saprophyticus .
Enterococcus faecalis .
Chlamydia trachomatis
.
Borrelia burgdorferi .
.20 ,73 - .
."
106 .
rhythm
.control
.
?
. 80
.lone atrial fibrillation
.
.
.
.
. .
?
.
.
. .
.
.
.
.
.16 30 .
) .(ICS
,-
.
. ?
. - 3
, .
. -
.
.
) ,(LABA .ICS
. ICS-
).(LABA
.21 35
.
.C39.8
,
. -
?
Campylobacter jejuni .
Shigella sonnei .
Salmonella non typhi
.
Entamoeba histolytica .
.22 29 ,
, .
, .
.17 15
. 3
128
126
. .
, ) x,y
(descents .
?
.Cirrhosis .
Nephrotic Syndrome .
Left-sided heart failure
.
Constrictive pericarditis .
.24 70 .
.
.-
, .
. ) (
.
?
. HLA-
.
. -NSAID-
). (allopurinol
. ,
.
.
.
.29 ,30
Hepatitis
.anti-HBs antibodies- :
.negative, HBsAg-positive, anti-Hbc-positive
.
?
. HBV-.
. .HBV-
. HBV-.
. .HCV
.30 ,84 .
.
, .
,38 , .
.60" ,
.40 , TSH .
?
. .
. ,
.
. ).(EPS
.
.TSH
.25 ) anion
(gap?
.
.
.
.
.
.Metformin
.
.
, .
Na+: 136 mmol/L (Normal 135 - :
pH: K+: 8.9 mmol/L (Normal 3.5-5) (145
.31 .
PPD 13 .
PPD- 6 . ,
. ?
. .
. .
.
. . PPD
15 .
. .
4 .
?
. .
. .
. Kayexalate .
. .
.27 ,76 .
.
.106/87 ,
, ,
, .
, ,shifting dullness -
.32 ,25 .
, " .
,
129
127
" .
.
?
US ..
. .
. .
....
,
. ,CRP<0.5 .16
?
. .
.(Azathioprine (Imuran .
. .TNF
. .
.33
?Staphylococcus aurous
. 1-8
.
. .
.
.
Staphylococcus aureus .
.
.39 40 .
Shirmer
.
?
pANCA .
anti LA ( SSA) .
dsDNA
.
anti centromer .
.34 36 .
.
Schober .
?
. .
.HLAB51 .
. .
. .NSAID
.40 ?Delirium
.
.
.
.
.
.
. ,
.
.35 ,79 .
.
) (Nasogastric tube .
?
. ''.
.
).(Suctions
.
.
.
).(PEG
.41 .
) (...
.Mycobacterium tuberculosis
.
?
.
).Tuberculin Skin Test (TST
.
.
.
.
. Isoniazide
.
.36 78 .
.
.
?
Aspirin .
Aspirin + Plavix .
Coumadin
.
. .
.42
?COPD
.
.
.
.COPD-
.
COPD
.
.
COPD
.
.37
?
Cystic fibrosis .
Usual Interstitial Pneumonitis (UIP) .
Eosinophilic Pneumonia
.
Emphysema .
.38 ,42 )(Crohn's Disease
20 .
. 5-
. .RLQ-CT-
20"
.43 -
?Diffuse large B-cell lymphoma
. rituximab
.cure-
130
128
.
.
.
) (relapse
.
.8;14
80%-
.
.49 ) (increment
6
, ?DIC
2000 .
5000 .
50000
.
10000 .
.44
)< (50% ?DVT
. .
. .
. .
. ".
.50 ,30
.HBV- ,
. HBV-DNA
600 ) ( ,
) AST (ALT- .
?
. .
. .Lamivudine-
. .Interferon alpha -
. .Tenofovir-
.45 54 ,
. - LV
LVEF .32%
.ACE
?
.Spironolactone (Aldacton) .
.Beta-blocker or Verapamil (Ikacor) .
Beta-blocker and Spironolactone
.
).(Aldacton
Verapamil (Ikacor) and Spironolactone
.
).(Aldacton
.51 ?
.
. .
. .
.
.
.
.
.46
)?(Rheumatoid Arthritis
. .
.
RF .
. -
.Methotrexate
.
.
.52 :
Specific gravity: 1.015, Protein: 1+, Blood:
Microscopy: 20-30 erythrocytes/hpf, 15-+2
.+++ 25 leukocytes/hpf, Eosinophils
?
. ,19 ,
.
. 65
) (OMEPRAZOLE .
. 55 ,
.
. 25 ,
.
.47 20 ,C40
.
. 20,000 -".
Streptococcus
pneumonia MIC < g/ml
.0.01
.IV penicillin G
,
. ,
?
.
.
.
.vancomycin
. .
. gentamicin .
.53 ACE
?
. 60
.
. 70
.
. 70 "
.
. 30
.
.48
?
. .
. Neisseria
.meningitides
. .hepatitis C virus
.54 ,
?
131
129
,
.
?
Prednisone .
Fentanyl patch .
(Acamol (Paracetamol .
(Voltaren (NSAID .
Glomerular Filtration Rate
((GFR.
.
.
.
.
.GFR-
.
.60
?HCV-
. HCV
.
. / / ,
.
. HCV
.
. HCV
Ribavirin- Interferon-
.
.55 ,42 ,
.
.
) .(VPB'S ?
. I
.
.
.
.
.
.
.
.61 ,30
. ,
.
.
.
TSH -Free T4 ,
Free T3 , .
?
Hashimotos thyroiditis .
Subacute thyroiditis .
Sick euthyroid syndrome .
Central hyperthyroidism .
.56 55 ,
.
160/100" , ,
.
),Creatinine: 95 mmol/L (Normal 60-110
)Na: ,pH: 7.5, HCO3: 28 mEq/L (18-24
145 mmol/L (135-145), K: 2.8 mmol/L
) .(3.5 5 " ,
?
. .
. .
. .
. CT .
.57
multiple myeloma monoclonal
gammopathy of undetermined
?(significance (MGUS
.
.
.
.
.
.
.IgA
.
.58
.
,
- ,
. NYHA
?
I .
II .
III .
IV .
.63 20
, .
3 .
?
. .
. 3.
CPK ..(Normal < 170) 700 ,
. .
.59 ,81
- ,
.Osteoarthritis
.64 50
" " ) obstructive sleep
.(apnea
.
132
130
, .
Prograf (FK-506), Prednisone, :
(Mycophenolate), Simovil )Cellcept
.(Simvastatin
. - .
,+++- ,
.
?
. .
. .
. -.
. .
- ,
SKIN TAGS , .
?
)Growth hormone (GH
.
)Insulin like growth factor-1 (IGF-1
.
Cortisol
.
Growth hormone releasing
.
(GHRH)hormone
.65 22
.
. :
(Na+: 137 mmol/L (Normal 135-145
(K+: 2.7 mmol/L (Normal 3.5-5
)pH: 7.30, HCO3:17 mEq/L (Normal 18-24
( Cl: 110 mmol/L (Normal 98-108
Urine electrolytes: Na:5 mmol/L, K:10
.mmol/day ?
.
.
.
.
.70
)
?(1
. 60 ),(Cloxacillin
. :
. :
, ,+ .
. 20 .
: C3 ,.
: ,.
. 17
.
: , ,
: .
. 65 )(Simvastatin
, .
:
, : , .
.
.
.
.
.66
?
.
, .
. "
.
.
.
. 2 3
.Light
.71 21 .
14
. MRI
) .(2
,
?
Prolactin .
Growth Hormone .
ACTH .
TSH .
.67 48 .PE -
.
+3 . :
,,
. +4 ,
.
?
Goodpasture's syndrome .
Wegener's granulomatosis .
Membranous nephropathy .
IgA nephropathy .
.72 32 10"
.2 , ,
) .(3
?
. 4-5
.
. 24.
. ACTH 7-8.
. MRI .
.68 21 -
.Mycoplasma Pneumomia
pan-agglutinin
4
37- . ?
. .anti-I
. -
.Mycoplasma
. .
. " .
.73
) ,(4 ?25
. C38 .
.
. . .
. HIV
.
. , , C39,
.
.69 ,55
Itraconazole-
.
133
131
.
?
.
.
.
.
.
.
.
.
.74 50
.
- .
" ) .(5
"?
. " .
. .I.V. Amiodarone (Procor)-
. .IV Magnesium
. I.V. Lidocaine
.75 19 ,
12- .
, ,
. Hemoglobin 6.7
.%g . .
) ?(6
.
.
.
.
.80 40
. MRI-
)
.(11
,HIV CD4 .40
?
. " Listeria
monocytogenes
Cerebral toxoplasmosis .
CNS Cytomegalovirus (CMV) infection .
Mycoplasma pneumonia encephalitis .
.76 ,66 ,
.
, .
" ,120/80 .60 "
) .(7
) ,(PRIMARY PCI
. ?
. .
.
.
.
) (.
. , ,
.
.81 35
. ,
. : ,
,c40 96 ," .110/70
. - ,
,%G11 ,L/10,000
.L 88,000 / .
?12
Babesia microti .
Plasmodium falciparum .
Borrelia recurrentis .
Ehrlichia canis .
.82 " ) (13
:
?
.
.
. .
. ) (Primary PCI
.
.
.
.77 41
. -
,
) .(8
.Uveitis
?
. .
. .
. .
ANA .
.78
?9
. ,
.
.
.
.
.
. ,SLE
.
.
62% .
) .(10 .
.
134
132
.85
?
..
. .
..
..
.93
SLE ?
. ).(arthritis
. ).(Pleuritis
. .
. .
.86
?
. D
.
.
.
. .
.
.
Gentamicin .94
?
. Listeria
.monocytogenes
.
.Staphylococcus aureus
. Enterococcus
.faecalis
. Bartonella
.henselae
.87
-Thalassemia ?
.
-.
. -.
.
-.
. Thalassemia.
.95 ?
.
.
.
.
.88
, ?
Prostacyclins .
ACE inhibitors .
.Phosphodiesterase-5 inhibitors .
.Endothelin antagonists .
.96
?
Cataract .
Hyperkalemia .
.Myopathy .
Osteoporosis .
.89
?
. 50 .
. 38 .
. 19 ,
.
. 30 - ,,
7 .
.97 H. Pylori-
?
Gastric Ulcer .
Gastro-Esophageal Reflux Disease .
MALT Lymphoma .
Gastric Carcinoma .
TIMI-risk score .98 Non-ST elevation acute
coronary syndrome
.90
) (Ulcerative Colitis ?
. .
.Prednisone .
. (Amino Salicylic Acid (5-ASA-5
. .TNF
,
.
, ?
. 150/90- .
. .
. 24
.
.
.50%
.91 Syndrome of
) Inappropriate ADH Secretion (SIADH
?
. 100/"
.
. 40/.
. - .
. .
.92 - ) Basic Activities of
(Daily Living, BADL ?
.
.
.
.
.
.
.
.
135
133
.1 .26
.2 .27
.3 .28
.4 .29
.5 .30
.6 .31
.7 .32
.8 .33
.9 .34
.10 .35
.11 .36
.12 .37
.13 .38
.14 .39
.15 .40
.16 .41
.17 .42
.18 ? .43
.19 .44
.20 .45
.21 .46
.22 .47
.23 .48
.24 .49
.25 .50
.51
.52
.53
.54
.55
.56
.57
.58
.59
.60
.61
.62
.63
.64
.65
.66
.67
.68
.69
.70
.71
.72
.73
.74
.75
.76
.77
.78
.79
.80
.81
.82
.83
.84
.85
.86
.87
.88
.89
.90
.91
.92
.93
.94
.95
.96
.97
.98
136
134
- 3000
.1
40
.
.
.
5" /.
MCV .88
. -
?
Coombs positive hemolytic anemia .
. .
. .
. .B 12
Anti endomesial antibodies .
.2
54 .
,
metatarsophalangeal joint - .
?
.
.
.
3-10
. allopurinol -
.3
.1 ,67
COPD 10- .
agonist Tiotropium -
.(bronchodilator)anticholinergic
,
)
( , 38
. , ,
24 , 89% .
"
.
. ?
. , agonist
, , .
. , agonist
, .
. , agonist
, , .
. agonist ,
.
. agonist ,
.CPAP-
.5 24
.
.
.
.
. -
?
methicillin susceptible Staphylococcus
.
.
.
.
.
aureus
methicillin resistant Staphylococcus
aureus
methicillin susceptible staphylococcus
epidermidis
Methicillin resistant Staphylococcus
epidermidis
Enterococcus faecium
.6
a ?
. )"( .
. .
. .
.
.
. .
.7 -
mosmol 600 ,
?
20 .
16 .
12
.
10 .
8 .
.8 58 20
,HIV " " .
viral load , , CD4 .150
.oral thrush
?
. .
. .
.
cd4 .
.
.
. acute HIV infection
.
.9
)?(TPN
. .
. -
. -
.
. .
.4
. ,
.
. ?
Psuedomonas aeroginosa .
Herpes simplex type II .
Q fever .
Vibrio vulnificus .
Clostridium perfingens .
.10
137
135
91 .
.
.myelodysplastic syndrome
?
.
.
.
.
.
1/20000.
.
.
.
.
.15 28 38.5 ,
.
.Shigella -
Shigella -
?
Shigella flexneri .
Shigella boydii .
Shigella sonnei .
Shigella dysenteriae .
Shigella suiss .
.11 30 .
, ,
.
.
.
?
. .
. .D-DIMERS
CT ..
. .
US . .
.16 ,25 , ,
, .
, ,
. .
.
.
?
. , CT .
. .
. .
. .
. MRI .
.12 72
' .
, , .
,
.
.
.
?
.
.
. "
.
. "
.
.
.
. " .
.17 45 ,
, ,
.
.
.
?
Allergic rhinitis and sinusitis .
mononeuritis multiplex .
glomerulonephritis .
Cardiac involvment .
Subcutaneous nodules .
.18
?(Systemic lupus erythemathosus (SLE
. 0.7 ,
, 70,000
,,
. 0.7 , ,
, 1800
. 1000 ,
, 70,000
,,
. 0.6 , 1000
, ,
. , , ,
, 70,000
.13
?
AMA .
PANCA .
US .
anti-smooth body antibodies .
MRCP .
.14 ,60 ,
.
?
.
.
. 3 3-
".
. ) 7-"(.
. .
. , 4".
.19
anti-TNF - Rheumatoid -
?arthritis
.
.
.
.
.
138
136
PTPTT -
355000 .
.
,
?
. V
. VII
. VIII
. X
. XII
.20
diffuse scleroderma - ?limited -
.
.
.
.
.
.21 45 ,
, .
186/98" , 20,000
, 1.6
"/" .
.
?
Hodgkin lymphoma .
Non-Hodgkin lymphoma .
Marginal zone lymphoma .
Chronic lymphocytic leukemia .
Hairy cell leukemia .
.26
?ACUTE STEMI
. .
. . 160/100" .
. .
..
. .
.27 40
, ,
210/127" .-
1.7"/" , 8.7/"
87,000 .
?
angiotensin converting enzyme inhibitors .
aspirin .
prednisone .
cyclophosphamid .
anti-TNF .
.22
. ?
. .
. ) (EUS
. octreoscan -
. PH
MRI ..
.28
?
Chlorambucil . .
Bleomycin . .
Melphanan . .
Cyclophosphamide .
Carboplatin .
.23 28
.
.
?
. , ,
. , ,
. , ,
. , ,
. , ,
.29 71 ,
.
- ,mEq/L 128
mosmol/Kg 120
.mEq/L 55 ,
, ?
.
.
.
.
.
.
.24 55 ,
.
. Q FEVER ) IGM-
.(IGG phase I ,TEE
. ?
. Q fever
.
.
.
.
.Duke's Criteria
. ,
.
. .Q fever endocarditis
.30 35 "
" , .
. .
.
?
.
.
.
.
.
.25
,
139
137
.
.
.
NaHCO3 .
.35 '
rheumatic fever ?
chorea .
erythema marginatum .
arthritis .
subcutaneous nodules .
group A streptococcus infection .
.31 ,80 , ,
, , .
CT . .
850 12 ,,
. CSF
.
?
. ,
, ,55
.
.
,
.
. .
.
.
.
.
.36 ,60
. ,
.
.
.mg/dL 15 PTH .
?
.
.
.
.
Volume -
.overload
. D
.32
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)( )(
,
.
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)'(
.
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5 ,
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)( ,
.
.37 62
22000 , 4500
17200 - .
.
.2
?
. INDUCTION MELPHALAN
Allogeneic stem cell transplantation .
Autologic stem cell transplantation .
.
Cyclophosphamide, daunorubicin .
)vincristine, prednisone (CHOP
.38 60
.
,
.
.sacroiliitis
, PND-
4 .
?
.
.
.
.
.
.33 , 80
.
,
. ,
?
.
.
.
.
.
.
.
.
.
.39
?
.
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.
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.
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.
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236
.
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.
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)?
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.
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.
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anterior uveitis . ?
psoriatic arthritis .
reactive arthritis .
ankylosing spondilitis .
.
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4
.
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.
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.
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.
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.
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.
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.
calcium gluconate .
.
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?
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240
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.
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.
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.
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136
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.
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241
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.
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.
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.
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- ) .
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.
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.
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.
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. ?
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.
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?
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. 5
24 , : ,126 -
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?
SIADH .
Compulsive Drinker .
Central DI .
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.115 T
?
.
. 70
. 30
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Marginal Artery Proximal LAD ,70%-
242
.25
.26
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? .74
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.106
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.108
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.113
.114
.115
.116
.117
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Daunarubicin
.
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.
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.
.
20 2 .
3
,
80 , 120
6
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.
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243
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.
.
.
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, ,12.4
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.
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1900 .
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.
.
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.
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.
.
.
.
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244
Intrahepatic Cholestasis
Hepatic Stenosis
Toxic Reaction
Idiosyncratic Reaction
Toxic & Idiosyncratic Reaction
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.
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, .
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.
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.
.
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150. ...Wide .
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.
.
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()
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02
245
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?
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.
.
.
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.
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.
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.
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.
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.
.
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.
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.
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.
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, . 240
?
Autoimmune Polyglandular Failure .
Hypothalamic Adrenal Insufficiency .
AIDS
.
.52 ,27
, ,
.
?
.
.
Meloidosis -
.
. 36
.59
?
.
.
.
.
.60 ?Polycystic Kidney Disease
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.
.
.
.
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.
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IgA Nephropathy .
Membranous Glomerulonephritis .
Membranoproliferative Glomerulopathy .
FSGS .
Amyloidosis .
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.
. 3 .
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.
= 64 ,PC02 = 84
,P02 ?
.
. Andexate IV
Naloxon IV
.
CT .
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246
Cyclophosphamides
IV
Cyclosporine
Infliximab IV
Leflunomide +
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.
.
.
.
.
03
.70 , .
ELISA .HIV-
?
. Acute HIV
. Viral Load
. CD4
.63 ,,
TSH .
?
.
CT .
FNA .
.
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p53 .
fas .
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.
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.
.
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.
. 24
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.
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.
.
.
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. ALT
. RNA HCV
.
.
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.
,
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.
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.
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.
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CT .
.
.
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, ,Hb=9.6 ,
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.
.
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.
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.
.
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.
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C3 pANCA . .
.
?
AntiGBM Disease .
Wegener Granulomatosis .
FSGN .
IgA Nephropathy .
.69
, antiHBs AgHBs Ag ,
antiHBe IgM , , HCV.
?
.
.
Lamivudin .
. Acute Hepatitis B
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. .270
04
247
80 .40
?
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.
DI .
DI .
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.
.
.
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APLA .
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. .
. .
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. ,
.
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.
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.
.
.
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.
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.
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.
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.
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6 .
2 .
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48
.
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.
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.
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248
05
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.
.
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.
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.
.
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,
,
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.
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,
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.
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.
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.
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.
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27 .
.
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.
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.
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249
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07
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.
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.
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? .12
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.26
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.28
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,
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.
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251
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272
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2005
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Idiopathic MDS is a disease of the elderly; the mean age at onset is 68 years.
:
RAEB1- ;5%- MDS-
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( 40% RAEB1/2) 10-19% RAEB2- 5-9%
Polyuria .1
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.10
MYELODYSPLASIA
DEFINITION
The myelodysplasias (MDS) are a heterogeneous group of hematologic disorders
broadly characterized by cytopenias associated with a dysmorphic (or abnormal
appearing) and usually cellular bone marrow, and consequent ineffective blood cell
production. A clinically useful nosology of these entities was first developed by the
French-American-British Cooperative Group in 1983. Five entities were defined:
refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS),
refractory anemia with excess blasts (RAEB), refractory anemia with excess blasts
in transformation (RAEB-t), and chronic myelomonocytic leukemia (CMML). The
World Health Organization classification (2002) recognizes that the distinction
between RAEB-t and acute myeloid leukemia is arbitrary and groups them together
as acute leukemia, notes that CMML behaves as a myeloproliferative disease, and
separates refractory anemias with dysmorphic change restricted to erythroid lineage
from those with multilineage changes (Table 94-5).
2006
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Most patients die as a result of complications of pancytopenia and not due to
leukemic transformation; perhaps one-third will succumb to other diseases
unrelated to their MDS
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Factor XI deficiency .23
In the absence of prophylactic antiretroviral therapy to the mother during .28
pregnancy, labor, and delivery, and to the fetus following birth (see below), the
probability of transmission of HIV from mother to infant/fetus ranges from 15 to
25% in industrialized countries and from 25 to 35% in developing countries. These
differences may relate to the adequacy of prenatal care as well as to the stage of
HIV disease and the general health of the mother during pregnancy. Higher rates
of transmission have been reported to be associated with many factors; some of
these are well proven by a number of studies, while others are considered to be
potential factors since various studies may have given divergent results. The bestdocumented factor that is associated with higher rates of transmission is the
presence of high maternal levels of plasma viremia. Low maternal CD4+ T cell
counts have also been associated with higher rates of transmission; however, since
low CD4+ T cell counts are often associated with high levels of plasma viremia, in
one study using multivariate analysis including plasma viral load and CD4+ T cell
count, only the level of plasma HIV RNA was significant.
:
HAART
HIV
.
C/I
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.
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.
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TB
. 9
" 15
.
:
The cutoff for a positive skin test (and thus for treatment) is related both to the
probability that the reaction represents true infection and to the likelihood that the
individual, if truly infected, will develop tuberculosis (Table 150-4). Thus positive
reactions for close contacts of infectious cases, persons with HIV1 infection,
persons receiving drugs that suppress the immune system, and previously untreated
persons whose chest radiograph is consistent with healed tuberculosis are defined
as an area of induration =5 mm in diameter. A 10-mm cutoff is used to define
positive reactions in most other at-risk persons. For persons with a very low risk of
developing tuberculosis if infected, a cutoff of 15 mm is used. Treatment should be
considered for persons from tuberculosis-endemic countries who have a history of
.BCG46 vaccination
321
289
Complete oral
Primaquine
absorption; active
compound not
known; t1/2: 7 h
Pharmacokinetic
Drug(s)
Properties
322
falciparum
Radical cure;
eradicates
hepatic forms
of P vivax
and P ovale;
kills all stages
of gametocyte
development
of P
Antimalarial
Activity
323
Nausea, vomiting,
diarrhea, abdominal
pain, hemolysis,
methemoglobinemia
Minor Toxicity
1232
Primaquine (0.5 mg of base/kg or 30 mg, daily adult dose) has proved safe and
effective in the prevention of drug-resistant falciparum and vivax malaria in adults.
Abdominal pain and oxidant hemolysis, the principal adverse effects, are not
common as long as the drug is taken with food and is not given to G6PD-deficient
persons. Primaquine should not be given to pregnant women or neonates.
, , . 4- 2
.32
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-' .34
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, low gradient .35
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70%
.
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- ,
.40
.
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.TG
.41
Beta-Adrenoceptor Blockers
While the abrupt administration of large doses of beta-adrenergic receptor blockers
can intensify HF, especially acute HF, the administration of gradually escalating
doses has been reported to improve the symptoms of HF, and to reduce allcause death, cardiovascular death, sudden death, rehospitalization for HF, and
pump failure death in patients with chronic heart failure already receiving ACE
inhibitors (Table 216-3). These drugs are indicated in patients with moderately
severe HF (classes II and III), but are not indicated with unstable HF, in hypotensive
patients (systolic pressure < 90 mmHg), in patients with severe fluid overload, in
patients who have required recent treatment with an intravenous inotropic agent, and
in patients with sinus bradycardia, atrioventricular block, or a bronchospastic
disorder.
Three beta-adrenergic blockers (metoprolol, bisoprolol and carvedilol) have been
shown to improve survival in patients with HF. The first two are selective and block
only 1 receptors, while the third blocks both 1 and 2 receptors as well as
receptors, thereby causing mild vasodilation. Carvedilol also appears to exert
antioxidant activity.
Before commencing beta-blocker therapy, patients should be stabilized on an ACE
inhibitor, diuretics and possibly digoxin. They should be begun in very low doses,
e.g., carvedilol 3.125 mg bid or metoprolol XL 12.5 mg qd and titrated upward
slowly every 2 to 4 weeks. During titration, the patients should be observed closely
for hypertension, bradycardia, and worsening HF. Approximately 15% of patients
Massive
hemolysis
in subjects
with severe
G6PD
deficiency
Major
Toxicity
,
" ,
.43
.
Shock Secondary to Right Ventricular Infarction 255 ,16 .46
(22 ) - 1456 " :
)
,15
.
(
cannot tolerate beta blockade, and an equal number cannot tolerate target doses
(carvedilol 25 mg bid and metoprolol XL 200 mg). In the latter, low-dose betablocker therapy is preferred to no therapy.
Once a maintenance dose has been achieved, administration of the beta blocker
should be continued indefinitely. If treatment of a patient on a beta blocker with a
positive inotropic agent is required, a phosphodiesterase III inhibitor (see below)
should be used.
290
325
<65
6575
>75
Aspirin or warfarin
Warfarin[target INR 2.5 (range 2.03.0)]
Aspirin
Warfarin[target INR 2.5 (range 2.03.0)]
Recommendations
324
:1347 '
Atrial flutter is usually less long-lived than is AF, although on occasion it may
persist for months to years. Often, if it lasts for more than a week, atrial flutter will
convert to AF. Systemic embolization is less common in atrial flutter than in AF.
Although atrial flutter is associated with a slightly lower risk of embolization than
AF, the same precautions should be followed in regard to anticoagulation as are
used with AF.
:
special considerations 230 16 .56
Diabetes Mellitus
The diabetic patient with hypertension is particularly challenging to treat because
multiple agents are usually needed to achieve goal blood pressure and because many
of the agents used to lower blood pressure can affect glucose metabolism adversely.
ACE inhibitors or angiotensin receptor blockers should be first-line therapy in
hypertensive individuals with type 2 diabetes. They have no known adverse effects
on glucose or lipid metabolism and minimize the development of diabetic
nephropathy by reducing renal vascular resistance and renal perfusion pressurethe
primary factor underlying renal deterioration in these patients (Chap. 323). Metaanalyses of clinical studies have demonstrated that setting a lower blood pressure
goal in diabetic patients is ideal to prevent progression of end-organ disease, with
current recommendations shifting from 130/85 mmHg downward to 130/80. The
average hypertensive diabetic patient will require at least three medications to
achieve appropriate control.
1353 ,16 .58
60-120 ,slow VT
Accelerated idioventricular rhythm
,
,- , .
,
, ,
) . .
.
.(
"
slow ,AIVR) Accelerated idioventricular rhythm - 1456 ' ,16 :
. 60-100 (ventricular tachycardia
.-
25%- ,STEMI
. ,
:1418 .59
This disorder results when the healing of an acute fibrinous or serofibrinous
pericarditis or a chronic pericardial effusion is followed by obliteration of the
pericardial cavity with the formation of granulation tissue. The latter gradually
contracts and forms a firm scar, encasing the heart and interfering with filling of the
ventricles.
Risk factors are prior transient ischemic attack, systemic embolus or stroke,
hypertension, poor left ventricular function, rheumatic mitral valve disease,
prosthetic heart valve, congestive heart failure.
Risk Factorsa
Age, years
291
concentrating ability. This defect usually does not improve with administration of
vasopressin and is therefore a form of acquired nephrogenic diabetes insipidus.
Disturbances in sodium chloride transport in the ascending limb of Henle and, in
azotemic patients, the osmotic (urea) diuresis per nephron lead to decreased
medullary hypertonicity and hence a concentrating defect. Partial obstruction,
therefore, may be associated with increased rather than decreased urine output.
Indeed, wide fluctuations in urine output in a patient with azotemia should always
raise the possibility of intermittent or partial urinary tract obstruction. If fluid intake
is inadequate, severe dehydration and hypernatremia may develop. Hesitancy and
straining to initiate the urinary stream, postvoid dribbling, urinary frequency, and
incontinence are common with obstruction at or below the level of the bladder.
(! 50% )
. IgA nephropathy
.82
.
1.018 < SG - Pre-renal ARF- .83
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CT .
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thoracentesis ;
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FMF 5% -
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FMF -
.
,erysipelase-like erythema FMF -
-
.5
, ,
,
.
,pleurisy , ,
326
.
ABC ,
( )
(
)
90 " )
.
.() ( 120
327
292
329
,
SSc- 5-40%- Anti-Polymerase I, II, III
SSc- 14%- Anti-Th RNP .
95-- ,
SSc- 5-10%- Anti-U1 RNP .
(anti-fibrillarin) Anti-U3 RNP .(MCTD)
-
100%
,
SSc- 5%-
SSc- 25%- Anti-PM/Scl ; "
,
.
Antinucleolar antibodies are relatively specific for SSc and are present in 20 to
30% of patients. Several antinucleolar antibodies have been associated with SSc:
Anti-RNA polymerases I, II, and III are found in patients with diffuse cutaneous
SSc who have a higher prevalence of renal and cardiac involvement. Anti-Th
RNP has been found in patients with limited cutaneous SSc, and anti-PM-Scl,
formerly referred to as anti-PM1, along with anti-Ku, may be found in a subset
of patients with overlapping features of limited cutaneous SSc and polymyositis.
Anti-U3 RNP (anti-fibrillarin) is also highly specific for SSc and may be
associated with skeletal muscle disease, bowel involvement, and pulmonary
arterial hypertension. Anti-U1 RNP is found in 5 to 10% of SSc patients and in
95 to 100% of those patients with the overlap syndrome of MCTD. The titers in
MCTD are usually high. Anti-SS-A (Ro) and/or anti-SS-B (La) are present in
those patients with overlap syndrome of SSc and Sjgren's syndrome.
hypertrophic Osteoarthropathy .113
.OA -
.114
)
,
.
,-tramadex (
.
.OA -
1962 ' ,10%-
.115
;1962 ' ,
X-
45 >
50 ;1963,
/
;1963-4 ,
1964 ,
.116
Vascular Occlusions
The prevalence of transient ischemic attacks, strokes, and myocardial infarctions is
increased in patients with SLE. These vascular events are increased in, but not
exclusive to, SLE patients with antibodies to phospholipids (aPL). Ischemia in the
brain can be caused by focal occlusion (either noninflammatory or associated with
vasculitis) or by embolization from carotid artery plaque or from fibrinous
vegetations of Libman-Sachs endocarditis. Appropriate tests for aPL (see below)
and for sources of emboli should be ordered in such patients to estimate the need for,
intensity of, and duration of anti-inflammatory and/or anticoagulant therapies. In
SLE, myocardial infarctions are primarily manifestations of accelerated
atherosclerosis. The increased risk for vascular events is as much as 50-fold in
women with SLE <45 years old compared to healthy women. Characteristics
associated with increased risk for atherosclerosis include older age, hypertension,
dyslipidemia, aPL, repeated high scores for disease activity, and high cumulative
doses of glucocorticoids. When it is most likely that an event results from clotting,
long-term anticoagulation is the therapy of choice. Two processes can occur at
oncevasculitis plus bland vascular occlusionsin which case it is appropriate to
treat with anticoagulation plus immunosuppression.
328
()
.
.VENULAR LEAKAGE
,
I.V
.
"
,
/
-
,
, /
.
: .110
,
) .
,
,
,
, .(
.
,
GRANULAR ,
-
.
.
SPARKLING
.()
"
.
, 2B
,.
.
POST CAPILLARY
293
330
331
Cardiac Manifestations
Pericarditis is the most frequent cardiac manifestation; it usually responds to antiinflammatory therapy and infrequently leads to tamponade. More serious cardiac
manifestations are myocarditis and fibrinous endocarditis of Libman-Sachs. The
endocardial involvement can lead to valvular insufficiencies, most commonly of
the mitral or aortic valves, or to embolic events. It has not been proved that
glucocorticoid or other immunosuppressive therapies lead to improvement of lupus
myocarditis or endocarditis, but it is usual practice to administer a trial of high-dose
steroids along with appropriate supportive therapy for heart failure, arrhythmia, or
embolic events. As discussed above, patients with SLE are at increased risk for
myocardial infarction, usually due to accelerated atherosclerosis.
. Ankylosing Spondylitis - .117
(
) : .118
,
,
.
,
,
:
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. 2-4
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,
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,
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, :
2022
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,
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.GI
,
ACTH
.
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,
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.
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:
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,
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) TT4
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.(2108
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35 mg/dL
A1C- 1% x
A1C ADA- " ,
x
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x
.(
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;
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(A1C-
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x
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,
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(
,)
.
294
130/ 85 mmHg
Blood pressure
Fasting glucose
333
.
.142
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.(
)
The most important viruses causing sporadic cases of encephalitis in .144
immunocompetent adults are HSV-1, VZV and, less commonly, enteroviruses.
.
HSV1 ...
.CSF - RBC - ,
EEG ,
: .145
.
,
,
.LP
MRI CT ,
"
. LP-
NSAIDS .
1646 .146
,
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(
)
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.148
.149
Side effects include the potential for an increased risk of serious infections.
Particularly notable is the capacity of TNF blockade to increase the risk of
developing reactivation of dormant tuberculosis. It is prudent to carry out
tuberculin skin testing and, if necessary, further evaluation with chest radiographs
before beginning therapy with an anti-TNF agent to limit the chance of inciting
Overweight and obesity are associated with insulin resistance and the metabolic syndrome.
However, the presence of abdominal obesity is more highly correlated with the metabolic
risk factors than is an elevated body-mass index (BMI). Therefore, the simple measure of
waist circumference is recommended to identify the BMI component of the metabolic
syndrome.
b
Some male patients can develop multiple metabolic risk factors when the waist
circumference is only marginally increased, e.g., 94102 cm (3739 in.). Such patients may
have a strong genetic contribution to insulin resistance. They should benefit from life-style
changes, similarly to men with categorical increases in waist circumference.
Men
Women
HDL cholesterol
Women
Triglycerides
Abdominal obesitya
225 ,
-
8 ,Online .141
:225-3 ,
332
2
.(
.
"
335 ,
14 ,-
.137
:
HMG-CoA reductase inhibitors are well tolerated and can be taken in tablet form
once a day. Potential side effects include dyspepsia, headaches, fatigue, and muscle
or joint pains. Severe myopathy and even rhabdomyolysis occurs rarely. The risk
of myopathy is increased by the presence of renal insufficiency and by
coadministration of drugs that interfere with the metabolism of HMG-CoA
reductase inhibitors, such as erythromycin and related antibiotics, antifungal
agents, immunosuppressive drugs, and fibric acid derivatives. Severe
myopathy can usually be avoided by careful patient selection, avoidance of
interacting drugs, and by instructing the patient to contact the physician
immediately in the event of unexplained muscle pain. In the event of muscle
symptoms, the plasma creatine phosphokinase (CPK) level should be obtained to
document the myopathy, but serum CPK levels do not need to be monitored on a
routine basis as an elevated CPK in the absence of symptoms does not predict the
development of myopathy and does not necessarily suggest the need for
discontinuing the drug.
,Atorvastatin ,HMG-CoA reductase inhibitors
(Link)
:Interactions
The risk of developing myopathy during therapy with HMG-CoA reductase
inhibitors ('statins') such as atorvastatin (CYP3A4 substrate) [5460] is
increased if coadministered with CYP3A4 inhibitors [5506]. Examples of
CYP3A4 inhibitors include but are not limited to: clarithromycin, erythromycin,
fluconazole, imatinib, STI-571, itraconazole, ketoconazole, troleandomycin, and
voriconazole.[4718] Itraconazole increases the AUC of atorvastatin by 2.5-fold,
which is substantially less than the effect of itraconazole on the AUC of simvastatin
and lovastatin (increased 19-fold and 20-fold, respectively).[5790] [5791] [5792] [5793]
Coadministration of atorvastatin with erythromycin increases atorvastatin
plasma concentrations by about 40%.[5460]
HMG-CoA reductase
:
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The UKPDS demonstrated that each percentage point reduction in A1C was associated
with a 35% reduction in microvascular complications. As in the DCCT, there was a
continuous relationship between glycemic control and development of complications.
Improved glycemic control did not conclusively reduce (nor worsen) cardiovascular
mortality but was associated with improvement with lipoprotein risk profiles, such as
reduced triglycerides and increased HDL.
One of the major findings of the UKPDS was that strict blood pressure control
significantly reduced both macro- and microvascular complications. In fact, the
The possibility of lymphoma must be considered whenever a patient with celiac sprue
previously doing well on a gluten-free diet is no longer responsive to gluten restriction
or a patient who presents with clinical and histopathologic features consistent with
celiac sprue does not respond to a gluten-free diet
90
Failure to Respond to Gluten Restriction
The most common cause of persistent symptoms in a patient who fulfills all the criteria
of the diagnosis of celiac sprue is continued intake of gluten. Gluten is ubiquitous, and
significant effort must be made to exclude all gluten from the diet... About 90% of
patients who have the characteristic findings of celiac sprue will respond to complete
dietary gluten restriction. The remainder constitute a heterogeneous group (whose
condition is often called refractory sprue) that includes some patients who (1) respond
to restriction of other dietary protein, e.g., soy; (2) respond to glucocorticoids; (3) are
"temporary," i.e., the clinical and morphologic findings disappear after several months
or years; or (4) fail to respond to all measures and have a fatal outcome, with or without
documented complications of celiac sprue, such as development of intestinal T cell
lymphoma.
83
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infections and atypical mycobacterial infections.
2007
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lack sensitivity thus if the first specimen is negative and diarrhea presists,testing of
additional stool spicimemens increase the likklihood of diagnosis. empirical treatment
is appropriate if CDAD is strongly sespected on clinical grounds
....
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MRI .
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antinuclear antibody .
anti dsDNA .
anti SM .
anti RO .
anti phospholipids .
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Cutaneous Systemic Sclerosis
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CHF .
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RV .
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HBsAb . anti HBc
.50 ,73 , :
68% 28,000
cd22, cd21 low grade -
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.
.
.
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.
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.
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120/80 32 - 91%
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.
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.
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.
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?
fusid, digoxin, spironolactone .
enalpril, atenolol, clopidogrel .
digoxin, fusid, Coumadin .
enalapril, fusif, hidralazine .
enalapril, fusid, spironolactone, carvedilol .
.46 , 24 ,
. .
?
.
.
.
.
.
.53
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.
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.47
.
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.
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.
.
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, . ?
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.
.
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colitis
. ,47 10
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.
,
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.
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.
.
.
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310
65
.
.
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.
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.
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?
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.
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.
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?
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.
.
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.65 ,
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PH = 7 .
.
LDH .
.
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, ( PTH 160) ,
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?
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.
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42% . ,
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G-CSF .
GM-CSF
.
.
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?
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.
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.
.59 ?
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.
.
.
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.
.
.
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. ,OA RA
. RF 20%10
,
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. Generalized
.61 .
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?
proximal RTA .
.
Conn's syndrome .
.
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ATRIAL FLUTTER .
WPW
.
.
.
.
.
.
.
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10%
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?
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.
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.
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, ramipril
. ?
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Furosemide .
Thiazide .
Hydralazine .
Diazoxide .
.84 AML ,
.
?
. 0.9% ,
.
.
.
312
Prone
Tidal Volumes
.85 .Na=158
12 ?
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146 .
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?
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.
.
.97 72 3 38.6
.
: ESR ..
: .T12 :
. ?
staph aureus .
group B strep .
E. coli .
salmonella typhi .
pseudomonas aeruginosa .
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.
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. :
.
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?
congenital lipodystrophy .
hairy cell leukemia .
myelodysplastic syndrome .
gaucher disease .
aplastic anemia .
.110 30 ,
,
LH+FSH . . MRI -
2.5 -" . ?
. ,
. .
. MRI
. DOPAMINE AGONISTs
MRI ,
. DOPAMINE AGONISTs
MRI
.104 ,60 ,
.
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200 30% ,
100 .
?
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PCR . (HSV) Herpes Simple CSF
.
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. HSV-ll
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?
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.
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90 . 37.8
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.
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- ?
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.
.124 48
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.
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?
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Goodpasture .
HSP
.
Sarcoidosis .
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.
.
.
.
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.
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.
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.
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NOMONORM
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315
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.
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. CD -
. CD4 200
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. ?
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CALCIUM CHANNEL BLOCKER .
THIAZIDE .
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. .
?
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.
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.
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11 . 0.9
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.
.
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?
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.
.1
.2
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.5
.6
.7
.8
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.15
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.20
.21
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70
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317
199
" .( ,372 ) 2565 ' ,'
: .23
IV
,
.
B
.
.
.CNS
"if PBP is suspected and multiple organisms :750 112 ,' : .22
including anaerobes are recovered from the peritoneal fluid, the diagnosis must be
reconsidered and source of secondary peritonitis sought"
.
198
1472 ' ,
: .16
214-6 1346 .
: .15
!%40 EF
,
.AF
.
LVEF < 40% and/or CHF
RF ( ) 1976 ( ) 1973 '.' : .14
.
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319 ) 2099 ' : .8
.
DI
.
318
201
SCLC- .566 ,': .44
.
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.
- 1500 ' ,' : .42
.
FEV1/FRC ,RV- ,TLC-
.( ,214 ) 1345 ' ,' : .41
.
3 1.8 INR
.
. 48-
.
48-
.40<
:1791 ' ,'
: .40
The most common cause of persistent symptoms in a patient who fulfills all the
criteria for diagnosing celiac sprue is continued intake of gluten. Gluten is ubiquitous,
and significant effort must be made to exclude all gluten from the diet. Use of rice in
place of wheat flour is very helpful, and several support groups provide important aid
to patients with celiac sprue and to their families. More than 90% of patients who
have the characteristic findings of celiac sprue will respond to complete dietary gluten
restriction. The remainder constitute a heterogeneous group (whose condition is often
called refractory sprue) that includes some patients who (1) respond to restriction of
other dietary protein, e.g., soy; (2) respond to glucocorticoids; (3) are "temporary"
(i.e., the clinical and morphologic findings disappear after several months or years);
or (4) fail to respond to all measures and have a fatal outcome, with or without
documented complications of celiac sprue, such as development of intestinal T cell
lymphoma.
200
high
:aortic regurgitation
. : .35
,decrescendo ,(...
?) blowing ,pitched
.(1400 16
)
3-
2 bisferiens pulse
,16
1305
.(HCM ) aortic regurgtaion
;
:
.(- 242 ) 1554 ' ,' : .34
;
;
;
;
(
)
.
.
" .(91 ) 599 ' / : .31
MCV- RDW-
.(
)
.
'
(
)
319
203
.
.
.(311 ) 2027 ' ,'
: .60
.
.
K
" .( 103 ) 692 ' ,'
'
: .59
.
-
.
, PTH- D .(331 ) 2248 ' ,' : .58
- .PTH-
( )
"
.
"
"
HPT
'
.PTHrP PTH-
.
"
.
PTH-
"
.590-591 ' , : .56
- ' .
.
.RBC
. ,
,
,
..
.PO
Manometry shows the basal LES pressure to be normal or elevated, and swallowinduced relaxation either does not occur or is reduced in degree, duration, and
consistency. The esophageal body shows an elevated resting pressure. In response to
swallows, primary peristaltic waves are replaced by simultaneous contractions (Fig.
286-3). These contractions may be of poor amplitude (classic achalasia) or of large
amplitude and long duration (vigorous achalasia). Cholecystokinin (CCK), which
normally causes a fall in the sphincter pressure, paradoxically causes contraction of
the LES (the CCK test). This paradoxical response occurs because, in achalasia, the
neurally transmitted inhibitory effect of CCK is absent and the direct excitatory effect
of CCK remains unopposed. Endoscopy is helpful in excluding the secondary causes
of achalasia, particularly gastric carcinoma.
A chest x-ray shows absence of the gastric air bubble and sometimes a tubular
mediastinal mass beside the aorta. An air-fluid level in the mediastinum in the upright
position represents retained food in the esophagus. Barium swallow shows esophageal
dilation, and in advanced cases the esophagus may become sigmoid. On fluoroscopy
with barium swallow, normal peristalsis is lost in the lower two-thirds of the
esophagus. The terminal part of the esophagus shows a persistent beaklike narrowing
representing the nonrelaxing LES (Fig. 286-1, panel 4).
286
:
202
:
:286 17
.' : .55
Achalasia affects patients of all ages and both sexes. Dysphagia, chest pain, and
regurgitation are the main symptoms. Dysphagia occurs early with both liquids and
solids and is worsened by emotional stress and hurried eating. Various maneuvers
designed to increase intraesophageal pressure, including the Valsalva maneuver, may
aid the passage of the bolus into the stomach. Regurgitation and pulmonary aspiration
occur because of retention of a large amount of saliva and ingested food in the
esophagus. Patients may complain of difficulty belching. The presence of
gastroesophageal reflux argues against achalasia; in patients with long-standing
heartburn, cessation of heartburn and appearance of dysphagia may suggest
development of achalasia, peptic stricture, or carcinoma on top of reflux esophagitis.
The course is usually chronic, with progressive dysphagia and weight loss over
months to years.
.(72- 19 ) 494- 121 ' ,'
: .53
.
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)
.
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, " .( ,239 ) 1532 ' ,'
: .51
30-
.
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: .50
.
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)
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205
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)
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: .93
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.
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: .86
.
)
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(ALL-
"
)
,ALL ,'
.(
, ,
:
.
, ,
,
.
.
"although granulomas are a pathognomic feature :1888 ' 17 ,' : .82
of CD, they are rarely found on mucosal biopsies."
(/ ) GIT
" :803 ' ,(?) : .80
,(
)
, .(/
) CNS
CI .(GATIFLOXACIN-
) / ,QT
.( ) 18 ,( )
DKA- .(323 ) 2160 ' ,' : .79
.
,
.5% 0.45%
."
204
RA
.'
: .77
.'
.( 222 ) 1415 ' ,' : .76
, ,
,
, ,
:
. ,
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:692 ' ,' : .75
.INR - ' ...
.(
,312 ) 2040 ' , : .74
-
;
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; :
.
;
2625 " -17 ,'
: .70
.(321 ) 2137 ' ,' : .69
,
.
90%-
:
.
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.
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.
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.(245 ) 1566 ' ,' : .65
/PF :
LDH ;0.6< LDH /PF LDH ;0.5<
.
.
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"
;7.2- PH ; : "
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.
;
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,
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,265 ) 1698 ' ,' : .61
RTA- . ,
:
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.
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321
207
,
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: .116
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'
.
" .(230- 6 ) 1480,33 ' ,' : .115
.
, "
.
ARB- ACE ,
)
.1345-1346 ' ,' : .114
.
(TEE "
65
, "
-
.
,
:
.( 214 ) 1345 ' , : .112
.TEE-
,
.(222 ) 1419 ' ,'
: .111
"
(1371)
.
SVCS.
.
.
" "
.(
) "
.
.( 216 ) 1375 ' ,' : .109
,
(CO )
.
. 50%
.(360 ) 2471 ' ,' : .108
, .2-20
.
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: .107
,
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.
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.
.
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13%)
;
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;(
2% 6%
10%
.
) 2 AIT
(
) 1 (AIT)
;(
.(
)
206
KSHV
HSV .( 173 ) 1120/1098 ' ' /' : .102
.( HHV8
) KS .(KS- )
.
.(274 ) 1755 ' ? : .101
,
.
.
.
.( 231 ) 1484 ' ,'
: .99
.
.
-
)
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.(
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(
.
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50%-
.(
,228 ) 1456 ' ,'
: .96
,
,
)
;(
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)
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.
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,
)
,(
.
.
.ICD
322
209
.
.1105 ' ,' : .136
, .PCP-
.HIB
( )
,' : .133
.
Approximately 90% of children and 50% of adults enter remission following 8 weeks
of high-dose oral glucocorticoids.
208
(' ,
)
.
"
1683 ' ,
: .125
"
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.
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HSP .
.'
'
.'
: .123
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- MM-
.(
,98 ) 659 ' ,' : .122
.( 9%-
MGUS-) MGUS
.MGUS-
BJ
.MM
,
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MNT-
.
.
.( ,283 ) 1816 ' ,'
: .119
K
.( 20 15 )
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)
,
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4 .
TSH T4 .
. ?
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. ,
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.
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US
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+ ,
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.
.
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. E
.2 82 . 1.8 :
, UREA 108 , CREATININE
.
- ,+ ,
.FeNa=0.49% 1.026 - SPECIFIC GRAVITY
?
Chronic Renal Failure .
Acute Tubular Necrosis .
Post Renal Azotemia .
Pre Renal Azotemia .
Acute on Chronic Renal Failure .
.9 + 60
Peripheral thrombophlebitis
?
CEA .
CA-125 .
CA19-9 .
ANA .
.10 35 5
. 10.
30 ,
, ,36.7 ,100 ,
- . 5000 20%
. ?
Drug reaction .
Hypereosinophilic syndrome .
Wegener .
.
.
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.
.
.
.
.
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.
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.
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.12 ,165 90 , ,142/88 -
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LDL - 145 .
. 95 -
HDL - 55 .
. 200 -
.
.5 ,180
?
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.
.
HbAlc .
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.
.
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3 . 3 ,
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. 3/6
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.
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. ?
72
323
.
.
.
CT
MRI
.21 25
. ,
ANA . anti dsDNA .
, .1+ ?
.
.
. RO
anti SM .
C3, C4 .
.14 ,72 . = Na
.120 mEQ/L ?
325
mEQ/L 10
286
.
.
.
.
TSH =11 U/L .
.23 ,30 .
MID .
.
?
.
. 600
. 600 300-
6
2 . CEFALEXIN
5 . CEEFALEXIN 1-
.24
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. RBBB ,130 ..
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.
. 88%
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38 . . .2
?
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.
.
.
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.
.
.+
.
.+
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,
.COPD ,110 ." .4
?
enoxaparin lmg/kg .
. ,
.19 68 ,
, ?
.
.
.
ERCP .
.27" Ca=12.3 .5 ?
.
.
.
.
.
.20 ?
.
.
CVA .
.
324
73
gestational HTN .
.28 .
,
, .
.P. falciparum
?
.
.
.
.
.
.36 ADPKD ,
?
.
renal vein thrombosis .
GN .
.
.29 ?
.
.
CCB .
. B
.37 ?anti-CCP -
.
. " RF
. 10%
.
.30 3 ,
DVT .
?
.
Anti-RhD .
Anti-mitochondrial antibodies (AMA( .
PANCA .
.38 4
. , HIV - CD4 .68
acid fast .
. 3
. ?
.
.
. ,
.
.
.31 30 .
.
.
, mg%74 ?
. 72
. peptidec
.
.32 HCV .
. .
,SAAG =1.2 WBC 500 60%
. ?
.
portal vein thrombosis .
.
SBP .
.
.40 ,
.
. ?
IgA nephropathy .
Goodpasture Syn .
Wegner .
Membrano proliferative .
.33 3.
." .6
?
ACS .
STEMI .
NSTEMI .
.
.
glomerolonephropathy
FSGN .
.41 80 OA
.UroSepsis
quinolone
. . ?
.
.
.
. -
. 300000
.34 .
.
.
?
lostran .
thiazide .
hydralazine .
diazoxude .
.42
?
.
. 4/6
opening snap
.
systolic click .
.35 25 ,
350 24 , 2+,
?
74
325
. HIV -
. DGI -
.43
?
sacroileitis .
uveitis
venous thrombosis .
pyoderma gangrenosum .
erythema nodosum .
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?
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prostate cancer .
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adult still's disease .
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- .
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?
.
.
.
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.
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.
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mixed metabolic acidosis with metabolic .
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.
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?
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.
.
.
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.
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AP=110, AST=40, ALT=38, .
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.
?
.
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?
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polycytemia vera .
autoimmune hemolytic anemia .
megaloblastic anemia .
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76
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?
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.
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.
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78
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.
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.
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24
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.
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.
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.
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.
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.
332
80
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.13
.14
.15
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.21
.22
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.24
.25
.26
.27
.28
.29
.30
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.32
.33
.34
.35
.36
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.41
.42
.43
.44
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.48
.49
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82
333
- 2010 '
.
.
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.
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.
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.142 .
CAD , .FAP- .2-2.5 INR
.
.
.
.
.143 .150,000 -CPK .
. 30%=EF , ?
.
IVIG .
.
380
.6 - MALT ,H. Pylori- . ?
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.
. PPI-
.
:
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.
.
.
.
.
:
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.
.
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:
subacute thyroditis
.2 , .90/40 ?
.
.
.
CT .
:
.8 ?
-N . 24
. 4-
.
.
. ,
: " arterial blood lactate levels among such patients with acute liver failure may distinguish
" patients highly likely to require liver transplantation '? ! )(
.? ' .' .
305-1 , Acetaminophen- Predictable and Dose-Related Toxicity, -
' - . ) ( ,
) ) .dose-related ' ' -
?! !!!
) ( " .
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. .
. ) (.
. .
. .
. - .
: )(848-849
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. ) 126 () ,
,(10 , ) ? 150 ?(
. ,
. 5%.
. 200 3%" 4
. FFP-
. + 5%
:?
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,80 AST 60, ALT HBsAG. anti HBcAG & anti HBs , ? AST
,60 ALT .150/90 .
.
. ) )B
.
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.
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NASH- US- .
.5 ,42 , , . .
. . ,
. ?
.
.
. Loperamide (Imodium
.
.
:
In those aged >40 years, an air-contrast barium enema or colonoscopy should
also be performed.
381
Metronidazole .
Fluconazole .
Ganciclovir .
.PPI -
:
.15 50 , , . . B,C.
.
:
ANA,
AST ALT 2
4
3" "
?
.
.
.
.
. TNF
:) ? 90% (
' . ,42-1 figure- . -
) ANA,SMA,LKM,SPEP ( , .
, . '.
, "" ,
,
.
, . .
.
) :(301
Strict diagnostic criteria have not been developed for most liver diseases, but liver biopsy
plays an important role in the diagnosis of autoimmune hepatitis, primary biliary cirrhosis,
nonalcoholic and alcoholic steatohepatitis, and Wilson's disease
) :(301-1
Liver biopsy in acute liver disease: Reserved for patients in whom the diagnosis remains unclear despite
medical evaluation.
.14 ,80 , . 10
, , ?
Acyclovir .
382
, , 50 15-25
, , ,
. '
... ,
: ) . (2.5 .
) ,1.1>SAAG - . ,2.5 - " - ,? ." -
'( ,. .
,
, ?
. .
.17 - ?HBV -
. 40
.
. HDV
. HBeAG
. ALT AST-
-
:- , 2- , 4- 3
Certain clinical and laboratory features suggest progression of acute hepatitis to chronic hepatitis: (1) lack
of complete resolution of clinical symptoms of anorexia, weight loss, fatigue, and the persistence of
hepatomegaly; (2) the presence of bridging/interface or multilobular hepatic necrosis on liver biopsy
during protracted, severe acute viral hepatitis; (3) failure of the serum aminotransferase, bilirubin, and
globulin levels to return to normal within 612 months after the acute illness; and (4) the persistence of
HBeAg for >3 months or HBsAg for >6 months after acute hepatitis.
- , AST- ALT- ...
'
- ' . .
:?
' )' 3126 (
3126 , " " ,
, -
...
OP PTH PAGET ' ?
.18 80 ,30% = EF , .
. . -
T3, T4 - normal. TSH 6.5
?
.
. 60" .
. " "
.
. } {O5 .
: , .
There are no universally accepted recommendations for the management of
subclinical hypothyroidism, but the most recently published guidelines do not
recommend routine treatment when TSH levels are below 10 mU/L.
?
TSH 4T
.
, ,
. ...30%=EF ?EF-
, EF-
.
383
. ACTH
CRH test.
:
.24 ,33 .
C-peptide . ?
.
. 2
.
factitious hypoglycemia .
Nonislet cell tumor .
:
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, " 130/80 140/85 .
.
.
. CCB
.
: ? (: (:
.25 " , . .
4.5" , )( .CT ?
. CT 6.
. .
. CT
.
: - , , )??(
, ,
... ? ' .
- ' - ) (342-12
, 342-12 ,adrenal incidentaloma .
- , 4":
However, size alone is of poor predictive value, with only 80% sensitivity and 60%
specificity for the differentiation of benign from malignant masses when using a 4-cm cutoff.
- 4 , " ..
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.
,
- .
.
,CCB - - .
- .. /
.
CT . ,
) , - 4 6" .
(.
? -' 342-12 '.
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.
.
.
.
384
.32 40 . -
3fT 4fT , TSH , . ?
.
. central-
.
US.
.
:
? :
Patients with serious bleeding need more aggressive treatment. These patients should be given
10 mg of vitamin K by slow IV infusion. Additional vitamin K should be given until the INR is in the
normal range. Treatment with vitamin K should be supplemented with fresh-frozen plasma as a
source of the vitamin Kdependent clotting proteins. For life-threatening bleeds, or if patients
cannot tolerate the volume load, prothrombin complex concentrates can be used.
??? PROTHROMBIN COMPLEX CONCENTRATE
, 8 PCC , C 2,7,9,10 .S- .
.36 ,mg/dl17 .
?
2 jak .
.
.
.
:) . ? HIGH CO ?( ,
?
.37 ?
ITP .
TTP .
. 12B
MDS .
.
:
.38 , - monoclonal peak , .8%
, , . ? ) gr 0.6
8% (
multiple myeloma .
smoldering myeloma .
monoclonal gammopathy of undetermined significance .
waldenstrom macroglobulinemia .
POEMS .
385
: )(
.39 , , , : LDH
?
.
CT .
PET-CT.
.
. ) - - )
:
) - ? CT ?(
, CT .
) ( + + <- .
.42 MM ) ( , ?
. paraprotein
. )RBC(
.
.
. ?
: ? Normocytic and normochromic anemia occurs in 80% of -
myeloma patients. It is usually related to the replacement of normal marrow by
expanding tumor cells, to the inhibition of hematopoiesis by factors made by the
tumor, and to reduced production of erythropoietin by the kidney
" , " ,paraprotein
-
.
.
.
.
. ] ]
43. 66 3 . 180,000 , .
? CLL
. )t(9,22
386
.
INR . PTT ,?
.
.
:
) (41
cox inhibitor.
.
:
.46 ?dabigatran
. protein C
.
. Xa
. 4-5
. INR
:
- 48. ADPKD , ?
.
.
.
.
.
:
.49 19 . , .Amoxicilline -
. , , .38
,130,000 BUN 30, CPK ,1.6 .145 .
,1.015=SG ,++++ . .
US- , , .
?
prerenal azotemia .
. IgA nephropathy
.
.
:
.50 , , . ?
FeNA . 1%
. 10
. 300
. 40
.45 "" ) (?
. gpII/III
. ADP
387
.
diabetic nephropathy .
2RTA .
. " HCV
.
:
" " ,
?
.
:?? ) . -' , , .500
300 (...500 .
' ) ( ,- .500 350- .
, ATN
. ,500-
300- -' . ...
44
The prerenal urine sediment is usually normal or has occasional hyaline and granular casts
300
ATN )
-( , 500- ) "
(.
.. , ) ( ..
. 300
.. .
.56 ?
Minimal change disease .
Focal Segmental .
MembranoProliferative .
Membranous .
) Focal proliferative . 100% (diffuse
:?
.57 17 , ?
.
.
. 24
CT.
. CPK
: , ' , . . ' . 44.
. '? ...
.52 ,60 - , . /
. ?
.
. ) (
.
.
.
: ) (2324
.58 , US - )?( . -
. ? .
?
.
.
.
388
?
diabetic nephropathy .
.
MM.
membranous nephropathy .
:'
.
. PH - .7.5
: ) (2386
. -
- UA
-
:
8 ,, , > .0.9" .130/80 ?
IGA NEPHROPATHY .
ALPORT .
LUPUS GRADE IV .
MEMBRANOUS .
.64 ?
.
.
.
.
. .
:
2301
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(
. ) Cl (89 -
.
) RTA. Cl ,89 - (...
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-+ 150 - ,
.
: ) ( ) '(
) : (
60 ,ACE INH , . ,hypertensive retinopathy II
5" .:
145
-
2.2
total protein 8
?HB 12
, , . 24 5 .
389
.
.
. ++
. , ,
.
: ) (1350 ? ??? 3 ) (
. ?? . .
. ??..
, )
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. ? , .
)( ) NSAIDs ?(
)(
)(
: (Uremic Pericarditis (
.67 .
. ,5 .60
?
.
.
.
. .
: . " .
.67 PPD ?
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.
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.
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.
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.
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. 40
.
390
: . 189-23
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!( . . .
39 ,70 . ?
. .
Ceftriaxone . ,
.
. , .IV
.
: . enteric fever - .1277
. , - -
72. , MSSA
. + oxacillin +
. + +
. + +
:
.73 ,43 2-3 . 3- ,38 LDH . 2
. 4200 3800.
3 . .
.
.
.
.
carcinomatous lymphangitis .
:? , ? ..
, 400 " ) ,4CD?( PCP ,?
,HIV- PCP- . PCP LDH
.80 ,23 , .
?
.
.
. +
.
:
.81 73 38 . .
, - 12,500-WBC , 80% . . ?
.
.
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.+
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. .
. .. , CNS .
.
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, ) (
( ,
.76 major ?Duke Criteria-
. ) (1:180
.
.
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.
391
. ) (
.
.
. ...
. ?
:
' - = , + ) (.
.82 .
C.difficile,10 ( , WBC- 13000 ( , .
, ? ) ? (
. PO
. PO
. IV
. IV
.+ PO
:
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. . 3 350 ,38.5 ,
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.
.
GCSF .
.
:
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, 3 , 5 .
.
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3-5 1 :
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.
NSAID .
.
.
.
:? )?(infectious arthritis
The synovial fluid is turbid, serosanguineous, or frankly purulent...
Prompt administration of systemic antibiotics and drainage of the involved joint
can prevent destruction of cartilage
.85 71 . 33 , , .. 90/60 ?
392
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. ACE
.
. PTHrP
:
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, ?
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..
..
. .TNF
..
:
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. 20"
.
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20 ? . ?
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) . - .
( ,
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... ,
) ( 60"
-326
When ocular signs and symptoms occur, consideration should be given for the use of
methylprednisolone 1000 mg daily for 3 days to protect remaining vision
96. ,35 . . , ,
, ?
MRI .
US .
.
.
:
.97 ,65 , . 13 .:
, 4C , , ?
. C
.
MM .
RA .
.
:
Persistent parotid gland enlargement, purpura, leukopenia, cryoglobulinemia, and low C4
complement levels are manifestations suggesting the development of lymphoma.
.98 ,RA / NSAID . DMARD.
.7 ?
.
. TNF
.
393
, , , IHD .. ?
??? .. ? ' .
,
.
.
' ANTI TNF - TNF- .
.PPD
DMARD TNF
.DMARD
.102 , ) ?( "
. ?
. ?
. 30'
.
.
.
:
? ,
) (
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. 12
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.
.
. "
.
.
:? ) . ' ,(... ' - -
!
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.
.
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. ) (..
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394
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..
.
.
.
. .
:
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, , . " . ?
.
.
.
. ICD
. ACE inhibitor
: . - 2:1 class A , ..
, . . AVB .
,
2:1 ?2
395
4 . -\
4
.115 - ":
Sulfonylurea .
.
acarbos.
rosiglitasone .
.
:
- " (-:
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.
. CCB FP -
. / -
. ) (
:
, - 34
.112 ,55 . 3-4 , .
." ,120/80 ,66}. { ?
) ( " .
. , ,
. NSAIDS-
.
.
:? ACS- .. ?prinzmetal ,prinzmental-
.
.117 MVR-
. 40%=EF )LVEDV=50 (LV
. 50=EF=70%, LVEDV
. " 30
. ) (?? 38 .. ) ( ( ,
.. .. ""???( , EF
38%63 LVEDV
: . ,?
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. BNP-
. BNP-
. BNP-
. BNP-
. BNP-
: ) (1906
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2S ,2P ,
. "
MS . "
."
.
ASD . ) (
:
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, :
.
VSD.
MR. ) MS ( - MS
PS .
HOCM .
:Pulsus Parvus et Tardus .
396
. ) (? COPD
. "
:
118
AS ) HOCM (
) Pulsus Parvus&Tardus "
" - , " ").
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. PAF
. CVA
. TEE
. 1".
. AF
: . .
.126 ?NSCLC-
.
. 10%
.
..
:Weight loss greater than 10% of total body weight is considered a bad prognostic sign. .
? YS5
- 89
Although incomplete resection rarely results in long-term survival, collected results indicate that
surgery alone in stage IIIA disease (N2 disease) is associated with a 1430% 5- year survival. The best
survival rate is seen in cases with minimal N2 disease and complete resection.
, YS 5-
,10% complete resection, -
,
,
, ,
.127 } . {CT ?
Ciprofloxacin .
Metronidazole .
Clindamycin .
Doxycycline .
: . . ? - ?
,
Antibiotics targeting the causative or presumptive pathogen (with Haemophilus influenzae
and
P. aeruginosa isolated commonly) should be administered in acute exacerbations
397
.
.
) ( - .
:? ? - -
, - ;Cor Pulmonale-
, ) 40 ( - risk factors" 34-2
- CT ) (.
, .
.133 19 , - ?
. COPD-
.
. HBV
.
:
.134 ? -ARDS - ?
. TV
.
. 100 120-
.
.
:
? ICU ? z .180
, . 2988 .
.130 62 . ?
.
.
.
.
.
:
cause ~75% of all malignant pleural effusions are lung carcinoma, breast carcinoma, and
lymphoma
.135 ?
. +
+ SABA .
+ N-acetyl cysteine .
+LABA .
. +
:
.136 ?
. 2PCO-
.
2pCO . 2PCO
2PO ." 90
: -
398
. ) ?)
.
. INR .
.
. .
:
.142 .
CAD , PAF. n- .2-2.5 INR
.
.
.
.
: , INR
- - - AF + ?
.:137
, , , . MASSIVE PE
?
.
LMWH .
.
DVT
? ) (?
)(
.139 .
?
.
.
.
ezetimibe .
:
.146
.
. CT
. 2 CA PNEUMNIA-
.147 , , 90" , ,5 .
.
RTA .
.
DKA .
. .
.141 ,60 . - .
. .48 ?
399
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..
..
..
.
2013
.9 , .:
- HBsAG
- HBc - IgM
- anti HAV IgM
- anti HCV
?
. B.
. A.
. A B.
. A B.
.2 ,20 , .
. Ulcerative Colitis -
?
p-ANCA .
.
. ) ?(
.
ASCA .
.3 50 . 10 , UC
. 2 .ALK-P - ?
SCLEROSING CHOLANGITIS .
..
.VIRAL HEPATITIS .
.TOXIC HEPATITIS .
.4 .
?
.
.
.
.
.-
.11 ),
(B12 :
. D-Xylose
.
. IgA
.
.12 60 . .70/40 ?
.
.
.
.
.5 ,55 . . -
,4.5 - ,2 .3 ?
.
.
.
.
.13 19 -" ) :
, ( . . ?US-
.
.
.
.
.6 ?PPI
- / .
- .
- .B12
- .Clostridium d-
.14 ,(?) 52 . ?
. H2 6
PPI . 8 .
. .PPI-
. .HP-
.7 ?
.
.
.
.
bacterial overgrowth .
400
.21 , 3 .
. ,TSH - 0.05 : T3 T4
. ?
.
Sheehan syndrom .
.
.
.16 45 . ,
. ," grave's , . enalapril ,
.
- ,39" ,70/40 130 , .
RT. MIDDLE LOBE PNEUMONIA :
" - , WBC 600 ,11 ,30 230
?
.
. .
. "
.
."
.22 ?
. 2
. CPK
.
.
.
.17 . .
,TSH 20, T3 0.5 .T4 ?
.
MRI .
. TPO -
US .
.23 " . , , .
' ." , 34 . . 25-
?
.
repaglinide .
.'
.
.19 ,70 .
. )( , , .
. :
TSH T3 , T4 -.
?
. .
. .
. .
. , .
.20 9 . .110
:
- TSH 0.05
401
.25 1 10 .
. rebound ,.
24 , ) (.
HCO3- 15, PH-7.15, Na - 124, K-4.5, GLU-400 :
?
CT .
CT
CT .
CT .
. , PTT ,
. , D dimer ,
PTT . D dimer , ,
. , ,
PTT . INR , ,
.
.25 ,80 , . : .
. .
TSH-54, T4- 0.6, T3- 1.1 :
?
T4 . .50-100
T3+T4 . .
T3 . .
T4 . .25-50
T4 . 150-200
.32 CLL ?
.
.
.
.
.
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?
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CT .
.
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. - ," ) 96/60
-" .(100/60 .MCV 64 ,5.5 ?
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.
.
.
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.28 ,28 . .
, 6.3 PH 7.1 400
?
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., CT .
. , IV
.35 ?
. .
.
.
. PTT 80
. INR 1.5-2.5
.29 )?(unfractionated
INR .
Bleeding time .
Thrombin Time .
Prothrombin Time .
partial Thromboplastin Time .
.30 ,60 ,NSAIDs , - .ACE-I
)?( . . .mcv 72
?
.
.
.
.
.
.31 ?
402
.36 55 . .
. 5 .4 INR ?
. .
. .
. .
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.
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. coombs
. coombs
.44 ?PTT
. ?XII
. VII
DIC .
.
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.
.
.
.
.39 ?CML-
.
. 70
.
.
.
.40 ,55 , .
. ,HB-8.8, MCV-108 :WBC-3000, LDH- ,
.900 ?
LDH .1
TSH .2
.3
.4
.5
.46 28 . 39
.
:
HB - 11
WBC - 120,000
THrombocyt - 80,000
LDH - 900
bilirubing -3.5 .
?
. /
. , TTP
.
. .
.
.47 , , , .
?
.
.
.
.43 75 3 . : .
: , ,total protein , , .
) .(multiple myeloma
-
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.2
.3
.4
.5 .
403
.49 ) (VF .
- ?
ST II III AVF ,
Ibutilide .
Vasopressin .
Flecainide .
Lidocaine .
Bretylium .
?
. .
Acute VSD .
Acute Mitral Regurgitation .
.
.
.56 ?
. AS ,70 ,
. ,60 ," ST
. ,50 ," LBBB
. ,19 ,"
.53 ?
. ,60 , LBBB "
. ,45 - ,
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. ,27 .
. ,47 VT.
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.58 NSTEMI .
. )3
?( .STEMI ?
restenosis . " warfarin
restenosis . "
.
in stent thrombosis . "
in stent thrombosis . " warfarin
404
. ACE-I
. NON DIHYDROPYRIDINE CCB
.
.
.60 30 , , , " ,
, , "?
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. .
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.
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, . .
?
.
.
.
.
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..
..
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. 7- .
. .
. .
. < 55
.66 STEMI .
, .
" ?
.64 75 . " .
?
Aspirin 325 mg/d .
Aspirin 325mg + Clopidogrel 75mg .
Clopidogrel 75mg.
Coumadin .
. -
.
.
.
.
.
.65 " . ?.
.
.
.
.
.
.67 ?
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. S2
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.
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405
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. ST 6' .
. .circumflex-
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? .
. .CT
.71 . .
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,120 135 .252
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.
.
. 50
.
?
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VERAPAMIL .2
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, ?
.
.
.
.
406
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. ?
.
.
.
.
PET-CT .
.
.
. C-ANCA -
.83 50 .
, ,70/40 ? PE
. ?
IVC FILTER .
.
. )(
?coumadin+clexane .
407
?
HSP.
.
RA .
FMF .
. .4.5
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. ?
.
.
.
.
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Cyclophosphamide.
NSAIDS .
.
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)( . ?
.
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.
.
: , . , ,
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. .
. IV PO
. IV
) . (...
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: - ." 180/98
.high -LDH , Cr- 2.0 , 7.8 -Hb" . . ?
.
ACE-I .
. , IV
. IV
. IV
.88 ?ANCA
.
.'
. '
IgA nephropathy .
.89 ?ANTI-TNF
Mantoux test .
HBs Ag .
HAV .
.94 70 , ,
ANA . , . ?
.
.
.
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? :
408
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.
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, .
?
(
( Amoxicilin
( IgA nephropathy
( Post streptococcal glumerulonephritis
.98 , .DVT ?
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..
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.99 PIP , RF .
CCP , . ?
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.
anti TNF .
.
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dipyrone .
.106 ,39 . .:
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.
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.
.
.
.
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. . .
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wegnaer .
good pasture .
IgA .
(Mambranous nephropathy) Membranous glomerulonephritis .
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. .71
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.5 - .10 - ?
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.
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C. Difficile .
.
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Goodpasture syndrome .
Wegener's granulomatosis .
Churg-Strauss .
.
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160 ' " . 90/60 ?
. PEG
. 0.9%
. 0.45%
. 5%
.113 ,
280 , 137 117 ,PH 7.25 10 .5.8" .120/80
?
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RTA4 .
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.123 ,70 . 39 ' ." ,' .
" lobar pneumonia- . ?
group A streptococcus .
pseudomonas .
mycoplasma pneumonia .
Staph aureus .
legionella .
.124 ,40 " , .
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. , Macrolides
.
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) , (
.
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.PH=7.42, PO2=40, PCO2=30 - .
?
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ARDS .
Cardiogenic pulmonary edema .
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. . .
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.
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.130 10 ?
411
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.
.
.
. " .
.
. .acute rheumatic fever-
. .
. 10- .3-4-
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. PO .
. IV
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.
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.
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CO . SVR.
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CO . SVR.
412
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.
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.3
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, ' .
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.
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.
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.11
.12
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.14
.15
.16
.17
.18
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: . ' , .MELD
...
? ... . .
. ,?
" 2565
The administration of oral contraceptive combinations of estrogenic
and progestational steroids leads to intrahepatic cholestasis with
pruritus and jaundice in a small number of patients weeks to months
after taking these agents .
:? ?
B ? HBc IgM " HBsAg" anti HBs B.
-Infrequently, in15% of patients with acute HBV infection, levels of
HBsAg are too low to be detected; in such cases, the presence of IgM
anti-HBc establishes the diagnosis of acute hepatitis B
Chapter 341:
.28
.29
.30
.31
.32
.33
? :?NSAID? ? ,"B12"
.
?-
.20
? : , "1 ,? .
. .0.5
! !! , " " - , "1 .
" 2- ,ACTH "-" 1
.
414
.21
.22
.23
.24
.25
II .25
.26
.27
.(AML ? ) :?2272
Hyperleukocytosis and the leukostasis syndrome associated with it is
a potentially fatal complication of acute leukemia (particularly myeloid
leukemia) that can occur when the peripheral blast cell count is
/100,000<mL .
At such high blast cell counts, blood viscosity is increased, blood flow
is slowed by aggregates of tumor cells, and the primitive myeloid
leukemic cells are capable of invading through the endothelium and
causing hemorrhage. Brain and lung are most commonly affected.
Patients with brain leukostasis may experience stupor, headache,
dizziness, tinnitus, visual disturbances, ataxia ,confusion ,coma, or
sudden death .
Plasma exchange remains the mainstay of treatment of : .
TTP
. . :
:
Chapter 245. ST-Segment Elevation Myocardial Infarction: "Pump
failure is now the primary cause of in-hospital death from STEMI"
.44
.45
.46
.47
.48
.49
.50
.51
.52
.53
.34
+ .5.5 + ? :.O .
. " , ,90/60 ..
30 " .? ?...
O- " ,
".
. 100/60
- - 45 )
- O - (
.
. ,60 -O ? ? :: . " Warfarin inhibits the vitamin K-dependent synthesis of biologically
active forms of the calcium-dependent clotting factors II ,VII ,IX and
X",
, K - ' -- . ," ' " .
.. -
: CKD - ' One example is warfarin anticoagulation for atrial fibrillation: the
decision to anticoagulate should be made on an individual basis in the
CKD patient, as there appears to be a greater risk of bleeding
complications.
6.5 ? . :
..... -
CD 20 . . . - .
. . .
? AML- MDS- LDH- 3-
.
. ,? ,
.
,T- PA- ,B12 .
.35
.36
.37
.38
.39
.40
.? .ATN - ? . .
.IGM ,10% MM VWD ,
:
415
.41
.42
.43
.54
.60
:? ?
Hypertensive patients have stiffer arteries, and arteriosclerotic
patients may have particularly high systolic blood pressures and wide
pulse pressures as a consequence of decreased vascular compliance
due to structural changes in the vascular wall. Vascular endothelial
function also modulates vascular tone. The vascular endothelium
synthesizes and releases a spectrum of vasoactive substances,
including nitric oxide, a potent vasodilator. Endothelium-dependent
vasodilation is impaired in hypertensive patients
) , . - -(.. !
: . . V5 V6 ! V2 V3 - . -
" , ...
?? :?
":
Contraindications to exercise stress testing include rest angina within
48 h, unstable
rhythm ,severe aortic stenosis ,acute myocarditis, uncontrolled heart
failure, severe pulmonary hypertension, and active infective
endocarditis .
AS AS . +'
..
" :2004
.55
.56
:.
? "?
" -
-
.
!!
, -
" , .
.61
.62
.63
.64
.65
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: . CHADS .
, .
= - / .
" , .
" .SAH
.(?RBBB +) AIVR .
LBBB .
:.
? A2 .
.67
.68
.69
.70
.71
.72
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.
-? ) . (
! "
.57
.58
.59
:? ARB .
? ACEI
ARB CCB, BB '
.
- ARB
? ? ?
416
.74
.75
.76
.77
.78
.79
.80
.81
.82
.83
.84
.85
.86
.87
.88
.89
.90
.91
.?? ? ?? PE . ? -- .
- CI
.
,( ' ) . - " : ... ,
.92
?. ? ) , : .133-3 .(1.4 ) ,(
,] . .""
. "
-Goodman & Gilman's The Pharmacological Basis of Therapeutics,
12e, Chapter 43:
Renal failure is another common comorbidity reported in patients
having lactic acidosis associated with metformin use, and decreased
glomerular filtration rates are thought to increase plasma metformin
levels by reducing clearance of drug from the circulation. There are no
consensus guidelines for renal contraindications for metformin use;
It is important to assess renal function before starting metformin
and to monitor function at least annually. Metformin should be
discontinued preemptively in situations where renal function could
.93
.94
.95
.96
.97
.98
.99
.100
:
" - ? MRSA ?
?
-( 314)
: , ,
Among patients with fatigue, pain, and autoantibodies of SLE, but
without major organ involvement, management can be directed to
suppression of symptoms. Analgesics and antimalarials are
mainstays. NSAIDs are useful analgesics/anti-inflammatories,
particularly for arthritis/arthralgias. However, two major issues
currently indicate caution in using NSAIDs. First, SLE patients
compared with the general population are at increased risk for NSAIDinduced aseptic meningitis, elevated serum transaminases,
hypertension, and renal dysfunction. Second, all NSAIDs, particularly
those that inhibit cyclooxygenase-2 specifically, may increase risk for
myocardial infarction. Acetaminophen to control pain may be a good
strategy, but NSAIDs are more effective in some patients. The relative
hazards of NSAIDs compared with low-dose glucocorticoid therapy
have not been established. Antimalarials (hydroxychloroquine,
chloroquine, and quinacrine) often reduce dermatitis, arthritis, and
.101
417
.104
.105
.114
.115
.116
. ) (.
2 BUN 260 . .
) ( , - ....
.106
.107
.108
.109
.110
.111
.112
.113
. .anion gap )
( .
.117
.118
.119
.120
.121
.122
.123
.124
.125
.
Routine baseline hepatic ALT testing based solely on an age of :
<years is optional and depends on individual concerns. Monthly 35
treatment is indicated for isoniazid biochemical monitoring during
patients whose baseline liver function tests yield abnormal results and
for persons at risk for hepatic disease, including the groups just
.mentioned
, ) ?( .
' ,
...
.
? ' - ,
US ..
.126
.127
.128
418
? - HIV 2. , .
- HIV
, :In HIV-infected persons ,isoniazid may be administered concurrently
with nucleoside reverse transcriptase inhibitors, protease inhibitors, or
NNRTIs.
) (..
...
HIV 9 6..129
.130
.131
.132
.133
.134
.135
.136
.137
.138
.139
..
""shifting the oxyhemoglobin dissociation curve to the left" - '' .
, ) (dissociatntion.
' , . shifting the oxyhemoglobin dissociation curve to the "" :
,""left ) ( ,
.140
.141
. !!! !!CO
. 2 , , . , ,
" ... ".
.
-The pathophysiology of carbon monoxide exposure is incompletely
understood. CO binds to hemoglobin with an affinity more than 200
times that of oxygen, and this not only directly reduces the oxygencarrying capacity of blood, but further promotes tissue hypoxia by
shifting the oxyhemoglobin dissociation curve to the left.
CO" : 200 ,
,
"
" . , , -
. ?
, CO
.
.
)( . , ' ,
!
.142
419
.
: ) (:)The ADA suggests these glycemic goals for hospitalized patients: (1
;in critically ill patients: glucose of 7.810.0 mmol/L or 140180 mg/dL
(2) in noncritically ill patients: pre-meal glucose <7.8 mmol/L (140
mg/dL) and at other times BG <10 mmol/L (180 mg/dL).
:http://www.ncbi.nlm.nih.gov/pubmed/19509383
:271
Erythrocyte transfusion is generally recommended when the blood
hemoglobin level decreases to 7 g/dL, with a target level of 9 g/dL in
adults
:More recently, a randomized clinical trial that compared vasopressin
plus norepinephrine with norepinephrine alone in 776 patients with
pressor-dependent septic shock found no difference between
treatment groups in the primary study outcome, 28-day mortality.
:Meta-analyses of recent clinical trials have concluded that
hydrocortisone therapy hastens recovery from septic shock without
increasing long-term survival.
? ... . )( .
, ,SECURE AIRWAY
= . .