1.

“AMPLE”
1. Allergies, the patient or family is asked whether the patient has a history of drug or food
allergies
2. Medication, asked about what drugs the patient is currently taking
3. Past Illness/Pregnancy, asked whether the patient has a history of systemic diseases
such as diabetes mellitus, hypertension, asthma, and heart disease, and asked if the
patient is a woman whether she is pregnant or not.
4. Last meal, ask the patient when was the last drink and meal,
5. Event/environment, which is asked how the environmental conditions are related when
the trauma event occurs
Reference
Advance Trauma And Live Support 9th Edition.

2.
Osteoprotegerin (OPG)
 Osteoprotegrin (OPG) belongs to the TNF receptor superfamily (TNFR)
 OPG has a function as an endogenous receptor antagonist that prevents the biologic
effects of RANKL, acting as an inhibitor in both remodeling and bone resorption
processes.
 OPG is synthesized in several cells including stromal cells, osteoblasts, vascular smooth
muscle cells, B lymphocytes and articular chondrocytes.(Simonet et al., 1997)
 OPG production by specific cells is modulated by several cytokines, vitamins, estrogens
and other molecules, thereby triggering osteoclasogenesis and bone resorption.
 OPG production is triggered by 1α,25-dihydroxyvitamin D3, estrogen, pro-inflammatory
cytokines such as interleukin-1 (IL-1) and TNF as well as transforming growth factor-
(TGF-β), where parathyroid hormone (PTH) and glucocorticoids inhibit OPG production.
(Thirunavukkarasu et al., 2001)
 The importance of OPG is illustrated in OPG-deficient mice, where osteoclast formation
is also impaired, and also in OPG-overexpressed mice, where severe osteopetrosis
develops with decreased osteoclast count (Kong et al., 1999)
 Furthermore, OPG can directly inhibit osteoclast activity, independently of RANKL
dependence, through interaction with receptors atypical of osteoclasts.
 Biological effects of OPG on bone cells include inhibition of late-stage osteoclast
differentiation, suppression of activation of mature osteoclasts and induction of apoptosis
in these cells.
RANK
 Activator receptor of Nuclear Factor Kappa (RANK) RANK, like OPG, is a TNFR
superfamily.
  RANK is believed to function as a natural receptor for RANKL and is also expressed in
several tissues such as musculoskeletal, thymus, liver, colon, mammary glands, prostate,
pancreas, and monocyte/macrophage linear cells including osteoclast precursors and
mature osteoclasts, B lymphocytes. and T, dendritic cells, fibroblasts and articular
chondrocytes. (Kearns et al., 2008).
 Activation of RANK will stimulate the differentiation of osteoclast precursors into
mature osteoclasts which will also activate mature osteoclasts.
 RANK activation by RANKL involves a long-range signaling cascade and will result in
an osteopetrotic phenotype of nuclear component-induced mice. (Takayanagi, 2007)
Reference:
Kong, Y. Y., Yoshida, H., Sarosi, I.. 1999. OPGL is a key regulator of osteoclastogenesis,
lymphocyte development and lymph-node organogenesis. Nature, 397, 315-23.
Simonet, W. S., Lacey, D. L., 1997. Osteoprotegerin: a novel secreted protein involved in the
regulation of bone density. Cell, 89, 309-19
Thirunavukkarasu, K., Miles, R. R. 2001. Stimulation of osteoprotegerin (OPG) gene expression
by transforming growth factorbeta (TGF-beta). Mapping of the OPG promoter region that
mediates TGF-beta effects.J Biol Chem, 276, 36241-50.

3.
Based on the study form Julie R. Zivin, Acute Renal Failure (ARF) can induce hypocalcemia.
This suggests that a shared mechanism for ICU-RC and ARP-associated hypocalcemia might
exist. The most compelling would be a derangement in the vitamin D-PTH axis, suggested by
the following data:
1. Decreased 1,25 dihydroxyvitamin D3 levels may develop during ARF and contribute to
the hypocalcemic state
2. Low 25(OH)-vitamin D3 levels are extremely common in hospitalized patient
populations
3. One study reported that both 25-and 1,25-vitamin D3 levels are decreased and PTH levels
are increased in septic hypocalcemic patients
4. Elevated PTH levels in critically ill patients have been associated with increased patient
mortality
However, it appears highly unlikely that ICU-HC is solely a consequence of low vitamin D
levels. For example, increased levels of calcitonin have been noted in ICU patients can
reportedly serve as a sensitive marker of sepsis. Hypocalcemia has also been associated with
markers of tissue inflammation, most notably tumor necrosis factor-a, interleukin-6, and C-
reactive protein, also point to a multifactorial basis for the hypocalcemic state.
Reference:
Zivin JR, Gooley T, Zager RA, Ryan MJ. Hypocalcemia: A pervasive metabolic
 abnormality in the critically ill. Am J Kidney Dis. 2001;37(4):689–98.

4.
Stiffness
Stiffness may be generalized (typically in systemic dis-orders such as rheumatoid arthritis and
ankylosing spondylitis) or localized to a particular joint. Patients often have difficulty in
distinguishing localized stiff-ness from painful movement; limitation of movement should never
be assumed until verified by examination.
Ask when it occurs: regular early morning stiff-ness of many joints is one of the cardinal
symptoms of rheumatoid arthritis, whereas transient stiffness of one or two joints after periods of
inactivity is typical of osteoarthritis.
Locking ‘Locking’ is the term applied to the sudden inability to complete a particular movement.
It suggests a mechanical block – for example, due to a loose body or a torn meniscus becoming
trapped between the articular surfaces of the knee. Unfortunately, patients tend to use the term
for any painful limitation of move-ment; much more reliable is a history of ‘unlocking’, when
the offending body slips out of the way.
Muscle Contratures
Contracture
If a muscle remains in a shortened state for a prolonged period, it develops a persistent
shortening that is resistant to stretching ( muscle contracture) . Such a contracture eventually
becomes irreversible. Muscle contractures also develop in certain diseases of muscle, such as
polymyositis, muscular dystrophy, and cerebral palsy. In addition, the muscle fibers of a necrotic
muscle are subsequently replaced by dense fibrous scar tissue, which undergoes progressive
fibrous contracture, resulting in the production of progressive joint deformities.
Reference
1. Apley & Solomons. System Of Orthopaedics And Trauma 10th Edition
2. Salter. Textbook of disorder and injuries of the musculoskeletal system 3rd edition