Table of contents :
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Chemical
elements
(below are listed alterations of plasma concentrations; see also
alterations
of
urinary concentrations).
When perfusion pressure falls, the homeostatic mechanisms of the
human
body tend to preserve euvolemia rather than concentration of
solutes
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plasma glucose (mg/dl) | > 250; 400-1,000 mg/dL or > 17 mmol/L (increased) | > 250 | > 250 |
arterial pH | 7.25–7.30 | 7.00–7.24 | <7.00 (>6.75) |
serum bicarbonate (mEq/l) | 15–18 | 10 to <15 | < 10 |
urine ketones (nitroprusside reaction method) | positive | positive | positive |
serum ketones (nitroprusside reaction method) | positive (3-27 mM/L (increased)) | positive | positive |
effective serum osmolality (mOsm/kg) = 2[measured Na (mEq/l)] + glucose (mg/dl)/18 | variable = 310-380 mOsm/kg (normal or decreased) | variable | variable |
anion gap = (Na+) - (Cl- + HCO3-) (mEq/l) | > 10 | > 12 | > 12 |
alteration in sensoria or mental obtundation | alert | alert/drowsy | stupor/coma![]() |
kalemia | 3.5-7 mEq/L (normal or increased) (potassium deficit = 3-5 mEq/kg | ||
natremia | 125-140 mEq/L (normal) (sodium deficit = 7-10 mEq/kg) | ||
bicarbonatemia | < 20 mEq/L | ||
uremia | 15-40 mg/dL | ||
water deficit | 6 (3-7) L = 100 ml/kg | ||
chloride deficit | 3-5 mEq/l | ||
phosphate deficit | 5-7 mmol/kg | ||
magnesium deficit | 1-2 mEq/kg | ||
calcium deficit | 1-2 mEq/kg |
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minimal urinary pH |
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% excretion of filtered HCO3- |
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potassiemia |
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Fanconi's
syndrome![]() |
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nephrolithiasis![]() ![]() |
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acid excretion in 24 hrs |
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urinary
anion gap (UAG)![]() |
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HCO3- requirement (mmol/kg/24 hrs) |
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Activity (muscle tone) | no movement, "floppy" tone | arms and legs flexed with little movement | active, spontaneous movement |
Pulse | absent | < 100 bpm | > 100 bpm |
Grimace (responsiveness or reflex irritability) | no response | facial movement only (grimace) | sneeze, cough, pulls away |
Appearance (skin color) | normal color all over (hands and feet are pink) | normal color (but hands and feet are bluish) | bluish-gray or pale all over |
Respiration (rate and effort) | absent | slow or irregular breathing | normal rate and effort or crying |
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exposure markers | [Pb]plasma [mg%] |
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[Ala]urine [mg/g creatinine] |
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> 15 | |
[zincoprotoporphyrine (ZPP)]RBC [mg/dL] |
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effect marker | activity ALA dehydrataseplasma [U] |
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urine osmolality | > 400 mOsm | < 350 mOsm |
natriuria | < 15 mEq/l | > 40 mEq/l |
sediment | negative | cylinders |
[urea]urine/[urea]plasma | > 8 | < 3 |
[creatinine]urine/[creatinine]plasma | > 40 | < 20 |
[urea/creatinine]plasma | > 10:1 | < 10:1 |
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type
I
/ chylomicronemia syndrome / essential familial
hyperlipemia / exogenous
hyperlipemia / familial fat-induced hyperlipemia /
Bürger-Grütz
syndrome (rare!)
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type
II
/ familial hypercholesterolemic xanthomatosis / hyper-b
-lipoproteinemia |
IIA :familial
hypercholesterolemia
(FH)
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heterozygote : 7-13 (275-500)
homozygote : > 13 (> 500) |
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normal |
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IIB / mixed hyperlipemia / combined
hyperlipidemia
: an abnormality that interferes with regulation of activity
of HMG CoA
reductase, the rate-controlling enzyme in cholesterol
biosynthesis
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type
III
/ familial dysbetalipoproteinemia / remnant
hyperlipidemia / remnant
removal disease / broad-beta disease :
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high | |||
type
IV,
carbohydrate-induced hyperlipoproteinemia / endogenous
hyperlipemia
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type V / combined fat-
and carbohydrate-induced
hyperlipemia / mixed hyperlipemia = type I + type IV
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4.4-4.7 mmol/L = 80-85 mg/dL | [insulin![]() |
3.6-3.9 mmol/L = 65-70 mg/dL | increased [glucagon![]() ![]() ![]() ![]() |
2.8-3.1 mmol/L = 50-55 mg/dL | neurogenic (autonomic) symptoms :
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< 28.5 mmol/L < 50 mg/dL | neuroglycopenic symptoms => hypoglycemic
encephalopathy![]() ![]() ![]() |
Naturally occurring
toxins(=>toxinology)
: nitrogen-containing heterocycles are termed alkaloids.
As compounds
of biological origin, toxins are often classed as biological
agents, but
they are not infectious and are more similar to chemicals with
respect
to their military potential for tactical use; they should be
considered
to be chemical agents. Therefore the Chemical
Weapons
Convention (CWC) (1993) also includes toxins as chemical agents,
and, specifically
includes toxins in its control regime along with other highly
toxic chemicals.
Toxins can be classified according to the targeted tissue(s) /
organ(s),
e.g. :
Prymnesiales Prymnesium
- Prymnesium parvum (golden algae)
=> secrete toxins that attack exposed cells in fish gills, causing inflammation, hemorrhaging and eventual suffocation. The algae, which have troubled western Texas waters for 2 decades, thrive in cooler temperatures and have killed fish weighing up to 50 pounds. Golden algae post some health threats to humans if infected fish are eaten. It also causes ecological damage by how fast it spreads. Algae, literally, can double and triple in quantity in 24 hours. While the devastation is greatest in the smaller lakes, those waters can be treated with chemicals, including copper-based algaecides. Golden algae are estuarine-based (saltwater-tolerant) organisms that are very small (10 mm long x 5 mm wide). They are generally oval shaped with 2 cup-shaped golden plastids running the length of each side of the cell. These tiny organisms, when in great number, can cause water to be discolored, ranging from yellow to coppery brown. They may be present in mud and cause problems with inland- or pond-raising of fish. Golden algae do not seem to go away as does red tide. Large concentrations of golden algae (blooms) can often be toxic to fish. The toxins affect the gills of the fish, which are the breathing system, thus limiting the fishes' ability to take in oxygen. Death is from asphyxiation, just as it is with red tide