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ELECTROLYTES TiKi TaKa _____________________ NOTES: ====== .

Human blood PH is m
antained at 7.35-7.45 by many mechanisms, the most importan t are the regulation
of CO2, bicarbonate and H atoms by lungs and kidney. . PH < 7.35 = acidosis whi
le PH > 7.45 = alkalosis. . PaCO2 & HCO3 can differentiate between respiratory a
nd metabolic acid base dis turbance. . Sometimes mixed acid-base disorders prese
nt with PH within normal range. . Normal HCO3 = 24 mEq/L and normal PaCO2 = 40 m
mHg. . Metabolic acid-base disturbance is due to primary change in HCO3 concentr
ation . . Respiratory acid-base disturbance is due to primary change in PaCO2. .
Primary rise in PaCO2 (respiratory acidosis) and drop of plasma HCO3 (metaboli
c acidosis). . Primary drop in PaCO3 (respiratory alkalosis) and rise in plasma
HCO3 (metabol ic alkalosis). .. HCO3 primary change (metabolic) while PaCO2 prim
ary change (Respiratory). .. Primary = the main change is in Paco2 or HCO3. .. C
ompensatory = slight change in the other item. .. i.e: PaCO2 = 45 & HCO3 = 35 -> metabolic .... PaCO2 = 26 & HCO3 = 28 --> res piratory .. if great change in b
oth PaCO2 & HCO3 --> think of mixed acid-base imbalance ( fix the formula & calc
ulate PaCO2 and compaire it with that of the case). . METABOLIC ACIDOSIS: ______
________________ . Decreased blood PH < 7.35. . Decreased blood HCO3 < 24 mEq/L
(1ry). . Decreased PaCO2 (Compensatory respiratory alkalosis), . PaCO2s in metab
olic acidosis is calculated by winter's formua: PaCO2 = 1.5 (H CO3) + 8 . Causes
: See below N.B: . Hyperventilation (tachypnea) is the mode of repiratory compen
sation for metab olic acidosis (to wash CO2). . Calculating the plasma anion gap
is the best next step in diagnosis of patien t's acid-base status, . due to it
narrow the diffrential diagnosis in case of metabolic acidosis e.g. A) Some of t
he most common cause of anion gap metabolic acidosis: - Lactic acidosis: Hypoxia
, poor tissue perfusion, mitochondrial dysfunction. - Ketoacidosis: Type 1 D.M,
starvation & alcoholism. - Methanol ingestion: Formic acid accumulation. - Ethyl
ene glycol ingestion: glycolic and oxalic acid accumulation. - Salicylates poiso
ning: causes mixed metabolic acidosis and respiratory alkal osis. - Uremia: Fail
ure to excrete (H) as NH4. B) Most common causes of normal anion gap metabolic a
cidosis: - RTA (renal tubular acidosis) --> has +ve urine anion gap (UAG). - Dia
rrhea --> has -ve urine anion gap (UAG). . METABOLIC ALKALOSIS: ________________

Increased blood PH > 7.45. Increased blood HCO3 > 24 mEq/L (1ry). Increased PaCO
2 (compensatory respiratory acidosis). PaCO2 in metabolic alkalosis is calculate
d by the formula: PaCO2 = (0.9 HCO3) 16 +,- 2. Causes; - Vomiting, diuretic --> V
olume depletion --> + Renin-aldosterone system. - Exogenous alkali intake. - min
eralocorticoids excess --> bicarbonate retention, H & K loss --> metabol ic alka
losis. . Metabolic alkalosis is divided into: 1- Saline responsive condition (wi
th urine chloride < 20 mEq/L) and volum dep letion, - due to GIT proton (H) loss
(vomiting), volume contraction or diuretics, - treated by normale saline. 2- Sa
line resistant condition (with urine chloride > 20 mEq/L) and volum expa nsion,
- Hyperaldosteronism, Barrter syndrome, Gitelman syndrome and excessive, b lack
liqurice ingestion. - Not treated by normal saline. . Hyperemesis gravidarum cau
ses volume depletion --> metabolic alkalosis with re spiratory compensation. . R
ESPIRATORY ACIDOSIS: ________________________ . Increased blood paCO2 > 40 mmHg
(1ry). . Increased blood HCO3 (Compensatory). . Decreased minute ventilation. (M
inute ventilation = Respiratory rate Tidal vo lume. . Caused by alveolar hypovent
ilation as: - Chest disese: COPD, Obstructive sleep apnea, silicosis, obesity. Neuromuscular disease: Myasthenia gravis, lambert-eaton, polymeilitis, G. b arr
e. - CNS disease: Stroke, infection, brain stem lesion. - Druge induced: anesthe
sia, Narcotics and sedatives. . RESPIRATORY ALKALOSIS: ________________________
. Decreased blood PaCO2 < 40 mm Hg. . Decreased blood HCO3 (compensatory). . Inc
reased minute ventilation (washing co2). . Caused by alveolar hyperventilation d
ue to: pneumonia, high altitude, anaemia , anxiety, pain, fever, pulm. embolism,
pleural effusion, atelectasis & Salicylate intoxication. . MIXED ACID-BASE DISO
RDERS (Metabolic acidosis and respiratory alkalosis) ___________________________
______________________________________________ . It may cause inappropriately no
rmale laboratory values. . Calculate the expected change in PaCO2 & HCO3 and com
paire it with the patien t measured values in the case, . To determine if a mixe
d disorder exists or a normale physiologic compensation has occured, . PaCO2s in
metabolic acidosis is calculated by winter's formua: PaCO2 = 1.5 (H CO3) + 8. .
Salicylates intoxications --> + Respiratory center --> Tachypnea and respirat o
ry alkalosis,
. . . . + .

. Also causes anion gap metabolic acidosis due to increased production and decr
eased renal elemination of organic acids as lactic and ketoacids. . ADRENAL INSU
FFICIENCY (Addison's disease): ____________________________________________ . No
n specific msnifestations: Anorexia, fatigue, GIT complains, weight loss an d hy
potension. . The most common electrolyte abnormality is HYPONATREMIA. . Also HYP
ERKALEMIA is common; due to decreased activation of aldosterone recep tors (with
mild hyperchloremic acidosis). . DIURETIC ABUSE: _________________ . Causes inc
reased excretion of water and electrolytes by the kidney. . Dehydration, weight
loss, orthostatic hypotension. . Hypokalemia and hyponatremia due to increased u
rinary excretion of Na & K --> increased urine Na & K. . Eating disorders may ca
use the patient abuse diuretics. . CAUSES OF ORTHOSTATIC HYPOTENSION: ---------------------------------. Decreased intravascular volume: Decreased fluid intake
, polyuria and diarrhea . . Decreased vascular tone: autonomic neuropathy or med
ications as (antihyperten sive and antipsychotics). . DIABETES INSIPIDUS: ______
_________________ . Causes euvolemic hypernatremia. . present with severe polyur
ia and mild hypernatremia. . Based on urine osmolality DI is of 2 types: - Compl
ete D.I: urine osmolality < 300 mosml/kg (Normally < 100 mosm/kg). - Incomplete
D.I: urine osmolality 300-400 mosm/kg. . Based on etiology D.I is of 2 types: Centeral D.I: decreased ADH release due to: CNS; trauma, hge, infection or tumor
. - Nephrogenic D.I: due resistance to ADH: common causes; hypercalcemia, sever
e hypokalemia, tubulointerstial renal disease, - medications as: Lithium(ttt of
bipolar disorder), demeclocycline, foscarnet , amphotricine and cidofovir. . N.B
:- Divalporic acid is used in bipolar disorder but doesn't cause D.I. - Dehydrat
ion --> HYPOVOLEMIC hypernatremia + increased urine osmolality. . PSYCHOGENIC PO
LYDIPSIAL: __________________________ . Excessive free water intake --> hyponatr
emia. . Patient with psychatric illness. . Like D.I euvolemic polyuria but psych
ogenic polydipsia (hyponatremia), wherea s D.I (hyppernatremia). . HYPONATREMIA:
_______________ . Serum sodium < 130 mEq/L. . Causes According to: ============

===================================================== - Serum osmolarity - Extra

cellular volume - Urine findings - Causes of hyponatremia ======================
========================================================== =====================
================================ 1) Normal ------. hyperproteinemia. . hyperlipi
demia. =========================================================================
======= ===================================================== 2) High (> 295 m0s
m/kg) - hyperglycemia. -------- Exogenous solutes (mannitol & radiocontrast). ================================
================================================ ===============================
======================== - Non renal salt loss: . Dehydration. - U Na < 10 . Vom
iting. - HYPOVOLEMIC . Diarrhea. ================================ ==============
========================================== - U Na > 20 - Renal salt loss: mEq/L
. Diuretics. . ACEIs. . Mineralocorticoids deficiency. 3) Low ==================
============================================== =================================
======================= (< 280 m0sm/kg) - psychogenic polydipsia. - Beer potoman
ia. Uosm < 300 - EUVOLEMIC ================================ ====================
==================================== - UNa >20 mEq/L - SIADH Uosm > 300 ========
========================================================== =====================
===================================== - CHF. - HYPERVOLEMIC - Hepatic failure. ------- U Na > 20 mEq/L mEq/L

- Nephrotic syndrome. ==========================================================

====================== =========================================================
= ... Hypovolemic hyponatremia is usually due to volume depletion --> decreased
ef fective arterial volume to the kidney --> ... --> increase Aldosterone, Renin
and ADH. . SIADH: ________ . Euvolemic hyponatremia. . Decreased serum osmolari
ty & increased urine osmolarity. . Increased urine sodium concentration. . Failu
re to correct with normal saline infusion. . DIAGNOSTIC CRITERIA OF SIADH: -----------------------------1- S.osm. < 270. 2- U.osm > S.osm. 3- U.Na > 20 mEq/L.
4- No hypovolemia. 5- Normal renal, adrenal & thyroid function. 6- No other know
n causes of hyponatremia. 7- No obvious stimulus (surgical, traumatic or painful
e) known to activate ADH release. . RENAL TUBULAR ACIDOSIS TYPE 4 (RTA TYPE 4):
______________________________________________ . Caused by Aldosterone deficienc
y or renal insensitivity to aldosterone. . Lack of aldosterone effect --> failur
e to secrete acids as NH4 and retention of potassium. . Causes NON ANION GAP MET
ABOLIC ACIDOSIS (i.e normale anion gap). . Hyperkalemia and renal insufficiency.
. Occur in diabetic nephropathy and worsened by drugs that inhibite Renin-aldos
terone system as: ACEIs & ARBs. .N.B: - Serum anion gap = S. Na - ( S. CL + S.
HCO3)... Normally (6-12) anion ga p if > 12. - Urine anion gap = U. Na - U. CL.
. Both DIARRHEA & RTA are associated with (normal anion gap metabolic acidosis).
. Both are difrentiated by Urine anion gap (UAG). . Acid excreted by the kidney
is buffered by NH4CL, so the more acid excreted; t he more chlorid found in uri
ne. . In RTA --> decreased acid secrtion --> decreased Chlorid in urine --> posi
tive UAG. . In Diarrhea --> intact kidney ability to excrete acids & diarrhea is
associate d with acidosis --> increased renal acid excretion --> --> increased
urine chlorid --> Negative UAG. . CHRONIC RENAL FAILURE --> decreased acid (NH4)
secretion & accumulation of org anic anions --> hypochloremic (anion gap) metab
olic acidosis. . furosemide --> volume depletion --> contraction metabolic alkal
osis (increased serum HCO3). . ADDISON DISEASE: __________________ . Caused by T
.B., haemorrhage.... . Decreased; cortisone, adrenal sex hormones and aldosteron
e secretion. . Normally; aldosterone acts on renal distal tubules to reabsorbe N
a in exchang

e with K & H ions. . Aldosterone difficiency --> loss of Na (hyponatremia) and r

etaining of K & H ( hyperkalemic metabolic acidosis). . i.e Normal anion gap hyp
erkalemic, Hyponatremic metabolic acidosis. . DRUGS CAUSING HYPERKALEMIA: ______
_______________________ . Non selective beta blockers --> unterfer with beta2 me
diated intracellular K uptake --> increase extracellular K. . ACEIs, ARBs & K sp
aring diuretics --> inhibition of aldosteron or the ENaC ch annel (epithelial Na
channel in the collecting tubules). . Cyclosporine --> blocks aldosterone activ
ity. . Heparin --> blocks aldosterone activity. . Digitalis --> inhibite Na-ATPa
se pump. . NSAIDs --> decrease renal perfusion --> decrease K delivered to colle
cting du cts. . Succinylcholine --> causes extracellular leakage of K through ac
tycholine rec eptors. . Trimetoprim --> block ENaC channel (Like K spairing diur
etics). --> Also trimethoprime causes competetive inhibition of renal tubular cr
eatinine secretion --> artificial rise in serum creatinine without change in GFR
. . In case of hyperkalemic patient with multiple drug therapy the best next ste
p after control hyperkalemia . by K binding resin as (sodium polystyeren sulfona
te) is review all his curren t medications (as one of these drugs maybe the caus
e of hyperkalemia). . POSTICTAL ANION GAP METABOLIC ACIDOSIS: __________________
__________________ . Due to lactic acidosis from increased production of lactic
acid by the muscle s & reduced hepatic uptake of lactate. . Usually transient &
resolve 60-90 miutes after seizures. . So, the best management in this patient i
s observation for 2 hours then repea te lab. examination. . if not resolved afte
r 2 hours --> look for other potential causes of metaboli c acidosis. .N.B.: IN
ANY PATIENT with acid base imbalance: the PH & PaCO2 are the 2 lab.val ues that
provide the best picture about acid-base status, as the bicarbonate can be calcu
lated from these 2 values using the henderson-h asselbalch equation. CORRECTION
OF HYPONATREMIA: ___________________________ 1- Asymptomatic or mildly symptomat
ic hyponatremia --> Normal saline. 2- Severe symptomatic hyponatremia --> rapid
increase in serum Na concentraion by hypertonic saline (3% saline). - Acute symp
tomatic hypernatremia is a medical emergency require rapid increase in serum Na
concentration. - Chronic hyponatremia require slow correction of serum Na concen
tration becaus e the brain cells had adjusted to the hyponatremic state, So, rap
id increase in serum Na can cause osmotic centeral pontine demyelinatio n syndro
me, so correction is done. by very slowly increase in serum Na (not more than 0.
5 mEq/L/h. SALYSIALATE TOXICITY: ____________________ . Suspected in patient wit
h triad of: fever, tinnitus and tachypnea (after drug

intoxication). . Causes mixed Respiratory alkalosis and anion gap metabolic acid
osis. . Explanation: - Aspirin stimulates respiratory center causing tachpnnea -> respiratory alka losis (CO2 wash). - Aspirin causes anion gap metabolic acido
sis by: . Uncoupling ofOxidative phosphorylation --> increasing O2 consumption b
y t issues & also hyperpyrexia. . Inhibites enzymes involved in carbohydrate and
lipid metabolism --> accum ulation of organic acids (pyruvate, lactate...). . I
mpaire renal function --> accumulation of organic acids. .N.B: - Normal acid-bas
e status --> PH 7.39-7.41, PaCO2 35-40 and HCO3 24. - Respiratory acidosis witho
ut compensation --> PH < 7.39, primary decrease in PaCO2 and normale HCO3. - Res
piratory acidosis with compensation --> PH < 7.39, primary decrease in PaC O2 an
d compensatory increase in HCO3. - Respiratory alkalosis with compensation --> P
H > 7.41, primary decrease in Pa CO2 and compensatory decrease in HCO3. - Respir
atory alkalosis without compensation --> PH > 7.41, primary decrease in PaCO2 an
d near normal HCO3 - Metabolic acidosis without compensation --> PH < 7.39, prim
ary decrease in HC O3 and near normale PaCO2. - Metabolic acidosis with compensa
tion --> PH < 7.39, primary decrease in HCO3 and compensatory decrease in PaCO2.
- Metabolic alkalosis with compensation --> PH > 7.41, primary increase in HCO3
and compensatory increase in PaCO2. - Metabolic alkalosis without compensation
--> PH > 7.41, primary increase in H CO3 and near normal PaCO2. .. HCO3 primary
change (metabolic) while PaCO2 primary change (Respiratory). .. Primary = the ma
in change is in Paco2 or HCO3. .. Compensatory = slight change in the other item
. .. if great change in both PaCO2 & HCO3 --> think of mixed acid-base imbalance
( fix the formula & calculate PaCO2 and compaire it with that of the case). . P
REGNANCY causes --> normal physiological chronic compensated respiratory alka lo
sis due to high progestrone level --> stimulate respiratory center --> Tachypnea
--> cons equent chronic mild respiratory alkalosis with metabolic compensation.
. It is common in late pregnancy due to increase of progesterone with the incre
a se of gestational age. . FAMILIAL HPOCALCURIC HYPERCALCEMIA: -----------------------------------. Increased serum calcium and increased/inappropriately norma
l PTH level are su specious for either: . PRIMARY HYPERPARATHYROIDISM -->normal
or increased urinary calcium excretion. . FAMILAR HYPOCALCURIC HYPERCALCEMIA -->
decreased urinary calcium excretion. . Ethylene glycol, Ethanol and Methanol: --------------------------------------. All of them cause metabolic acidosis wit
h an anion gap and an osmolar gap. . But Ethylene glycol --> calcium oxalate (re
ctangular, envelope shaped crystal s) in urine. .N.B: how to calculate osmolar g
ap ?? - 1st calculate serum osmolarit = {2Na + Glu/18 + BUN/2.8}.

- Then calculate osmolar gap = observed osmolarity (case) - calculated osmolari

iting: --------------------------------------------------------------. Mechanism
: 2 phases; - Generation phase: Vomiting --> loss of gastric fluid containing HC
L , NaCL and water. - the loss of H ions as HCL --> unbalanced retention of HCO3
(because of the loss of gastric acidity --> no stimulus for HCO3 release by the
pancreas), - HCO3 is instead retained in the blood --> metabolic alkalosis. - M
aintenance phase: Vomiting --> volum loss & decreased ECV --> decreased re nal p
erfusion --> activation of renin-angiotensin-aldosterone system. - Aldosterone -> retain water and excrete H & K in urine --> hypokalemia and contraction metab
olic alkalosis. . the 1st step in managementis to retore the ECF Volume by iv no
rmal saline & K . . this will decrease activation of renin-aldosterone system by
restoring proper renal perfusion. . i.e the step in management of volume contra
vtion metabolic alkalosis --> norm al saline and k. . DIABETIC KETOACIDOSIS (DKA
): -----------------------------. Causes anion gap metabolic acidosis. . Common
in type I DM ( blood gluc. > 250-600 mg/dl) less common in type II. . Polyuria,
polydipsia, abdomenal pain, nausea and vomiting mimic surgical abd omen. . PRIMA
RY POLYDIPSIA: --------------------. Problem of excessive water intake common in
schizophrenic patients. . Normal functioning kidney --> excrete diluted urine (
of low specific gravity < 1.003) i.e low osmolarity. . Dx: withholding water int
ake --> increased urine osmolarity & specific gravit y --> confirm diagnosis. .
Adminstration of phenohiazines to schizophrenia --> increase thirst sensation -> wores primary polydipsia & hyonatremia. . N.B.: - Nephrogenic diabetes insipid
us (DI) due to lithium (ADH resistance) --> loss water --> hypernatremia & maxim
ally diluted. - Centeral DI --> loss water --> hypernatremia & maximally diluted
. - to distinguish between central and nephrogenic DI --> exogenous ADH --> if c
o rrected = central DI, if not corrected = Nephrogenic DI. - SIADH --> excessive
free water retention --> hyponatremia & concentrated urin e. - Carbamazebine in
tensify kidney responce to ADH --> free water retention & hyp onatremia --> as S
IADH. . ALCOHOLICS refractory hypokalemia: -----------------------------------.
Chronic alcoholics --> multiple electrolyte imbalance --> hypokalemia, hypoma gn
esemia, hyponatremia.

. Mg is important cofactor for K uptake and maintenance of intracellular K leve

l. . So refractory hypokalemia is due to hypomagnesemia, so correction of hypoma
gn esemia is essential to correct hypokalemia. . BOWEL ISCHEMIA AND METABOLIC AC
IDOSIS: ---------------------------------------. common in patients with asthero
sclerosis and peripheral vascular disease. . Acute abdomenal pain, nausea, vomit
ing, hypoactive bowel sounds and abdomenal tenderness. . Mechanism: bowel ischem
ia --> accumulation of lactic acid from anaerobic meta bolism --> lactic acidosi
s --> metabolic acidosis with anion gap. . N.B.: DKA --> blood glucose > 250 - 6
00 mg/dl. . HYPERNATREMIA: ---------------. The most common cause is hypovolemia
. . Mild cases can be treated by 5% Dextrose in 0.45% saline. . Severe cases -->
initially treated with IV normal saline 0.9% then switch to half normal saline
0.45%, . when the volume deficite has been restored inorder to better replace th
e free fluid loss. . GASTRIC OUTLET OBSTRUCTION: ---------------------------. du
e to prepyloric peptic ulcer --> scaring & fibrosis --> obstruction. . causes se
vere vomiting --> volume contraction --> hypokalemic, hypocholeremic , metabolic
alkalosis. . Emergent ttt is NAOGASTRIC suction to decompress the stomach, then
hydration with sodium chloride and K replacement. . MANGEMENT OF HYPERKALEMIA:
3 steps --------------------------1- Membrane stabilization (normalize cells ele
ctrical activity) with calcium gl uconate. 2- Drive K intracellular: Insulinee/g
lucose administration is the most rapid wa y to decrease serum K level, also B2
agonist (Albutrol) shift K intracellular. 3- Remove K from the body: Sodium poly
steren sulfonate (Kalyexalate) bind K in GIT, FUROSEMIDE loop diuretic leads to
loss of K in urine, RENAL Dialysis is the most definitive way to remove K from t
he body in Renal failure. . Shifting K intracellularly is more rapid than removi
ng it from the body. . Insuline/glucose is more rapid than any other method. . H
YPOCALCEMIA: --------------. May occur during or immediately following major sur
gery due to repeated blood transfusion. . Due to volume expansion and hypoalbumi
nemia, so usually asymptomatic because the ionized calcium is normal. . When ion
ized calcium is decreased (due to binding with citrate of repeated tr ansfusion)
--> symptoms appears. . Hyperactive tendone reflexes, muscle cramps and rarely
convulsions. . N.B.:

- hypomagnesemia may mimic hypocalcemia because it causes decrease PTH secret io

n and decrease peripheral response to PTH. - Hypokalemia --> muscle weakness, cr
amps may be flaccid paralysis if severe hypokalemia. EKG shows U wave in severe
hypokalemia. - Hyperkalemia --> muscle weakness, flaccid paralysis if severe hyp
erkalemia --> EKG changes, maybe a systole. - Hyponatremia --> a symptomatic, bu
t if prolonged --> weakness, lethargy, de lirium and seizures. - Hypermagnesemia
--> if mild --> decreased deep tendone reflexes, if severe --> lost deep tendon
e reflexes, muscle paralysis & may cardiac arrest. . CARBON MONOXIDE POISONING:
---------------------------. After exposure to fire (house ....). . CO --> decre
ase delivery of O2 to tissue by 2 mechanisms: - binds to hemoglobine 260 times t
han O2 --> displace o2 frome Hb --> decreas e O2 carrying by the blood. - causes
shift of the oxyhemoglobine dissociation curve to the left --> decre ase unload
ing of O2 from Hb in the tissue. . this increase the anaerobic metabolism --> in
crease lactic acid production -> anion gap metabolic acidosis. . this type of la
ctic acidosis due to decrease O2 delivery to tissue is calle t ype A lactic acid
osis. . It occurs in CO poisoning and circulatory failure. . LOOP DIURETICS: ---------------. Frequently used in cirrhotic patients with volume overload and as
cities. . Potential side effects are --> Hypokalemia, metabolic alkalosis, prere
nal ren al failure . HYPERCALCEMIA: ---------------. Manifested by nonspecific s
ymptoms --> abd. pain, constipation, polyuria and neuropsychatric ilness. . TTT:
1st IV normal saline 0.9% --> increase renal excretion of Ca by decreasi ng ca
reabsorption at the proximal tubules. . Then LOOP diuretics --> inhibite Ca reab
sorption at loop of henel. . treatment of the cause of hypercalcemia. . SUCCINYL
CHOLINE: -----------------. Is a depolarising neuromuscular blocker that can cau
se life threating hyperka lemia. . It should not be used in patient with or at h
igh risk of hyperkalemia such as (burn, crush injury patient & patient with demy
linating syndromes. . Non depolarizing agents as vecuronium and rocuronium are b
etter used. CALCIUM LEVEL IN HYPOALBUMINEMIA: --------------------------------.
Only 45% of circulating ca is free and physiologically active (ionized ca). . th
e remainder is bound to albumin with a ration 0.8 mg/dl Ca per 1 gm albumin . .
thus every reduction in serum albumin 1 gm/dl leads to reduction in serum Ca by
0.8 mg/dl though the ionized Ca level doesn't changed. . For patient with abnorm
al serum albumin concentration (as liver disease) acor rect ca level is calculat
ed by: Corrected Ca = 0.8 (normal albumin - measured albumin) + measure d ca.

. Normal albumin = 4 gm/dl. . CUCHING'S SYNDROME: ------------------. Caused by

excess corticosteroids intake as in brochial asthma or edogenous ad renal hypers
ecretion of cortisone. . Manifested by: trunkal obesity, weight gain, easy bruis
ing, proximal muscle w eakness, hpertension, hyperglycemia, acne, . Osteopenia,
osteoprosis, cataract. . HYPERNATREMIA AND HYPOKALEMIA (common). SEPTIC SHOCK: -----------. History of sepsis with hypotension, fever, oliguria and acidosis. .
due to hpotension & hypoperfusion --> anaerobic metabolism --> lactic acidosi s
. . IV normal saline 0.9 % is the 1st step in treatment metabolic acidosis of se
p tic shock. . with or without vassopressorfor hypotension & antibiotics for inf
ection. Dr. HISHAM ELKILANY. _________________________