Finals IB - Water and Electrolyte Balance Supplementary Lecture

7/21/2019 Finals IB - Water and Electrolyte Balance Supplementary Lecture

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WATER AND

ELECTROLYTESBALANCE


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WATER BALANCE

Water constitutes about 60% of bodyweight in men and 50% in women.

2/3rdof water is in ICF (about 28L).

1/3rdis in ECF (about 14L) Blood plasma,interstitial fluids, lymph and transcellularfluids (free fluid in pleural, pericardial and

peritoneal cavities CSF and digestivesecretions).

93% of plasma volume is water and 7% isproteins.


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TOTAL BODY WATER AND ITS

COMPONENTS

TOTAL BODY

WATER IN 70

Kg

INTRACELLULAR EXTRA CELLULAR

4245 L

(60 %)

2426 L 1819 L

INTERSTITIAL:1314 L

PLASMA : 55.5 L


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WATER BALANCE IN THE ADULTS

IN TAKE OUT PUT

BEVERAGES = 1500 mL

WATER IN FOOD = 600 mL

METABOLIC WATER= 400 mL

TOTAL = 2500 mL

URINE = 1500 mL

SKIN LOSS = 500 mL

(SWEAT / INSENSIBLE)

LUNGS = 400 mL

FECES = 100 mLTOTAL = 2500 mL


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WATER BALANCE

Water balance is maintained by theelectrolyte balance and is controlled bythe Antidiuretic Hormone (ADH)

secreted from posterior pituitary byacting on renal tubules for the control ofwater reabsorption in response to bodywater intake / loss.


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WATER BALANCE

Proximal Renal Convoluted Tubules &

Collecting Ducts membranes have

small integral proteins with hydrophilic

Aquaporin Channels AQP1, AQP2,

AQP3, AQP4 & AQP6 which open

under the influence of ADH to

facilitate water reabsorption in order to

maintain water balance.


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WATER BALANCE

Water content of ICF and ECF iscontrolled by differences in theosmotic pressure across the cell

membrane plasma which are verypermeable to water but the osmolalitybetween the two must be equal otherwise the water will move from lowerosmolality to high osmolality until newequilibrium is attained.


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WATER BALANCE

WATER DEPLETION : occurs in variety

of diseases like diarrhea, vomiting, fever,

burns etc.

The loss of water increases plasmaosmolality and causes dehydration of ICF

specially of

CNS tissues as water moves from ICF toECF which more dangerous than ECF

dehydration & may result in coma and

death in severe cases.


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WATER BALANCE

Body responds with stimulation ofthirst which increases the intake of

water and stimulation of ADH release

which increases water reabsorptionfrom kidneys thereby restoring the

water balance.


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HOMEOSTATIC CORRECTION OF

WATER DEPLETION

8 ADH + H2O VOLUME 1

-

THIRST RENAL BLOOD FLOW 2

+ A+

7 HYPOTHALAMIC + RENIN RELEASE 3

OSMOLALITY

B +

ANGIOTENSIN II 4

+

6 [ Na+] + ALDOSTERONE 5


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LOSS OF BODY WATER

HEMOCONCENTRATION

RELEASE OF ADH THIRST

INCREASED REABSORPTION INCREASED

OF WATER IN THE WATER INTAKE

RENAL TUBULES

PLASMA TONICITY/VOLUME RESTORED


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WATER BALANCE

WATER EXCESS : occurs rarely

specially in those patients who are on

Intravenous(IV) fluids and in some

Psychiatric diseases.

The excess of water decreases plasma

osmolality and causes over hydration.


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WATER BALANCE

Body responds with inhibition ofthirst which decreases the intake of

water and inhibition of ADH release

which decreases water reabsorptionfrom kidneys thereby restoring the

water balance.


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HOMEOSTATIC CORECTION OF

WATER EXCESS

8 ADH + H2O VOLUME 1

- THIRST +

- RENAL BLOOD FLOW 2

A-

7 HYPOTHALAMIC - RENIN 3

OSMOLALITY

B -

ANGIOTENSIN 4

- -

6 [ Na+] - ALDOSTERONE 5


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EXCESSIVE WATER DRINKING

HEMODILUTION

INHIBITION OF ADH INHIBITION OF THIRST

DECREASED TUBULAR LESS WATER INTAKE

REABSORPTION OF WATER;

GREATER WATER LOSS

PLASMA TONICITY/VOLUME RESTORED


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WATER BALANCE

ABNORMALITY OF ADH DIABETESINSIPIDUS:

Rare disease of posterior pituitary resulting

in loss of ADH secretion.

The loss of water increases plasma

osmolality and causes dehydration of ICF.


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WATER BALANCE

Body tries to respond with

stimulation of thirst which increases

the intake of water but due to

disease of ADH there is no increase

reabsorption of water from the

kidneys so the balance is not

restored and patient continues to

excrete a large amount of urine

although he is dehydrated.


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RESULTS OF ADH DEFECIENCY

8 ADH - H2O VOLUME 1

BLOCK -THIRST RENAL BLOOD FLOW 2

+ A

+

7 HYPOTHALAMIC + RENIN 3

OSMOLALITY

B +

ANGIOTENSIN 4

+ +

6 [ Na+] + ALDOSTERONE 5


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COMPOSITION OF THE BODY FLUIDS

EXTRA CELLULAR FLUIDS INTRACELLULAR FLUIDS

ANIONS CATIONS ANIONS CATIONS

Cl =100 mmol/L

HCO3=26mmol/L

ORGANIC

IONS =3 mmol/L

PHOSPHATE = 1

mmol/L

SULPHATE = 0.5

mmol/LPLASMA PROTEINS=

16 mmol/L

SODIUM = 140

mmol/L

K+= 4.5 mmol/LCa 2+= 1.3

mmol/L

Mg 2+=

0.7mmol/L

PHOSPHATE = 126

HCO3= 10

SULPHATE = 10

ORGANIC IONS = 05

PROTEINATE = 40

As mmol / Kg of

WATER

K+= 165

Mg+= 14

Na+= 12

Ca+= very less

As mmol / Kg

of WATER


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SODIUM

THE MOST ABUNDANT CATION OF

ECF, 140-142 mmol/L REPRESENTINGHALF OF OSMOTIC STRENGTH OFPLASMA AND THEREFORE PLAYSIMPORTANT ROLE IN DISTRIBUTION

OF WATER AND MAINTAINANCE OFOSMOTIC PRESSURE IN ECF, WHEREAS IN ICF IT IS ONLY 10-20 mmol/L.1/3rdIS PRESENT IN SKELETON ASINORGANIC PORTION.


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SODIUM

NORMAL DAILY INTAKE IS 130-260

mmol (8-15 gm) WHERE AS BODY

REQUIRES ONLY 2-5 mmol. THE

REST IS EXCRETED IN URINE ,

SWEAT, GIT SECRETIONS ETC.

EXCESS INTAKE:

HYPERTENTION.


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SODIUMIT ENTERS THE CELLS

THROUGH ATP DEPENDENTSODIUM POTASSIUM ATPasePUMP.

IT IS REABSORBED FROM

RENAL TUBULES UNDER THEEFFECT OF ALDOSTERONE, AHORMONE SECRETED BY

ADRENAL CORTEX.ACTH

ANDDEOXYCORTICOSTERONEMAYALSO CAUSE RENALREABSORPTION TO SOME

EXTENT.


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SODIUM

FUNCTIONS

MAINTAINANCE OF PLASMAOSMOTIC PRESSURE AND VOLUME.DECREASED Na+RESULTS IN

DECREASED PLASMA VOLUMELEADING TO DECREASED CARDIACOUT PUT AND HYPOTENSION.

PLAYS IN IMPORTANT ROLE INREGULATION OF NERVE

EXCITABILITY.


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SODIUM

DUE TO ITS ASSOCIATION WITH

CHLORIDE, IT SERVES AS ANIMPORTANT SOURCE OF Cl-FORFORMATION OF HCl IN GASTRICJUICE AND IN TRANSPORT OFCARBON DIOXIDE FROM TISSUES TOTHE LUNGS.

INVOLVED IN EXCHANGE FOR H ION

EXCRETION FROM KIDNEYSTHEREFORE HELPS IN THEREGULATION OF BLOOD pH AND

NORMAL ACID BASE BALANCEOFBODY.


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RENIN-ANGIOTENSIN SYSTEM RENIN IS A PROTEOLYTIC ENZYME

SECRETED BY JUXTAGLOMERULAR

APPARATUS ADJACENT TO RENAL

GLOMERULI.

IT SPLITS A DECAPEPTIDE,

ANGIOTENSIN-IFROM -2 GLOBULIN.

ANOTHER PEPTIDASE ANGIOTENSIN

CONVERTING ENZYME (ACE) PRESENT

MOSTLY IN LUNGS CONVERTS IT INTO A

HORMONE ANGIOTENSIN-II WHICH

HAS 2 IMPORTANT SYSTEM IC

FUNCTIONS.


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RENIN-ANGIOTENSIN SYSTEM

1.ACTS DIRECTLY ON CAPPILARY WALLS

CAUSING VASOCONSTRICTIONTHEREBY MAINTAINS BLOOD PRESSURE.

2.STIMULATES CELLS OF ZONA

GLOMERULOSAIN

ADRENAL CORTEXTOSYNTHESIZE AND SECRET

MINERALOCORTICOID HORMONE

ALDOSTERONE.


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ALDOSTERONE

NORMAL PLASMA LEVELS

SUPINE 29 mg / dL.

URINARY EXCREATION = 2026

mg / dL.FUNCTIONS

INCREASE RETENTION /

REABSORPTION OF Na+THROUGH

DECREASED EXCRETION FROM

KIDNEYS.

ALDOSTERONE


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INCREASE EXCRETION OF K+, H+,

NH4.

SIMILAR EFFECTS ON IONIC

TRANSPORT IN SWEAT GLANDS,

SALIVARY GLANDS ANDINTESTINAL MUCOSA.

DEOXYCORTICOSTERONE ALSO

AFFECTS BUT 30 - 50 TIMES LESSPOTENT THAN ALDOSTERONE.

ALDOSTERONE


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SODIUM

ABNORMALITIES

1. HYPONATRAEMIA: DECREASE IN

PLASMA SODIUM DUE TO ACUTE

URAEMIA, VOLUME DEPLETION,

DIURETIC TREATMENT, ADRENAL

INSUFFICENCY (ADDISON ,S

DISEASE), ADH ABNORMALITIES,INCREASED ECF VOLUME WITH

OEDEMA, CONGESTIVE CARDIAC

FAILURE AND RENAL DISEASES.

SODIUM


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SODIUM

CLINICAL FEATURES:

CELLULAR OVERHYDRATION

SPECIALLY OF CNS LEADING TO

HEADACHE, CONFUSION,

FITS,DECREASED CARDIACOUTPUT, HYPOTENSION AND EVEN

DEATH MAY OCCUR.

SODIUM


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SODIUM

2. HYPERNATRAEMIA:

EXCESS OF PLASMA SODIUMCAUSED BY DECREASED INTAKEOF WATER, UNCONSCIOUSNESS,DAMAGE TO THIRST CENTRE,EXCESSIVE WATER LOSS AS INDIABETES INSIPIDUS,GLYCOSURIA, EXCESSIVE INTAKE

OF Na+

IN DIET OR IN DRUGS,EXCESSIVE RETENTION OF Na+ASIN CUSHING,S SYNDROME ANDCONN,S SYNDROME.

SO


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SODIUMCLINICAL FEATURES:

HYPERVOLAEMIALEADING TOMILD- MODERATE TO SEVEREHYPERTENSION WITH OEDEMAAND IN SEVERE CASESHEADACHE (THROBING)DYSPNOEA AND OTHER EFFECTSON CVS LIKE CONGESTIVE

CARDIAC FAI LURE(CCF).

DISORDERS OF ALDOSTERONE


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DISORDERS OF ALDOSTERONE

PRIMARY ALDOSTERONISM

(CONN,S SYNDROME).ADENOMAS OF GLOMERULOSA

CELLS.

CLINICAL FEATURES

Na+ RETENTION AND

HYPERTENTIONK+ LOSS AND ALKALOSIS.

DISORDERS OF


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DISORDERS OF

ALDOSTERONE

MUSCLES PARASTHESIAS,WEAKNESS, PARALYSIS.

POLYDIPSIA, POLYURIAAND

TETANY.

TREATMENT

REMOVAL OF TUMOURAND

SPIRANOLACTONE(ALDECTONE)

THERAPY.


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SECONDARY ALDOSTERONISM

RENAL ARTERY STENOSIS :

HYPERPLASIA AND HYPERFUNCTION OFJUXTAGLOMERULAR CELLS.

CIRRHOSIS OF LIVER,CARDIACFAILURE, NEPHROTIC SYNDROME.

RENIN AND ANGIOTENSIN II.

SIGNS AND SYMPTOMS SAME AS IN

PRIMARY.

CHLORIDE


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CHLORIDE

PRESENT IN CLOSE ASSOCIATION WITH

SODIUM AND THEREFORE FUNCTIONS

SIMILAR TO IT I.E

MAINTAINANCE OF WATER AND

ELECTROLYTES BALANCE.

PLASMA OSMOTIC PRESSURE.

ACID BASE BALANCE: IN TRANSPORT OF

CO2FROM TISSUE TO LUNGS IN ALSO IN

THE EXCRETION OF NH4IONS.

CHLORIDE


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CHLORIDE

FORMATION OF HCl IN THE

GASTRIC JUICETHE MAIN SOURCE IS DRINKING

WATER & TO SOME EXTENT

VEGETABLES AND FRUITSIN VOMITING THERE IS MORE

LOSS OF CHLORIDE AND

COMPENSATORY INCREASE INHCO3

- : HYPOCHLOREMIC

ALKALOSIS.


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POTASSIUM

THE MOST ABUNDANT CATION OF ICF.DAILY REQUIREMENT IS 2-4 gm

PRESENT IN FRUITS, VEGETABLES,

MEATS, GRAINS & MILK.FOUND MOSTLY INSIDE THE CELL, LIKE

MUSCLE CELLS.


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POTASSIUMFUNCTIONS

NERVE ACTIVITY IN SKLETAL &

CARDIAC MUSCLE.

PART OF Na+ / K+ ATPASE OF

SODIUM PUMP IN TISSUES.

REQUIRED FOR MANY ENZYME

REACTIONS LIKE GLCOGEN

SYNTHASE.

COMPETES WITH H+ FOR

EXCHANGE WITH Na+ IN KIDNEYS.

POTASSIUM


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POTASSIUM

ABNORMALITIES

HYPERKALEMIA ; NORMALLY THEEFFICIENT RENAL EXCREATION DOESNOT RESULT IN HYPERKALEMIA, BUT

MAY BE SEEN IN FOLLOWING CONDITIONRENAL FAILURE.

FEVERS ; EXCESSIVE BREAK DOWN OFBODY PROTEINS AN RELEASE OF K+.

INJURY OR INFECTION OF THE MUSCLES.

LYSIS OF TUMOURS.

ADDISON,S DISEASE.


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POTASSIUM

CLINICAL FEATURE

WEAKNES AND NUMBNESS OFMUSCLES TINGLING OF

EXTREMITIES.BROAD QRS COMPLEX WITH

PEAKED T WAVE AND NO PWAVE. ARRHYTHMIAS LIKEBRADYCARDIA APPEAR ANDHEART MAY STOCK DIASTOLE.


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POTASSIUM

2. HYPOKALEMIA: NORMALLY NOTOBSERVED BUT MAY BE PRESENT IN

DECREASED INTAKE , PROLONG

INFUSION OF K+ FREE IV FLUIDS.INCREASED RENAL LOSS LIKE IN

RENAL DISEASES , DIURETICS ,

METABOLIC ALKALOSIS AND EXCESS

OF ALDOSTERONE.

LOSS FROM GIT AS IN VOMITING

DIARRHEA.


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POTASSIUM

CLINICAL FEATUREANOREXIA , NAUSEA AND MAY BE

PARALYTIC ILEUS.

MUSCLE WEAKNES MENTALDEPRESSION.

ECG CHANGES LIKE INVERSION OF

T WAVE.RAPID IRREGULAR PULSE AND

HYPOTENSION.


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ANDROGENS

DHEA AND ANDROSTENEDIONEWEAKER ANDROGENS.

ANABOLIC EFFECTS INRETENSION OF Na+ , P , K , ClAND PROTEINS.

INCREASE SECRETION MAYCAUSE MUSCULINIZATION INFEMALES AND FEMINIZATION

IN MALES.


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LAB DIAGNOSIS

INCREASE PLASMA CORTISOL,

ACTH.

LOSS OF DIURNAL RHYTHM.INCREASE URINARY CORTISOL.

GLUCORTCOID SUPPRESSION.

+ IN CUSHING,S DISEASE.

- IN CUSHING,S SYNDROM.


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TREATMENT

REMOVAL OF TUMOUR TISSUE.

METYRAPONE ANDAMINOGLUTETHIMIDE, TO

BLOCK CORTISOL SYNTHESIS.

K+REPLACEMENT.

Finals IB - Water and Electrolyte Balance Supplementary Lecture

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