BASIC PRINCIPLES OF CELL INJURY & ADAPTATION

B.Pharmacy 2nd Semester Pathophysiology - UNIT 1
INTRODUCTION
HOMEOSTASIS
COMPONENTS AND TYPES OF FEEDBACK SYSTEMS
PATHOGENESIS (REVERSIBLE & IRREVERSIBLE)
MORPHOLOGY OF CELL INJURY
CELL SWELLING
INTRACELLULAR ACCUMULATION
CALCIFICATION
ENZYME LEAKAGE AND CELL DEATH
ACIDOSIS & ALKALOSIS
ELECTROLYTE IMBALANCE

1. BASIC
PRINCIPLES OF
CELL INJURY

2. Cellinjuryandadaptationarefundamentalconceptsinunderstandingthe
responseofcellstovariousstressesandinsults.Let'sdelveintoeachofthese
aspects:
Introduction:
Cellinjuryreferstothestructuralorfunctionalabnormalitiesthatresultwhen
cellsareexposedtoharmfulstimuli.Adaptation,ontheotherhand,isthe
abilityofcellstomodifytheirstructureorfunctioninresponsetothesestimuli,
aimingtomaintainhomeostasis.
Definitions:
CellInjury:Structuralorfunctionalchangesincellsduetovariousstressors.
Adaptation:Cellularresponsetostressaimedatmaintainingorrestoring
homeostasis.

3. Homeostasis:
•Homeostasisisthemaintenanceofstableinternalconditionswithinan
organismdespiteexternalchanges.Incellularterms,itinvolves
regulatingvariablessuchaspH,temperature,andionconcentrations
toensureoptimalfunction.
Components and Types of Feedback Systems:
HOMEOSTASIS

4. •Stimuli:These are changes in the internal or external environment that disrupt the
body's equilibrium. For example, a rise in body temperature due to hot weather.
•Receptor:Specialized cells or sensory organs detect changes in stimuli and send
signals to the control center. In our example, sensory receptors in the skin detect the
temperature change.
•Control Center:The control center receives information from the receptors and
determines the appropriate response. In this case, the control center could be the
hypothalamus in the brain.
•Effector:Effectors are structures, typically muscles or glands, that carry out the
response instructed by the control center. In our example, sweat glands are effectors
that produce sweat to cool down the body.
Components of Homeostasis:

5. Feedbacksystemsarecrucialinmaintaininghomeostasis.Therearetwo
maintypes:
NegativeFeedback:Workstocounteractdeviationsfromthesetpoint,
restoringhomeostasis(e.g.,bloodglucoserise).
PositiveFeedback:Amplifiesdeviationsfromthesetpoint,potentially
leadingtoacascadeofevents(e.g.,bloodclotting).
Types of Homeostasis:

6. NegativeFeedback-BloodGlucoseRise:
Stimulus:Increased blood glucose levels after a meal.
Receptor:Specialized cells in the pancreas called beta cells sense the elevated
blood glucose levels.
Control Center: The control center in this scenario is the pancreas. It receives
input from the beta cells and initiates a response.
Effector:The effector in this case is the release of insulin by the pancreas into the
bloodstream.
Response:Insulin facilitates the uptake of glucose by cells, promotes its
conversion into glycogen for storage, and enhances glucose utilization in
tissues, thus lowering blood glucose levels.
Example:Afterconsumingamealrichincarbohydrates,bloodglucoselevelsrise.
Betacellsinthepancreasdetectthisincreaseandreleaseinsulin.Insulinthen
promptscellsthroughoutthebodytotakeupglucosefromthebloodstream,
reducingbloodglucoselevelsbacktothenormalrange.

7. PositiveFeedback-BloodCoagulation:
Stimulus:Injury leading to blood vessel damage.
Receptor: Platelets and damaged endothelial cells in the blood vessel wall detect
the injury.
Control Center:The liver synthesizes and releases clotting factors into the
bloodstream in response to signals from the damaged tissue.
Effector:Platelets aggregate at the site of injury, and clotting factors catalyze the
formation of fibrin, a protein mesh that stabilizes the clot.
Response:Clot formation reinforces the initial platelet plug, preventing further
blood loss at the injury site.
Example:Whenyousustainacut,damagedbloodvesselwallsexposecollagen
fibersandtissuefactors.Plateletsadheretotheexposedcollagenandrelease
chemicalsthatattractmoreplatelets.Asplateletsaggregate,theyrelease
additionalclottingfactors,leadingtotheformationofabloodclot.Thisclotting
cascadecontinuesuntiltheclotisstabilizedandbleedingstops.

10. CELL INJURY

12. Mechanisms of Necrosiss and
Apoptosis

13. Differences between necrosis &
apoptosis

25. Pathogenesis:
ATP depletion disrupts cellular energy metabolism, compromising various
ATP-dependent processes essential for cell function and survival.
Consequences:
Reduced ATP levels impair the activity of ATP-dependent ion pumps, such
as the sodium-potassium pump, leading to intracellular accumulation of
sodium and calcium ions and extracellular accumulation of potassium
ions.
Disruption of ATP-dependent processes affects protein synthesis, ion
homeostasis, and maintenance of membrane integrity.
Effects:
Cellular functions dependent on ATP, such as protein synthesis, ion
transport, and maintenance of membrane potential, are impaired. This
leads to cellular swelling, loss of microvilli, and alterations in organelle
structure and function.
PATHOGENESIS OF CELL INJURY (REVERSIBLE)
ATP Depletion:

27. Damage to Mitochondria:
Pathogenesis:
•MitochondriaarecrucialorganellesinvolvedinATPproduction,calcium
homeostasis,andregulationofapoptoticpathways.Damage to
mitochondriadisruptscellularenergymetabolismandcalcium
homeostasis,contributingtoreversiblecellinjury.
Consequences:
•Mitochondrialdamageimpairsoxidativephosphorylation,reducingATP
productionandincreasingthegenerationofreactiveoxygenspecies(ROS).
•Dysfunctionofmitochondrialcalciumtransportmechanismsleadsto
cytosoliccalciumoverload,activatingcalcium-dependentenzymesand
promotingcellularinjury.
Effects:
•DecreasedATPproductioncompromisescellularenergystores,while
increasedROSgenerationcontributestooxidativestressandcellular
damage.Calciumoverloadfurtherexacerbatescellularinjurybyactivating
deleteriousenzymesandapoptoticpathways.

28. Changes in Ion and Water Influx:
Pathogenesis:
•Alterationsinionandwaterinfluxdisruptcellularosmoticbalanceand
membraneintegrity,leadingtocellularswellinganddysfunction.
Consequences:
•Increasedintracellularcalciumlevels,resultingfromATPdepletionand
mitochondrialdysfunction,activatephospholipasesandproteases,leading
tomembranedamageandincreasedpermeability.
•Dysregulationofionchannelsandpumpsdisruptsionhomeostasis,
resultinginintracellularaccumulationofsodiumandwaterand
extracellularlossofpotassium.
Effects:
•Cellularswelling,alsoknownashydropiccellularchangeorvacuolar
degeneration,occursduetotheinfluxofwaterandions.Thisleadsto
swellingoforganelles,dilatationoftheendoplasmicreticulum,and
formationofcytoplasmicvacuoles,compromisingcellularstructureand
function.

29. Insummary,reversiblecellinjuryinvolvesmultipleinterconnected
mechanisms,includingATPdepletion,damagetomitochondria,and
alterationsinionandwaterinflux.Thesemechanismscontributeto
cellulardysfunctionandstructuralchanges,whichcanbereversedifthe
injuriousstimuliareremovedpromptly.Understandingthesemechanisms
isessentialforelucidatingthepathogenesisofreversiblecellinjuryand
developingstrategiesforinterventionandprevention.

32. IRREVERSIBLE CELL INJURY

33. MitochondrialDamage:
Pathogenesis:
Mitochondriaplayacrucialroleincellularenergyproduction,calcium
homeostasis,andapoptosis.DamagetomitochondriadisruptsATP
synthesis,increasesreactiveoxygenspecies(ROS)production,and
promotesmitochondrialpermeabilitytransition,triggeringapoptosis.
Consequences:
ATPdepletioncompromisescellularenergystores,leadingtodysfunctionof
ATP-dependentprocesses.IncreasedROSproductioncausesoxidative
damagetocellularcomponents,exacerbatingcellularinjury.Mitochondrial
permeabilitytransitionporeopeningresultsinreleaseofpro-apoptotic
factors,initiatingapoptoticcelldeath.

34. MembraneDamage:
Pathogenesis:
Membranedamagedisruptscellularintegrityandfunction,leadingto
leakageofcellularcontentsandlossofosmoticbalance.
Consequences:
Lossofmembraneintegrityallowsinfluxofionsandwaterintothecell,
leadingtocellularswellinganddysfunction.Leakageofintracellular
contents,suchasenzymesandions,intotheextracellularspace
activatesinflammatoryresponsesandcontributestotissuedamage.

35. CytoskeletalDamage:
Pathogenesis:
Thecytoskeletonprovidesstructuralsupport,maintainscellshape,and
mediatesintracellulartransportandsignaling.Damagetothecytoskeleton
disruptstheseessentialfunctions.
Consequences:
Cytoskeletaldamagecompromisescellularintegrityandstability,leadingto
lossofcellshapeandstructuralintegrity.Disruptionofintracellular
transportimpairscellularfunctionsandcontributestocelldysfunctionand
death.

36. NuclearDamage:
•Pyknosis:Condensationofchromatinwithinthenucleus,resultingin
shrinkageandincreasedbasophilia.
•Karyorrhexis:Fragmentationofthenucleusintosmaller,irregularlyshaped
fragments.
•Karyolysis:Dissolutionofnuclearchromatin,resultinginlossofnuclear
stainingandstructure.
Consequences:
NucleardamagedisruptsDNAintegrityandgeneexpression,impairing
essentialcellularprocessessuchasreplicationandtranscription.
Fragmentationanddissolutionofthenucleusarecharacteristicfeaturesof
irreversiblecellinjuryandapoptosis.

37. LysosomalDamage:
Pathogenesis:
Lysosomescontainhydrolyticenzymesinvolvedinintracellulardigestion
andrecyclingofcellularcomponents.Damagetolysosomalmembranes
leadstoleakageoftheseenzymesintothecytoplasm.
Consequences:
Releaseoflysosomalenzymesintothecytoplasmresultsinautodigestion
ofcellularorganellesandstructures,leadingtofurthercellulardamage
anddysfunction.

38. CellDeathandPhagocytosis:
Pathogenesis:Irreversiblecellinjuryculminatesincelldeath,whichcan
occurvianecrosisorapoptosis.Necrosisischaracterizedbycellularswelling,
ruptureofthecellmembrane,andreleaseofcellularcontents,elicitingan
inflammatoryresponse.Apoptosis,orprogrammedcelldeath,isaregulated
processinvolvingactivationofcaspasesandfragmentationofthecellinto
apoptoticbodies.
Consequences:Celldeatheliminatesdamagedcellsandpreventsfurther
tissuedamage.Phagocyticcells,suchasmacrophages,engulfandremove
apoptoticcellsandcellulardebris,contributingtotissuerepairand
resolutionofinflammation.

39. Insummary,irreversiblecellinjuryinvolvesextensivedamageto
cellularstructuresandfunctions,leadingtoirreversiblechangessuch
asmitochondrialdysfunction,membrane damage,cytoskeletal
disruption,nuclearalterations,lysosomaldamage,andultimately,cell
death.Understandingthesemechanismsiscrucialforelucidatingthe
pathogenesisofirreversiblecellinjuryanddevelopingstrategiesfor
interventionandtreatment.

48. Morphology of cell injury –Adaptive changes
(Atrophy, Hypertrophy, hyperplasia,
Metaplasia, Dysplasia)

49. Cellinjurycanleadtovariousadaptivechangesascellsstriveto
maintainhomeostasisinresponsetoenvironmentalstressors.
Theseadaptivechanges includeatrophy,hypertrophy,
hyperplasia,metaplasia,anddysplasia.

50. 1.Atrophy
Definition:Atrophyisadecreaseincellsizeandfunctionalcapacityduetoareductionin
cellsubstance.
Types:
PhysiologicalAtrophy:Normalprocessofaging(e.g.,thymusglandatrophyinchildren).
PathologicalAtrophy:Duetoinadequatenutrition,disuse,diminishedbloodsupply,or
denervation.
Causes:
Disuse:Muscleatrophyfromprolongedimmobilization;Denervation:Lossofnervesupply
leadingtomuscleatrophy;Ischemia:Reducedbloodsupplytotissues(e.g.,cerebral
atrophyduetoatherosclerosis);Malnutrition:Inadequatenutritionleadingtogeneral
wasting(e.g.,cachexiainchronicdiseases);Lossofendocrinestimulation:Hormonal
changes(e.g.,endometrialatrophypost-menopause).
Mechanism:
-Decreasedproteinsynthesisandincreasedproteindegradation,primarilythroughthe
ubiquitin-proteasomepathway.
-Autophagy,wherecellcomponentsaredegradedbylysosomes.
Examples:
-Muscleatrophyinalimbimmobilizedbyacast.
-BrainatrophyinAlzheimer’sdisease.

51. 2.Hypertrophy
Definition:Hypertrophyisanincreaseincellsizeandfunctionalcapacitywithoutan
increaseincellnumber.
Types:
-PhysiologicalHypertrophy:Duetoincreasedfunctionaldemandorhormonal
stimulation(e.g.,skeletalmusclehypertrophywithexercise).
-PathologicalHypertrophy:Duetoabnormalstressordiseaseconditions(e.g.,
cardiachypertrophyduetohypertension).
Causes:
-Increasedworkload:E.g.,weightliftingleadingtoskeletalmusclehypertrophy.
-Hormonalstimulation:E.g.,uterinehypertrophyduringpregnancy.
Mechanism:
-Increasedproteinsynthesisandorganellenumberwithincells.
-Activationofgrowthfactorsandsignaltransductionpathways(e.g.,IGF-1inmuscle
cells).
Examples:
-Leftventricularhypertrophyinresponsetochronichypertension.
-Skeletalmusclehypertrophyinresponsetoresistancetraining.

52. 3.Hyperplasia
Definition:Hyperplasia is an increase in the number of cells in an organ or tissue, leading
to increased mass.
Types:
-**Physiological Hyperplasia**: Hormonal (e.g., breast enlargement during pregnancy) or
compensatory (e.g., liver regeneration after partial hepatectomy).
-**Pathological Hyperplasia**: Due to excessive hormonal stimulation or growth factors
(e.g., benign prostatic hyperplasia).
Causes:
-**Hormonal**: E.g., estrogen-induced endometrial hyperplasia.
-**Compensatory**: Following tissue damage or partial organ removal.
-**Chronic irritation**: E.g., callus formation on skin.
Mechanism:
-Increased cellular proliferation driven by growth factors and hormones.
-Activation of stem cells and increased mitotic activity.
Examples:
-Endometrial hyperplasia due to prolonged estrogen stimulation.
-Compensatory liver hyperplasia after partial resection.

53. 4.Metaplasia
**Definition**:Metaplasiaisareversiblechangeinwhichonedifferentiatedcelltypeis
replacedbyanothercelltype.
**Types**:
-**SquamousMetaplasia**:Replacementofglandularepitheliumbysquamous
epithelium(e.g.,intherespiratorytractduetosmoking).
-**ColumnarMetaplasia**:Replacementofsquamousepitheliumbycolumnar
epithelium(e.g.,Barrett'sesophagus).
**Causes**:
-**Chronicirritationorinflammation**:Leadingtoreplacementbyacelltypebetter
suitedtowithstandthestress.
-**VitaminAdeficiency**:Leadingtosquamousmetaplasiainvariousepithelial
tissues.
**Mechanism**:
-Reprogrammingofstemcellsintheaffectedtissue.
-Cytokines,growthfactors,andextracellularmatrixcomponents drivethe
differentiationofstemcellstothenewcelltype.
**Examples**:
-Squamousmetaplasiaofbronchialepitheliuminsmokers.
-Barrett’sesophagusduetochronicgastroesophagealrefluxdisease(GERD).

54. 5. Dysplasia
**Definition**: Dysplasia is an abnormal proliferation of cells that is characterized by
changes in cell size, shape, and organization. It is often considered a precancerous
condition.
**Types**:
-**Mild, Moderate, Severe Dysplasia**: Based on the degree of abnormal cellular and
architectural features.
-**Carcinoma in situ**: Severe dysplasia involving the full thickness of the epithelium but
not invading the basement membrane.
**Causes**:
-**Chronic irritation or inflammation**: E.g., cervical dysplasia due to human
papillomavirus (HPV) infection.
-**Genetic mutations**: Leading to disruption in normal cell regulatory mechanisms.
**Mechanism**:
-Genetic and epigenetic changes leading to loss of normal control of cellular growth and
differentiation.
-Accumulation of mutations in oncogenes and tumor suppressor genes.
**Examples**:
-Cervical dysplasia detected by Pap smear.
-Dysplasia in the bronchial epithelium of smokers.

56. CellSwelling
Definition:Cellswelling,alsoknownashydropicswellingoroncosis,occurs
whencellstakeinexcesswaterduetoaninabilitytomaintainionicandfluid
homeostasis.
Mechanism:
Injury:Physical,chemical,orbiologicalfactorsdamagethecellmembraneor
disruptcellularmetabolism.
IonicImbalance:Damagetoionpumps(e.g.,Na+/K+ATPase)leadstoan
accumulationofsodiuminsidethecell.
OsmoticImbalance:Waterfollowssodiumintothecell,leadingtoswelling.
Examples:
HypoxicInjury:Inconditionslikeischemia(restrictedbloodflow),cellslack
oxygen,leadingtoATPdepletionandimpairedionpumpfunction.
ToxicInjury:Exposuretotoxinssuchasbacterialtoxinsordrugscandamage
cellularmembranes.

57. IntracellularAccumulation
Definition:Thisreferstothebuild-upofsubstanceswithincellsduetometabolic
derangements.
TypesandExamples:
Lipids:
Steatosis:Accumulationoftriglyceridesinlivercells,commonlyseeninalcoholabuseor
obesity.
Atherosclerosis:Cholesterolaccumulatesinmacrophagesandsmoothmusclecellswithin
arterialwalls.
Proteins:
MalloryBodies:Aggregatesofdamagedintermediatefilamentsinlivercells,oftenseenin
alcoholicliverdisease.
Amyloidosis:Accumulationofmisfoldedproteinsformingamyloiddepositsinvarioustissues.
Glycogen:
GlycogenStorageDiseases:GeneticdisorderslikePompedisease,whereglycogenaccumulates
intissuesduetoenzymedeficiencies.
Pigments:
Melanin:Increasedmelanininskincellsleadingtohyperpigmentationdisorderslikemelasma.
Hemosiderin:Accumulationofiron-containingpigmentinconditionslikehemochromatosis.

58. Calcification
Definition:Pathologicaldepositionofcalciumsaltsintissues.
Types:
DystrophicCalcification:Occursindamagedornecrotictissues.
Example:Calcificationinatheroscleroticplaquesordamagedheartvalves.
MetastaticCalcification:Occursinnormaltissuesduetohypercalcemia(elevated
bloodcalciumlevels).
Example:Calcificationinthelungs,kidneys,andstomach dueto
hyperparathyroidismorchronickidneydisease.

59. Enzyme Leakage
Definition: Release of intracellular enzymes into the extracellular space due to cell
membrane damage.
Clinical Significance:
Enzyme levels in blood can indicate tissue damage or disease.
Examples:
ALT/AST (Alanine/ Aspartate Aminotransferase): Elevated in liver damage.
CK-MB (Creatine Kinase-MB): Elevated in myocardial infarction.
Amylase/Lipase: Elevated in pancreatitis.

60. CellDeath
Types:
Necrosis:
Definition:Uncontrolledcelldeathresultingfromsevereinjury.
Characteristics:Cellswelling,plasmamembranerupture,inflammation.
Examples:Myocardialinfarction,gangrene.
Apoptosis:
Definition:Programmedcelldeath,aregulatedprocess.
Characteristics:Cellshrinkage,nuclearfragmentation,noinflammation.
Examples:Embryonicdevelopment,removalofdamagedcells.

61. Acidosis & Alkalosis
Definition:
Acidosis: Excessive acidity in the blood and other body tissues (pH < 7.35).
Alkalosis: Excessive alkalinity in the blood and other body tissues (pH > 7.45).
Types and Causes:
•Metabolic Acidosis:
Cause: Increased acid production or loss of bicarbonate.
Examples: Diabetic ketoacidosis, lactic acidosis, renal failure.
•Respiratory Acidosis:
Cause: Accumulation of CO2 due to hypoventilation.
Examples: Chronic obstructive pulmonary disease (COPD), drug overdose.
•Metabolic Alkalosis:
Cause: Loss of acid or excessive bicarbonate.
Examples: Vomiting, diuretic use, hypokalemia.
•Respiratory Alkalosis:
Cause: Excessive loss of CO2 due to hyperventilation.
Examples: Anxiety, high altitude, fever.

62. Electrolytes
Definition:Electrolytesaremineralsinyourbodythathaveanelectriccharge.Theyarepresentinyour
blood,urine,tissues,andotherbodyfluidsandareessentialforvariousphysiologicalfunctionssuchas:
KeyElectrolytesandTheirNormalValues:
1.Sodium(Na+):NormalRange:135-145mEq/L.
Functions:Maintainsfluidbalance,essentialfor
nerveandmusclefunction.
2.Potassium(K+):NormalRange:3.5-5.0mEq/L.
Functions:Crucialforheartfunction,muscle
contractions,andnervesignals.
3.Calcium(Ca2+):NormalRange:8.5-10.2mg/dL.
Functions:Importantforbonehealth,muscle
function,andnervesignaling.
4.Magnesium (Mg2+):NormalRange:1.7-2.2
mg/dL.
Functions:Involvedinover300biochemical
reactions,includingmuscleandnervefunction.
5.Chloride(Cl-):NormalRange:96-106
mEq/L.
Functions:Helpsmaintainfluidbalanceandis
anessentialcomponentofstomachacid.
6.Bicarbonate(HCO3-):NormalRange:22-28
mEq/L.
Functions:MaintainspHbalanceintheblood.
7.Phosphate(PO4-):NormalRange:2.5-4.5
mg/dL.
Functions:Importantforbonehealth,energy
production,andcellfunction.

63. Electrolyte Imbalance
Definition:Electrolyteimbalanceoccurswhenthelevelsofelectrolytesin
yourbodyaretoohighortoolow.Thiscandisruptnormalbodilyfunctions
andmayleadtoserioushealthissues.
CausesofElectrolyteImbalance:
Dehydration:Duetoexcessivesweating,vomiting,ordiarrhea.
KidneyDisease:Impairedkidneyfunctioncanaffectelectrolytelevels.
Medications:Diuretics,laxatives,andcertainmedicationscanalter
electrolytelevels.
ChronicDiseases:Conditionslikediabetesandheartdisease.
Malnutrition:Inadequateintakeofessentialnutrients.
Hormonal Imbalances:DisorderslikeAddison’sdiseaseor
hyperaldosteronism.

64. SymptomsofElectrolyteImbalance:
SodiumImbalance:
Hypernatremia(HighSodium):Thirst,confusion,muscletwitching,seizures.
Hyponatremia(LowSodium):Nausea,headache,confusion,seizures,coma.

PotassiumImbalance:
Hyperkalemia(HighPotassium):Muscleweakness,fatigue,irregularheartbeats,cardiac
arrest.
Hypokalemia(LowPotassium):Musclecramps,weakness,arrhythmias,constipation.
CalciumImbalance:
Hypercalcemia(HighCalcium):Nausea,vomiting,constipation,kidneystones,confusion.
Hypocalcemia(LowCalcium):Musclecramps,numbness,tingling,seizures,arrhythmias.
MagnesiumImbalance:
Hypermagnesemia (HighMagnesium):Nausea,vomiting,muscleweakness,lowblood
pressure,respiratorydepression.
Hypomagnesemia(LowMagnesium):Tremors,musclecramps,seizures,arrhythmias.

65. ChlorideImbalance:
Hyperchloremia(HighChloride):Fatigue,muscleweakness,excessivethirst,high
bloodpressure.
Hypochloremia(LowChloride):Dehydration,weakness,difficultybreathing,
confusion.
BicarbonateImbalance:
MetabolicAcidosis(LowBicarbonate):Rapidbreathing,fatigue,confusion,shock.
MetabolicAlkalosis(HighBicarbonate):Muscletwitching,handtremors,
dizziness,arrhythmias.
PhosphateImbalance:
Hyperphosphatemia(HighPhosphate):Itching,jointpain,musclecramps,weak
bones.
Hypophosphatemia (LowPhosphate):Muscleweakness,bonepain,confusion,
seizures.

66. MalabsorptionandElectrolyteImbalance
Malabsorption:
Malabsorptionreferstothebody'sinabilitytoproperlyabsorbnutrients,including
electrolytes,fromthegastrointestinaltract.Thiscanleadtoelectrolyteimbalancesdueto
inadequateintakeorabsorption.
CausesofMalabsorption:
CeliacDisease:Damagetothesmallintestine'slining,reducingnutrientabsorption.
Crohn’sDisease:Inflammationofthedigestivetractaffectingabsorption.
ChronicPancreatitis:Impairedenzymeproduction,affectingdigestionandabsorption.
LactoseIntolerance:Inabilitytodigestlactose,leadingtogastrointestinalsymptoms
andpotentialnutrientmalabsorption.
BariatricSurgery:Surgicalproceduresforweightlosscanalterdigestionand
absorption.

67. SymptomsofMalabsorption:
•Diarrhea
•Weightloss
•Bloatingandgas
•Fatigue
•Musclecramps.
•Anemia(duetoiron,folate,orvitaminB12deficiency)
•Bonepainorosteoporosis(duetocalciumandvitaminDdeficiency)
Conclusion:
Electrolytesplayacriticalroleinmaintainingvariousbodilyfunctions.Imbalancescan
resultfromawiderangeofcauses,includingdehydration,kidneydisease,medications,
andmalabsorption.Recognizingthesymptomsandunderstandingtheunderlyingcauses
arecrucialfortheeffectivemanagementandtreatmentofelectrolyteimbalances.Proper
hydration,nutrition,andmedicalinterventionarekeytorestoringandmaintaining
electrolytebalance.

68. THANK YOU