2. Introduction to Pathology (Greek Word)
Pathos = Suffering
Logos = Study
Definition:
It is the scientific study of structure and function of the body in disease.
(or)
Pathology consists of the abnormalities that occur in normal anatomy and
physiology leading to disease.
It mainly involves the investigation of the causes of disease and associated changes
at the levels of cells, tissues, and organs, which in turn give rise to the
presenting signs and symptoms of the patient.
3. Important terms in pathology and medicine:
1) Patient: Is the person affected by disease.
2) Lesions: Are the characteristic changes in tissues and cells produced by
disease in an individual (or) experimental animal.
3) Morphology: It consists of examination of diseased tissues (Blood & Urine
Tests)
4) Etiology: Includes the underlying causes and modifying factors. (Why of
Disease)
Eg: Diseases with unknown etiology: Hypertension, Diabetes, Cancer etc.
5) Pathogenesis: Refers to the steps in the development of disease. (How of
Disease)
4. Cell Injury
Definition: It is defined as a variety of stresses a cell encounters as a result of
changes in its Internal and external environment.
(Stress may be Physiologic (or) Pathologic stimuli)
6. Causes of Cell Injury
1. Hypoxia
Causes:
a. Ischemia
b. Inadequate oxygenation of the blood
c. Reduction in the oxygen-carrying capacity of the blood
2. Chemical Agents
a. glucose, salt or oxygen
b. poisons
c. environmental toxins
d. social “stimuli”
e. therapeutic drugs
3. Physical agents- trauma, extremes of temperature, radiation, electric
shock, & sudden changes in atmospheric pressure
4. Infectious agents
7. Cont……….
5.Immunologic reactions
Example: anaphylactic reaction to a
foreign protein or a drug reaction to self antigens
6.Genetic defects
• Examples are genetic malformations associated with
Down Syndrome, sickle cell anemia & inborn errors
of metabolism
7.Nutritional Imbalances
8. Pathogenesis of cell injury
• General principles of pathogenesis
1. Type, duration and severity of injurious agents
2. Type, status and adaptability of target cell
3. Underlying intracellular phenomena
eg. Mitochondrial damage, cell wall damage, free
radicals
4. Morphological consequences
eg. Ultrastrucal changes, swelling
10
9. Reversible Cell Injury
• If the hypoxic or ischemic effect is for short duration,
the effects may be reversible on rapid restoration of
circulation.
• Some of the sequential biochemical and ultra-
structural changes in reversible cell injury are as
under:
i) Depletion of ATP:
ATP is the primary requirement for the synthesis of
lipid, protein, cell membrane etc.
In human body ATP is produce by aerobic and
anaerobic process.
10. Cont…
Aerobic process is carried out by mitochondria and
anaerobic ATP is produce by the glucose/glycogen.
In the ischemic condition, the supply of oxygen and
Glucose both are affected. So, decrease the production of
ATP. Due to this effect protein synthesis, cell membrane
formation, lipid synthesis process get affected and it
leads to cell injury.
Due to insufficiencies of oxygen supply RBC disorder,
Heart disease, Lungs Disease will form. Generally
anaerobic cell injury are less severe than the aerobic cell
injury.
11. Cont…
ii) Intracellular lactic acidosis & nuclear clumping:
Due to low oxygen supply aerobic ATP formation
process get affected and mitochondria fails to work.
So anaerobic glycolytic pathway start to produce ATP.
This results in rapid depletion of glycogen and
accumulate lactic acid.
It lower the intracellular pH due to intracellular
acidosis and produce clumping of nuclear chromatin.
This effect release the lysosomes and it produce
cellular digestion.
12. iii) Effect on plasma membrane:
Plasma membrane required phospholipid for continuous repair
but due to lack of ATP fatty acid not form the phospholipids. Due
to this effects plasma membrane pumps get affected and the
regulation of calcium, sodium and potassium get affected.
a.) Failure of Na+ -K+ ATPase pump:
Na+ -K+ ATPase pump is useful for the exchange of Na+ inside
to outside and K + outside to inside from the cell.
Lower ATP level affect the activity of this pump and Na+
get accumulate inside the cell and potassium out of the cell.
13. Cont…
Accumulation of Na+ inside the cell retain the water and
increase intracellular water level and hydropic swelling
occur due to disruption in osmotic pressure.
b.) Failure of Ca++ pump:
Accumulation of Na+ inside the cell produce affect in the
intracellular level of Ca++.
Excess Ca++ accumulate inside the cell as well as into
the mitochondria leads to reversible cell damage.
14. iv.) Decrease protein synthesis:
• Lack of oxygen effect disturb the intracellular
osmotic balance of the cell so endoplasmic reticulum
and golgi apparatus swell up.
• So the ribosome detach from the granular
endoplasmic reticulum and it get inactive.
• This effect decrease the synthesis of protein.
15. Irreversible Cell Injury
• Long lasting/persistence ischemic or hypoxic effect
produce cell death or irreversible damage.
• If cell fails to reverse mitochondrial function as well as
disturbance in cell membrane/plasma membrane function
cause irreversible cell injury.
i.) Ca+ influx produce excitotoxicity into the cell:
Large amount of intracellular Ca++ produce damage in
mitochondrial cell wall as well as excitotoxicity
(activation of number of enzymes like phospholipase,
endonuclease, protease etc.). This effect damage the cell
structure such as component of cytoskeleton, plasma
membrane, DNA etc.
16. Cont…
a.) Effect of activated phospholipase:
Activated phospholipase degrade the membrane
phospholipids which is the main constituent of plasma
membrane. As well as due to lack of ATP generation new
phospholipid will not form and it exaggerate the effects.
b.) Effect of activated protease:
Activated protease damage the cytoskeleton of
the cell membrane leads to irreversible cell injury.
c.) Effect of activated endonuclease:
Activated endonuclease damage the nucleoprotein
as per below process:
- Condense or clumps the nucleus
- Produce fragments of nucleus
- Dissolve the nucleus
17. ii.) Low pH of cell activate and release the lysosomal
hydrolytic enzyme:
• Lack of oxygen decrease the intracellular pH and it
activate or release the lysosomal hydrolytic enzyme
like lactic dehydrogenase (LDH), Creatine kinase
(CK), hydrolase, RNAse, DNAse, glycosidase,
phosphatase, lipase, amylase etc.
• Activation of this enzyme digest the cellular
components through the phagocytic effects and cause
the irreversible cell injury.
18. Pathogenesis and Mechanisms of cell
Injury:
1. ATP depletion or Hypoxia
2. Loss of calcium homeostasis
3. Oxidative stress (excess Reactive Oxygen
Species)
4. Damage to mitochondria, and increased
permeability of membranes
19. 1. ATP depletion or Hypoxia:
Hypoxia first causes loss of phosphorylation in mitochondria and
decrease the production of ATP which is a source for energy.
Loss of ATP (which is a energy source) has widespread effects on
many systems in the cell.
for example: Neurons and cardiac myocytes are rapidly injured by
ATP decreases that occur as a consequence of ischemic injury. A
major component of the injury is the alteration of membrane
permeability caused by decreased activity of ATP-dependent ionic
pumps.
Decreased ATP results in increased anaerobic glycolysis,
accumulation of lactic acid, and therefore decreased intracellular
pH.
Decreased ATP causes decreased action of Na+ / K+ pumps in the
cell membranes, leading to increased Na+ and water within the cell
(cell swelling).
20. 2. Injury produced by loss of calcium
homeostasis:
Cytosolic free calcium is kept at concentrations that
are at least 10-fold lower than the extracellular
levels.
Mitochondria and endoplasmic reticulum keep
intracellular calcium under control.
If the intracellular calcium level may rise it produces:
– Increase Glutamate Release.
– Activation of protease and lipases, causing membrane
damage.
– It Activate Nitric oxide and Reactive oxygen species
which increase the oxidative stress and damage the cell.
21. 3. Oxidative stress (excess Reactive
Oxygen Species):
Cells generate reactive oxygen forms as
byproducts of metabolic reactions that reduce
molecular oxygen to water.
These reactive forms, called reactive oxygen
species, can damage lipids, proteins and DNA.
22. 4. Damage to mitochondria, and increased
permeability of membranes:
Mitochondria are important primary or secondary targets for most
agents that cause cell injury. Alterations in mitochondrial
membrane permeability generally lead to apoptosis. Loss of the
capacity of the plasma membrane to maintain a proper ionic
balance between the intra-and extracellular compartments.
Distribution in mitochondrial function produces:
– Reduce ATP Synthesis so it decreases the formation of energy
for the cellular activity.
– Increase the accumulation of intracellular calcium in
endoplasmic reticulum.
– Formation of Reactive oxygen species also enhanced.
– These all mechanism may lead to damage the cell and produce
cellular injury.
23. Outcomes of Cell Injury
CELL INJURY / CELL STRESS
ACUTE CHRONIC
CELL DEATH CELL
REVERSIBLE
ADAPTATIONS
NORMAL CELL
11
24. Mechanisms of Cell Injury
➢ ATP depletion: failure of energy-dependent functions
reversible Injury necrosis
➢Mitochondrial damage: ATP depletion failure of energy-
dependent cellular functions ultimately necrosis;
under some conditions, leakage of proteins that causes apoptosis
➢Influx of calcium: activation of enzymes that damage cellular
components and may also trigger apoptosis
➢Accumulation of reactive oxygen species: covalent modifications of
cellular proteins, lipids, nucleic acids
➢Increased permeability of cellular membranes: may affect plasma
membrane, lysosomal membranes, mitochondrial membranes;
typically culminates in necrosis
➢Accumulations of damaged DNA and misfolded proteins triggers
apoptosis
25. •
All stresses & noxious influences exert their effects first at the
molecular or biochemical level
•
Cellular function is lost far before cell death occurs and the
morphologic changes of cell injury (or death) lag far behind both
•
Ultrastructural Changes of Reversible Cell injury
Alteration in plasma membrane reflecting disturbance in ion
and volume regulation induced by loss of ATP
2. Mitochondrial changes
3. Endoplasmic reticulum changes
4. Nuclear alterations
Morphology of cell and tissue injury
26. PLASMA MEMBRANE ALTERATIONS
Cellular swelling
Formation of cytoplasmic
blebs
Blunting and distortion of
microvilli
Deterioration and loosening
of intercellular attachments
27. Mithochondrial Changes
Early it appears condensed as a
result of loss of matrix protein
following loss of ATP
Followed by swelling due to
ionic shifts
Amorphous densities which
correlate with the onset of
irreversibility
Finally, rupture of membrane
followed by progressing
increased calcification
28. Dilation
Detachment of
ribosomes and
dissociation of
polysomes with
decreased protein
synthesis
Progressive
fragmentation and
formation of
intracellular
aggregates of myelin
figures
Endoplasmic Reticulum Changes
30. Cellular Adaptations to Stress:
Adaptations are reversible changes in the number, size,
phenotype, metabolic activity, or functions of cells in response to
changes in their environment.
Cellular Adaptations
Physiologic
adaptations
Pathologic
adaptations
31. Physiologic adaptations: Usually represent responses of cells to
normal stimulation by hormones (Eg: The hormone-induced
enlargement of breast and uterus during pregancy.)
Pathologic adaptations: are responses to stress that allow cells t
modulate their structure and function and thus escape injury.
Types of Cellular adaptations
Hypertrophy (Increase in Cell size)
Hyperplasia (Increase in Cell number)
Atrophy & (Decrease in Cell size or Cell shrinkage)
Metaplasia (Change of one form of cell to other, Eg: Columnar
epithelium to Simple Squamous epithelium.)
33. It is decrease size
and weight of an
organ due to
decreased size and
number of its
component cells
Atrophy
34. Hyperplasia
• Is an increase in
the absolute number
of cells, in response
to a stimulus or
persistent cell
injury. It may be
physiological or
pathological.
35. Metaplasia
• A reversible change in which one
mature/adult cell type (epithelial or
mesenchymal) is replaced by another
mature cell type of the same category.
36. Dysplasia:
• Means 'disordered cellular development'.
• Often accompanied with metaplasia and hyperplasia.
• Often occurs in epithelial cells.
• Observed charactertics are
– Increased number of layers of epithelial cells
– Increased mitotic activity
– Disorderly arrangement of cells from basel layer to
surface layer.
– Cellular and nuclear pleomorphism (variability in the
size, shape and staining of cells and/or their nuclei.)
37. Morphology of Reversible Cell Injury
The two main morphological correlates of reversible cell injury
are:
Cellular Swelling : it is the result of failure of energy-
dependent ion pumps in the plasma membrane, leading to an in
ability to maintain ionic and fluid homeostasis. Cellular swelling
the first manifestation of almost all forms of cell injury to cells, is
a reversible alteration that may be difficult to appreciate with the
light microscope, but it may be apparent at the level of the whole
organ.
Eg: It causes increase in weight of organ.
38. Fatty change: It occurs in hypoxic injury and in various forms
of toxic or metabolic injury and is manifested by the appearance
of small or large lipid vacuoles in the cytoplasm.
It is principally encountered in cells participating in fat
metabolism (e.g., hepatocytes, myocardial cells) and is also
reversible.
Other morphological characteristic includes:
Plasma membrane blebbing and loss of microvilli,
Mitochondrial swelling,
Dilation of the ER,
Eosinophilia.
39. Morphology of Irreversible Cell Injury
Autolysis (i.e. self-digestion) is disintegration of cell by its own
hydrolytic enzymes liberated from lysosomes. Autolysis is rapid
in some tissues rich in hydrolytic enzymes such as in the
pancreas, and gastric mucosa; intermediate in tissues like the
heart, liver and kidney; and slow in fibrous tissue.
Heterolysis is disintegration of cell by the hydrolytic enzymes
liberated from inflammatory mediators like Neutrophils etc.,
Necrosis is a series of morphological changes which occurs in
a lethally injured cell.
Apoptosis is also known as Programmed Cell death.
40. Morphology of Necrosis
Necrosis is the type of cell death that is associated with loss
of membrane integrity and leakage of cellular contents
resulting in dissolution of cells, largely resulting from the
degradative action of enzymes on lethally injured cells.
(Or)
It is a spectrum of morphological changes that follow cell
death in living due to progressive degradation action of
enzyme (present with in the cell) on lethally injured cell.
41. Morphological changes are due to:
1) Intracellular protein denaturation.
E.g. Both structural and functional proteins.
2) Enzymatic digestion of severely injured cell.
E.g. Leading to Autolysis & Heterolysis.
3) Loss of integrity of plasma membrane of necrotic cell.
Necrosis is characterized by changes in the cytoplasm and
nuclei of the injured cells.
42.
43. Patterns of Tissue Necrosis
Coagulative Necrosis:
A form of tissue necrosis in which the component
cells are dead but the basic tissue architecture is preserved for at least
several days. It is characteristics of infarcts ( areas of ischemic necrosis)
in all solid organs except the brain
A wedge-shaped kidney
Infarct (yellow) with
preservation of the
outlines
44. Liquefactive Necrosis
• When the rate of dissolution of the necrotic cells considerably
faster than the rate of repair, the resulting morphologic
appearance is termed as liquefactive necrosis.
• Commonly occur due to ischaemic injury and bacterial or fungal
infections.
• Common examples are infaract brain and abscess cavity.
46. Caseous Necrosis
• The term caseous (cheese-
like) derived from the friable
white appearance of the
area of necrosis.
• It is a combination of
coagulative and liquefactive
necrosis.
• It is found in the center of
foci of tuberculous
infections.
47. Fat necrosis
• It is a special form of cell death occuring two
anatomical different locations but
morphologically similar leisons.
• It specifically affects the adipose tissue and
most commonly results from pancreatitis or
trauma.
• The unique feature determining this type of
necrosis is the presence of triglycerides in
adipose tissue.
48. Fibrinoid Necrosis
• It is a type of connective tissue necrosis seen
particularly in autoimmune disease in which
collagen and smooth muscle are affected for
example in polyarteriitis nodosa, Arthus
reaction etc.
• This necrosis occurs when complexes of
antigens and antibodies are deposited on
walls of arteries and called as fibrinoid.
49. Gangrenous Necrosis
• It is a type of secondary necrosis modified by
invasion of bacterial agents.
• The term gangrene is commonly used in clinical
practice to describe a condition when extensive
tissue necrosis is complicated by bacterial
infection.
• There are 3 major types of gangrene:
Dry gangrene
Wet gangrene
Gas gangrene
50. Cont…..
1. Dry gangrene: This form of gangrene begins in the
distal part of a limb due to ischemia. For example:
toes and feet of an old patient due to
atherosclerosis.
2. Wet gangrene: It results from severe bacterial
infection of necrotic area most commonly it occurs
in the extremities due to arterial obstruction, but
also in the internal organs such as in intestine.
3. Gas gangrene: This is a wound infection caused by
Clostridium perfringes and other types of Clostridia.
This bacteria gain entry into the tissues through
open contaminated wounds. It produces various
toxins.
51.
52. Cell Death
• It is a state of irreversible injury. It may occur in the living body
or focal change (i.e. autolysis, necrosis and apoptosis) and the
changes that follow it (i.e. gangrene and pathologic
calcification) or result in end of the life (somatic death) .
Autolysis (self digestion) – Disintegration of the cell by
its own hydrolytic enzymes liberated from lysosomes. It can
occur in the living body when it is surrounded by inflammatory
reaction but the term is generally used for postmortem change
in which there is complete absence of surrounding
inflammatory response.
• It is rapid in some tissues rich in hydrolytic
enzymes such as in the pancreas and gastric mucosa ;
intermediate in tissues like the heart, liver and kidney; and slow
in fibrous tissue.
53. Apoptosis
A type of cell death referred to as a single
(programmed) cell death.
It is an important mechanism for the removal
of cells as occurs in cells with irreparable DNA
damage (from viruses, free radicals,
chemical….etc), protecting against neoplastic
transformation.
55. What are the differences between necrosis and
apoptosis
Necrosis Apoptosis
Definition Death of group of cells within the
living tissue
Single (programmed) cell
death
Causes Always Pathological May be pathological or
physiological
Nucleus Pyknosis, karyorrhexix and
karyolysis
Regular fragmentation of
the DNA
Cytoplasm Swells Shrinks
Cell
membrane
Dissolves Blebs forming apoptotic
bodies
Surrounding
inflammation
Present Absent
56. Homeostasis
• The mechanism by which the constancy of the internal environment is
maintained and ensured is called homeostasis.
• The body is said to be in homeostasis when its cellular needs are
adequately meet and functional activities are occurring smoothly.
• Virtually every organ system plays a role in maintaining the internal
environment.
• The normal composition of internal environment consists of the
following components:
1. Water- Water is the principal and essential constituent of the body.
The total body water in normal adult male comprises -50-70%
(average 60%) of the body weight and about 10% less in a normal
adult female (average 50%). The total body water (average 60%) is
distributed into 2 main compartments of body fluids separated from
each other by membranes freely permeable to water. These are as
under:
• a.) Intracellular fluid compartment: This comprises about 33% of the
body weight, the bulk of which is contained in the muscles.
57. • b.) Extracellular fluid compartment: This constitute
the remaining 27% of body weight containing water.
2. Electrolytes: The concentration of cations (positively
charged) and anions (negatively charged) is different in
intracellular and extracellular fluids:
In the intracellular fluid, the main cations are
potassium and magnesium and the main anions are
phosphates and proteins. It has low concentration of
sodium and chloride.
In the extracellular fluid, the predominant cation is
sodium and the principal anions are chlorides and
bicarbonate. Besides these, a small proportion of non-
diffusible proteins and some diffusible nutrients and
metabolites such as glucose and urea are present in the
ECF.
58. A homeostatic regulatory mechanism
consists of 5 parts:
1. Receptors: It respond to a stimulus. It monitors change in
control condition and sent the input information to control
center via sensory receptor.
2. Sensory neurons: It receives information from receptor and
sends input messages to integrated center.
3. Integrated center: It analyze the incoming messages and
send the reply via motor receptor(brain and spinal cord).
4. Motor receptor: It send the reply coming from integrated
center to effector.
5. Effectors are the cell or organ that responds according to
output command of the control center via motor receptor.
59. Types of feedback System
Receptor, sensory neurons, integrated system, motor receptor and
effector form mainly two kinds of feedback mechanisms.
1. Negative feedback:
When the response of effectors opposes the original stimulus, it
is called negative feedback because it negates the stimulus.
An example of negative feedback is the temperature thermostat
in your home.
Temperature sensors turn the air conditioner off and on to
maintain air temperature within a specific, limited range.
60. In the same way, the brain controls normal body-temperature
homeostasis by negative feedback.
– Some stimulus (Stress) disrupts homeostasis (control condition) by
an increase in body temperature.
– Due to this condition thermo receptors (temperature sensitive
receptors) in the skin and brain activate and send input message via
nerve impulse to control center.
– Control center analyze the input message and send output message
to effectors (skin).
– Effectors according to output message of control center increases
sweating from sweat glands causes increased heat loss by
evaporation.
– Finally, decreases the temperature in the form of response and
normalize the body temperature (control condition).
61. 2. Positive feedback:
The effector adds to the initial stimulus instead of negating it, speeding
up the process.
– Labor contraction is the example of positive feedback system.
– Labor contractions force baby’s head or body into birth canal.
– It produces effect on control condition and increases distention of
cervix of uterus.
– It activates the stretch receptors of cervix and send input message to
control center via sensory nerve impulse.
– Control center activates the hypothalamus and pituitary gland and
send the output message to increase oxytocin secretion in blood.
– Oxytocin produces their effect on to the effector (cervix of
uterus) and cause distention of cervix of uterus than the normal
value to push the baby further into birth canal.
– Birth of the baby decreases distention of cervix of uterus and
interrupts positive feedback cycle.
62. Intracellular Accumulations:
• Intracellular accumulation of substances in abnormal amounts
can occur within the cytoplasm (especially lysosomes) or nucleus
of the cell.
• It can be divided into 3 groups:
Accumulation of constituents of normal cell metabolism
produced in excess e.g. accumulations of lipids (fatty change,
cholesterol deposits) proteins and carbohydrates.
Accumulation of abnormal substances produced as a result of
abnormal metabolism due to lack of some enzymes e.g. storage
diseases or inborn errors of metabolism.
Accumulation of pigments e.g. endogenous pigments under
special circumstances and exogenous pigments due to lack of
enzymatic mechanisms to degrade the substances or transport
them to other sites.
63. ACID BASE IMBALANCE
Metabolic process of cell produce carbon dioxide and metabolic acid. Carbon
dioxde combine with the water molecules (H2O) to form bicarbonate
(H2CO3). Metabolic product excreted via kidney and lungs. Kidney excreted
metabolic acid and lungs excreted CO2. This factor maintain the blood pH
between 7.3 to 7.4.
• Serum concentration of bicarbonate and partial pressure of CO2 that
determines the concentration of carbonic acid play a main role in
maintaining the blood pH. Alteration in the blood bicarbonate levels
produce either metabolic acidosis or alkalosis.
• Alteration in pCO2 produce respiratory acidosis or alkalosis.
64. Metabolic acidosis:
In the blood increase the amount of H+ ions and decrease the
bicarbonate HCO3- ion level due to metabolic process decrease
the pH of blood. This occurs in the following conditions:
- Production of large amount of lactic acid due to vigorous
exercise, shock like condition
- Uncontrolled diabetes mellitus
- Starvation
- Chronic renal failure
- Therapeutics administration of ammonium chloride or
acetazolamide.
• High level of H+ ions in metabolic acidosis stimulate the
respiratory centre and it increase the rate of breathing with deep
respiration. Bicarbonate level in the plasma get fall.
65. Metabolic alkalosis:
• Increase the level of bicarbonate HCO3- ions and decrease the
amount of H+ ions in the blood rise the pH of blood and it is known
as metabolic alkalosis.
• This occurs in the following conditions:
- Sever and prolonged vomiting
- Administration of alkaline salts like sodium bicarbonate.
- Hypokalemia such as cushing’s syndromes, increase secretion of
aldosterone
• Clinically, metabolic alkalosis is characterized by depression of
respiration, depressed function with uraemia and increase
bicarbonate excretion in the urine. Bicarbonate level in the blood
get increased.
66. Respiratory acidosis:
• Rise in pCo2 level in the lungs decrease the blood pH and it is
known as respiratory acidosis.
• This occurs in the following conditions:
- Air obstruction as occur in chronic bronchitis, asthma like
condition
- Restricted thoracic movement in pregnancy, ascites like conditions
- Impaired neuromuscular functions like poliomyelitis, polyneuritis.
If there is severe retention of CO2 patient may develop
confusion, drowsiness and coma. The arterial pCO2 level get rise.
67. Respiratory alkalosis:
• Decrease in the pCO2 level in the lungs (excess removal of
CO2) rise the blood pH and it is known as respiratory
alkalosis.
• This occurs in the following conditions:
- Hysterical over breathing
- Working at high temperature
- At high altitude
- Meningitis, encephalitis
- Salicylate intoxication
•Peripheral vasoconstriction, consequent pallor, lightheadedness and tetany
like characteristics are the identical mark for the respiratory alkalosis. The
arterial pCO2 level get decreased.
68. Calcification
Extracellular accumulation or deposition of calcium is also known as
calcification.
Calcification of soft tissue (arteries, cartilage, etc) can be caused by
Vitamin K deficiency or by poor calcium absorption due to a high
calcium/vitamin D ratio.
There are mostly two types of calcification;
1. Dystrophic calcification:
Dystrophic calcification refers to the deposition of calcium salts in
dead or dying tissues.
Dystrophic calcification occurs in the presence of normal levels of
serum calcium (around 10 mg/100 ml).
İt is mostly seen in the necrotic area and produce atheromas.
İt also affect the heart or artery valve by producing stenosis
69. 2.Metastatic calcification:
The deposition of calcium salts in normal tissues is known as metastatic
calcification.
Metastatic calcification can occur widely throughout the body but
principally affects the interstitial tissues of the vasculature, kidneys, lungs,
and gastric mucosa.
The usual causes of the hypercalcemia include:
a.Hyperparathyroidism, either primary or secondary,
b.Vitamin-D intoxication,
c.Deficiency of magnesium and
d.Hypercalcemia of malignancy.
Some basic symptoms of the calcifications are:
Tartar on teeth Kidney stones
Gall stones Calluses
Heterotopic bone
70. Electrolytes
• An electrolyte is a substance that conducts electricity
when dissolved in water. They are essential for a
number of bodily functions.
• The main electrolytes in the human body are sodium,
potassium, calcium, bicarbonate, magnesium, chloride,
phosphate etc.
• Intracellular compartment has higher concentration of
potassium, calcium, magnesium and phosphate ions in
the blood.
• While extracellular fluid has higher concentration of
sodium chloride, bicarbonate etc.
• Balance between these electrolytes inside the body is
essential for maintaining the good health.
71. Cont….
• Calcium
Calcium is a vital mineral that your body uses to stabilize blood pressure
and control skeletal muscle contraction. It’s also used to build strong
bones and teeth.
• Chloride
Chloride is necessary for maintaining the proper balance of bodily fluids.
• Magnesium
Magnesium is a critical mineral that regulates many important functions,
such as muscle contraction, heart rhythm, nerve function.
• Potassium
Potassium is particularly important for regulating heart function. It also
helps maintain healthy nerves and muscles.
• Sodium
Sodium is needed in the body to maintain fluid balance and is critical for
normal body function. It also helps to regulate nerve function and
muscle contraction.
• Phosphate
The kidneys, bones, and intestines work to balance phosphate levels in
the body. Phosphate is necessary for a wide variety of functions and
interacts closely with calcium
72. Electrolyte Imbalance
There are many causes for an electrolyte imbalance which include:
• Loss of body fluids from prolonged vomiting, diarrhoea,
sweating or high fever.
• Inadequate diet and lack of vitamins from food.
• Malabsorption - your body may be unable to absorb these
electrolytes due to a variety of stomach disorders, medications
(i.e. furosemide,hydrocortisone).
• Hormonal or endocrine disorders.
• Kidney disease.
• A complication of chemotherapy is tumor lysis syndrome. This
occurs when your body breaks down tumor cells rapidly after
chemotherapy, causing a low blood calcium level, high blood
potassium levels, and other electrolyte abnormalities.
