I am a professional pharmacist. These slides provide for pharmacy department students. These slides describe pathology topics.

1. LECTURES IN PATHOLOGY
by
DR. AMIR RIAZ
Consultant Physician
&
Assistant Professor LCPS Lahore

2. DEFINITIONS
• PATHOLOGY
– It is the scientific study of disease.
• DISEASE
– The bodily condition when some variations occur in
structure and functions of various body organs from the
normal.
– Therefore Pathology is the study of abnormal variations
of structure and functions in the body. It is also called
as Morbid Anatomy & Physiology.

3. ANATOMY &
PHYSIOLOGY
Normal organization of
structure & functions of
various body parts
DISEASE
Abnormality in structure
and functions of body
PATHOLOGY
Study of abnormal
Causes (etiology)
Mechanism (pathogenesis)
Manifestations
(clinical features)
Progress (sequels)
CLINICAL PRACTICE
Medicine &
Surgery
Diagnosis
Treatment & Prophylaxis
(Pharmacology)
Follow-up
Manifestations of Disease
Damage done by harmful agent + Body reaction against it = Disease
Broad Groups of Disease
INFLAMMATORY DEGENERATIVE NEOPLASTIC

4. CAUSES OF DISEASE
• Genetically determined diseases
– Chromosomal abnormalities (Mutations)
Causes:
• Radiation • Chemicals • Infective agents
– Autosomal or X-linked disorders.
– Susceptibility to some diseases
• Human Leukocyte Antigen (HLA) System
• Blood Group

5. • Acquired diseases
– Physical Agents
• Trauma, Radiation, Heat & Cold, Electricity
– Chemical Poisons
• Acids, Alkalis, Toxic substances, Organic chemicals
– Nutritional Deficiencies
• Proteins, Fats, Carbohydrates, Vitamins, Minerals,
Fluids & Electrolytes, Oxygen
CAUSES OF DISEASE (cont…)

6. • Acquired diseases (cont…)
– Infections & Infestations
• Bacterial, Viral, Fungal, Protozoal, Parasites
– Abnormal Immunological Reactions
• Hypersensitivity
• Autoimmunity
– Psychological Factors
CAUSES OF DISEASE (cont…)

7. • Methods in Pathology
– Examination of body fluids.
• Blood, Plasma & Serum
• Urine & Stool
• CSF, Pleural, Pericardial & Peritoneal fluids
– Biochemical tests.
– Serological tests.
– Biopsy – Autopsy
– Macroscopic Examination
– Microscopic Examination
Histology, Cytology, Electron Microscopy
Immunology, Molecular Biology, Genetic studies

8. Cell Injury
Noxious agent visible changes in cell
(severity & duration of insult)
• Causes
– Reduced Oxygenation
• Respiratory, Cardiovascular diseases, Anemia
– Physical Agents
• Trauma, Heat or Cold, Radiations
– Chemical Agents
– Toxins
• Bacterial, Plants, Animals
– Microorganisms
– Abnormal Immunological Reactions

9. Cell Injury
• Types
– Necrosis
– Cloudy Swelling
– Fatty Change
– Atrophy
– Degenerations
– Calcification
– Pigmentation

10. Necrosis
• Cell death due to lack of blood supply.
Swelling of
cell memb.
Nuclear
disruption
Cytoplasmic
damage
Release of
enzymes
Types of Necrosis
• Coagulative necrosis • Colliqutative necrosis
• Caseative necrosis • Necrobiosis

11. Necrosis
Coagulative
• Solid organs
(heart, kidneys, spleen)
• Cytoplasmic &
Nuclear changes seen
• Cell shape retained
• Fibrosis
• Gangrene less
common
Colliquitive
• Hollow or Soft organs
(brain, intestine, lugs)
• Cellular changes with
fluid & pigments
• Cell shape & strc. Lost
• Fibrosis
• Gangrene more
common
Gangrene - complication of necrosis, tissue invaded
by putrefactive organisms  (foul smelling gas)

12. Caseation
• Different type
• Necrotic tissue has a
yellowish cheesy
appearance & greasy
to touch
• Commonly seen in
chronic infections like
Tuberculosis
• Fibrosis / Calcification
may occur at site
Necrobiosis
• Special type
• Single or few cells
involved in gradual
but progressive cell
damage, various stages
seen of which few can
be reversed
• Areas of damage close
to noxius agent & area
of recovery at others
Necrosis

13. Cloudy Swelling
• Mildest form of cell
damage
• Reversible
• Organ swells up
• Pale or boiled appearance
of cell
• E/M- mitochondria
swollen & beaded,
granular cytoplasm,
mitochondria break down

14. Fatty Change
• Accumulation of fat in non-fatty tissues & organs
which have high metabolic rate e.g; liver, skeletal
muscles, heart, kidneys.
• Any kind of metabolic derangement can cause it.
( Obesity, Starvation, Diabetes Mellitus )
Damaging Agent
Interfere ē cell enzymes
 utilization of fats in cell
Accumulation
of fat in cells
 food intake, starvation
 mobilization of fat
from adipose tissue
Fatty degeneration
(nucleus is central)
Fatty infiltration
(nucleus - on side)

15. Atrophy
• Simple decrease in cell size & number leading to
shrinkage of effected tissue or organ.
Causes
• Age - old age called “Senile Atrophy”.
• Gradual reduction in blood supply.
• Reduction in functional activity-“Disuse atrophy”.
• Interrupted nerve supply - loss of function of organ.
• Endocrine deficiencies -  metabolic functions.
• Pressure effects - cellular compression e.g; tumors
• Nutritional deficiencies. • Effect of toxins

16. Degeneration
• Accumulation of abnormal kind of substances in
the cellular matrix leading to cellular dysfunction.
Types
• Hyaline degeneration:
– hyaline material and fibers are deposited.
• Mucoid degeneration:
– deposition of mucin and mucopolysaccharides.
• Amyloid degeneration:(sp. type ē dif. Subtypes)
– a waxy substances mixture of proteins &
mucopolysaccharides is deposited at various
sites in tissues

17. Calcification
• Dystrophic
• Local deposits occur
– Necrotic tissue e.g;
caseous lesions of T.B,
old infarcts, old pus
collection, dead parasites,
old thrombi.
– Tissues undergoing
slow degeneration
• Metastatic
• Increase in blood Ca.
–  Ca absorption
due to  vitamin D
–  mobilization of
Ca from bones
 PTH, tumors, &
metabolic disease
• Ca deposits in tissues
on arterial side of CVS
•Abnormal deposition of calcium salts in tissues.

18. Pigmentation
• Endogenous
• Abnormal deposition
of normal pigments of
the body
• Melanin- cholasma,
Addison’s disease.
• Bilirubin- liver disease
• Iron containing pigmt.
Hemosiderin
Haemoblobin
Haematin, Lipofuscin.
• Exogenous
• Pigment from outside,
inhaled, ingested or
injected in the body.
• Lungs- inhaled matter
coal dust, silica, asbestos
• Ingestion of heavy
metals- lead, silver,
mercury, arsenic
• Tatooing
• Pigment- injection site

19. INFLAMMATION
• It is the dynamic process by which living
tissues react to injury. (vascular &
connective tissue are concerned)
Causes
• Physical • Chemical
• Infective • Immunological
• Vascular or Hormonal
Types
• Acute • Subacute • Chronic

20. Acute Inflammation (continued)
Classical Signs
• REDNESS (Rubor)
• HEAT (Calor)
• SWELLING (Tumor)
• PAIN (Dolor)
• LOSS OF
FUNCTION
(Functio laesa)
Essential Features
• HYPERAEMIA
• EXUDATION
• EMIGRATION OF
LEUKOCYTES

21. Acute Inflammation (continued)
• Events in inflammation
– Lewis’s Tripple Response
FLUSH, FLARE & WEAL
Injury
Damaged cells
Chemical Mediators
Vascular Dilatation
Hyperaemia
– Vasoconstriction
– Vasodilatation
• Capillary
• Arteriolar
Hyperaemia - explains
REDNESS & HEAT
Direct effect
on vessels
Nervous reaction
(axon reflex)
Mechanism

22. Acute Inflammation (continued)
Exudation
• Second important feature of Ac. Inflammation
Swelling – Tumor
• Vasodilatation → hyperaemia → ↑hydrostatic
pressure → opening of capillary pores → fluid
accumulation in area → swelling.
Movement of Proteins in area → ↑osmotic
pressure → ↑ fluid accumulation.
• Proteins degradation by enzymes → products;
Chemotaxis, Vasodilators

23. Acute Inflammation (continued)
Emigration of Leukocytes
• Movement of WBCs from capillaries to area
• Neutrophils, Monocytes & Macrophages,
Lymphocytes, Basophils & Eosinophils
• Specific cells at some sp. Sites e.g.
– Ac. Inflammation – Polys, Macrophages
– Ch. Inflammation – Lymphocytes, Monocytes
– Allergic reactions – Eosino & Basophils, Mast cells
• Margination – WBCs move closer to vessel wall.
• Pavement – WBCs stick to walls closer to cap. pores.

24. Acute Inflammation (continued)
• Diapedesis – movement of WBCs
– Pseudopodial projections → invaginate in gap
junctions & move out with Amoeboid movement.
• Functions of Leukocytes;
– Phagocytosis
– Proteolysis – (pus formation)
– Coagulation cascade activation
– Release of chemical mediators
• Prostaglandins
• Vasoactive amines (histamine & serotonin)
• Leukotrines & Interleukins
• Complement components
• Kinin system components
• Bacterial end products

25. Acute Inflammation (continued)
• CHEMOTAXIS
Movement of WBCs in inflammatory area in
response to certain chemical agent.
– Complement components
– Bacterial products
– Lymphokines
– Protein degradation products
• PHAGOCYTOSIS
Ingestion of foreign bodies & debris by
Polymorphs & Macrophages
– Opsonization – antibodies of natural or specific
type
– Complement components
– Presence of other cells in area
– Activity is better in solid than hollow organs

26. Persistent irritation
INFLAMMATION
ACUTE SUBACUTE CHRONIC
Suppuration
Pus formation
Drainage
NORMAL
HEALING
HEALING ē
SCARRING
Caseation Granuloma
Calcification
Organization
Fibrosis
Resolution
Inflammation (continued)

27. Inflammation (continued)
• NOMENCLATURE
Add suffix “itis” to the name of organ;
– Liver – Hepa- Hepatitis. Appendix – Appendicitis
– Stomach – Gastro – Gastritits. Colon - Colitis.
– Kidney – Nephro – Nephritis. Tonsil – Tonsillitis.
• INFLAMMATION - SPECIAL TYPES
• Catarrhal Inflammation
• Pseudo-membranous Inflammation
• Exudative Inflammation
– Serous type − Exudative type
– Suppurative type − Haemorrhagic type

28. Inflammation (continued)
• Some Specific Terminologies
• Resolution – complete restoration of normal
conditions
– Minimal cell death
– Rapid elimination of casual agent
– Favorable local conditions
Mechanism
– Degradation of fibrin by enzymes
– Removal of fluid & exudate by circulation
– Removal of debris by phagosytosis & lymphatics
– Restoration of normal vascularity & hemodynamic

29. Specific Terminologies (continued)
• Suppuration – formation of Pus
• Abscess – collection of pus at any site
– Infection by Pyogenic bacteria (pus forming)
– Character different for different bacteria
– Outcome variable at different sites
• Epithelial surfaces – slough out to form “Ulcer”
• Internal organs – Abscess → surgical drainage or
removal → resolution
→ extend in tissue plains → “Sinus” or “Fistula”
Treatment → resolution & normal healing
No therapy → delayed healing & organization

30. Specific Terminologies (continued)
• EMPYEMA – collection of pus in body cavity or
hollow organs, e.g, gall bladder
• SINUS – a tract extending from a cavity to surface
• FISTULA – a track between two cavities or
epithelial surfaces (Congenital or Acquired)
• ULCER – break in covering epithelium after tissue
necrosis & replaced by inflammatory tissue
- Simple (Acute or Chronic) - Malignant
• HEALING – restoration of normal tissue after the
inflammatory process
• ORGANIZATION – excess grannulation tissue
leading to fibrosis & scar formation
• CELLULITIS – inflammation in tissue planes

31. Chronic Inflammation
• Prolonged course, onset may be Primary or Follows Acute
inflammatory reaction.
• Causes:
– slowly growing organisms.
– low virulance of organisms.
– persistance of harmful agent.
– poor resistance of host.
• Features:
– Lymphocytes, macrophages & plasma cells in the area.
– Proliferation of capillaries lead to Grannulation tissue.
– Proliferation of fibroblast lead to Fibrosis.
– Formation of caseating or non-caseating “GRANULOMA”.
• Tuberculosis, Sarcoidosis, Leprosy, Crhon’s Disease.

32. Tuberculosis
• Chronic infection caused by ‘Mycobacterium
Tuberculosis” (resistant waxy material in structure).
• A bascillus resistant to bleaching by Acid or Alcohol after staining red
with Carbol Fuchsin therefore known as
“AFB - Acid or Alcohol Fast Bascillus”.
• Microaerophilic, grow in special media & conditions.
• Slowly growing, spore forming, can live dormant in tissues &
enviorment for years.
• Tubercle formation - characteristic “Caseating Granuloma”.
• Infection is common in;
– Malnutrition & poor Hygienic conditions.
– Lack of BCG vaccination.
– Immunocompromised host, AIDS or Drugs

33. Tuberculosis
• Types of Infections (clinical):
– Primary T.B - first infection of mycobacteria in tissues (usually
Lungs) - small focus of caseative tubercle known as Primary or
Ghon’s Focus. AFB spread to Local lymph nodes & cause
caseation. Pri. Focus + caseating Lymph node is called, “Primary
or Ghon’s Complex.
– It may hel by calcification or fibrosis, or may spread to other
tissues & organs locally or via lymphatics/blood stream.
– Miliary T.B - generalized spread of Mycobacteria by blood
stream throughout body forming small multiple tubercles like
millet seeds (milium).
– Post-Primary or Re-Infection T.B - reactivation of primary
focus or reinfection with AFB leads to slow gradual tissue
destruction & distant spread by lymphatics or blood.

34. Tuberculosis
• Variations of T.B infection
– Exudative T.B - in serous cavities, pleura, pericardium etc.
– Cold Abscess - in solid organs, lymph nodes, bones etc.
– Fibrotic T.B - in lungs, GIT, tubes etc.
– Acute Caseating / Non-reactive T.B - massive caseation in case of
massive infection.
• Clinical Features
– General - malaise, fever, night sweats, weight loss, cough
– Specific - related to organ involved, e.g,
• Lungs - cough, hemoptysis, breathlessness.
• Pleura - chest pain, cough, breathlessness.
• Bone & Joint - aches pains,swelling & fractures.
• Brain - headache, vomiting, fits, coma, Neurological deficiet.
• Lymph Nodes - swelling, mass formation, local compression.

35. Tuberculosis
• Diagnosis
– Blood Exam.  ESR,  Hemoglobin,  lymphocytes.
– Sputum Exam. For AFB.
– X-Ray Chest, Bones & Joints.
– Mantoux Test.
– Lymph node or Tissue Biopsy.
– Examination of Exudative fluid.
– Mycodot test on Blood for AFB.
– PCR (polymerase chain reaction) for Mycobacterial DNA.
• Treatment
– General - good hygiene & nutrition, good living conditions.
– Specific - BCG - Vaccination & Chemoprophylaxis.
– Drug therapy - Anti-tuberulous drugs in combination for
prolonged period of time.

36. Leprosy
• Slowly progressive chronic inflammation affecting
peripheral nerves caused by “Mycobacterium Laprae”.
• An Acid or Alcohol Fast Bascillus – AFB.
• Spread by – nasal secretions, prolonged close contact.
• Spectrum of disease varies depending upon immune
status of the host.
– Lepromatous leprosy
– Borderline lepromatous
– Boerderline borderline
– Borderline tuberculoid
– Tuberculoid leprosy.

37. Leprosy
•Lepromatous
•Disfiguring nodularity of
skin Leonine Facies.
•Late nerve involvement.
•Organisms in tissues +
plasma cells, lylmphocytes &
macrophages.
•Mycobacteria can be isolated.
•Cell mediated immunity is
absent.
•Treatment is difficult.
•Tuberculoid
•Focal areas of anasthesia
damaging nerves.
•Early nerve involvement.
•Basic lesion is Follicular
Granuloma.
•Organism not isolated easily.
•Cell mediated immunity is
well developed.
•Response to therapy is good.

38. Syphilis
• Venereal or Sexually transmitted disease (STD).
• Traponema Pallidum – spirochete.
• Highly invasive & live in tissues for years.
• Dark field illumination, Silver staining &
Immunoflourescence techniques.
• Types of Clinical Disease
– Primary Syphilis – T.P enter tissues & invades to blood
stream. In 3 weeks Primary lesion a nodule at site of
entry appears “Hard Chancre”. Ulcer with secretions
contains spirochetes stained with special techniques.
Lymph nodes enlarge, hard & painless. If not treated in
2-3 months disease spreads in body to next stage.

39. – Secondary Syphilis – generalized skin rash (pox).
Ulceration of mucous membranes. Generalized
Lymphadenopathy, fever, anemia & individual organ
and tissue damage.
– Tertiary (Late) Syphilis – many years after Primary or
Secondary lesions. Spirochetes scanty but tissue
damage is extensive.
• Gumma in solid organs.
• Syphilitic aortitis.
• Neurosyphilis – Meningovascular or Parencymal. GIP & Tabes
• Congenital syphilis – transplacental spread of disease.
– Diagnosis – special staining, Immunological tests.
– Treatment – Prevention & Penicillin therapy.
Syphilis

40. VIRUSES
• Smallest micro-organisms in nature(size in nm) not visible
by Light microscope only seen with Electron microscope.
• Virus Particle = “Virion”, central core of genetic material
DNA or RNA & protein capsule - Capsid.
• Can not replicate itself, depends on host cell’s metabolic
processes - “Obligatory Intracellular Paracite”.
• Mechanism of Disease
– virus invades cell & enters into nucleus  incorporates its
DNA/RNA in cell genetic material  protein & DNAsynthesis of
cell stops  formation of Viral DNA/RNA & proteins  cell
death  vrial replication   viral count  invasion of other cells
– different viruses invade different specific cells & produce various
clininicopathological diseases.

41. VIRUSES
• Acute Infection - in three stages.
– Incubation Period - Viral invasion & replication in host cells, local
spread of viruses in tissues & to lymph nodes, tissue damage.
– Primary Viremia - viruses enter into blood & spread to other body
tissues & distant lymph nodes causing futher cell death & viremia.
– Secondary Viremia - generalized spread throughout body, damage
to other organs & tissues  disseminated disease.
• Body Reaction to Viral Infections
– activation of Immune system  formation of Antibodies &
Sensitized Lympocytes & release of Interferon.
• Variations in Viral Infections
– Latent viruses (herpes)  Slow viruses (Kuru)  Oncogenic (EBV)
• Treatment -
– Immunization (active/passive), Anti-Viral drugs & Interferon.

42. NEOPLASIA
• Neoplasia - new growth, non-cancerous or cancerous.
• Pre-Cancerous Lesions.
– HYPERPLASIA - excess proliferation leading to an increase in
number of cells & increase in size of the tissue/organ.
Causes, chronic irritation, excess hormones.
– HYPERTROPHY - increase in size of cells & tissue without any
increase in number of cells. It is due to increased functional
activity of any tissue.
– ATROPHY - simple decrease in size of cells leading to shrinkage
of tissues & organs.
– METAPLASIA - change of one type of tissue to another type of
different tissue at a place. There may be associated hyperplasia.
Usual cause is chronic irritation.
– DYSPLASIA - disordered cellular development leading to
abnormal & variable number of cells with change in shape,
arrangement & increased mitosis. It is a Pre-malignant condition.

43. NEOPLASIA
• Neoplastic Growth - abnormal proliferation of cells in
a tissue or organ leading to new growth formation.
• Features:
– Progression.
– Purposeless.
– Regardless of surrounding tissue.
– Not related to body needs.
– Parasitic in nature.
• Classification.
– Clinical - (behavior & morbidity) - Benign & Malignant.
– Histological - according to origin from type of tissue.
• Epithelia & Glands -
• Mesodermic / Connective tissue -
• Neural Ectoderm
• Hemopoietic tissue -
• Lymphoid tissue -

44. FEATURES BENIGN MALIGNANT
Rate of Growth Slow progression Usually rapid progress
Shape of
Growth
Well demarcated
often encapsulated
Irregular illdefined &
non-capsulated
Relationship to
srrounding
Merely compress
normal tissues
Invade & destroy normal
tissues
Spread of
Growth
Remains locallized Local & distant spread
via, lymph, blood &
serous cavities –
METASTASIS.
NEOPLASIA
(CLINICAL FEATURES)

45. • DIFFERENTIATED
• Similar to their parent of origin
in shape & structure.
• Evidence of normal function.
• Nuclei of same size & shape.
• Infrequent Mitotic figures.
• Signifies a Simple Growth.
• Course & Prognosis is Good
• UNDIFFERENTIATED
• Shape & structure differ from
original cells.
• Abnormal function.
• Abnormal Nuclear
configuration & appearance.
• Abnormal Mitosis.
• Signifies a Malignant Growth.
• Course & Prognosis is Poor.
NEOPLASIA
(Classification of Tumor Cells according to their Appearance)

46. CARCINOGENS
Physical agents.
Chemical agents.
Viruses.
Normal Cell Susceptible cell
Mutant cell
Loss of identity
Increased mitosis
Co-factors
Hereditary & Age
Environment
Hormonal Status
Chronic Irritation
Host reaction successful
Restoration of Normal
cells
Host reaction failure
continued proliferation
MALIGNANCY

47. PROTEINS
• Polypeptides of Amino Acids.
• Essential A.A – not formed in body, deficient in vegetable
proteins, found in animal proteins, must be present in diet.
• Non-Essential A.A – can be formed in body, not an
essential component of diet.
• Daily Allowance of Proteins = 0.75 Grams/kg.
• Approximately 40 – 50 Grams/day. 15% of Dietary intake.
• Requirement depend upon “Nitrogen Balance”.
• Proteins required (Grams) = Urinary Nitrogen x 6.25.
• Urinary Urea = 80 – 90 % of Nitrogen.
• Adequate energy intake is essential in addition to Proteins
for normal growth otherwise proteins are utilized for
Gluconeogenesis.

48. Protein Energy Malnutrition (PEM)
• Malnutrition – poor food intake or imbalanced diet.
• Starvation – drought, war, environmental conditions may
lead to deficiency of Energy or deficiency of Proteins.
• Causes of PEM – (multiple)
– Trauma or Surgery - Infections or Sepsis.
– G.I disorders - Malbsorptioon.
– Chronic Illness - Metabolic diseases.
– Malignancy - Dementia.
– Psychological diseases - Anorexia Nervosa.
• Simple Malnutrition – common in adults.
– Muscle wasting, low body mass, weight loss, apathy & lethargy.
–  Immunity,  resistance to infections. (G.I & Respiratory tract)

49. • Severe Malnutrition – common in children < 5 years age.
• Demography – Developing countries, Drought & War.
• Marasmus – most common severe PEM in children.
– Child looks emaciated, muscle wasting & loss of body fat with no
edema (albumin is normal, muscle supply amino acids).
– Thin dry sparse hairs. Diarrhea is frequent & anorexia & apathy.
• Kawashirkor – common in infants displaced from breast
feeding & deficient in weaning foods.
– Sever anorexia & apathy. Generalized edema ( albumin). Skin
pigmentation & thickening. Hairs dry sparse & discolored.
Distended abdomen with hepatomegaly & ascites.
Protein Energy Malnutrition (PEM)

50. • DIAGNOSIS
– Clinical Examination.
– MUAC – Mid upper arm circumference( <12.5 cm).
• INVESTIGATIONS
– Blood Counts. - Stool examination.
– Electrolytes. - Malaria parasite.
– Serum Albumin. - Chest X-Ray.
• TREATMENT
– AIMS – to improve protein intake, energy supplement & control of
infections.
– Resuscitation – correction of fluids & electrolytes (ORS or I.Vs).
Antibiotics, Antihelmintics & Antimalarials.
Protein Energy Malnutrition (PEM)

51. • TREATMENT (continued)
– Refeeding – controlled calculated diet replacement, 100
Kcal/kg/dday with 0.6 Grams/ks of proteins. DISCO. Oral feeding
or PEG feeding or TPN.
– Supplements – Iron, Folic acid, Vitamins & Minerals.
– Rehabilitation – Balanced dietary intake, Identification of
deficiencies & Infections with specific therapy.
– Prevention – Education of Balanced Diet & Good Nutrition. Food
supplementation. Childhood Immunization. Special diet in
Pregnancy & Lactation. Family Planning & Child spacing.
• PROGNOSIS
– 50 % Mortatility in Severe PEM. Can be lowered to 1 – 2 % with
earlier detection & prompt treatment.
Protein Energy Malnutrition (PEM)

52. VITAMINS
• Very important food constituent essential for various
enzymatic processes in the body.
• Classification
– Fat Soluble vitamins – A, D, E & K.
– Water Soluble vitamins – B1, B2, B6, B12, Niacin, Folic acid & C.
• VITAMIN – A (Retinol, Retinoids & -Carotene)
– Present in body as ester with long chain Fatty Acids.
– Source – Liver, Milk, Butter, Cheese, Egg youlk, Fishoil,
Vegetable (-Carotene).
– Metabolism – absorbed in gut & converted to retinaldehyde then
reduced to retinol (vitamin – A). 6g -Carotene = 1 g Retinol.
– Functions – present in rod & cones of retina (vision), cellular
proliferation, synthesis of glycoproteins,

53. • VITAMIN – A (continued)
– Deficiency – Xerophthalmia (dry eyes, corneal ulcers,scars &
infection), Night Blindness.
– Treatment – Retinol palmitate 30 mg orally or I.M for 2 days.
Therapy for Infections & Malnutrition.
– Prevention – vitamin A supplemented food, Dairy products, Green
leafy vegetables.
– Latest Research – Protection against Cancer, Low risk of
Cardiovascular diseases, beneficial in Skin diseases (Acne).
– Adverse Effects – (>300 mg in Adults & >100 mg in Children)
– Liver & bone damage, Hair loss, Diiplopia, Teratogenic effect –
birth defects (.3mg/day in pregnancy)
VITAMINS

54. • VITAMIN – D (Cholecalciferol or Vitamin D3)
– Metabolism - 7 – Hydrocholesterol in Skin under Sunlight 
Choleclaciferol bind to vitamin D binding protein  Liver & 25
hydroxylation takes place  25 hydroxy cholecalciferol (25-OH
D3)  Kidneys & 1 – 25 hydroxylation  1 – 25 di-hydroxy
cholecalciferol (1, 25 – OH D3) active vitamin D3.
– Actions – Calcium & Bone metabolism. ( PTH & Calcitonin).
– Causes of Deficiency – dietary deficiency, lack of exposure to
sunlight, low absorption from gut (phytates), Drugs, Renal
diseases, Congenital enzyme defects, Malignancies.
– Clinical Manifestations
• Rickets in children. & Osteomalacia in Adults.
VITAMINS

55. • RICKETS – seen in Children.
– Neonatal rickets- skull bone abnormality.
– Long bone deformities, splaying of bone ends.
– Ricketic rosary & Harrison’s sulcus.
– Bowing of legs & Pseudo fractures.
– Myopathy (muscle weakness).
• OSTEOMALACIA – seen in Adults.
– Muscle & Bone pains, tnderness.
– Psudofractures – Looser’s zones.
– Proximal Myopathy – waddling gait.
– Tetany & hypocalcemia.
• Investigations – Serum Calcium & Alkaline
phosphatase, Bone X-Rays & Bone biopsy.
VITAMIN – D (continued)

56. • Treatment
–  vitamin D intake (400 I.U/day) + Calcium
supplements.
–  exposure to Sunlight.
– Oral or Injectable vitamin D preperations.
• Prevention
– Balanced diet with Vitamin D supplements in growing
kids & good exposure to Sunlight.
VITAMIN – D (continued)

57. • Very important role in Coagulation mechanism.
– Absorbed from gut & stored in Liver, helps in
synthesis of Clotting factors (II, VII, IX & X).
– Sources – Green leafy vegetables, Seed oils & Dairy
products.
– Deficiency lead to Hemorrhagic tendencies &
Clotting disorders.
– Causes -  transfer of Vitamin K through Placenta,
 Vitamin K in Breast milk,  Vitamin K stores in
Liver, Cholestatic jaundice, Drugs (vit. K antagonists).
– Treatment – Vitamin K orally or injections
(10 mg/day).
– Prevention – Dietary modification, Treatment of
underlying defects or disease.
VITAMIN – K (Phylloquinone)

58. •  - Tocopherol present in 90% of Human Body.
– Functions – Anti-oxidant properties, Membrane
stability, cell proliferation & growth,  incidence of
Cardiovascular diseases.
– Sources – Vegetables, Seed oils, Cereals, Nuts, Animal
products.
– Absorbed with fatty acids. Daily requirement 7 – 10
mg/day.
• Deficiency – Hemolytic anemia, Neurological signs,
Cardiovascular diseases.
– Treatment – vitamin E supplements as  - Tocopherol.
– Prevention – dietary modification.
VITAMIN – E
(Tocopherols/Tocoretinoles)

59. • Vitamin B1 – Thiamin
• Vitamin B2 – Riboflavin
• Vitamin B6 – Pyridoxine
• Vitamin B12 – Cobalamin
• Vitamin B1, B6, B12 – B-complex.
• Niacin – Nicotinic Acid
• Folate – Folic Acid
• Vitamin C – Ascorbic Acid
Water Soluble Vutamins

60. Vitamin B1 – Thiamin
• Essential co-factor for Carbohydrate metabolism.
• Source – Cereals, Grains, Beans, Nuts.
• Body has small stores, deficiency develops quickly &
directly related to Carbohydrate intake in diet.
• Deficiency – Alcoholics, Starvation, Polished rice.
• Beri Beri – presents as, Muscle weakness, Edema,
Ascites, Neuropathy – Wernicke-Korsakoff syndrome,
Heart failure due to Cardiomyopathy.
• Treatment – Thiamine 50 mg I/M x 3 days followed by
25 mg / day orally.
• Prevention – Dietary advise.

61. • Co-factor for many Oxidative processes in cell.
• Source – Dairy products, Offals, Leafy vegetables.
– (not destroyed by cooking)
• Deficiency – (rare) Angular stomatitis, Red tongue,
Dermatitis, Eye diseases.
• Treatment – Riboflavin 5mg / day orally.
Vitamin B2 – Riboflavin

62. • Co-factor in metabolism of Amino acids.
• Source – Plant & Animal foodstuff.
• Deficiency – extremely rare, Polyneuropathy.
• Drug Interaction – INH, Hydralazine, Pnecillamine.
• Treatment – Pyridoxine – 10 – 50 mg / day orally.
• Prolonged use may cause toxicity.
Vitamin B6 – Pyridoxine

63. • Co-enzyme in conversion of Amino acids & DNA
synthesis in association with Folic acid.
• Source – Meat, Egg, Fish, Milk, (not in plants).
• Metabolism – 5-30 g in diet, only 2-3 g absorbed.
Released in stomach attaches to Intrinsic factor &
absorbed from distal Ileum, attaches to plasma proteins,
goes to Liver & stored.
• Deficiency – occurs over 2 years, body stores are
large.
• Causes - Pernicious Anemia (def. Intrinsic factor),
Malabpsorption, Pancreatic & Ileal disease, Drugs.
• Features – Anemia, Neuropathy, Spinal cord
degeneration, Sensory loss, Muscle weakness,
Paraplegia,, Dementia.
• Treatment – Hydroxycobalamin 1000 g I/M x 3 wk.
Vitamin B12 – Cobalamin

64. • Found in Neucleotides (NAD & NADP).
• Source – Plants, Meat, Offal, Fish & Bran.
• Deficiency – Malnutrition & deficient diet – Pllegra.
Dermatitis, Diarrhea, Dementia.
• Treatment – Nicotinamide – 300 mg / day / week
then 50 mg / day.
• Increased Protein content in diet & treatment of
Malnutrition.
Niacin – Nicotinic Acid

65. • Essential for formation of DNA.
• Source – Green vegetables, Liver, Kidney. Cooking
destroys 60 – 90 %. Daily requirement 100 g.
• Deficiency – common, occurs in 4 months.
– Megaloblstic anemia, glossitis.
• Causes – Poor diet, excessive cooking of food,
Pregnancy, Drugs (sulfonamides).
• Treatment – Check serum Folate levels. Folic acid –
5mg / day orally, Food supplement, Folate therapy in
Pregnancy.
Folate – Folic Acid

66. • Simple sugar & reducing agent, formation of
Collagen, & cellular function.
• Source – Guava, Citrus fruits, Vegetables.
– Lost in water, cooking, storage of food & alkalis.
• Deficiency -  in Asians, Smokers & poor intake of
food in Infants & Old age.
• “SCURVY” – weakness, muscle pain, abnormal hairs,
swollen & bleeding gums, bruising of skin & hair
follicles, delayed wound healing, anemia.
• Treatment – Ascorbic acid – 250 mg / day orally.
Food supplement, fruits & juices.
Vitamin C – Ascorbic Acid