GROUP 3
• MAZERA JOHN BUGUTA – SMAZJO2111
• ONESMUS PTOO – SMWOPT1831
• NANDABI KHISA ALBERT – SNANKH2111
• LOCHINGAMOI GILBERT – SLOCGI2111
• MANDELA ELIJA MOGOA – SMANMO2021
• CELESTINE NAASISHO – SNAACE2111
• ERIC MUTEGI – SMUTGI2121
• ESTHER NYABUTO - SNYAKW1711
• NORAH LODEYA CHESINON – SLODCH2111
• SILAS KIPLAGAT – SKIPSI2111
• MOGOA IAN OMWENGA - SMOGIA2111
PIGMENTATION
DISORDERS
INTRODUCTION.
• A skin pigmentation disorder is a condition that
affects the color of the skin and can be caused by
diseases that affect the discoloration of the skin like
melasma and vitiligo.
• Pigmentation disorders can be exogenous or endogenous.
• ENDOGENOUS PIGMENTATION
• Endogenous pigments are characterized as hematogenous which originate from blood and non-hematogenous
which originate from non-blood, fat or fat-like, and non fat-like substances.
• MELANIN PIGMENTATION
• The skin gets it colour from a pigment called Melanin which is made by special cells in the skin called
Melanocytes. When these cells are damaged or unhealthy, it affects melanin production.
• Melanin disorders can be Hyperpigmentation or Hypopigmentation.
• Hypopigmentation : Low amount of Melanin in the skin which can cause Vitiligo, Pityriasis Alba, Tinear
Versicolor and Post Inflammatory Hypopigmentaion.
• Hyperpigmentation : High amount of Melanin in the skin which can cause Melasma, Ephelides, Solar
Lentigines, Post Inflammatory Hyperpigmentation and Café au lait macules.
• Melanin is a normal pigment found in the form of fine brown granules in the skin, choroid of the eye, adrenal
medulla & sometimes in the meninges.
• Its produced by melanocytes, after secretion of the pigment, its taken up by adjacent epidermal cells &
phagocytic melanophores in the underlying dermis.
• Melanocyte stimulating hormone stimulates
production of melanin in the skin & probably also
an increase of melanocytes.
• The secretion of MSH is monitored by adreno-
cortical hormones.
• In addition, adrenal catecholamines appear to
inhibit the formation of pigment at a local skin
level.
1. addison’s disease
• Generalised melanosis is a characteristic of this
condition which involves the destruction of the
adrenals, thus removing the inhibitory adrenal
control.
• Secretion of MSH proceeds unopposed.
Pigmentation is seen on exposed skin surface &
those subject to local irritation including squamous
mucous surfaces s.a the mouth.
2. chloasma
• Patches of melanotic pigmentation appear on the
skin of the face, breasts & genitalia due to
increased secretion of MSH.
• Most common in pregnancy.
3. jaundice
• Occurs due to bilirubin (iron- free pigment).
• When the bilirubin content of the serum rises above
34umol/L, jaundice appears. This can be brought about
by an abnormality in one of 3 main ways:
i)post-hepatic (obstructive) jaundice
• Obstruction of bile ducts is commonly due to gall stones
in the major ducts, tumor compression or occasionally,
fibrosis involving the small intra-hepatic ducts.
• The bile canaliculi become distended with
conjugated bilirubin which is reabsorbed.
Conjugated bilirubin is water soluble & is excreted
in the urine.
• Jaundice occurs in pregnancy & following steroid &
other drug therapy due to changes in the walls of
canaliculi causing intra-hepatic stasis of bile without
large duct obstruction (cholestatic jaundice).
ii) pre-hepatic jaundice
• Occurs in increased destruction of red cells as in haemolytic
anaemia.
• In these conditions the excessive amount of pigment has not
passed through the liver for conjugation. Its held in solution in
the plasma in combination with albumin.
• In adults the pigment may have little effect, but in the newborn
it can crystallise out in the tissues & in the brain causing
necrosis.
• Because of the size of the bilirubinalbumin molecule, the
pigment doesn’t appear in the urine.
iii) hepato- cellular jaundice
• Liver cell damage (occurring most commonly in
hepatitis) is the essential feature.
4. HAEMOSIDERIN
• The iron derived from red cell breakdown is held in
the spleen, liver & marrow combined with apoferritin.
• In the plasma its transported by transferrin. The two
mechanisms maintain an equilibrium between the
iron contents in these 3 sites.
• When the amount of iron within the cells becomes
excessive & overloads the ferritin system, its
deposited in a brown granular form haemosiderin.
• This occurs in 2 situations:
i. Local breakdown of red cells in tissues e.g in
internal haemorrhage or the colour changes in a
‘black’ eye.
ii. Visceral siderosis; this is seen in the liver, spleen
& sometimes the kidneys in cases of haemolytic
anemia. The change is most strikingly seen in the
liver which becomes deep brown.
Haemochromatosis (bronzed
diabetes)
• The absorption of iron from the intestine is
controlled by the ferritin- transferrin mechanism
already mentioned.
• The ferritin content of the intestinal epithelium,
iron saturation of the plasma, stores of iron in the
liver & spleen & the demand for iron by the bone
marrow form a balancing mechanism preventing
overloading of any part of the system.
• In haemochromatosis, a genetic disorder the absorption of iron is
virtually uncontrolled. The system becomes overloaded & iron is
deposited as haemosiderin in many sites, the main ones being:
Pancreas- associated with fibrosis which may destroy islet tissue=
diabetes mellitus.
Liver- usually associated with fibrosis (cirrhosis)
Skin- mainly around sweat glands. Excessive melanin is also
deposited hence this condition is sometimes termed bronzed diabetes.
Heart muscle
Mesenteric lymph nodes of the intestine.
5. LIPOFUSCIN
• “wear & tear pigment” is an insoluble brownish yellow granular
intracellular material that is seen in a variety of tissues (the
heart, liver & brain) as a function of age or atrophy.
• Consists of complexes of lipid & protein that derive from the
free radical catalyzed peroxidation of polyunsaturated lipids of
subcellular membranes.
• Its not injurious to the cell but is important as a marker of past
free radical injury.
• The brown pigment when present in large amounts, imparts an
appearance to the tissue that is called brown atrophy.
6. Vitiligo.
• This is a skin disorder that causes the skin to loose
its colour in patches which usually get bigger with
time. Smooth white areas(Macules) appear on a
person’s skin and hair turns white if Vitiligo
invades a place with hairs.
• The condition occurs when Melanocytes are
destroyed by the body’s immune system.
7. Melasma.
• This is a common skin disorder characterized by gray-
brown discolored patches of skin on areas of the face
exposed to sun. Sometimes called ‘’Mask of
Preganancy’’ as it frequently affects pregnant women.
• Melasma is caused by Radiation, Light( UV, Visible, or
Infrared), Genetics, Hypothyroidism, Contraceptive
therapy, and antiseizure medications.
• Foods rich in Vitamin D are advised to keep and
maintain the skin in healthy condition.
8. Albinism.
• This is a rare genetic condition caused by
mutations of genes that affect the amount of
melanin the body produces and is characterized by
congenital reduction or absence of melanin
pigment. It results from defective production of
Melanin from Thyrosine through a complex
pathway of metabolic reactions.
EXOGENOUS
PIGMENTATION
• Exogenous Pigments are characterized as agents
containing color that are formed outside the body
but found within tissues. Examples include Carbon,
Asbestos fibres, Tattoo ink and metals.
• These pigments maybe introduced by inhalation,
ingestion or injection.
• The most important are those introduced by
inhalation of dusts in industrial processes.
inhalation
• The commonest substances inhaled are coal dust (carbon)-
black & stone dust (silica)- grey.
• When inhaled, its phagocytosed by alveolar macrophages&
transported through lymphatic channels to the regional tracheo-
bronchial lymph nodes.
• Aggregates of the pigment blacken the draining lymph nodes &
pulmonary parenchyma (anthracosis).
• Heavy accumulations may induce emphysema or a fibroblastic
reaction that can result in a serious lung disease (coal workers’
pneumoconiosis)
ingestion
• Pigmentation can be caused by chronic ingestion of
metals s.a silver/ lead. In both, the skin has a
metallic hue & in the case of lead a blue line
appears on the gums due to interaction between
lead & sulphurettred hydrogen.
• Excessive intake of carrots can lead to yellowish
red skin pigmentation caused by carotene.
injection
• Tattooing is the most striking example of
pigmentation following injection.
• REFERENCES.
• Klatt,Edward.C et al, Review of Pathology, 4th Edition,
2014, Pg 643.
• [Link]
tion-disorders/Reviewed-on-May-2021
• [Link]
athophysiology/Reviewed-on-February-2020
THE END.
