PATHOPHYSIOLOGY OF SHOCK

Shock occurs when the metabolic needs of cells are not being met
because of inadequate blood flow. It could be as a result of reduction
in the circulation of blood or problem from cardiac output. This
causes tissue hypoxia, an inadequate supply of nutrients and the
accumulation of waste products.
TYPES OF SHOCK
1. Hypovolaemic shock: this occurs when the blood volume is
reduced by 15 to 25. Reduced venous return and in turn
cardiac output may occur.
2. Cardiogenic shock: this occur in acute heart disease when the
damaged heart muscles cannot maintain an adequate cardiac
output, e.g in myocardial infarction.
3. Septic shock,bacteriaemic or endotoxin: this is caused by severe
infections in which endotoxins are released into the circulation
from dead Gram- negative bacteria e.g entrobacteria
4. Neurogenic shock, vasovagal attack, fainting): the causes
include sudden acute pain, severe emotional experience, spinal
anastesthesia and spinal cord damage. Parasympathetic nerve
impulses reduce the heart rate, and in turn, the cardiac output.
5. Anaphylactic shock: in allergic an antigen interacts with an
antibody and a variety of responses can occur. In severe cases,
the chemicals released, e.g histamine, bradykinin, produce wide
spread vasodilation and constriction of bronchiolar smooth
muscle ( bronchospasm).the vasoconstriction profound reduces
the venous return and cardiac output resulting in tissue
hypoxia. Bronchospasm reduces the amount of air entering the
lungs, increasing tissue hypoxia

PATHOPHYSIOLOGY OF ESSENTIAL OR PRIMARY HYPERTENSION

Hypertension can be defined simply as a persistent rise in the blood
pressure above the individual limit.
The three main factors to be considered as the cause of primary
hypertension are:
(a) Emotion: in any prolonged and source emotional or stress in situation,
there is physiologic release of excessive amounts of adrenalin
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 (epinophine) and noradrenalin (Nerepinephrine) at the meeting point of
nerves. As a result of excessive stimulation of the sympathetic nervous
system.
Thetwo hormoness released are vasoconstrictors i.e narrowing the blood
vessels and also increase peripheral existence. This invariably increases
blood pressure (hypertension).
(b) Age: with ageing the arteries becomes hardening leading to the
thickening and narrowing of the blood vessels. the vessels become less
elastic. This lead to increased peripheral resistance consequently
increase blood pressure.
(c) Obesity: in an obese individual, there is increase deposition of
cholesterols in form of accumulation or fatty plague. with lead to the
thickening and narrowing of the blood vessels and cause increase blood
pressure.

EFFECT OF PRIMARY HYPERTENSION.

The manifestation of primary hypertension depend on the effects of
prolonged elevated pressure on blood vessels in various organs and tissues as
well as the increased work load on the heart. The persistent increase in the
arterial system causes the covering of blood vessels with blood to undergo
increase in the size (hypertrophy) which lead to hardening and narrowing of
the blood vessels which cause hypertension.
The effect on this could be traced to the sclerotic changes ( hardening of
soft tissues) in the blood arteries supplying blood to the heart (coronary
arteries). It leadsto diminished blood and oxygen supply to the middle layer on
of the heart (myocarduim) causing angina pectoris or suffocation coronary
thrombosis with sub-sternal [Link] also causes increased left ventricular
contraction with full and bounding pulse initially to force blood through the
narrowed coronary artery to the middle layer of the heat, which lead to heart
failure and blood will be congested in the heart, also leads to pulmonary
congestion with paroxysmal attacks of night difficult breathing (dyspnoea) due
to left heart failure. The left of the heart later fails (congestive heart failure)
causing severe venous congestion and generalized is odema.
The effect on the cerebral arteries is to make them to rupture leading to
cerebral haemorrhage (cerebrovascular accident) with all its manifestation.
the sclerotic effect on renal blood vessels is the gradual is regular flow of
blood to the kidney(renal is chaemia) and renal damage leading to renal
failure.
It effect on renal blood vessels causes rupturing of retinal vessels. The eyes
accumulates the fluid (oademetous) leading to blindness and blurring of the
vision.

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 PATHOPHYSIOLOGY OF SECONDARY OR NONE ESSSENTIAL
HYPERTENSION.
kidneys are the commonest causes of secondary hypertension. In any
kidney disease where there is kidney damage or reduced renal blood flow, this
lead to the release of rennin by the renal juxtaglomerulus apparatus. Renin act
on angiotensinogen (hypertensinogen) which is present in the alpha globulin
fraction of the plasma protein to form angiotensin [Link] 1 combines
with an unknown enzyme in the lungs to form a vasoconstrictor called
ansiontension ll. This causes widespread vasoconstriction of the blood vessels
and consequently increase in blood pressure.

PATHOPHYSIOLOGY OF CONGESTIVE CARDIAC FAILURE

The heart is the only pumping organ circulating blood to all parts of the
body to meet the metabolic needs of the blood tissue heart failure can be
caused by conditions that interfere with it’s pumping function such causes may
include hypertension, inadequate of blood to the heart (ischaemic heart
disease valvular heart disease; pulmonary heart disease etc. Whenever one
side of the heart is affected, the other side will invariably be affected soonest
where about and prompt treatment is not instituted.
In a situation where hypertension or Aortic valve stenosis is the cause, the
myocardium of the left ventricle become hypertrophied (enlargement) weak
and fails to pump sufficient blood to the systemic circulation. Oxygenated
blood then accumulates within the left ventricle. The congestion of this blood
extends backwards to the left atrium and then into the pulmonary circulation
the congestion within the lungs bloods to the filling up of the lungs aveoli with
serous fluid causing accumulation as the plural cavity (hydrothorax). The
pulmonary with excessive accumulation of fluid will impair the exchange in the
lungs causing the characteristics respiratory embarrassment like
orthophoeabreathlessness that prevent lie down and cough .the patient may
cough out blood in severe pulmonary congestion due to rupturing of the
pulmonary capillaries and arterioles.
The pulmonary Oedema leads to congestion of blood within the
pulmonary arteries and then two result ventricle .The right
ventricles becomes enlarged before filing to pump
deoxygenated blood to the lungs for Oxygenated, similar
hypertrophy and failure occurs with the myocardium in the
right atrium leads to it’s congestion. Congestion in the right
Atrium leads to increased pressure and congestion of blood
within the superior and inferior vana-cava causing venous
congestion.
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 Congestion within the superior vena- cava causes the distension of the
jugular veins in the Neck as a Pathophysiology characteristic sign. The
venouscongestion causes escape of fluid from the vascular system into the
interstitial spaces leading to generalized edema (anasarca) which becomes
evident as sacral edema while in sitting position and pedal oedema(feet and
Ankles) while standing up.
Escape of fluid into the peritoneal cavity leads to Ascites. The congestion
within abdominal organs causes Anorexia. Anorexia may also result from drug
toxicity (like digoxin ) or nonstimulating dietary prescriptions . The stomach
and intestinal congestion produces manifestation of blood into the heart
causes a low cardiac output . Reduced cardiac output coupled with kidneys
congestion lead to reduced renal blood flow resulting into diminished urinary
output (Oliguria ).
Reduced renal blood flow leads to the release of an enzyme called . Renin by
the renal juxtaglomerular cells . Renin leads to the formation of angiotensin ii
(vasoconstrictor) . Angiotensin ii stimulates the mineralo-corticold part of
Adrenal cortex to release Aldosterone , which causes reabsorption of sodium
and consequently water reabsorption from the renal tubules into the blood
stream aggravating the Oedema. The patient may present with subnormal
temperature due to reduced heat production from decreased metabolism
caused by reduced blood and oxygen circulation to the body tissues . At the
terminal stage , the patient goes into coma due to impaired cerebral
functions caused by inadequate blood and oxygen supply to the brain tissue
.
PATHOLOGY OF SICKLE CELL ANAEMIA
Sickle cell Anaemia is a hereditary blood disorder caused by the
presence of an abnormal Hemoglobin-S in the Red Blood cells, making the Red
Blood Cells to assume an abnormal sickle shape white can be to the ahemolyse
leading to ehmolyseanemia. During the Biochemical formation of the normal
Haemoglobinmolecule ([Link]-A) in a normal individual witch normal
Haemolobin blood cells, it has been discovered according to Green (1978) and
Ganong(1977) that the Amino Acid Glutamic acide) assumes the sixth position
among the 146 Amino acid residues in each Beta polypeptide chain of globin
from each parent.
The main abnormality of the sickle Red Blood cells, therefore, is in the
formation of the Globin portion of the Haemoglobin molecule. In individuals
with sickle cell disease, it has been discovered that it is the identical Mutant
Genes inherited from the two parents, according to Ganong. (1977) that have
the replacement of Amino-Acid glutamine by Amino-Acid valine in each Beta
Polypeptide chain, thereby causing the formation of the abnormal Hemoglobin-
S is the affected child.
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Hemoglobin-S is very insoluble at low blood oxygen tensions and when the
blood is acidic thereby causing the formation of firmer crystals and
precipitation within the Red Blood cells. Hemoglobin-S at this time causes a
distortion in the shape of the Red Blood cells that this disease has derived its
name.
The precipitation Hemoglobincauses the Red cell me membrane to
be more fragile and breakdown (haemolyse) easily . Severe and continuous
haemolysis leads to sickle cell Anemia (with all its manifestation) as well as
increased bilirubin in the blood stream. Excess bilirubin causes the hemolytic
jaundice.
The abnormal sickle Red blood cells increase the viscosity of the blood causing
a sluggish blood flow and thrombi formation in blood capillaries. The victim
experience an acute episode call crisis characterized by severe haemolytic
anemia and pains, especially in the presence of an infection
(e.g. Malaria) ,stress , dehydration , exposure to cold , hypoxia and acidosis .
This crisis further increases the blood viscosity leading to circulatory
sluggishness and thereafter thrombosis.
The thrombosis promotes intravascular Occlusion which causes oxygen
tissue deprivation and an accumulation of acid waste products, leading to
swelling loss of function and pains at the joints and muscles. The vascular
occlusion in the mesentery covering abdominal organs leads to acute
abdominal pains, while that of the renal blood vessels cause destruction of
kidney enthrones leading to renal failure. The occlusion of cerebral arteries can
cause cerebralthrombosis or embolism leading to stroke with hemiplegic. The
occlusion of the tiny blood vessels supplying periosteumof the digests of the
hands feed causes their painful swelling (Dactylitis).
The sickle cell patient may suffer from cholelithiasis due to accumulate of
bilirubin in biliary tracts from haemolysedsickle cells. Such is also prone to leg
ulcer at the level of mallelous due to peripheral stasis and vascular occlusions.
He or she can be prone to osteomyelitis and other secondary infections. Fever
is also common due to presence of any secondary infection. There is usually
hyperplasia of the red bone marrow and enlargement of the liver and spleen
partly due to excessive reticulocytes formation (reticulocytosis) in them and
partly due to more engulfing of thehaemolysed red cells by the kuppfer cells.

RESPIRATORY SYSTEM
PATHOLOGY OF BRONCHIAL ASTHMA
Bronchial Asthma, according to Roper (1970) is defined as an attack of
Breathlessness associated with bronchial obstruction or spasm and
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characterized by expiratory wheeze. In a normal situation, the bronchial trees
are always patent for easy passage of air to and from the alveoli of the lungs.
Whenever any of the offending agent or stimuli gets to the bronchi either
trough inhalation or ingestion or their mere physical presence before the
victim, this causes the release of chemical mediators like Histamine,
Prostaglandins and other slow-reacting substance of Anaphylaxis in response to
the antigen. These chemical mediators act on receptor sites on the membrane
of the bronchial smooth muscle. This contraction causes constriction of the
bronchial trees leading to their narrowing.
The presence of the antigen within the bronchi and bronchioles
stimulates the mucus-secreting glands in their ciliated epithelium to produce
more mucus, in an attempt to dilute and sweep away the antigen. The
presence of more mucus further aggravates the narrowing of these bronchial
trees. The presence of the mucus and broncho-constriction obstructs the easy
expulsion of carbon-dioxide through these air passage ways causing the
characteristic wheezy breathing with expiratory dyspnoea ([Link]
breathing). The expiratory dyspnoea leads to accumulation of carbon-dioxide in
the blood stream causing cyanosis.
The broncho-constriction causes the usual painful tightness (i.e feeling of
suffocation) experienced in the chest. It is this feeling of suffocation that makes
the patient to be anxious. The anxiety, expiratory dyspnoea and feeling of
suffocation lead to insomnia. The presence of the offending agent along the
respiratory tracts initiates the cough reflex. The sputum produced during the
coughing is usually scanty and thick. The excess carbon-dioxide in the blood
stream stimulates the respiratory centre in the medulla oblongata leading to
increasing respiration. The difficulty in breathing makes the heart to beat faster
to pump more deoxygenated blood to the Lungs for Oxygenation. This causes
an increase in pulse rates. Since the victim will now be restless due to
respiratory difficulty, more muscle glycogen will be consumed leading to the
release of more heat causing a slight increase in the body temperature. Excess
of this heat leads to more production of the characteristic sweat (perspiration)
to expel heat from the body.
In adults, efforts will be made to sit up, bend forward and throw
their heads backward, in order to use all the accessory muscles of respiration in
an attempt to over come the embarrassing expiratory dyspnoea.

PATHOPHYSIOLOGY OF PNEUMONIA
Pneumonia is the inflammatory of the Lung tissue, in which the alveoli
are usually filled with inflammatory exudates. Whenever the pneumococcal or
any of the organisms causing pneumonia enter the Lungs, they will inflame the
Lungs, tissue (including the bronchioles and alveoli) causing the formation of

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inflammatory exudates. These exudates containing plasma, cellular Debris,
causative organisms and their toxins and the blood cells startsfillings up the
Alveoli.
The inflammatory exudates later make the alveoli and even the whole
Lung tissue to become consolidated with patches. This consolidation impairs
the gaseous exchange between the alveoli and the surrounding blood
capillaries, leading to dyspnoea. Since enough oxygen cannot diffuse into the
blood stream as a result of alveolar consolidation, this then leads to cyanosis.
As a result of low oxygen content in the blood circulation , the heart beats to
pump sufficient blood to thr diseased lungs for Oxygenation to meet the
oxygen needs of the body tissues. This leads to increase pulse rates
(Tachycardia) which will be full and bounding
The consolidation of the Lung tissue interferes with the expiration of
carbon-dioxide leading to its accumulation in the blood stream brings about
fast respiration with flaring nose.
When this infection spreads to the pleurae covering the, pleurae become
inflamed leading to pleurisy which brings about the characteristic chest pain.
The chest pain is felt more during coughing or inspiration, when the Lungs will
expand and rub against the stretched and inflamed pleurae. It is the chest pain
felt especially in deep inspiration that causes the shallow respiration. The
presence of the exudatesand bacterial toxins within the bronchioles serve
asforeign matters irritating the bronchial lining to produce mucus and set up
cough reflex, in order to get rid of these foreign matters. At first the cough will
be dry, painful and unproductive and later becomes less painful but productive
of sputum.
In Bronchopneumonia, the sputum is tenacious, blood streaked and
mucopurulent. The microorganisms and their toxins causing any disease
including pneumonia serve as pyrogenscapable of producing fever. When these
pyrogens enter the blood stream, they first react with the Leucocytes forming
another substance called endogenous pyrogens. The endogenous pyrogens, on
circulating to the brain, then stimulate the heat regulatingcentre in the
hypothalamus by resetting the thermostat in this centre, causing more heat
production in the body and consequently a higher body temperature. The body
temperature will be continue to increase as long as the pyrogens are present
resulting into shivering, headache, malaise and anorexia. In Infants and young
children there can be convulsion due to the immaturity and instability of the
heat regulating centreand the nervoussystemgenerally to cope with the
continuous fever. With the administration of appropriate antibiotics, the
pyrogen will be destroyed and their concentration greatlyreduced. The
thermostat level is then lowered leading to stimulation of the body heat-
dissipating responses, in form of peripheral vasodilatation, sweating and

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evaporation to the sweat. This leads to cooling of the body and return to
normal of the body temperature.
In serve cases of pneumonia where the body temperature has risen
above 40.5°C, there is danger of brain cellular damage characterized by
disorientation and delirium. As at this time the heat regulating centre in the
hypothalamus is losing its capacity to regulate the temperature, resulting into
continuous fever until death occurs. Death most often occurs when the
temperature has risen between 43.4°C to 44.4°C

PATHOLOGY OF PULMONARY TUBERCULOSIS

When the TubercleBacilli enter the Lungs the inhalation of the
droplets containing these micro-organism, they will set up a chronic
inflammation of the Lungs tissues and the pleurae covering the lungs.
Inflammation of the Pleurae leads to pleurisy which is characterized
by chest [Link] inflammation of the Lungs tissues (Pneurmonities)
leads to the formation of the TUBERCLE(i.e collection of lungs
tissue,phagocyte cells, fibroblasts and lymphocytes) around the
Tubercle Bacilli.
If the body immunity is high, the Tubercle Bacilli will be destroyed by the
Tubercle, and the lung wound heals by fibrous tissue. Where the body
immunity is very low, the Tubercle breaks down to from cassation (i.e Cheesy
mass). The cassation will liquefy to from pus part of the sputum.
The presence of the Tubercle Bacilli along the respiratory tract and lungs
brings about the cough reflex to get the bacilli out of the respiratory system.
The coughing of the sputum containing pus and the bacilli leads to the creation
of cavities in the lungs. The distortion of the normal anatomical structure of the
lung tissue by the bacilli based on the creation of various cavities and the
formation of some scar tissues in the lungs invariably impairs the normal
gaseous exchange within the lung causing [Link] to low
intake of oxygen from the lungs into the blood stream causing cyanosis.
The low oxygen content in the blood steam due to dyspnoea
consequently stimulates the heart to faster to circulate more blood to the lung
for oxygenation. This leads to increase pulse rate. The dyspnoeasimilarly
interferes with the release of adequate volume of carbon- dioxide out of the
Lungs leading to its increase in the blood stream. Increasecarbon- dioxide
respiration.
The destruction of the blood vessel the lung by the Tubercle bacilli leads
to haemoptysis. Prolonged haemoptysis leads to Anemia, body weakness and
body wasting with loss of body weight. In women, prolonged anemia may also
lead to amenorrhea. The presence of the tubercle Bacilli and their toxin in the

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blood stream leads to profuse night sweating, especially and presumably due
to increase basal metabolic rate this time.
The increase basal metabolic rate also accounts for the veering pyrexia which
gets lowered in the morning.
A times, some patties may develop Erythematic Nod sum (i.e a bluish –
red raised lesions of about 2.5cm in diameter) on the anterior aspect of the leg,
as a result of allergic reaction to the tuberculosis in other parts of the body.

PATHOPHYSIOLOGY OF COMMON COLD

A cold develops when viruses get into Nasal cavities and start to attack the
Nasal mucosa. The viruses penetrate mucosa cells and begin to proliferate. The
immune reaction induced consists of an increase in blood circulation and a
swelling of the Nasal mucosa. The Airways narrow. At the same time, the Nose
produces more secretionin order to rinse out the viruses. This secretion
gradually becomes viscous and can no longer flow through the narrow airways.
The Nose then becomes congested

THE DIGESTIVE SYSTEM

PATHOPHYSIOLOGY OF PEPTIC ULCER
Peptic ulcer the ulceration or erosion of the mucous membrane of the
stomach and the proximal part of the Duodenum by the digestive action of
Hydrochloric acid and [Link] part of the Gastro-intestinal Mucosa is prone
to peptic ulcer, once it comes in contact with the Gastric secretion containing
Hydrochloric Acid and Pepsin.
In Non peptic ulcer individuals, thought there Is secretion of hydrochloric Acid
and pepsin by their Gastric glands, yet they don’t experience peptic ulceration
due to the following naturals body defensive mechanisms like:
- There is enough secretion of mucus by the Gastro-intestinal Mucosa to
dilute Acid-pepsin secretion and also to coat the mucosa preventing it
from digestive action of Acid-pepsin.
- The strong alkalinity of the Bile, Pancreatic and intestinal juices in the
Duodenum, in addition helps to neutralize the Acid-pepsin, reducing its
digestive and erosive power on the duodenal wall.
- The healthy state of the Gastro-intestinal mucosa itself with a good
blood supply and quick regenerative ability of its cells also serves as a
protective mechanism against the Acid pepsin.
- Peptic ulcer occurs, therefore, in an individual when there is an
imbalance between the said body’s natural defensive mechanism and

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 the hydrochloric Acid-pepsin secretion, or when there is excessive
production of Acid-pepsin, or when the naturals Defensive mechanism
are ineffective against the digestive action of Acid-pepsin. The
Hydrochloric Acid and pepsin start eroding the Gastric mucosaor
duodena mucosa leading to Gastric ulcer or Duodenal ulcer respectively.
This is worsened when there is no food in the stomach to neutralize the
Acid-pepsin.
- The erosionof the nerve ending in the Gastro-Duodenal mucosa leading
to the sensation of pain which characteristically felt in the epigastria as
Epigastria pains. This pain is severely felt 1-1 1/2 hours in Gastric ulcer
patient after the intake of coarse or seasoned foods into the stomach,
due to the churning movement of the stomach on the food, making the
food to irritate the ulcerated part. Intakes of food in food in these case
doses not relieve pain.
The pains is felt 2-31/2 hour after the intake of food in duodenal ulcer patient
after the expiration of the neutralizing affect of this food on the Acid-pepsin.
Hence, intake of food relieves pains in duodenal ulcer. The quick onset of
epigastria pains in Gastric ulcer patient makes the patient to lose appetites for
food (Anorexia). The delay in the onset of epigastria pains (2-3 1/2 hours) in
duodenal ulcer patient stimulates such to develop more appetite for food
(anorexia). The delay in the onset of epigastric pain (2-3 1/2hour) in duodenal
ulcer patient stimulates such to develop more appetite for food thereby
increasing the body weight. The pain disturbs the duodenal ulcer patient’s
sleep in the nigh, since such does not eat food to neutralize the acid-pepsin
around that time. This makes the acid to erode the mucosa of the duodenum.
The presence of the ulcer in the pyloric portion of the stomach is usually
accompanied with inflammation, Oedema and scar tissue formation leading to
narrowing of the lumen of the pylorus. This narrowing will invariably delay the
emptying of the food into the duodenum causing vomiting. Prolonged vomiting
and anorexia lead to dehydration and loss of body weight, as seen above with
gastric ulcer patient.
The erosion of the blood versels in the submusosa lining of the stomach or
Duodenum by Acid-pepsin leads to internal Hemorrhage which can manifest as
Haematemesisin Gastric ulcer or Melaenain both Gastric and Duodenal ulcers.
Prolonged internal hemorrhage leads to anemia with all its signs and
symptoms. The erosion of the four lavers of the stomach or Duodenum leads to
Gastric or Duodenal perforation. Traces of the partially digested food materials
and some microorganisms then sip through the perforated part to infect the
peritoneum causing peritonitis with its fatal manifestation.

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 PATHOLOGY OF INTESTINAL OBSTRUCTION
Intestinal obstruction is the obstruction to the passage of the intestinal
content, which can either be acute affecting the small intestine or chronic
particularly affecting the large intestine. The presence of an obstruction,
irrespective of the cause and location will block the lumen of the intestine
preventing the passage of the content within the intestine. This leads to the
accumulation of the contents which change to fluid and gas above the
obstruction causing abdominal distension. The presence of the accumulated
materials above the obstruction exerts pressure on and even irritates the
nerve endings in the intestinal Mucosa and submucosa causing the colicky
abdominal pains. This pain may also be due to the intestinal spasms in an
attempt to force the contents through the obstruction.
In the small intestine, this obstruction causes distension as a result of
accumulated food which overflows backwards into the stomach. The
improperly digested food starts irritating the gastric and Esophageal mucosa
causing the vomiting. The vomitus initially contains the stomach contents
and later bile which has flown down and mixed with the food in the
intestine. The vomitus may even be brown and faecal in nature due to
excessive fluid and gas accumulating from the intestine.
Prolonged vomiting leads to dehydration as well as fluid and electrolyte
[Link] presents with sunken eyes, hollow cheek and dry
skin [Link] vomiting can also lead to hypovolaemia and consequently
hypovolaemicshock with its manifestation like subnormal temperature,
rapid but feeble pulse, cold clammy skin and pallor.
The presence of the obstruction at any point in the intestine does not
permit further formation of faces, apart from the previously formed ones
which had been passed out. This leads to constipation in which no fecal
matter or gas (i.e flatus) is passed out of the Anus. In a situation where the
obstruction is not promptly removed surgically, the pressure exerted by the
accumulated contents on the tiny blood vessels in the intestinal sub mucosa
can lead to is chimera followed by gangrene, necrosis and perforation of
intestinal wall.
The escape of the infected intestinal content through the perforated part
can infect the peritoneum leading to peritonitis. The irritation of the serous
peritoneum by infected content causes more secretion of serous fluid into
the peritoneal cavity leading to As cites. Peritonitis causes generalized
abdominal tenderness and rigidity. The absorption of the septic materials
into the bloodstream through the perforated part leads to septicemia with
pyrexia and increase pulse rates. The skin becomes hot with flushed cheeks.
Where this situation is not promptly arrested both medically and surgically,
the patient goes into delirium and dies.

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 PATHOPHYSILOGY OF GASTRO-ENTERITIS
Gastro-enteritis is the inflammation of the mucous membrane of the
stomach and the intestine. Whenever the causative micro-organism gain
entrance into the Gastro-intestinal tract, they will irritate or inflame the
andredness of the mucosa. The toxins produced by these organism irritate
the nerve ending in the mucosa leading to severe abdominal cramp with
abdominal tenderness. The abdominal cramp makes the patient to prostrate
and restless.
The inflammation of the gastric mucosa by the bacteria and their toxins
cause the frequent vomiting, while inflammation of the intestinal mucosa by
the bacteria antitoxins cause the release of excessive amount of fluid and
electrolytes by the small intestine leading to the frequent passage of
explosive, watery, unformed and offensive stools called Diarrhea. The
essence of the Diarrhea and vomiting is to serve as body defense
mechanism to get rid of the bacteria and their toxins along this tract.
Profuse diarrhea and vomiting lead to dehydration manifesting as sunken
eyes, loss of skintug or,depressed fontanel’s (in children) and loss of body
weight. The loss of fluids and electrolytes including glucose causes the
general body weakness. The loss of these materials from the body will also
cause hypovolaemia leading to Anemia and hypovolemic or Oligarchic shock
characterized by low Blood pressure, and fast but but feeble pulse. There
will be but feeble pulse. There will be fast, sighing and shallow respiration
due to acidosis caused by hypernatraemiaresulting from dehydration. The
patient’s skin will be cold and clammy due to constriction of the peripheral
blood vessel reducing blood supply to the skin. The body temperature
becomes subnormal due to hypovolaemiain which less blood carrying less
heat flows to vital centers. Severe dehydration leads to reduced renal blood
flow causing very low output of urines (Oliguria), which is highly
concentrated. In extreme cases, there may be no urine production (Anuria)
due to onset of renal failure.
The excessive loss of body fluids stimulates the thirst centre in the
hypothalamus, ,which invariably makes the victim to be highly thirsty and
eager to drink water in an attempt to compensate for the lost fluids from
the body. Where adequate and prompt replacement of fluids and
electrolytes loss is not made, and the infection remains untreated, the
victim goes into heart failure, renal failure and coma.

PATHOPHYSIOLOGY OF CHOLERA
Cholera is a modifiable and internationally quarantinabledisease caused
by vibro cholerae and characterized by profuse vomiting and dehydrating
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diarrhea with rice water stools, muscular cramps and marked toxemia.
Whenever the vibrato cholera gains entrance into the Gastrointestinal tract
through contaminated foods and drinks by infected faces or vomits, they
will irritate of inflame the stomach and the intestinal mucosa.
The inflammation causes the swelling and redness of the mucosa. The
toxins produced by these organisms irritate the nerve endings in the
mucosa leading to severe abdominal cramp with prostration.
The irritation of the gastric mucosa by these organisms and their toxins
causes the frequent vomiting; while irritation of intestinal mucosa by the
bacterial enter toxins cause and the release of excessive amount of fluids
and electrolytes by the smalls intestinal leading to the frequent passage of
unformed and offensive rice water stools. The essence of the Diarrhea and
vomiting is to serve as body defense mechanism to get rid of the bacterial
toxins along this tract.
NB The other effects of diarrhea and vomiting in cholera are exactly as
discussed under Gastro-enteritis above.

PATHOPHYSIOGY OF APPENDICTIS
The vermiform Appendix is a reticule-endothelial organ containing more
lymphoid tissue for the formation of lymphocytes. Since lymphocytes help
to invade the microorganism and neutralize their toxins, Appendix,
therefore, provides local protection of the body.
Appendix communicates with the caucus through a lumen. One of the
commonest causes of Appendicitis is an obstruction of the lumen either by
foreign body, facecloth (i.e hard faces) or kinking of the Appendix itself.
This obstruction prevents drainage of materials in the Appendix into the
caecum. The foreign body or facecloth containing microorganisminflame the
Appendix mucosa causing Appendicitis.
There will be increased blood supply (hyperemia) containing more white
blood cells (Leucocytosis) to the appendix to arrest the situation. The
increased blood supply coupled with the inflammatory exudates and the
already accumulated materials within the Appendix lead to its swelling. The
redness as a sign of inflammation due to hyperemia appears at this initial
stage.
The accumulated and irritating materials exert pressure on the
intraluminar nerve ending s both in the mucosa and submucosa layer of the
appendix causing sudden colicky abdominal pain, which radiates from the
umbilicus to the right iliac fossa of the abdominalcavity, where the pain
settles and remains constant instead of being intermittent before setting in
the right iliac fossa.

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 The accumulation of the inflammatory exudates makes the appendix
tender on palpation, which also makes the muscular wall of appendix rigid
around the right iliac fossa. The vitim finds it difficult to extend the thigh at
the hip join, since active movement of this thigh initiates the pain in the
right iliac fossa. Hence the victim prefer to walk slowly and gently.
In mild cases and where the body resistance is high, the inflammation
subsides and healing of the inflamed appendix takes place. In severe cases
where the body resistance is low and the virulence of the microorganisms is
high, this leads to suppuration and abscess formation and further
[Link] then appears light yellowish at this stage.
In severe cases again, increased congestion within the appendix or its
kinking exerts pressure on intraluminar vessels causing ischemaemia.
Appendix then becomes gangrenous appearinggreenish or black in color and
later perforates or ruptures .the infected material then escape into the
peritoneum causing either localized or generalized peritonitis, and into the
blood stream causing septicemia(bacteriacemia) with all their fatal
manifestations like rigor, tachycardia, vomiting, furred tongue etc.
Adhesions may even binding appendix to the neighboring organs and
abdominal wall leading to the presence of appendix mass.
Where the ilio-caecal junction which is very close to the opening of the
Appendix into the caecum is obstructed by either the faecolith or cancer,
there will be an accompanying constipation. Occasionally there can be
diarrhea where the inflamed appendix lies in the pelvic region and irritating
the rectum. The victim may present with dysuria where the tip of the
inflamed Appendix lies very close to the urinary blader or commencement
of the Urethra.

PATHOLOGY OF HEMORRHOIDS
A hemorrhoids is varicosity (i.e dilatation and tortuousity) of the rectal
and Anal Veins. All causes of hemorrhoids create a continual pressure and
resistance to the forward (upward)flow of venous blood within the rectal and
Anal Veins. This resistance causes the stagnation or pooling of venous blood
leading to dilatation and tortuousity of rectal and anal veins.
The accumulation of venous blood in these veins causes local swelling.
This swelling can press on the nerve endings in the rectum and anal canal,
leading to serve pains. This pain becomes worse on defecation, making the
victim to ignore defecation. More water is then absorbed from the faecesin the
pelviccolon making the faeces to become hard. This leads to constipation. Any
attempt made by the victim to expel this hard faeces through the rectum and
anal canal, makes the dilated and tortuous veins to rupture leading to escape
of bright red blood through the Anus. Prolonged bleeding can lead to anemia.

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 A little crack in these dilated and tortuous veins paves way for infection
leading to anal discharge. Irritation of the anal mucosa by the anal discharges
causes the usual itching of the anal region called Pruritus [Link] continual
congestion of venous blood within the recto-anal veins leads to poor oxygen
and nutrient supplies to the muscular layer of the lower rectum and anal canal.
These make these musclesto beweak. The greaterpressure exertedby the
contracting abdominal muscles and lowering of the diaphragm on defecation,
especially of hard faces, causes the prolapsed of the rectum outside the
externalanal sphincter.
The return of the prolapsed to its normal place depends on the degree of
hemorrhoids. For instance in the first Degree hemorrhoid, the prolapsed will be
seen with a proctoscope inside the [Link] the second Degree hemorrhoid,
prolapsed will be seen outside the Anus on defecation but returns inside
spontaneously after defecation. In the third degree hemorrhoid, the prolapsed
will remain outside the Anus, even after defecation unless it is pushed back into
the rectum with finger. The presence of the prolapsed outside the anus causes
the victima great physical discomfort from pains and inability to walk properly,
for fear of not wanting to injure the prolapsed rectum.

PATHOLOGY OF HERNIAS
Hernia, according to fish (1974) is the protrusion of an organ or part of an
organ through an opening in the wall of the cavity in which it lies. Though
Hernia can occur at any part of the body, yet abdominal hernias are the most
frequent. Hernias irrespective of the causes invariably lead to the escape (i.e
protrusion) of an organ part of an organ through an opening in the covering
wall. This protrusion that is initiated by prolonged slight, moderate or serve
strains like in coughing, crying (in babies), defeating or micturition will bring
about swelling around the affected area.
The pathophysiology of some the existing Hernias is as discussed below:
Inguinal Hernia:This is the protrusion of part of any abdominal organ through
the inguinal canal that fails to obliterate after the migration of testes into the
scrotum. This occurs during the development of a male child before birth, or in
some cases during infancy or early childhood. The failure of the obliteration of
this canal permits the escape of part of the intestine through this canal towards
the scrotum causing a swelling around the inguinal region ([Link] groin). An
impulse will be felt in the swollen part on coughing, since coughing further
increases intra-abdominal pressure and consequently increase in pressure of
blood within the blood vessels being trapped in the narrowed inguinal canal.
Inguinal hernia is said to be direct when the protruded organ through the
inguinal canal does not lead to the scrotum but causing a swelling of thegroin

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alone. It is said to be indirect inguinal hernia when the protruded organ leads
to the scrotum, causing swelling of the scrotum and the groin.
In a situation where the hole in the inguinal canal is big, it means the
protruded organ can be pushed back easily into the abdominal cavity using a
digital pressure on the swollen part. This type is called reducible inguinal
Hernia. Where the hole is very small, this leads to strangulation of the
abdominal organ that has protruded and the pushing back of this organ
becomes difficult. This type is called irreducible inguinal hernia, and which will
conspicuously lead to strangulated hernia.
Strangulated Hernia: This is the type in which the blood supply to the
protruded organ is impaired due to the constriction of this organ by the
narrowed inguinal canal. Since the nerves in the walls of the protruded organ
are compressed due to strangulation, this leads to severe abdominal pain
which worsens on screaming that further causes increase in intra abdominal
pressure. Prolonged severe pain can leadto neurogenic shock.
The constricted blood vessels in the walls of the strangulated organ
causes lack of blood supply to a part of this organ leading to gangrene and
necrosis of the [Link] can rupture or perforate causing the
escape of the content in the protruded organ into the peritoneal sac covering it
leading to peritonitis, while prolonged hemorrhage leads to anaemia and
hypovolaemic shock.
Diaphragmatic Hernia: This is the protrusionof abdominal organ like the
stomach, intestine or Liver through a weak spot in the Diaphragmatic muscles.
In a baby with this type of hernia due to a defect usually in the left sides of the
diaphragm, this then permits the protrusion of any of the mentioned organs
above through the weak spot in the diaphragm into the thoracic cavity.
Abnormal presence of any abdominal organ in the thoracic cavity causes a
displacement of the heart of the heart to the right and compression of the
Lungs. The Lungs compression interferes with normal respiration causing
cyanotic attacks.
Hiatus Hernia: This is the protrusion of the stomach through the Esophageal
Hiatus (i.e Opening) into the thoracic cavity due to a defect in the
diaphragmatic muscles surrounding the lower part of the Esophagus. The cause
of this type of hernia is a defect in the diaphragmatic muscles, such that these
muscles do not fit in closely around the lower end of the Esophagus as the
Esophagus passes through the diaphragm. This abnormal gap (i.e hiatus or
opening) created between the Esophagus and the weakened diaphragmatic
muscles then permits the upward protrusion of the stomach into the thoracic
cavity. The cardiac sphincter control is then impaired allowing a reflux of gastric
secretions and food, mucus and even blood.

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 Prolonged vomiting leads to loss of body weight and body weakness. The
regurgitation of the Acid-pepsin from the stomach into the lower part of the
Esophagus will ulcerate or erode this part causing Esophagitis with burring
substernal pains. The gradual healing of the ulcerate part of the Esophagus
leads to scarring and narrowing causing Esophageal stenosis. This stenosis
leads to dysphagia, with accumulation of food above the stenosedpart. The
above stenosedpart will later ferment producing foul smell in to the mouth.
Further stenosis worsens the regulation of food unless the stenosis is corrected
surgically along with herniorrhaphy.

PATHOPHYSIOLOGY OF PERITONITIS
Peritonitis is the inflammation of the peritoneum. The peritoneum is the largest
and delicate serous membrane, which lines the abdominal and pelvic cavities
and covering either partially or wholly the organs contained in these cavities.
Whenever an infection spreads to the peritoneum either from within
([Link] of any of the abdominal or pelvic organs it lines) or without
([Link] to gunshot wound), the peritoneum becomes inflamed causing
peritonitis.
The presence of microorganisms or contents from a perforated organ
into the peritoneum will irritate the serous layersof the peritoneum, causing
more secretion of serous fluid into the peritoneal cavity to dilute the offending
agents. This leads to abdominal distension. The escape of the fluid contents
from the perforated organ into the peritoneal cavity further compounds the
abdominal distention. The escape of the fluid contents from the perforated
organ into the peritoneal cavity further compounds the abdominal distension.
The entrance of microorganisms and their toxins into the blood stream
through any damaged blood vessel, either in Omentum or perforated organ
leads to septicemia. The microorganisms and their toxins serve as pyrogens and
endogenous pyrogens resetting the thermostat in the heat regulating centre in
the hypothalamus. This leads to more production of body heat leading to
higher body temperature with rigor.
The irritation of the nerve ending by bacterial toxins in the portion of the
peritoneum called Omentum will cause serve and generalized abdominal pain,
tenderness and abdominal rigidity the greater Omentum presents a defensive
mechanism by trying to wall off the inflamed part of any perforated abdominal
organ, in order to prevent the spread of infection. This furthercauses
abdominal rigidity
Where the spread of the infection to the peritoneum is from the
perforated stomach, the presence of the bacteria and their toxins will irritate
the gastric mucosa causing vomiting prolonged vomiting leads to body weight
loss, fluid and electrolyte imbalance and dehydration with all its signs and

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symptoms like sunken eyes, hollow cheeks, loss of skin Tugor etc. The vomitus
initially will contain undigested food in the stomach and finally bile stained and
foul being describe as faecal vomit, when the intestinal contents are
regurgitated on account of the paralysis of the inflamed intestine.
The prolonged vomiting leads hypovolaemic shock with rapid but feebie
pulse the respiration becomes shallow and fast due to the inability of the lungs
to expand fully as a result of the distended abdomen the temperature becomes
subnormal due to shock no faeces or flatus will be passed out in the later stage,
since the stomach and part of small intestinal contents have been vomited,
coupled with the paralyzed and inflamed intestine
At a later stage, where prompt and adequate relief measure are not
provided, the continuous accumulation of the bacterial toxins will poison the
brain tissue causing brain damage and coma

PATHOPHYSIOLOGY OF VIRAL HEPATITIS

Viral hepatitis is the inflammation of the liver tissue by viruses. The three types
of viruses involved are virus “A, virus” “B, Non-A and Non-Bvirus”. The virus “A”
causing infective Hepatitis gains entrance into the body through faeco-oral
route; virus “B” causing Homologous serum Hepatitis enter the body through
injections (e.g. contaminated needles, blood transfusion, mosquito bites etc).
the Non-A virus causing syndrome similar to infective hepatitis enters through
faeco-oral route, while Non-B virus present syndrome and mode of entry
similar to Hepatitis “B”.
Whenever any of these viruses gains entry into the body, it will attack the
liver cells causing inflammation (hepatitis) and necrosis of the liver tissue the
presence of these viruses and their toxins as pyrogens and endogenous
pyrogens in the blood stream will reset the thermostat in heat regulating
centre in the hypothalamus causing increase in body temperature (pyrexia)
These viruses proliferate within the liver tissue causing more
inflammation and swelling that lead to heptomegaly. Some liver cells become
necrosed due to serous attack by these viruses and their toxins. The
Necrosedhepatic cell will interfere with normal bile formation and obstruct
even the bile flow formed by the living liver cells, causing intrahepatic
obstructive jaundice. The obstruction to bile flow into the extrabiliary tract
causes accumulation of bilirubin in the blood stream leading to jaundice. Excess
of this bilirubin is excretedin the urine as urobilinogencausing dark colored
urine. Since bile containing bilirubin can not reach the intestine to color the
faeces brown due to intrahepatic biliary obstruction, the faeces then become
pale or clay colored.
The irritation and poisoning of the nerve endings within the hepatic cells
leads to abdominal tenderness and pains within the right hypochondriac region

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of the abdominal cavity. The irritation of the gastro-intestinal mucosa
especially by virus “A” or Non-A virus causes abdominal discomfort with
increased peristaltic movement leading to diarrhea, while some may present
with constipation. Irritation of the gastric mucosa leads to nausea and
vomiting. The onset of nausea and vomiting leads to Anorexia, loss of body
weight and general malaise.
The presence of these viruses and their toxins in the blood stream causes
the various irritations leading to headache backache and joint pains. Prolonged
intra-hepatic biliary obstruction causes the accumulation of bile salts (sodium
taurocholate and sodium Glycocholate) in the blood stream which then irritate
the coetaneousnerves causing pruritus. Prolonged inflammation and necrosis
of liver tissue leads gradually to cirrhosis of the liver. Since the diseased liver
can no longer metabolizedcarbohydrate, fat and protein properly, this leads to
malaise, mucles wasting and body weight loss. The prolonged intrahepatic
obstruction by scar tissue resulting from inflammation can affect the inflow of
blood from the portal vein. The backflow of this blood into the spleen leads to
splenomegaly.
The bile salts in the bile normally help in the absorption of vitamin Kin
the intestine to be used by the liver to form blood clothing factor called
prothrombin. Since these bile salts can not flow to the intestine due to chronic
intrahepatic biliary obstruction coupled with the fact that the diseased liver can
not manufacture prothrombin, all these lead to spontaneous bleeding, under
the skin causes the small purpuric spots called petechiae. Prolonged bleeding
leads to Anaemia. In advanced cases, since the liver can not convert ammonia
to urea, this causes ammonia toxicity that can poison the brain tissue leading to
hepatic coma.

PATHOPHYSIOLOGY OF LIVER CIRRHOSIS

Cirrhosis of the liver is a chronic, diffuse and degenerative disease affecting the
liver tissue, in which there is destruction of parenchyma cells, leading to
excessive formation of dense fibrous tissue. The liver initially becomes enlarged
(Hepatomegaly)due to fatty infiltration of the Liver, especially in cirrhosis
caused by chronic alcoholism. Later there three will be extensive necrosis
irrespective of the cause, leading to considerable scarring of the Liver tissue.
After a prolonged period, the scar tissue over rides the liver [Link] the
scar tissue contracts, the liver becomes small with rough [Link] rough
surfaces described as HOBNAIL SURFACES are due to small projecting nodules
of regenerated liver cells.
The late clinical manifestations of liver cirrhosis are partly due to the
chronic failure in liver functions, and partly due to obstruction to both the

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portal circulation into the Liver and bile flow into the biliary tracts. In normal
situations, the portal vein helps to drain blood from abdominal organs into the
Liver. In portal cirrhosis, the obstruction to the portal circulation causes the
backflow of blood within the portal vein. This leads to increase pressure within
the portal venous system causing portal [Link] then flows back
into the abdominal organs causing their congestion.
The congestion of blood in the spleen leads in the stomach and
Esophagus causes their varies and weakening predisposing them to rupturing.
The rupturing of the Oesophagealsand gastric veins leads to haematemesis,
and melaena. Congestion in the vessels of abdominal organs generally leads to
digestive disturbances like chronic dyspepsia and changes in bowel habits like
constipation or diarrhea. Congestion within the mesenteric veins like Recta and
Anal veins causes Hemorrhoids. Prolonged bleeding leads to Anaemia.
In Biliary cirrhosis due to obstruction in the biliarytracts to bile flow, this
causes backflow of bile containing bilirubin (bile pigment) into the systemic
circulation. Accumulation of bilirubin in the blood steam leads to severe
jaundice. Since the bile containing bilirubin can not enter the intestine as
stercobilin to colour the faeces brown, the faeces then becomes claycoloured.
Excess of bilirubin is excreted in the Urine as Urobilinogen making the Urine to
be dark brown or coffee-coloured. Bile contains Bile salts (sodium Taurocholate
and sodium Glycocholate). Accumulation of bile salts in the blood stream under
the skin will irritate the cutaneous sensory nerves causing pruritus.
The Liver dysfunction due to its cirrhosis manifest in various forms.
For example, the inability to manufacture enough prothrombin needed
for blood clotting leads to spontaneous bleeding tendencies like epistaxis,
melaena, haematuria and haematemesisetc. The bleeding under the skin can
give rise to small purpuric spots called petechiaewhile the bigger ones are
called ecchymoses. Since the cirrhotic liver can not manufacture enough
plasma proteins like serum albumin, this causes a reduction in the colloidal
osmotic pressure of the blood leading toOedema. Oedemaaggravated by the
systemic venous congestion due to portal hypertension, leading to escape of
fluid into peritoneal cavity causing Ascites; into pleural cavity causing
hydrothorax, and into the pericardial cavity leading to pericardial effusion
The necrotic Liver cells release the Live cells enzyme called serum
glutamic Oxalate Transaminase and serumGlutmicpyritic Transaminase into the
blood stream. In advanced case, there can be gynaecomastia (breast
enlargement males) and testicular atrophy due to inability of the diseased liver
cannot destroy the antidiuretic hormone and Aldosterone in circulation, as it
used to do under normal condition, these hormones then accumulate in the
blood stream promoting the reabsorption of water and sodium respectively
tubules into the blood stream, resulting into Oedema.

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 The cirrhotic patient presents with lassitude, weakness and muscle
wasting due to the impaired protein metabolism and carbohydrate storage as
liver glycogen. At the terminal stage, the liver will be unable to convert
Ammonia, resulting from the breakdown of Amino acids, to urea. This leads to
ammonia toxicity irritating the brain tissue causing hepatic.

PATHOPHYSIOL OF PRIMARY LIVER CELL CARCINOMA

According to Royle and walsh (1992), Benign and primary malignant
neoplasms are rare in the liver but that the liver is a frequent site of metastasis;
moreso ifthe malignancy is in the abdominal cavity. The presence of cancer in
the liver causes an enlargement of the liver (hepatomegaly). The cancerous
cells destroy the liver tissue causing an impairement in the liver functions. Since
cancer causes toxemia, according to roper (1978), the toxins will irritate the
nerve ending within the liver and its neighborhood leading to dull aching pain
within the right hypochondriac region of the abdominal cavity. The cancer can
cause intrahepatic obstruction to blood from hepatic artery and the portal vein
into the liver as well as outflow of bile the liver.
The obstruction to portal flow causes back flow of blood to all abdominal
organs leading to increases blood pressure within the portal vein and its
tributaries causing portal hypertension and congestion in abdominal organs.
The congestion of blood within the spleen leadsto splenomegaly, while the
dilatation or congestion and rupturing of the gastric and Oesophageal veins
lead to Haematemesis and malaena. Prolonged bleeding leads to Anaemia. The
increase pressure within the portal vein and its tributaries forces fluid in
circulation into the peritoneal cavity causing Ascites. Since the diseased Liver
cannot manufacture prothrombin needed for blood clothing, this leads to
prothrombindeficiency disease. This will subject the victim to bleeding
tendencies like purpura, epistaxis, Malaena etc. after sustaining minor injuries.
The congestion in all veins draining into the portal vein especially along
the Digestive system leads to anorexia, flatulence, and abdominal discomfort.
Prolonged anorexia coupled with an impairment in protein metabolism and
carbohydrate storage as Liver glycogen lead to weakness and muscle wasting.
An obstruction at the portal Hepatitis impairs the outflow of bile through
extrabiliary tracts into the intestine to color the faeces brown. This causes the
clay-colouredfaeces. Since the Liver cells can not take up the bilirubin formed
by the spleen (during haemolysis) due to obstruction to portal flow at the
portal hepatis by the cancer, bilirubin then accumulates in the blood stream
causing jaundice. Excess of this bilirubin will then be excreted in the urine as
urobilinogen making the urine dark or coffee-coloured. In advanced stage, the
Liver will be unable to convert ammonia, resulting from the breakdown of

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amino-aids, to Urea. This leads to Ammonia toxicity irritating the brain tissue
and causing hepatic coma.

PATHOLOGY OF PRIMARY LIVER CELL CARCINOMA

According to Royale and Walsh (1992), Benign and primary malignant
neoplasm’s are rare; in the Liver but that the liver is a frequent site of
metastasis; more so if the malignancy is in the abdominal cavity. The presence
of cancer in the Liver causes an enlargement of the Liver (Hepatomegaly). The
cancerous cells destroy the Liver the tissue causing impairment in the liver
functions. Since cancer causes toxemia, according to Roper (1978), the toxins
willirritate the nerve endings within the Liver and its neighbor hood leadings to
dull aching pain within the right hypochondriac region of the abdominal
cavity. The cancer can cause intrahepatic obstruction to blood flow from
hepatic artery and the portal vein into the liver as well as outflow of bile from
the liver.
The obstruction to portal flow causes back flow of blood to all abdominal
organs leading to increase blood pressure within the portal vein and its
tributaries causing portal hypertension and congestion in abdominal organs.
The congestion of blood within the spleen leads to splenomegaly, while the
dilatation or congestion and rupturing of the gastric and esophageal veins
leadto haematemesis and malaena prolonged bleeding leads to anaemia the
increase. Pressure within the portal vein and its tributaries forces fluid in
circulation into the peritoneal cavity causing Ascites. Since the diseased Liver
cannot manufacture prothrombin needed for blood clotting, this leads to
prothrombin deficiency disease. This will subject the victim to bleeding
tendencies like purpura, epitasis,Melaenaect after sustaining minor injuries.
The congestion in all veins draining into the portal vein especially along
the Digestive system leads to anorexia, flatulence, and abdominal discomfort.
Prolonged anorexiacoupled with an impairment in proteins metabolismand
carbohydrate storage as Live glycogen lead to weakness and muscle wasting.
An obstruction at the portalHepaticimpaired the outflow of bile through
extrabiliarytracts into the intestinal to colour the faecesbrown. This causes the
clay-colouredfaeces. Since the liver cells can not take up the bilirubin formed
by the spleen ( duringheamolysis) due to obstruction to portal flow at the
portal hepatic by the cancer, bilirubin then accumulates in the blood stream
causing jaundice. Excess of this bilirubin will then be excreted in the urine as
urobilinogen making the urine to be dark or coffee-coloured. In advanced
stage, the liver will be unable to convert ammonia, resulting from the
breakdown of amino-acids, to urea. This leads to ammonia toxicity irritating the
brain tissue and causing hepatic coma.

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 PATHOPHYSIOLOGY OF CARDIOSPASM ( ACHALASIA)
Achalasia is the spasm of the muscle at the muscle at the cardiac end of the
esophagus leading to inability of the cardiac orifice to open correctly. After the
bolus of food has been swallowed into the Esophagus, the foode becomes
really held up at the cardio-esophageal junction. The muscular layer of the
Esophagus starts contracting vigorously to push the food through the
constricted part into the stomach. After sometime, the Esophagus becomes the
hypertrophied and dilates above the site of the stricture. This bsituation bring
about dysphagia and regurgitation of food.
Initially, only solids are held up and which can only pass through with the
help of a drink when sufficient pressure has been mounted. This stricture
impairs the nutrition making the patient to lose body weight gradually.
Vomiting of the offensive, stale food occurs especially when sleeping thereby
causing pulmonary complications as a result of aspiration of fragment of the
vomitus into the [Link] excessive cough which may occur as a result of the
aspiration of part of the vomitus in recumbent position can disturb the night
sleep as nocturnal wakefulness. Tracheitis as a pulmonary complication
resulting from aspiration of vomitus will manifest as substernal pain.
The accumulation of food above the cardio-esophageal junction makes
the patient to have a sensation of food sticking in the lower part of the
esophagus. In serve stage, the prolonged irritation of esophageal mucosa by
the offensive, stale food may lead to esophageal carcinoma.

PATHOPHYSIOLOGY OF PYLORIC STNOSIS

Pyloric stnosis is the narrowing of the pyloric orifice (pylorus) through which
the stomach opens into the Duodenum. Irrespective of the cause of the
narrowing of the pylorus (either as a congenital abnormality or as a
complication of the duodenal ulcer or by cancer), this prevents the food from
leaving the stomacheasily through this narrowed part into the duodenum. This
causes accumulation of food and fluid in the stomach.
The progressive fullness of the stomach causes Anorexia and
abdominaldistension. The stomach muscles start contracting vigorously to push
the food through the narrowed pyloric orifice into the duodenum. This strong
muscular contraction of the stomach is shown as visible peristalsis from the left
side of the epigastrium to the right side.
The progressive fullness of the stomach due to pyloric stenosis, coupled
with the vigorous contraction of the stomach muscles leads to projectiles
vomitingto relieve the stomach of its distension. Excessive vomiting leads to
loss of body weight, fluid and electrolyte imbalance and signs of dehydration.
The excessive loss of calcium leads to tetany characterized by carpo-pedal

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spasm; while impaired bowel movement due to the pyloric stenosis causes
constipation.

PATHOPHYSIOLOGY OF AMOEBIC DYSENTERY. (AMOEBIASIS)

Amoebiasis is a chronic inflammatory and ulcerative bacterial infection of
the large intestine, which is caused by the protozoa called
entamoebahistolytica,, and characterized by diarrhea with blood and mucus
accompanied with dull colicky abdominal pains. Amoebiasis is contacted
through the faeco-oral route (i.e through contaminated foods and drinks by
infected). The entamoeba Histolytica is found in man in the vegetative or active
forme exhibiting active amoeboid movements. This vegetative form invades or
erodes the wall of the colon produsing ulcers.
Where the blood vessels in the submucosa layer are invaded, this causes
the release of blood into the intestine. The presence of these bacteria and the
ulcers will irritate the intestinal mucosa leading to increase peristaltic
movement of the colon causing diarrhea with blood and mucus and abdominal
pain .The excess mucus in the stool is a defensive mechanism initiated by the
goblet cells in the intestinal mucosa secreting more mucus to wash out the
bacteria and their toxin. The abdominal pain is caused by the irritation of the
neve endings of meissner’s plexus of nerves in the submucosa layer of the
colon by the bacteria and their toxins.
The systemic spread of these bacteria from the colon via the portal
circulation to the liver leads to amoebic Hepatitis which can result to amoebic
Abscess causing more abdominal pain within the right hypochondriac region of
the abdominal cavity. The frequency of the diarrhea with blood causes loss of
body weight, Aneamia, malaise and dehydration. Within the colon, these
bacteria encyst and it is these cysts that are passed out in the human faeces
which are ineffective to other human beings. When the encysted organismsare
swallowed again through the contaminated vegetables or fruits or food, they
are destroyed by the digestive juices of upper digestive tract; the cysts being
able to survive until they reach the large intestine where these bacteria hatch
from the destroyed cysts and then develop into the natured vegetative forme
again.

PATHOPHYSIOLOGY OF OBSTRUCTIVE JAUNDICE

The obstructive jaundice is a type of jaundice which is caused by an
obstruction to the free flow of bile either within the liver the biliary tract into
the [Link] bile which is secreted by the liver contains the bile salts and
the bile pigment (bilirubin), among other constituents in a normal situation.
Whenever there is an intrahepatic or extrahepatic biliary obstruction, this
prevents easy flow of bile into the Duodenum. The bile pigment (bilirubin) in
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the bile helps to colour the faeces brown in the colon in normal helth. Since
bile containing bilirubin can mot enter the duodenum as a result of the
obstruction, this therefore, makes the faeces to be claycoured or putty-
coloured.
Or Due to extrabiliary obstruction, for example, there is back flow of the
bile through the liver into the blood stream. On passing through the liver,
bilirubin in the bile combines with the glucuronic acid in the liver to form a
water-soluble bilirubin (I.e conjugated bilirubin ) compound .This leaves the
liver through the Hepatic veins to the systemic circulation .Excess of bilirubin in
the blood stream, therefore, causes the severe jaundice.
When excess of this bilirubin circulates to e kidneys, it will be excreted as
urobilin in the urine giving the urine the dark-brown coffee colour. Bile contains
the bile salts called sodium Taurocholateglycocholate. Excess of these bile salts
in the blood stream under the skin will irritate the cutaneous nerve endings
causing the [Link] mere sigh of fatty food by the victim causes the
nausea and vomiting as a psychological relief, since bile cannot reach the
duodenum to emulsify fat. Bile salts help in the absorption of vitamin K from
the small intestine into the blood stream, and to the liver to be stored. Vitamin
K is used by the liver to manufacture a blood clotting factor called protrombin.
An obstruction to the flow of bile into the intestine, therefore, leads to
protrombin deficiency disease which manifests as persistent bleeding after a
minor injury. This deficiency also causes an increase in the blood clotting time.
The prolonged bleeding leads to aneamia with all its manifestations.

TYPES OF JAUNDICE
1. Heamolytic jaundice: this is due to increased haemolysis of red blood
cells in the spleen. The Bilirubin is increased and if hypoxia develops
the efficiency of hepatocyte activity is reduced.
2. Obstructive jaundice : obstruction to the flow of bile in biliary tract
caused by gall stone,tumour of the head of pancreasefibrous of the
bile ducts.
3. Hepatocellular jaundice : this is the result of damage to the liver by
viral infections, toxic substances of drugs,amoebiasis ( amoebic
dysentery), cirrhosis of the liver.

GENITO-URINARY SYSTEM
PATHOPHYSIOLOGY OF NEPHRITIC SYNDROM
in normal situation, the glomeruli of the nephrons of the kineys do not
filter constituents of the blood with a higher molecular weight of 68000 and
above into the bowman’s capsule. The constituents that are not filtered include
blood cells and plasma proteins. The constituents of the blood being filtered

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are those with molecular weight lower than 68000. These include water, food
substance (e.g glucose, amino acid, fatty acids), inorganic and metabolic wastes
like Uric, URIC Acid, creatinine etc.
in disease conditions, most of the causes of Nephritic syndrome and up
with inflammation and damage to the glomeruli. The damage to the glomeruli
leads to increased permeability of the glomeruli to plasma proteins. The
excess escape of albumin (as part of plasma proteins) in the urine causes
severe albuminuria .severealbuminiria leads to hypoalbuminaemia.
Hypoalbuminaemia causes a reduction in the colloidal osmotic pressure of the
blood leading to serious escape of fluid from extracellular spaces (i.e within
blood vessels ) into the intercellular spaces causing severe oedema. The
rucduced colloidal osmotic pressure of the blood also leads to escape of fluid
into the peritoneal cavity causing as cites. The escape of fluid into the pleural
cavity leads to pleural effusion(i.e hydrothorax), while excess of this fluid in the
pericardial cavity causes pericardial effusion. The hydrothorax interferes with
the gaseous exchange in the lungs causing the dyspnoea. The severe loss of
gamma globulin (immunoglobulin) as part of the plasma protein lost in the
urine leads to a reduction in the patient’s body immunity, thereby making such
to be prone to secondary infection. The severe oedema brings about an
increase in body weight.
It is being speculated that thehypoproteinemiadue to serve albuminuria
appears to stimulate the liver to produce more cholesterol since cholesterol is
usually produced in the relation to albumin to maintain the albumin
concentration in the blood stream. More production of cholesterol or lipid into
the blood stream therefore causes hypercholesterolemia ([Link]).
In advanced or untreated cases of Nephritic syndrome, the prolonged
reduced colloidal osmotic pressure of the blood which causes failure of
reabsorption of water from the tissue into the blood stream leads to
[Link] to reduced renal blood flow, which also
stimulates the Juxtaglomerular Apparatus in the nephrons to release an
enzymes called Renin into the blood stream. The release of Renin finally leads
to the formation of a vasoconstrictor called Angiotensin Il which causes
increase in blood pressure.
Angiotensin Il stimulates the mineralo-corticoid section of Adrenal cortex
to produce aldosterone promotes the reabsorption of sodium from renal
tubules into the blood stream, causing hypermatraemia which invariably
increases the osmotic pressure of the blood. This then stimulates the
Osmoreceptors in hypothalamus. The hypothalamus stimulates the posterior
pituitary to release Antidiuretic hormonetichormone into the blood stream to
promote reabsorption of water from the renal tabulates into the blood stream.
This causes oliguria and hypervolaemiaworsening the hypertention. These are

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seen more where Nephrotic syndrome has become complicated with renal
failure.

PATHOPHYSIOLOGY OF ACUTE NEPHRITIS (Acute Glomerulo-

Nephritis or Bright’s disease)
Acute Glomerulo-nephritis, according to Royal and Walsh (1992) is a
diffuse,uninfectious inflammation of the Glomeruli of both kidneys. The
glomeruli of the nephrons are usually injured by immunological processes.
These immunological processes may involve the trapping of antigen-antibody
complexes (which are formed extra-renally) in the glomeruli and invariably
inflaming the glomeruli, or the antibodies being formed in the glomerular
basement membrane against an antigen initiating the inflammation of the
glomeruli. Most often, the cause is by the Betahaemolyticstreptococci.
Whenever any of the above causes occurs, the glomeruli become
inflamed and partially obstructed by the antigen-antibody complexes. The scar
tissue that usually follows inflammatory process can also obstruct the
glomeruli. This obstruction reduces the glomerular blood flow leading reduced
glomerular filtration, which invariably causes oliguria. The same glomeruli may
even rupture causing the escape of blood into the renal tubules leading to
haematuria. The scanty urine is usually dark, concentrated and smoky in colour
due to the presence of blood in it.
The inflamed glomeruli become more permeable leading to the escape
of plasma proteins into the Bowman’s
capsules which ultimately causes mild Albuminuria, with some grandular
casts in the urine. Albuminuria causes a reduction in plasma proteins leading to
a fall in colloidal osmotic pressure of the blood. The reduction in colloidal
osmotic pressure causes the escape and accumulation of extracellular fluid into
the intercellular spaces leading to oedema. This oedema is first noticed around
the orbital cavities (periorbitaloedema) and around the ankles. In serve cases,
fluid may accumulate in the pleural cavity causing pleural effusion and in the
peritoneal cavity causing Ascites. The pleural effusioncan interfere with normal
gaseous exchange in the lungs causing dyspnoea.
The reduced glomerular blood flow stimulates the juxtaglomerular
Apparatus in the nephrons to release an enzyme called Renin. Renin then
initiates the Renin-angiotensin-Aldosterone system leading to increase in the
blood pressure that is seen in this disease. Since the kidneys are located within
the posterior part of the abdominal cavity behind the peritoneum, the
inflammation of these kidneys causes pain and tenderness in the back.
One of the functions of the kidneys is to excrete the metabolic wastes
like Urea, Uric acid, and creatinineet. In the Urine. Since the glomeruli are now
inflamed and partially obstructed,the reduce glomerular filtration due to this

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obstruction accounts for the retention and an increase in the urea and
creatinine levels in the blood stream. The presence of the Beta
haemolyticstreptococci as causative organisms including their toxins serve as
pyrogensand endogenous pyrogens in the blood stream. The endogenous
pyrogens and endogenous pyrogensreset the thermostat in the heat regulating
centrein the hypothalamus leading to more production of heat causing the
pyrexia.
The onset of increase blood pressure (hypertension) manifests as
headacheand vomiting which may even lead to convulsions (hypertensive
encephalopathy). The body presents a defensive mechanism by producing anti-
streptolysin). O titre to neutralize the toxins produced by the Beta
haemolyticstrecocci. The presence of these organisms in the nasal or throat
swab coupled with an elevation in anti-streptolysins O titre in the blood stream
serve as some diagnostic measures. At the terminal stage when prompt and
adequate medical attention is not sought, the victim may go into renal failure
(uraemia) and heart failure.

PTHOPHYSIOLOGY OF RENAL FAILURE

Renalfailure id the serve interruption of the kidney function leading to
serve renal dysfunction, and which may be acute or chronic. The causes of
Acute Renal Failure may be pre-renal (e.g. inadequate renal perfusion resulting
from conditions leading to decreased renal blood flow); intra-renal (e;g actual
or renal diseases like glumerulo-nephritis etc) and extra-renal (e.g Uretic calculi
or cancer, prostate enlargement etc). The chronic Renal Failure is caused by
progressive decrease of both kidneys which may be any of the causes of acute
renal failure. Renal Failure, according to Royale and Walsh (1992), is caused by
renal tubular necrosis from inadequate blood supply, hypoxia or inflammation
of the glomeruli.
Any of the causes of renal failure will bring about a decrease in glomerlar
filtration leading to a decrease in urine output (oligura), or no urine production
(Anuria) depending on the severity. Oliguria or Anuria causes retention of
sodium and water in blood stream and the body imbalance. The retention of
sodium and water in blood stream and the body tissues causes Oedema and
over hydration and consequently Hypertension, Heart failure and pulmonary
Oedema. The pulmonary Oedema interferes with normal respiration causing
dypnoea.
The retention of potassium leads to hyperkalaemiacausing cardiac
Arrythmias, cardiac arrest and muscular weakness. The retention of hydrogen
ions from metabolism leads to metabolic acidosis which will continue to
stimulate the respiratory centrecausing rapid, deep and noisy respiration ca!
ledkussmaul’srespiration with Acidotic odour of breath.

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 The retention of phosphates in the skin leads to pruritus. Thepresence of
retained urea in the Gastro-intestinal tract breaks down to from Ammonia
which is very irritating to the Gastro-intestinal mucosa causing nausea,
vomiting, hiccough and Haematemesis. The victim presents with Urea frost
([Link] powder) on the sking surfaces due to the deposition of white crystals
of urea on skin surfaces. This is usually first seen around the mouth. The toxic
effect of Urea on the bone marrow leads to diminished platelets formation
called thrombocytopenia causing bleeding tendencies.
The bleeding under the skin give rise to small purpuric spots called
petechiase, while larder ones are Ecchymoses. Prolonged bleeding leads to
Anaemia becomes pronounced since the diseased kidneys can no longer
produce the hormone called Erythropoeietin which assits in erythropoiesis. The
presence of pulmonary Oedema coupled with inability of the victim to cough
out the retained secretion along the respiratory tract due to general weakness
of the body, therefore, make the victim prone to secondary infection like
pneumonia. The retrained metabolic wastes irritate the central Nervous system
causing severe headache, confusion, convulsions, drowsiness, disorientation
and ureamiccoma.

PATHOPHYSIOLOGY OF URETHRAL STRICTURE

Urethral stricture is the narrowing of the urethra thereby preventing
easy outflow of urine from the urinary bladder. The cause of the urethral
stricture may be due to scar tissue formation resulting from urethral infection
([Link] infection) or trauma. The cause may even be due to tumour of
the urethra. The presence of the stricture prevents easy passage of urine from
the urinary bladder throughthe urethra. This leads to urinary retention in the
bladder. Where the stricture is incomplete, there will be frequent passage of
small amount urine which will be painful (dysuria). Dribbling of urine also
occurs. If this stricture is as a result of urethritis caused by the pathogenic
organisms called Neisseriagonorrhoeae, there will be passage of purulent
urethral discharge with some itching and burning sensations around the
urethral meat us. The inflameduretha becomes red and swollen.
The incomplete or incomplete Urethra stricture makes the urine to
accumulate in the urinary bladder causing distended urinary bladder,
accompanied by the sensation of fullness. This also results into distended lower
abdomen with severe pain. Since the retained urine in the bladder contains a
lot of toxic wastes, these can infect the bladder causing cystitis. Where the
victim is not relieved of this stricture on time, the full bladder causes backflow

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of urine through the ureters to the pelves of the kidneyscausing
Hydronephrosis. This invariably leads to pyelonephritis end finally renal failure.
The distended and painful bladder, due to inability to pass urine, makes
the victim anxious, restless and to perspire profusely while making efforts to
maturate. In severe stage, the onset of renal failure, with all its manifestations,
causes retention of metabolicwastes (like urea and other nitrogenous
substance ) in the blood stream resulting into uraemia. This will finally lead to
ureamic coma.

PATHOPHYSIOLOGY OF BENIGN PROSTATIC HYPERTROPHY

The prostate gland is an accessory organ of male reproductive system,
which is located below the urinary bladder and surrounding the
commencement of the [Link] normal circusmstances, the prostate gland
does not hinder the out flow of urine from the urinary bladder through the
urethra. Whenever this gland enlarges as seen in benign prostatic hypertrophy
(otherwise calls benign hyperplasia of the prostate or carcinoma of the
prostate), it will then strangulate the neck of the bladder thereby interfering
with the easy outlet of urine from the bladder into the urethra. This leads to
urinary retention within the bladder. The urinary bladder become infected due
to the retained urine, causing inflammation of the bladder called cystitis.
In most cases, this enlargement is insidious in onset and the victim will
be conscious of an increasing difficulty in urine. Where the obstruction to
urinary outflow is nearly complete, the stream of urine during maturation will
be reduced in force and quantity. This leads to dribbling of urine and frequency
of micturition. In some patients where the acute retention occurs, this leads to
distension with of the lower abdomen with severe pain and distress due to
inability to pass the urine. The enlarged prostate may exert pressure on nerves
causing backpain and scartica.
The urinary retention leads to backflow of urine into the ureters causing
their abnormal distension with urine called hydroureter. This further leads to
distension of the renal pelvis with urine causing
[Link] the atrophy of the kidney
tissue leading to renal failure with all its manifestation.

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NOTE WELL:the increase production of prostatic secretion which
invariability leads to an increase in the blood serum level of Acid phosphatase
isvery suggestive of carcinoma of the prostate.

PATHOPHYSIOLOGY OF HYDROCELE
Hydrocele is a collection of fluid in the tunicavaginalis(sac) surrounding
the testis and epididymis. This surgical condition may occur due to
inflammation, local injury or a neoplasm of the tunica Vaginalis.
More often, the cause is idiopathic. In some babies, the cause of Hydrocele has
been traced to a late closure of the processusvaginalisor vaginal process (i.e
continuation of the peritoneal cavity of the abdomen around the testis in the
scrotum), which may later close spontaneously. The processes vaginalis later
becomes the tunica vaginalisafter the processusvaginalis has been princhedoff
from the peritoneal cavity of the abdomen due to constriction of the inguinal
canal.
Due to the continual incomplete closure of the processusvaginalis, up to
young adult age, there remains a connection therefore between the peritoneal
cavity of the abdomen and the Tunica vaginal. This connection will allow the
serous fluid in the peritoneal cavity to circulate down and accumulate within
the Tunicavaginalis.
The infection or Neoplasm or local injury to the existing processusvaginalis
will inflame this vaginalis causing more secretion of the serous fluid and its
accumulation around the Testis. This leads to the leads to the characteristic
swelling of the scrotum, which will later be very large,unsigh and
uncomfortable. The victim then seeks surgical attention in the hospital, where a
surgical removal of the Tunica vaginalis called hydrocelectromy will be done

PATHOSIOLOGY OF BREAST CANCER

Breast cancer is the growth of malignant tumor in the women’s breasts. The
causes of breast cancer like in any other part of the body are not known. Breast
cancer, affecting the body, begins when any of the special genes called
Oncogenes found in very normal cell are Activated or excited by radiation,
chemicals, viral infection or continual irritation or friction. These Ontogenesis
then produce proteins that transform a normal cell which does not divide in to
cancerous cell that grows out of control.
The cancer cells then spreads by breaking through a barrier called the
basement membrane which surrounds all tissues. The cancer cells then crawl
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into the blood stream or the lymphatic system and carried to distant parts of
the body. They leave the blood stream and lodge in a small capillary and again
burrow through the basement membrane. The moment these cancer cells
settle in new tissues, they start forming a new tumour.
The abnormal growth of cancer cells in the breast leads to Oversized and
shapeless breast which gives the victim a cosmetic disfigurement of the breast,
backache and feeling of fatigue. This makes the victim to become worried. The
presence of cancer brings about lump in the breast which is usually detected on
breast palpation by the victim herself. This lump or breast mass is usually hard
and non painful at first. Initially the lump will be mobile but late becoming fixed
or firm. The hardness and firmness are due to the formation of fibrous capsules
and shrinkage.
When the cancer spreads to the maxillary lymph nodes, it causes the
small nodular swellings in the armpit. This may serve as the first warning, in
addition to the feeling of a lump in the victim’s breast. The infiltration of the
axillary lump nodes also leads to limph oedema of the breasts, causing
lymphatic obstruction in the breast as well as changes in the smooth physical
appearance of the skin. The breast skin become pulled in, giving the
appearance of an orange.
The infiltration and destruction of the lactiferous ducts causes the
retraction of breast nipple. The infiltration of blood vessels in the breast leads
to their destruction and bleeding from the breast nipple. Prolonged bleeding
leads to Anaemia. In advance cases, there can be development of boil which
will later breakdown to become breast ulcer that refuses to heal. The ulcer
later spreads to destroy the entire breast tissue. Other changes that occur
depend on the metastasis of these cancer cells to other organs in the body.

PATHOPHYSIOLOGY OF AIDS
Acquired immune Deficiency Syndrome (AIDS) is a fatal disease of vital origin,
which attacks principally the blood system, rendering the immune (defense)
components powerless against other infections or disease. It is caused by a
virus now called Human immunodeficiency virus (HIV). Whenever the AID s virus
now called HIV-1 enters the human body, it starts selecting cells to attach itself
to. These are the cells with a special receptor known as the CD4 antigen. This
receptor (CD4 antigen) is present on cells in the body’s immune system, the
helper T Lymphocytes and on some macrophages. The cells lining the intestine
(bowel epithelium) and in the brain (microphages cells) also support the
growth of HIV.
The moment the HIV has made contact with CD4 antigen-carrying cells, it
sheds its lipid coat and injects its RNA in to human cells. This single-stranded
RNA then makes a copy of itself with the use of an enzyme called reverse
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transcriptase. This result in double stranded DNA which then inserts itself into
human cell DNA. Since HIV becomes part of the human cell’s genetic material,
infection of the cell is irreversible. Hence AIpomDS becomes an incurable
disease.
The AIDS virus has the ability to remain dormant for months, or even
years but where the human infected by the body’s immune system when
fighting another disease, the HIV then begins to multiply to infect more humans
cells. The HIV DNA Start to instruct the human cell to produceviral component,
such as viral proteins and RNA which are the two main components of HIV. The
viral proteins migrate of the surface of the infected cell, where they stieck out
through its outen the [Link] by a process known as
budding,multitudes of new viruses detach themselves from the infected
host(human) cells, and are taken away into the blood stream to attach to other
cells with CD4 receptors. The increased multiplication of AIDS virus leads to
progressive destruction of infected human cells, thus destroying the body’s
immune system and decreasing its ability to fight secondary infections.
Where the brain tissue is infected by AIDS virus, the multiplication of this
virus in the brain leads to encephalopathy resulting into [Link]
presence of AIDS viruses in the blood stream leads specifically to the
destruction of the whiteblood cells like lumphocytes,neutrophils and
monocytes which act as body soldiers, thereby causing a severe reduction in
the body immunity making the victim more susceptible to secondary infections
or opportunistic infections such as pneumocystis carinii pneumonia(causing
severe cough and chest probems) and kaposi’ssarcroma(cancer on surface of
the skingorin the mouth).
Infection of the intestinal mucosa leads to its destruction resulting into
persistent and frequent (chronic) diarrhea and malabsorption of food
substances causing gradual dehydration with loss of body weight, malaise and
[Link] form of AIDS with extensive stooping is called WET AIDS. The
progressive and severe body weight loss gives AIDS a name called slim Disease.
The presence of HIV in the body sets up infection and inflammation in
the body causing increase basal metabolic rate with more heat production
leading to chronic fever and profuse night sweaing. Infection of the lymph
nodes in the neck,armpit and groin leads to their swelling(lymphadenopathy).
This gives rise to a form of AIDS called DRY AIDS. IT is the untreatable chronic
diarrhea leading to hypovolaemic shock, coupled with Dementia resulting from
encephalopathy that makes the victim go into coma and death.

PATHOPHYSIOLOGY OF POLIOMYLITIS
Poliomyelitis, according to familusi (1983) is an infective disease

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 Caused by an enterovirus known as the poliovirus; while lucas and gilles
(1977) defined it as an acute febrile illness classically resultingin a in
flaccid [Link] pathophysiology of poliomyelitis can be presented in
two ways. The manifestations of the effects of the poliohe
manifestations of the effects of the polio viruses before attacking the
central nervous system are grouped under pre paralytic or non
paralyticstate;while those that manifest during the involvement of the
central nervous system are grouped under paralytic stage.

PARALYTIC STAGE(paralytic poliomyelitis).

Whenever the polioviruses gain entry into the body through the
nasopharynx or the alimentary tract through the ingestion of
contaminated foods and drinks by infected faeces, these viruses then
proliferate in the gastro intestinal tract and lymphoid tissues, before
invading the blood stream and finally the central nervous system.
The presence of polioviruses along the gastro intestinal tract causes the
irritation of the gastric and intestinal mucosa leading to vomiting and
diarrhea respectively. Some victims may experience [Link]
inflammation of the oro pharynx and oral tonsils leads to pharyngitis and
tonsillitis respectively causing the sorethroat,while irritation of the
nasopharynx causes the coryza.

paralytic stage: (paralytic poliomyelitis).

Some of these polioviruses will get absorbed in the Gastro-intestinal tract
into the blood stream and irritate meninges of the brain and the spinal cord.
The irritation of the meninges around the cervical region causes the neck pain
experienced on flexing or stretching the inflamed meninges. This makes the
victim to prefer to hold the neck without flexing on extending it. This causes
the characteristic stiffness of the neck.
Irritation of the meninges around the thoraco-lumbar regions causes the
backache and stiffness of the back. Involvement of the meninges around the
sacral region of the spinal cord brings about inability to straighten the knee
when the hip is flexed. This causes the positive kerning’s sign like in meningitis.
The irritation of the meninges covering the brain causes excessive secretion of
the cerebro-spinal fluid leading to increased intracranial pressure and then
headache.
On reaching the central Nervous system, polioviruses have affinity for the
motor cells in the anterior Horns of the spinal cord, as well as the motor nuclei

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of the brains stem causing serious damages in these areas, which lead to the
characteristic poliomyelitis muscular paralysis.
The involvement of the spinal cord causes the paralysis of the muscles
supplied by the spinal nerve. This types of paralysis is called spinal paralysis.
Infection of the brains stem causes the paralysis of the muscles supplied by the
cranial nerves. This types of paralysis is called Bulbar paralysis.
The infection of the anterior horn cells of the cervical and Lumbo-sacrel
segments of the spinal cord causes the flaccid paralysis of the upper and lower
limbs respectively. There is wasting of the affected muscles, as well as loss of
cutaneous and tendon reflexes. The worst hit muscles in the lower limbs are
the quadriceps femoris, harmstrings, peronei and anterior tibialmuscules.
The involvement of the 3rd, 4th and 5thcervical segment of the spinal cord
causes paralysis of the diaphragm and consequently respiratory paralysis.
Infection of the thoracic portion of the spinal cord leads to paralysis of the
thoracic muscles. Paralysis of thoracic muscles causes respiratory difficulties.
The infection of the Lumbosacral enlargement of the spinal cords causes
urinary retention. Infection of the 9 th, 10th and 11thcranical nerves causes
hoarseness and weakness of the voice, laryngeal stridor and dysphagia leads to
accumulation of saliva around the oropharynx which may incidentally flow into
the Larynx causing respiratoryembarrassment. Involvement of the respiratory
and cardiac centrein the medullaablongata may causes alteration in normal
rates and depth of respiration as well a rise or fall in the blood pressure
respectively.

PATHOPHYSIOLOGY OF MENINGITIS
In normal health, the meninges act as protective coverings preventing
the microorganisms from infecting the Brains and the spinal cord. Whenever
any of the causative organisms (i.g Bacteria) gain entrance into the meninges,
the meninges become inflamed leading to meningitis,. The viral type of
meningitis is usually insidious in onest, while that of bacterial type is more
sudden.
Whenever this infection spreads to the to the ventricles of the brains, the
choroid plexuses within the villi of the ependyma lining the ventricles of the
brains start to secrete more cerebrospinal Fluid (CSF) in an attempt to flush out
the offending organisms and toxins. This leads to increased CSF production and
its circulation within and around the Brains and spinal cords.
The infection of the CSFby pyogenic organisms (e.g staphylococcus,
Meningococcal, streptococcus and influenza) makes the CSF to become

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purulent and cloudy or milky in colouras opposed to its colouless nature. This
cloudiness and increased volume of CSF invariably increases the pressure of
CSF within and around the brains causing increased intracranial pressure and
increased blood pressure. The increase intracranial pressure couple with
continual irritation of brains tissue by microorganisms and their toxins leads to
severe headache and patient beingirritable. Irritation of the vomiting central in
the hypothalamus leads to nausea and vomiting. Prolonged vomiting leads to
dehydration.
Infection of the heat regulating centre in thehypothalamus leads to
continuous pyrexia, resulting into Fits in adults or convulsion in children.
Irritation of the visual centre the neck region of the meaning covering the
spinal cord is irritated or inflame and the neck is flexed forcibly, the victim
experience severe neck pain. Hence he prefers to straighten the neck always
leading to the characteristic neck rigidity (stiffness of the neck). Similar
irritation of the meanings around the sacral segment of the spinal cord brings
about inabilityto straighten the knee when theis flexed. This is the
characteristic positive kerning’s sign of meningitis in which the victim
experiences serve pain when the knee is forcibly straightened, while the hip is
flexed. Hence he prefers to flex the knee.
In another development, the victim will prefer to flex the hip and the
knee to reduce the pain being felt in response to forward flexion of the neck.
This refers to another characteristic sign of meningitis called Brudzinski’s sign.
The flexion of the inflamed meninges in the thoracic and lumbar segments of
the spinal cord causes the severe back pain. In response to the presence of
microorganism s and their Toxins, the Recticulo-endothelial Organs (e.g bone
marrow, spleen, Liver) produce more white blood cells to combat this infection.
This leads to increase Leucocytes count (Leucocytosis) of the CSF. In untreated
cases, the meningitis patient become confused, drowsy and goes into coma,
due to involvement of all vital centers in the brain.

PATHOPHYSIOLOGY OF TETANUS
Tetanus is caused by the exotoxins produced by the bacilli called
clostridium [Link] bacilli gain entrance into a deep and contaminated
wound. The exotoxins produced at the wound site are tetanospasmin and
tetanolysin. These exotoxins poison the motor end-plates at this site causing
the initial local muscular weakness near the site before the generalised body
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spasm. Later the local motor nerves become stimulated by these exotoxins
leading to violent muscular spasm within the neighbourhood of the injury . The
tetanospasmin then gets absorbed by the motor end-plates at the site of
infection and travels along the motor nerves to the central nervous system
([Link] , and and spinal cord ) and the peripheral nerves . The clostridium
tetani remain at the infection ( wound site ) germinating and multiplying in an
anaerobic environment, rather than spreading through the body tissues or
invadind the blood stream . The tetanospasmin leaves the spinal cord through
the anterior horn cell and motor nerves to settle at the neuromuscular
junctions . Released form the nerves endings at these junctions are the
chemical transmitters called acetylcholine and an enzyme called cholinesterase
.Acetylcholine causes muscular contraction , while cholinesterase hydrolyses
acetylcholine into choline and acetic acid these by neutralizing the contractiig
effect of acetylcholine . The presence of tetanospasmin at the neuromuscular
junction suppresses the action of cholinesterase there by promoting the
contracting effect of acetylcholine , causing the characteristic violent muscular
contracting (muscle spasms or muscular rigidity ) seen in titanic patients.

The irritation or stimulation of the motor nerve cells of facial muscles of

mastication ( e.g masseter , temporalis, pterygoid muscles ) by Exotoxins causes
another characteristic sigh called trismus ( i.e lockjaw ). Lockjaw
impairsfeeding . The effect of exotoxins on other facial muscles like Orbicularis
Oculi and levatorpalpebaesuperioris ( muscles surrounding the orbital cavity
and orbicularis Oris( surrounding the mouth ) causes the raising of the
eyebrows and pulling outwards of the corners of the mouth producing a forced
smile called Risussardonicus .
The stimulation or irritation of the motor nerves of the neck muscles
causes the painful stiffness of the neck and the throwing backward of the
head . The irritation of the motor nerves of the posterior muscles of the trunk
(Back) causes the tonic spasm leading to arching of the back called
opisthotonus, while its effect on the laryngeal muscles causes laryngeal spasm
leading to dispnoea and cyanosis .The tetanosin travels through the blood
steam causing haemolysis . The presence of exotoxins in the blood steam
serves as pyrogen and endogenous pyrogen resetting the thermostat in the
regulating centre in the hypothalamus causing more heat production leading to
pyrexia.

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 Any mild stimulus or disturbance in form of external noises , touch,
light,feeding,nursing procedures etc precipitates the generalized painful body
spasms .The paroxysms of body spasm may last of seconds or minutes leading
to death form exhaustion and laryngeal spasm

PATHOPHYSIUOLOGY OF PARAPLEGIA
Paraplegia is the paralysis of the legs or lower half of the body. Paraplegia
occurs as a result of injury to the lumbo-sacral regions of the spinal cord
The nature of this paralysis depends on the section of the motor nerve
pathways that are affected . In a situation where the upper motor neurone is
injured , this brings about flaccid paralysis and absence of reflexes initially
which will be followed later by spastic paralysis .
In case of injured to the lower motor neurone , the reflex Arc will be
interrupted leading to flaccid paralysis and loss sensations. When the spinal
cord is exposed to sudden and severe mechanical injury, there will be sudden
interruption of initiating and regulatory impulses between the higher centre
and the cord below the site of injury. This leads to impairment in the
transmission of impulses to and from the neurons below the injury site. This
causes loss of muscle tone (flaccid paralysis), loss of sensations and absence of
reflexes below the site of injury. Since the Unary bladder and bowel are
supplied by branches from the spinal cord, and in as much as the spinal cord
reflexes to these organs are suppressed, micturiction and defecation become
suppressed leading to unary retention with overflow and constipation
respectively. The retention of urine in the bladder can predispose the patient to
infections leading to diseases like cystitis, pyelonephritis and renal failure.
The loss of bladder muscles tone usually remains for some time before
Hyper-reflexia occurs in which the bladder becomes hypertonic leading to
frequent unary incontinence. It is this incontinence that will discourage the
patient from having adequate intake of fluid with the hope that it will reduce
the frequency of micturition. This later predisposes the patient to unary tract
infection and renal calculi formation.
The suppression of reflexes to the Gastro-intestinal tract causes the
atomicity (weakness) of the involuntary muscles along this tract leading to
paralytic illus. The weakness of the large intestine especially the pelvic colon
and rectum causes the suppression of defecation leading to constipation.

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Constipation is further aggravated by patient’s immobility due to paraplegia.
Where this situation is not reduced, prolonged constipation can lead to fecal
impaction and abdominal distension.
Renal calculi may develop due to calcium moving out of immobilized
bones. This is the essence of restricting calcium intake by this type of patient,
but encouraging the intake of grape and apple by this type of acid urine that
reduces the precipitation of calcium and formation of renal calculi. The acid
urine will also inhibit the growth of microorganisms and thereby preventing
unary tract infection. The movement of calcium from immobilized bones can
lead to softening of the bones called Osteoporosis.
Paraplegic patient is very prone to Decubitus ulcer (pressure sore) due to
changes in vasomotor tone, impairment of tissue perfusion, unavoidable
immobility and the loss of cutaneous sensations which will all serve as
contributory factors to tissue break down (pressure sore). All these factors are
assisted by continual pressure, moisture or friction that may exist between the
patient bony prominent areas and the bedlinens due to prolonged immobility.
With reference to injury to the upper motor neurone, paraplegia is
usually accompanied by physical discomfort as a result of pains radiating along
the spinalnerves that originate at the level of injury. This physical discomfort is
usually aggravated by the spasticity of the muscle caused by injury to upper
motor neurone. The continual spasticity may lead to contractures and
deformities of the legs. The paralyzed muscles can become atrophied due to
lack of nerve impulses to the affected muscles.
Thrombophlebitis may occur due to stagnation of blood on lower
extremities caused by poor venous return. Poor venous return obviously is as a
result of prolonged immobility and lack of pumping or milking action of
paralyzed skeletal muscles. Thrombophlebitis is characterized by local Oedema,
redness, warmth, tenderness and red streaks of the lower extremities. There
can be insomnia due to prolonged anxiety, unavoidable immobility,
dependency and necessary frequent re-positioning to prevent development of
bedsore. Infertility may also be experienced due to testicular atrophy,
decreased production of sperm and infrequency of ejaculation as a result of
suppression of nerve impulses to the reproductive organs due to spinal injury.
There may be traumatic psychological feelings of anger, grief, resentment,
frustration and depression due to paraplegia.

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 PSYCHOPATHOLOGY OF SCHIZOPHRENIA
(SCHIZOPHRENIC DISORDERS)
This is major psychiatric disturbance that includes a wide range of
severely disordered behaviors. This disorder involves disorganization of a
previous level of functioning like language and communication, content of
thought, perception, affect, sense of self, volition, relationship with the
external wold and motor behavior. C.T scans, according to Goldman (1988)
have indicated presence of enlarged lateral ventricle and atrophy of the frontal
cortex in victims with chronic schizophrenia. There is also decreased utilization
of prefrontal cordial areas. It has also been shown by the magnetic resonance
imaging studies that the frontal lobes of schizophrenic patients are smaller
than normal, thereby hindering the normal functional capacities of the centres
within this portion of the cerebral cortex. The frontal lobe controls voluntary
muscle movements, speech, behavior, character, emotional states and
intelligence.
The disorder of the Broca’s or motor speech area leads to disturbance in
language communication in from of circumstantialities (i.e irrelevant detours in
speech, so that the conversion fails to reach the anticipated goal). There is
complete incoherence of speech called word salad with a mixture of words
lacking meaning and logical coherence. The voice may be monotonous while
the face will be immobile.
The disorder and possible smallness of the frontal lobe of the cerebral
cortex leads to disturbances in content of thought causing incorrect conclusion
like delusion of grandiose, persecutory delusion and somatic delusion (i.e.
something is rotting inside his or her body). There are disturbance in
perception such as auditory, visual, tactile and olfactory hallucinations. Victim
can shift from tears to joy for no obvious reason. The disorder and smallness of
frontal lobe makes the victim function poorly in significant areas of routine
daily living, such as work and social relations. There is lack of concern for sell
care. There is sense of being different and separate from others leading to
intense loneliness.
The disturbance in the motor behavioral aspect of the frontal lobe causes
decrease reaction to the environment to almost total reduction of movement
and activity. There is catatonic stupor in which the victim acts like a Zombie. A
timeshe or her becomes wildly aggressive and difficult to control.

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 Recent studies using position emission tomography have proved that the
number of dopamine receptors in the Basal Ganglia of patients with chronic
schizophrenia is markedly elevated, according to Goldman(1988),thus causing a
reduction in the amount of a neurochemical transmitter called Dopamine in the
brain. Since Dopamine helps to relax skeletal muscles while an opposing
transmitter called Acetylcholine helps to contract the skeletal muscles, decease
Dopamine therefore enables acetylcholine to exert a greater effect bringing
about muscular spasm of extrinsic eye muscles portrayed in schizophrenic
patient in from of eye movements seen especially when the eyes tract a
moving object

PSYCHOPATHOLOGY OF DEPRESSION
According to Goldman (1988), Depression is a psychomotor retardation
in which the victims present with extensive paranoid or nihilistic delusion and
hallucinations. There are suggestions that a catecholamine neuro-transmitter
called Dopamine which is closely related to Adrenaline and noradrenaline is
functionally decreased in some cases of major Depression, thereby causing a
general feeling of malaise with loss of energy.
More recently, it has been hypothesized that Depression is associated
with cholinergic dominance. Since cholinergic applies to parasympathetic
nerves, and in as much as parasympathetic stimulation has a tendency to slow
down body processes except the digestion and absorption of food cholinergic
dominance therefore can account for slowing down of body processes in
depressed victims. This not withstanding, there have been reports that
Monoamine Oxidase (MAO) and catecho-O-methyltransferase(COMT), the
enzymes important in monoamine metabolism are lower in depressed patients.
Physiologically speaking, the monoamine Oxidase is an enzyme which inhibits
or prevents the breakdown of serotonin and catecholamine’s in the brain. A
reduced amount of monoamine oxidase therefore will lead to more breaking
down of serotonin and catecholamine. Since serotonin stimulates proper
functioning of smooth muscles, while catecholamines (i.e Adrenaline,
Noradrenalin and isoprenaline) are for biochemical transmission of nerve
impulses particularlyin sympathetic system playing an important role in mood
regulation, the excessive breakdown of serotonin and catecholamine due to
reduced monoamine oxidase therefore will lead to mood disturbances.

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 The mood disturbances include despair, pessimism, sadness, apathy
tearfulness, walking about weeping and wringing; hands, smiles are rare, there
is poor concentration due to preoccupation; there is feeling of too wretched to
pay attention to what goes on and there is slowness in thought; thinking and
talking about suicide;and poor stimulation of smooth muscles causing
impotence, frigidity and loss of libido.
The depression of thefrontal lobe of the cerebral cortex concerned with
reasoning, intelligence, memory and sense of responsibility leads to indecision,
irritability, self doubt, while depression of the hypothalamus containing the
sleep centre causes sleep disturbance in form of early waking and lying awake.

PSYCHOPATHOLOGY OF EPILEPSY
Epilepsy is a chronic disorder characterized by recurring manifestation of
abnormal, rapid and uncontrolled neuronal electrical discharges within the
brain, characterized by sensory motor and autonomic disturbances and
changes in the level of consciousness. There is abnormal conversion of the
potential energy (position) of the neurons into kinetic energy (of
motion).Greater attention has been paid to Gamma Amino Butyric Acid (GABA)
and Acetylcholine having opposite effects upon the brain excitability, so that an
imbalance between these two substance within the brain could be one factor
predisposing to seizure production. The balance between acetylcholine
(excitatory) and GABA (inhibitory) may be upset for instance by pyridoxine
deficiency as the latter substance is essential for the synthesis of GABA. The
more the release of Acetylcholine in the presence of reduced or lack of GABA
leads to overstimulation of the muscles causing spasms or seizures.
The manifestation of Epilepsy depend on the areas or vital centres of the
brain that are affected. The cerebral cortex lesions disorder leads to sudden
cessation of activity, momentary absence of consciousness and starring blankly
into space seen in petit mal Epilepsy.A times the petit mal episodes are
unnoticed by the victim, while attention and learning are negatively affected
due to disorders of the frontal lobe and Temporal lobe of the brain.
Occasionally in petit mal, the victim may present a few involuntary movements
and failing down due to disorder either in the posterior lobe of the cerebellum
or Temporal lobe and even a characteristic of a chorea disorder in Basal
Ganglia. The rolling of the eyes upwards in petit mal may be due to injury to
flocculonodularlobe of the cerebellum.

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 In Grand (major) Mal Epilepsy, the victim used to experience irritability,
tension and headache before the episode due to disorders affecting the
Thalamic and cortical areasof the Brain. In the Aura stage of Grand mal
Epilepsy, a lesion or disorder in the thalamic portion can lead to numbness or
tingling sensations in an area of the body, since all of the sensory impulse in the
thalamus before being relayed on to the cerebral cortex. The victim in the Aura
stage can go into sudden loss of consciousness at all levels.
In the tonic phase of Grand mal epilepsy, the victim may fall down due to
a lesion or disorder affecting the flocculondular lobe of the cerebellum. There
can also be tonic spasm of the muscles causing rigidity of the body due to
either Basal Ganglia orcerebellar disorder, since these are the areas in the brain
that are concerned with body balancing and normal muscles tone. There is
involuntary cry due to sudden contraction of thoracic and muscles forcing air
through the spastic glottis. There can also be temporary cessation of
respiration leading to cyanosis where the disorder affects the respiratory
centre in the medulla oblongata. The jaws are fixed with the hands clenched
due to Basal ganglia and cerebella lesions causing strong contraction of
massetermuscle on the lateral parts of the face and muscles of the hands
respectively. The eyes may be widely open with the pupils dilated due to
lesions affecting the visceral efferent fibres in the cerebral cortex, which are
concerned with adjustment of the size of the eye pupils.
In the clonic phase of Grand mal epilepsy, there are irregular jerky
movement which are characteristicof cerebellar disorder or chorea disorder in
Basal Ganglia. At this stage, the respiration is re-established but stertorous
possibly due to respiration centre in the medulla oblongata being able to regain
its respiratory functions. The victim blows out frothy saliva which can not be
swallowed due to spasm of the muscles of the face like masseter muscle on the
salivary glands and the excessive functioning of the tongue, lips and oral
mucosa due to spasm of the masseter musclecausing locking of the Jaws.
Unary incontinence is common in clonicphase as a result of cerebral
cortex disorder, since all activities of the body including the process of urine
formation and micturition which are regulated though the visceral efferent or
autonomic nerves are influenced by impulses from the cerebral cortex. The
faecal incontinence rarely occurs which may be due to the reason advanced for
unary incontinence above.

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 The victim later goes into deep sleep for several hours due to a disorder
effecting the sleep centre in the anterior hypothalamus. He or she wakes up
with no memory of seizure based on disorder of the frontal lobe of the cerebral
cortex that is concerned with memory, intelligence and reasoning. The victim
may be confused on regaining consciousness where the cerebral cortex has not
yet regained its full normal functioning. Some victims may be aggressive or
violent where the disorder affect the Limbic system of cerebrum, which plays a
considerable part in emotional life that has effect on human behavior.
THE ENDOCRINE SYSTEM
PATHOPHYSIOLOGY OF SIMPLE OR ENDEMIC GOITRE
Goitre is an enlargement of the thyroid Gland. Goitre can be simple or
toxic. The simple goitre, according to Roper (1978) is an enlargement of the
goitre in which the patient does not show any signs of excessive thyroid
activity. In a normal situation, the ingested iodine in the food is taken up by the
thyroid Gland to manufacture its hormones called thyroxin and
triiodothyronine. These hormones are used for normal mental and physical
development and control of basal metabolic rate in the body.
The deficient of iodine in the diet or the blood stream causes deficient
production of thyroxineand Triiodothyronineby the Thyroidgland. The
deficiency of these hormones in the blood stream stimulates the anterior Lobe
of the pituitary Gland to produce its hormones called Thyroid stimulating
Hormones (TSH). The increase production of TSH is to stimulate the Thyroid
gland to produce adequate Thyroid hormone. The effect of this Thyroid gland
Stimulation leads to the increase in the number and size of the follicles in the
Thyroid Gland, as well as the accumulation of viscid fluid called colloid within
this gland. All these leads to the enlargement of the Thyroid Gland called
simple goitre.
The prolonged iodine deficiency and excessive stimulation of the Thyroid
Gland by the TSH lead to the development of nodules containing grossly
distended follicles. The initial effect of the Goitre is the cosmetic disfigurement
it poses on the victim, giving such a victim a lot of embarrassment. It can also
causes compression and displacement of larynx, Trachea and the oesophagus.
The comprssion of the Larynx and Trachea give rise to manifestation of
respiratoryobstruction like cough,dyspnoea, stridor, cyanosis and restlessness.
There is cough probably due to the accumulation of mucus above the
obstruction there by initiating the cough reflex to expel [Link] due
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to interference with the free flow of air within the lower respiratory tract by
the obstruction. Dyspnoea leads to cyanosis since enough oxygen can not each
the alveoli of the Lungs for gaseous [Link] carbon dioxide then
accumulates in the alveoli and the blood stream, since it can not be freely
expelled through the obstruction.
The forceful passage of air through the obstruction causes the harsh breathing
sound called stridor. The victim becomes restless because of the choking being
experienced as a result of the respiratory obstruction. The compression of the
Esophagus leads to Dysphagia, while a compression of the recurrent Laryngeals
nerves may leads to hoarseness of the voice.

PATHOPHYSIOLGY OF THYROTOXICOSIS
Thyrotoxicosis, according to Royle and walsh(1992) may be called
Hyperthyroidism or toxic goitre or exophthalmic goitre or Grave’s disease. It is
worthy of note, however that it is Hyperthyroidismassociates with
Exophthalmos that is called exophthalmic goitre or Grave’s disease .
Thyrotoxicosis is a condition in which there is over production of the
Thyroid Hormone called Tyroxine, as a result of excessive stimulation of the
Thyroid gland by over production of the Thyroid stimulating Hormone from the
Anterior Lobe of the pituitary Gland. The excess of the Thyroxine in the blood
stream causes increase in the Basal Metabolic Rate in the body increase in the
Basal Metabolic Rate requires more oxygen to oxidize glucose to supply the
needed energy by the body tissue. Since the blood helps to.

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