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ADVANCED MEDICAL SCIENCE
1. Define Anorexia. What can it be caused by?
2. What are the 3 major mechanisms by which diarrhoea
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can be characterised?
Briefly outline the pathophysiology of jaundice.
Outline the pathophysiology of cirrhosis.
How does colorectal cancer develop?
Outline the pathophysiologic changes that can occur
with colorectal cancer.
Draw and explain the bowel changes that unfold with
Crohn’s disease.
How is non-viral hepatitis different from viral hepatitis.
Outline the pathophysiology of Irritable bowel
syndrome.
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10. Distinguish between hyperplasia and hypertrophy.
11. List the characteristics of cancerous tissue which differentiate it from
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normal tissue.
Identify 1 cause and 1 pathophysiologic change for the genetic
disorder, Haemophilia.
Differentiate between autosomal disorders and Sex-linked disorders.
Provide 1 example for each pathophysiologic concept.
Define the term intracellular accumulations and outline how each
category differs.
Identify two outcomes of cell injury and outline their differences.
Describe in detail the differences between a benign neoplasm and a
malignant neoplasm.
Outline the condition ALL and identify which chromosomal disorder
it is most likely to develop in.
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Characterised by bulging pouches (diverticula) in GI wall that
pushes mucosal lining through surrounding muscle.
Classified by two clinical forms:
Diverticulosis (diverticula are present but do not cause symptoms)
Diverticulitis (diverticula are inflamed; may cause potentially fatal
obstruction, infection or haemorrhage)
Pathophysiology: Diverticula probably result from high
intraluminal pressure on an area of weakness in the GI wall, where
blood vessels enter. In diverticulitis, retained undigested food and
bacteria accumulate in the diverticular sac. This hard mass cuts off
the blood supply to the thin walls of the sac, making them more
susceptible to attack by colonic bacteria. Inflammation follows and
may lead to perforation, abscess, peritonitis, obstruction or
haemorrhage.
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4. Causes:
- Diminished colonic motility and increased intraluminal pressure.
- Low-fibre diet
- Defects in colon wall strengthen.
5. Pathophysiologic changes:
- Inflammation of the diverticula
- Trapping of bacteria-rich stool in diverticula: Often accompanied by
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low-grade fever.
Rupture of diverticula and subsequent inflammation and infection.
Sepsis
Rupture of diverticula near vessel: Microscopic or massive
haemorrhage.
Intestinal obstruction.
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Backflow of gastric or duodenal contents (or both) into oesophagus
and past lower oesophageal sphincter (LES), without associated
belching or vomiting.
2. Reflux of gastric contents causes acute epigastric pain, usually after
meals.
3. Pathophysiology: Hormonal fluctuations, mechanical stress, and the
effects of certain foods and drugs can decrease LES pressure. When
LES pressure falls and intra-abdominal or intragastric pressure rises,
the normally contracted LES relaxes inappropriately and allows
reflux of gastric acid or bile secretions into the lower oesophagus.
There, the reflux irritates and inflames the oesophageal mucosa,
causing pyrosis. Persistent inflammation can cause LES pressure to
decrease further, possibly triggering a recurrent cycle of reflux and
pyrosis.
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4. Causes:
- Weakened oesophageal sphincter
- Increased abdominal pressure
- Hiatal hernia
- Medications
- Food, alcohol or cigarettes
- Nasogastric intubation for more than 4 days
5. Pathophysiologic changes:
- Increased abdominal pressure and oesophageal
irritation.
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Addison's disease, also called adrenal hypofunction or adrenal
insufficiency, occurs in two forms: primary and secondary. It is
a relatively uncommon disorder that occurs in people of all
ages and in both sexes. Either primary or secondary Addison’s
disease can progress to adrenal crisis.
2. The primary form of Addison’s disease originates within the
adrenal glands. It is characterised by decreased
mineralocorticoid, glucocorticoid, and androgen secretion.
The secondary form of Addison’s disease is caused by a
disorder outside the gland, such as a pituitary tumour with
corticotrophin deficiency. In secondary forms of the disorder,
aldosterone secretion may be affected.
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Pathophysiology: In primary Addison’s disease, more than 90
percent of both adrenal glands are destroyed. Massive destruction
usually results from an autoimmune process whereby circulating
antibodies attack adrenal tissue. Destruction of the gland may also
be idiopathic. Other causes of primary Addison’s disease include:
Tuberculosis
Removal of both adrenal glands
Haemorrhage into the adrenal gland
Neoplasms
Infections, such as HIV, histoplasmosis, meningococcal pneumonia,
and cytomegalovirus.
In rare cases, a familial tendency.
Pathophysiology: Secondary Addison’s disease may result from:
Hypopituitarism
Removal of a non-endocrine corticotrophin-secreting tumour
Disorders of hypothalamic-pituitary function that diminish the
production of corticotrophin.
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Cushing's syndrome is a cluster of physical abnormalities caused
when the adrenal glands secrete excess glucocorticoids. It may also be
caused by excessive androgen secretion. When glucocorticoid excess
is due to pituitary-dependent conditions, its is called Cushing’s
syndrome.
Pathophysiology: Cushing’s syndrome appears in 3 forms:
Primary: caused by a disease of the adrenal cortex.
Secondary: caused by hyperfunction of corticotrophin-secreting cells
of the anterior pituitary gland.
Tertiary: caused by hypothalamic dysfunction or injury.
In about 70 percent of patients, Cushing’s syndrome results from an
excess of corticotrophin. This leads to hyperplasia of the adrenal
cortex. Corticotrophin overproduction may stem from:
Pituitary hypersecretion
A corticotrophin producing tumour in another organ
Administration of synthetic glucocorticoids
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4. Complications associated with Cushing’s syndrome are caused by the
effects of cortisol, the principal glucocorticoid. These complications
may include:
- Osteoporosis and pathologic fractures
- Peptic ulcer
- Lipdosis
- Impaired glucose tolerance
5. Frequent infections or slow wound healing due to decreased
lymphocyte production and suppressed antibody formation may
occur. Suppressed inflammatory response may mask infection.
6. Hypertension due to sodium and water retention is common in
Cushing's syndrome. It may lead to ischemic heart disease and heart
failure.
7. Menstrual disturbances and sexual dysfunction also occur because of
increased adrenal androgen secretion. Decreased ability to handle
stress may result in psychiatric problems ranging from mood swings
to psychosis.
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Diabetes insipidus is a disorder of water metabolism caused by a deficiency
of ADH. The absence of ADH allows filtered water to be excreted in the
urine instead of reabsorbed. The disease causes excessive urination and
excessive thirst and fluid intake. It may first appear in childhood or early
adulthood and is more common in men than in women.
Pathophysiology: Some drugs as well as injury to the posterior pituitary
gland can cause abnormalities in ADH secretion. A less common cause is a
failure of the kidneys to respond to ADH. Lesions of the hypothalamus,
infundibular stem, and posterior pituitary gland can also interfere with
ADH synthesis, transport or release. Lesions may be caused by brain
tumour, removal of the pituitary gland, aneurysm, thrombus,
immunologic disorder or infection.
Normally ADH is synthesised in the hypothalamus and then stored in the
PPG. Once it is released into the general circulation, ADH increases the
water permeability of the distal and collecting tubules of the kidneys,
causing water reabsorption.
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4. What to look for:
- Abrupt onset of extreme polyuria (usually 4 to 16L/day of dilute
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urine, but sometimes as much as 30 L/day.
Polydipsia and consumption of extraordinarily large volumes of fluid.
In severe cases, fatigue occurs because sleep is interrupted by the
need to void and drink fluids. Children often have enuresis, sleep
disturbances, irritability, anorexia, and decreased weight gain and
linear growth.
Weight loss
Dizziness
Weakness
Constipation
Increased serum sodium and osmolality
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Diabetes mellitus is a disease in which the body does not produce or
properly use insulin, leading to hyperglycaemia.
The disease occurs in two primary forms:
Type 1
Type 2
Several secondary forms also exist, caused by conditions such as
pancreatic disease, pregnancy, hormonal or genetic problems, and
certain drugs or chemicals.
Pathophysiology:
In Type I diabetes, the beta cells in the pancreas are destroyed or
suppressed. Type I diabetes is subdivided into idiopathic and
immune-mediated types.
A local or organ specific deficit may induce an autoimmune attack on
beta cells. This attack, in turn, causes an inflammatory response in
the pancreas called insulitis. By the time the disease becomes
apparent, 80 percent of the beta cells are disabled.
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5. With the idiopathic form, patients have a permanent insulin
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deficiency and are prone to ketoacidosis. However, there is no
evidence of autoimmunity.
Type 2 diabetes may be caused by the following:
Resistance to insulin action in target tissues
Abnormal insulin secretion
Inappropriate hepatic gluconeogenesis (overproduction of glucose)
Type 2 diabetes may also develop as a consequence of obesity and a
sedentary lifestyle. The pancreas produces some insulin, but it is
either too little or ineffective. The following factors contribute to its
development:
Impaired insulin secretion
Inappropriate hepatic glucose production
Peripheral insulin receptor insensitivity
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7. Pathophysiologic Changes:
- High serum osmolality caused by high serum glucose levels: polyuria,
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polydipsia.
Depleted cellular storage of CHO, Protein and Fat (polyphagia).
Prevention of normal metabolism of CHO, Fat and Protein caused by
impaired or absent insulin function.
Low intracellular glucose levels: Headache, fatigue, lethargy, reduced
energy levels.
Electrolyte imbalances: muscle cramps, irritability, and emotional
lability.
Glucose induced swelling: Vision changes (blurring).
Neural tissue damage: numbness and tingling.
Hyperglycaemia: Slowly healing skin infections or wounds; skin
itching.
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A goitre is an enlargement of the thyroid gland. It is not caused by
inflammation or neoplasm and not initially associated with
hyperthyroidism or hypothyroidism. This condition is commonly
referred to as non-toxic goitre. It is classified in two ways:
endemic, caused by a lack of iodine in the diet.
Sporadic, related to ingestion of certain drugs or food and occurring
randomly.
Non-toxic goitre is most common in females, especially during
adolescence, pregnancy, and menopause. At these times, the
demand for thyroid hormone increases.
Toxic goitre arises from long-standing non-toxic goitre and occurs in
the elderly. The enlarged thyroid gland develops small rounded
masses and secretes excess thyroid hormone.
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4. Pathophysiology: Non-toxic goitre occurs when the thyroid gland
cannot secrete enough thyroid hormone to meet metabolic needs.
As a result, the thyroid mass increases to compensate. This usually
overcomes mild to moderate hormonal impairment.
5. TSH levels in non-toxic goitre are generally normal. Enlargement of
the gland probably results from impaired hormone production in
the thyroid and depleted iodine, which increases the thyroid gland’s
reaction to TSH.
6. Endemic goitre usually results from inadequate dietary intake of
iodine, which leads to inadequate synthesis of thyroid hormone. In
Japan, goitre resulting from iodine excess from excessive ingestion
of seaweed has been found.
7. Sporadic goitre commonly results from ingestion of large amounts
of goitrogenic foods or use of goitrogenic drugs.
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When thyroid hormone is overproduced, it creates a metabolic
imbalance called hyperthyroidism. Excess thyroid hormone can
cause various thyroid disorders; Grave’s disease is the most
common.
2. Pathophysiology: In Grave’s disease, thyroid stimulating antibodies
bind to and stimulate the TSH receptors of the thyroid gland. The
trigger for this autoimmune response is unclear, it may have several
causes. Genetic factors may play a part; the disease tends to occur in
identical twins. Immunologic factors may also be the culprit; the
disease occasionally coexists with other autoimmune endocrine
abnormalities, such as Type I diabetes mellitus, thyroiditis and
hyperparathyroidism.
- Grave’s disease is also associated with the production of several
autoantibodies formed because of a defect in suppressor T
lymphocyte function.
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3. What to look
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for:
An enlarged thyroid
Exophthalmos
Nervousness
Heat intolerance
Weight loss, despite increased appetite
Excessive sweating
Diarrhoea
Tremors
palpitations
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In thyroid hormone deficiency in adults, metabolic processes slow
down. This is due to a deficit in T3 and T4, which regulate
metabolism. The disorder is most prevalent in woman and people
with Down Syndrome.
Hypothyroidism is classified as primary or secondary. The primary
form stems from a disorder of the thyroid gland itself. The secondary
form stems from a failure to stimulate normal thyroid function.
Pathophysiology: Primary hypothyroidism has several possible
causes:
Thyroidectomy
Inflammation from radiation therapy
Amyloidosis and Sarcoidosis
Hashimoto’s thyroiditis
Secondary hypothyroidism is caused by a failure to stimulate normal
thyroid function.
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4. What to look for:
- Energy loss
- Fatigue
- Forgetfulness
- Sensitivity to cold
- Unexplained weight gain
- Constipation
- As the disease progresses: anorexia, decreased libido, menorrhagia,
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paraesthesia, joint stiffness, muscle cramping.
CNS
Integumentary System
Cardiovascular System
GI Symptoms
Reproductive System
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