ALHT106 Lecture Notes - Lecture 6: Benign Prostatic Hyperplasia, Ischemia, Metaplasia
Pathophysiology introduction:
Pathophysiology- physiology of altered health; study of structural and functional changes in the
body that occur with disease, and causes, manifestations and progression of the disease
Pathology- study of structural changes in cells, tissues and organs
Physiology- study of human body function
Also focuses on mechanisms that underlie the disease which can provide background for
treatment
Disease- the interruption, cessation, or disorder of a body system or organ structure
Disease process:
-Aetiology (causes)
-Risk factors (inherited, environment and lifestyle
-Pathogenesis (progression/development of disease)
-Morphologic changes (structural- functional changes)
-Clinical manifestations (signs and symptoms)
-Diagnosis (based on aetiology, morphological changes and clinical manifestations)
-Clinical course (treatment program)
Aetiology:
-Disease-causing agents can cause disease to a single organ or a number of organs or systems
-Most diseases are multifactorial:
-disease without a single cause
-Risk factors: multiple factors that predispose individuals to increased chance of disease
development
Aetiological agents:
-Chemical stimuli: e.g poisons, alcohol, acids, alkaline substances, pollution, smoking, some
foods, carbon monoxide, insecticides, trace metals e.g. lead or mercury
-Can injure cell membrane or other cell structures, block enzymes, coagulate proteins, disrupt
osmosis and ionic balance
-Physical stimuli: e.g. trauma, burns, radiation, electricity, extremes of temperature
-Radiation creates heat- thermal burns; DNA mutations; interrupts replications; kills cells
-Extreme cold disrupts cell membranes; stops enzyme action; causes vasoconstriction; increases
blood viscosity. Extreme heat may- burns and coagulation of proteins in tissues and blood
vessels
-Nutritional stimuli: e.g. lack of vitamin D- loss of bone mass and Rickets. Osteopaenia or
Osteoporosis; lack of B vitamins reduces mitochondrial ATP production; lack of vitamin K-
haemostats problems (insufficient production of 4 clotting factors by liver cells)
-Infectious stimuli: infectious microorganisms e.g. viruses, bacteria
-Genetic stimuli: e.g. inheritance of a mutated/disease allele- defective protein formed or
insufficient/excess amount of protein formed
-Increasing age- reduction in body system function- risk factor for many (all?) diseases
-Intracellular accumulations: e/g/ interfere with normal cell function; cause toxicity effects
Congenital vs Acquired disease:
-The causes of disease may be congenital or acquired
-Congenital: defects present at birth:
-causes include genetic factors and/or environment (viral, maternal drug use/alcohol use/
smoking, irradiation or intrauterine crowding)
-Acquired: caused by an event that occurs at birth:
-Injury, exposure, insufficient nutrition, hypoxia, ischaemia, immune response, neoplasia
Internal or external disease:
-Disease can arise from within the body or be due to an outside agent
-Internally e.g. genetic or metabolic agents (e.g. hyperlipidaemia, excess cortisol secretion);
hypoxia and ischaemia
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-Externally: e.g. via UV exposure, physical impact and cancerous agents
-If aetiology cannot be determined, it is referred to as an idiopathic disease
-If disease results directly from medical treatment, it is an iatrogenic condition e.g. heart disease
arising from medication prescribed
Clinical manifestations:
-Signs: observable or measurable conditions in the body arising from the disease e.g. rash, fever,
vomiting, fracture, diaphoresis, microscope analysis of cell/ tissue changes
-Symptoms: subjective experiences of the person e.g. pain (headache, nausea, feeling faint)
Pathogenesis and morphology:
-Pathogenesis: sequence of cell and tissue events/changes that take place from time of initial
contact wiht an astrological agent until ultimate expression of the disease
-i.e. how the disease process evolves
-Morphology: fundamental structure or form of cells or tissue
-Gross anatomical
-Microscopic
-Lesion is discontinuity of a body organ or tissue
Definitions:
Hypoxic: insufficient oxygen supply to cells/tissues
Ischameia: insufficient blood flow to cells/tissues
Necrosis: death of cells/tissues (often from hypoxia, ischaemia, presence of microorganisms or
toxins)
Hypoxia and ischaemia- cell injury or death (necrosis) if not corrected
Cell injury:
-When confronted with stress, cells may undergo adaptive changes to survive
-When stress is overwhelming or adaption ineffective the cell can be injured or die
-If stressor removed in time, adapted cell can revert back to normal
Stress on cells:
-Cells continually exposed to changing and potentially damaging conditions: need to adapt to
these changes in the internal environment to maintain homeostasis
-Cells adapt to increased work demands by changing in:
-Size (atrophy and hypertrophy)
-Number (hyperplasia)
-Form (metaplasia)
Intracellular accumulations:
-Normal body substances in excess: lipids, proteins, carbohydrates, melanin etc.
-Abnormal endogenous products: abnormal synthesis; toxins from pathogens
-Exogenous products: environmental agents e.g. silica and pigments not broke. down by the cell;
mainly stored in lysosomes or accumulate in nucleus
Cell adaptions:
Atrophy: decrease in cell size
Hypertrophy: increase in cell size
Hyperplasia: increase in number of cells
Metaplasia: replacement of adult cells
Dysplasia: deranged cell growth of a specific tissue
Atrophy:
Shrinkage of cell size due to inactivity/decreased workload
Examples: broken limb in a cast- atrophy of muscles from lack of use while the cast is on; or
astronauts in space (unless they do resistance-type exercises)
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Hypertrophy:
-Hypertrophy: increase in cell size from increased workload
-Examples are enlargement of uterus during pregnancy, increased exercise or workload on the
heart- left ventricle hypertrophy (largest workload demands on LV)
-Pathological example is undiagnosed hypertension
Hyperplasia:
-Hyperplasia: increase in cell number in tissue capable of mitotic division (not including cancer)
-Controlled process in response to stimuli:
-Hormonal e.g. changes during pregnancy, excessive hormonal stimulation or effects of growth
factors
-Compensatory e.g. liver regrowth after surgery
-Examples: benign prostatic hyperplasia; adrenocortical hyperplasia- cushion’s syndrome
Metaplasia:
-Reversible change in which one cell is replaced by another
-Usually in response to chronic irritation or inflammation
-Cells cannot change their primary tissue type
-Example: with long-term exposure to cigarette smoke or other airway irritation, ciliated, columnar
epithelial cells in airways change to stratified, squamous epithelium (Multiple layers provide
more protection)
Dysplasia:
-Deranged cell growth of a specific tissue that results inc ells that vary in size, shape and
organisation
-Can be associated with chronic irritation or inflammation
-Possible precursor for cancer
-Can revert back to normal tissue
Inflammatory disorders:
-Normal inflammation (Acute) first stage of healing and productive body response; abnormalities
during inflammation and healing include excess fibrinous exudate- adhesions or excess scar
tissue formation (hypertrophic or keloid)
-Prolonged/chronic inflammation (2+ weeks) causes ongoing destruction of health cells/tissues
-Allergic/hypersensitive responses can trigger ongoing inflammation via repeated exposure to a
trigger- release of histamine from mast cells; re-exposure causes the allergen to bind to IgE that
are now on mast cell membranes- degranulation; histamine triggers the inflammatory response
-Autoimmune disorders also create a chronic inflammatory response in certain tissues-d
destruction of the tissue and loss of function
-Examples include synovial membrane and articular cartilage destroyed in rheumatoid arthritis,
and insulin-producing cells of the pancreas destroyed in type I DM
Healing disorders:
-Include poor or delayed healing, insufficient collagen formation, excess scar tissue formation,
adhesions, insufficient leucocytes
-Can arise from hypoxia, ischaemia, wound contamination by debris, foreign bodies or pathogens
-Poor quality connective tissue or insufficient collagen may arise from lack of vitamin C
-Metabolic disorders such as excess cortisol secretion reduce both inflammatory and specific
defence responses while metabolic syndrome and type II DM may put a person in a pro-
inflammatory state and/or delay healing
Immune and infectious disorders:
1. Caused by replication of a pathogenic microbe in/on body; microbes kill healthy cells in
infection process. Some microbes e.g. bacteria or fungi can produce toxins which can harm/kill
cells, or trigger abnormal responses in the body e.g abnormal clotting
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Document Summary
Pathophysiology- physiology of altered health; study of structural and functional changes in the body that occur with disease, and causes, manifestations and progression of the disease. Pathology- study of structural changes in cells, tissues and organs. Also focuses on mechanisms that underlie the disease which can provide background for treatment. Disease- the interruption, cessation, or disorder of a body system or organ structure. Diagnosis (based on aetiology, morphological changes and clinical manifestations) Disease-causing agents can cause disease to a single organ or a number of organs or systems. Risk factors: multiple factors that predispose individuals to increased chance of disease development. Chemical stimuli: e. g poisons, alcohol, acids, alkaline substances, pollution, smoking, some foods, carbon monoxide, insecticides, trace metals e. g. lead or mercury. Can injure cell membrane or other cell structures, block enzymes, coagulate proteins, disrupt osmosis and ionic balance. Physical stimuli: e. g. trauma, burns, radiation, electricity, extremes of temperature. Radiation creates heat- thermal burns; dna mutations; interrupts replications; kills cells.
