Showing posts with label Pathophysiology. Show all posts
Congestive Heart Failure
- Congestive Heart Failure
Right ventricular failure occurs when the right ventricle is unable to pump blood into the pulmonary circulation. Less blood is oxygenated and pressure increases in the right atrium and systemic venous circulation, which results in edema of the extremities.
Left ventricular failure occurs when the left ventricle in unable to pump blood into systemic circulation. Pressure increases in the left atrium and pulmonary veins; then the lungs become congested with blood, causing elevated pulmonary pressure and pulmonary edema.
To compensate, the cardiac muscle hypertrophies eventually resulting in decreased ventricular compliance. Decreased compliance requires higher filling pressure to produce the same stroke volume. Increased muscle mass impedes oxygenation of the heart muscle, which leads to decreased contraction force and heart failure.
As cardiac output fails, stretch receptors and baroreceptors stimulate the sympathetic nervous system, releasing catecholamines that increase the force and rate of myocardial contraction.
This causes increased systemic resistance, increased venous return, and reduced blood flow to the limbs, viscera and kidneys.
Sweating results from sympathetic cholinergic fibers, there is extra work for the heart muscle, and there is less systemic blood flow.
The renal system responds by releasing renin-angiotensin, which sets off a chain of events – vasoconstriction, leading to increased aldosterone release, causing sodium and water retention and, in turn, increasing preload. Finally, sodium and water retention becomes excessive, resulting in signs of systemic venous congestion and fluid overload.
image from content.onlinejacc.org
image from content.onlinejacc.org
Tag :
Pathophysiology,
Pathophysiology of Dementia
Primary Dementia
Primary dementias are degenerative disorders that are progressive, irreversible, and not due to any other condition. Specific disorders are dementia of the Alzheimer’s type (DAT) and vascular dementia (formerly multi-infarct dementia). Dementia of Alzheimer’s type demonstrates progression of symptoms from the initial stage, which is characterized by mild cognitive deficits in the area of short-term memory and accomplishment of goal-directed activity, to the final stage in which profound impairment occurs in the areas of cognition and self-care abilities. Research is ongoing. Dementia of Alzheimer’s type believed to have multiple causative factors.
1. Genetic Factors:
- Familial Alzheimer’s disease is associated with abnormal genes on chromosomes 1, 14, and 21. In particular, with genes located on these chromosomes (1 and 14) that encode for amyloid precursor protein which leads to mutation of the amyloid beta-peptide in plaques.
- A specific cholesterol-bearing protein, apolipoprotein E4 (Apoe4), is found on chromosome 19 twice as often as people with DAT as in general population.
2. Biochemical and brain structure factors:
- The neurotransmitter acetylcholine has been implicated in terms of relative deficit and/or receptor abnormalities as related to Alzheimer’s disease.
- Autopsy findings reveal presence of brain changes, that is, the presence of amyloid plaques and neurofibrillary.
- Additional areas of investigation includes: slow viral infection, autoimmune processes, and head trauma.
Secondary Dementia
Occur as a result of another pathologic process.
1. Infection-related dementias
- Acquired immunodeficiency syndrome
- Chronic meningitis
- Creutzfeldt-Jakob disease
- Progressive multifocal leukoencephalopathy
- Postencephalitic dementia syndrome
- Syphilis
- Subacute sclerosing panencephalitis
Tuberculosis
2. Subcortical degenerative disorders
- Huntington’s disease
- Parkinson’s disease
- Wilson’s disease
- Thalamic dementia
3. Hydrocephalus
4. Vascular dementias
5. Traumatic conditions, such as post traumatic encephalopathy and subdural hematoma.
6. Neoplastic dementias
4. Vascular dementias
5. Traumatic conditions, such as post traumatic encephalopathy and subdural hematoma.
6. Neoplastic dementias
- Glioma
- Meningioma
- Meningeal carcinomatosis
- Metastatic deposits
7. Inflammatory conditions, such as sarcoidosis, systemic lupus erythematous, and temporal arteritis.
8. Toxic conditions, such as alcohol-related syndrome and iatrogenic dementias
9. Metabolic disorders
8. Toxic conditions, such as alcohol-related syndrome and iatrogenic dementias
9. Metabolic disorders
- Anemia’s
- Deficiency states
- Cardiac or pulmonary failure
- Hepatic encephalopathy
- Porphyria
- Uremia
Tag :
Pathophysiology,
Hypoparathyroidism
Hypoparathyroidism is a condition where a marked decrease, reduction or diminished secretion of parathyroid hormones is noted. This disorder occurs less frequently than hyperparathyroidism. A genetic factor is sometimes involved in the occurrence of this disorder where the kidneys develop insensitivity to parathyroid hormones leading to a condition known aspseudohypoparathyroidism (HPH).
Parathyroid glands are small nodular endocrine tissue located at the posterior surface of the thyroid glands. There are around 2-8 glands found on the on the thyroid lobes. However, typically four to six are found. These glands are responsible for the production ofparathyroid hormones. The chief cells of parathyroid glands synthesize this peptide hormone that is also called aparathormone (PTH). Only few of these hormones are stored because after it is synthesized, secretion follows immediately. The main function of parathormone (PTH) is to regulate the serum calcium level. That is why this is the most important regulator of maintaining the blood homeostasis in relation to calcium level. The secretion of PTH is relatively dependent on calcium concentration. Very low degree of serum calcium stimulates the parathyroid glands to synthesize and increase the secretion of parathormone. Normal serum calcium level is 9-11 mg/dl. Any drop below the minimum range
Increase levels of parathormones would increase calcium levels. Thus, PTH is also called a hypercalcemic hormone. The one that acts opposite to PTH is called calcitonin which is secreted by the thyroid glands that causes increase deposition of calcium in the bones and low in the blood plasma. Thereby, calcitonin is called a hypocalcemic hormone. The feedback interaction between these two hormones is very vital in achieving calcium homeostasis in blood.
Increase levels of parathormones would increase calcium levels. Thus, PTH is also called a hypercalcemic hormone. The one that acts opposite to PTH is called calcitonin which is secreted by the thyroid glands that causes increase deposition of calcium in the bones and low in the blood plasma. Thereby, calcitonin is called a hypocalcemic hormone. The feedback interaction between these two hormones is very vital in achieving calcium homeostasis in blood.
The mechanisms on how calcium is elevated with increase PTH secretion are the following:
- Osteoclast activation
Result: release of calcium deposited in bones
When calcium levels drop parathyroid hormones activates osteoclasts inside the bone. Osteoclasts are cells that stimulate bone cell destruction. This is primarily done by the body to cause a breakdown in the bone matrix so that calcium from the bone will be released to the blood, making more calcium available.
- Increase renal excretion of Phosphate (PO4)
Result: decrease phosphate levels
Increase parathormone secretion due to low calcium level triggers the body to undergo another mechanism which is the escalation of phosphate elimination in kidneys. This is effective in maintaining calcium in plasma because when calcium and phosphate are both elevated, they are incorporated into the bones. Presence of calcium alone does not have this effect, therefore, elimination of phosphate would prevent calcium bone deposition and the calcium released from the bones remains in the extracellular fluid (ECF).
- Increase retention of calcium by the kidney
Result: increase calcium in extracellular fluid (ECF)
- Vitamin D activation
Result: increase calcium absorption in the intestinal tract
This mechanism will lead to the addition of calcium in the blood plasma from the diet or food intake of a person. Vitamin D is a fat soluble vitamin that is needed for the absorption of calcium. Without this vitamin, calcium will not be used by the body. If a person’s diet contains enough calcium such as milk products, green leafy vegetables, shrimp, salmon, clams, tofu, legumes and fortified orange juice he/she will just excrete the calcium on the condition that vitamin D is lacking. Foods rich in Vitamin D are dairy products, eggs, and fatty fish. Once PTH is present this vitamin found in the gastrointestinal tract will be activated thereby, increasing calcium absorption.
Etiology
- Surgical removal of parathyroid gland or parathyroidectomy
- Neck surgery such as radical neck dissection
- Autoimmune disease
- Genetic or hereditary factor where kidneys are insensitive to parathyroid glands
- Elevation of phosphate levels
- Impaired gastrointestinal tract absorption
- Decrease Vitamin D in the diet
A resulting low calcium concentration in the plasma (hypocalcemia) due to the mentioned etiological factors can cause extreme weakness, defective muscular function and altered mental processes.
image source from www.netterimages.com
image source from www.netterimages.com
Tag :
Pathophysiology,
Turner Syndrome
Definition
Turner syndrome or Ullrich-Turner syndrome is a chromosomal inability where one or all parts of a sex chromosome are absent. It is also called Gonadal dysgenesis. This abnormality is a genetic disorder that affects a girl’s development.
Frequency
- Affects about 1 in every 2500 live-born girls worldwide
- Turner syndrome only occur in females
- Turner syndrome is present at conception or following the first cell division and remains throughout life
Risk Factors
- Genetic predisposition
- Females
Pathophysiology
Normally, females have two X chromosomes – XX. In Turnersyndrome, one those X chromosome either is absent or has missing components or has an abnormality. The effects of the condition vary widely among girls with Turner syndrome. It all depends on how many of the body’s cells are affected by the changes to the X chromosome.
Signs and Symptoms
Signs and Symptoms
- Short stature. Girls with Turner syndrome who aren’t treated for short stature reach an average height of about 4 feet 7 inches (1.4 meters).
- Lymphedema (swelling) of the hands and feet (edema or extra fluid in the hands and feet)
- Broad chest and widely spaced nipples
- Low hairline at the back of the neck
- Low-set ears. Differently shaped ears that are set lower on the sides of the head than usual
- Reproductive sterility
- Underdeveloped ovaries gonadal streak. Turner syndromeprevents the ovaries from developing properly, which affects a girl’s sexual development and the ability to have children.
- Amenorrhea or the absence of menstrual period. Because the ovaries are responsible for making the hormones that control breast growth and menstruation, most girls with Turnersyndrome will not go through all of the changes associated with puberty unless they get treatment for the condition.
- Obesity and increased weight
- Shield shaped thorax
- Shortened metacarpal
- Small fingernails
- Webbed neck (extra folds of skin extending from the tops of the shoulders to the sides of the neck)
- Poor breast development
- Horseshoe kidney
- Visual impairments of sclera, cornea and glaucoma
- Ear infections
- Hearing loss
- Hips are not much bigger than the waist (high waist-to-hip ratio)
- Has problems with concentration, memory and attention
- Has problems with math, social skills and spatial relations
- Abnormal bone development (especially the bones of the hands and elbows)
- A larger than usual number of moles on the skin
Diagnosis
- Amniocentesis (during pregnancy)
- Karyotype or a chromosome analysis – test of choice
Treatment
There is no cure for Turner’s syndrome. However, the symptoms can be managed by the following:
- Growth hormone
- Estrogen replacement therapy
image from hubpages.com
Tag :
Pathophysiology,
Cell Injury
CAUSES OF CELL INJURY
Causes of cell injury are summarized into three components. Injury of the cell occurs as a result of:
Causes of cell injury are summarized into three components. Injury of the cell occurs as a result of:
- A DEFICIENCY of substances that are vital to the cell
- A presence of substances that inhibit with cell function. This is noted in cases of POISONING or INTOXICATION
- The loss of the cell’s structural integrity such as in cases of physical injuries or also termed as TRAUMA.
DEFICIENCY
The life process of a cell is derived from a variety of chemical requirements, need for an energy supply and from its complex metabolism. Deficiency of these factors may contribute to inhibition of cell function hence, causing cell injury. Factors that may produce a deficiency of essential nutrients vital for the cell’s life process are the following:
- Primary nutrient deficiency
A lack of nutrients necessary for cell’s life process is called a primary nutrient deficiency. In cases where an individual is suffering from starvation a lack of dietary energy sources will result to cellular injury. Even in cases where an individual’s diet is adequate and even excessive in providing energy sources but when a certain nutrient is lacking cellular injury would still be the result. For instance, a person who lacks thiamine in his diet will result to damage on the nervous tissue as this vitamin is required for the normal carbohydrate metabolism in the tissue.
- Secondary Nutrient Deficiency
A secondary nutrient deficiency results from the inability of the body to absorb the substances that are present in the diet. In this case, the person’s diet is adequate not only in energy sources but also in vitamins and nutrients. However, there is a problem in the absorption of the substances that will still result to cell injury.
- Genetic defects
Injurious cell deficiencies can also arise as a result of genetic defects. The metabolic pathways of the cell contain substances that synthesized based on the encoded information from the genes that are present in the chromosomes. (See section on Anatomy and Physiology of Cells). Once chromosomes are damaged or injured a decline in metabolic intermediate occurs and the cell function is then compromised due to the lack or deficiency of these intermediates. Aside from that genetic control of metabolism is defective or inadequate when genetic defects are present. Thus, the resulting phenomenon is – CELL INJURY.
- Infection
Deficiency state leading to cellular injury can also be caused by viral actions. Following infection of a cell by a certain virus, the virus causes the cells to produce new virus particles that are then released from the infected cell. Aside from that, infectious agents utilize the needed nutrients that the cell must use for its processes. Some cells may survive this situation however, a disruption in the cell’s metabolism occurs when a heavy demand for key metabolites in the production of new viral particles that results to cellular injury.
INTOXICATION or POISONING
Cell injury also occurs as a result of poisoning. Toxins are injurious substances that produce cell intoxication. Toxins could either be exogenous or endogenous.
- Exogenous Toxins
Exogenous toxins are of external origins can be characterized as being of biological or non-biological origin.
- Biological exogenous toxins – these are produced by living organisms which are commonly microorganisms. These microorganisms serve as agents of infection and they gain access to body tissues and release injurious substances inside the body. Most commonly bacteria are sources of biologicaltoxins, however, other microorganisms such as the fungi and protozoa can also produce toxins that may cause an injury to the cells.
- Non-biological exogenous toxins – these are injurious chemicals that originate outside the body. When these substances (chemicals) are inhaled or swallowed they cause a massive cell injury and damage. Many therapeutic drugs are highly effective at prescribed doses. However, the same drugs can be fatal in higher doses.
- Endogenous Toxins
Endogenous toxins are injurious substances that arise inside the cells. These toxins are formed in two ways:
- Genetic defect which causes a toxic substance to be constantly produced. Intoxification in this way could either be direct or indirect. An example of direct intoxification due to a genetic defect is in case of Huntington’s disease, wherein a toxic substance causes a neurological dysfunction.
In indirect genetic intoxification the product of a genetic defect, which by itself not toxic, activates an alternative metabolite pathways wherein the products are toxic. For example in case of PKU toxic phenylketones are formed because of the interference in the normal neurological development.
- Impaired circulation that allows metabolic by-products to accumulate to toxic levels. Normally, cells produce substances at normal levels. For example, carbon dioxide and bilirubin. However, when these substances are not removed from the cells and excreted out of the body their levels rises and can cause extensive damage to the cells. Cell injury from these accumulated substances that are normally tolerated in normal levels is secondary to the impaired circulation that has interfered with their normal removal in the cell.
TRAUMA
Trauma is a physical injury. Physical disruption of cells is results to cellular injury or damage. Trauma can be caused by the following factors:
- Hypothermia
Hypothermia is defined as a decreased in the body temperature. Extreme cold injures the cells as a result of ice crystal formation in the water of the cytoplasm. Typically, this damage is noted on frostbite.
- Hyperthermia
Hyperthermia is the opposite of hypothermia wherein there is an increased in the body temperature. Extreme heat damages the cells by disrupting the cell proteins. Presence of excessive heat causes the proteins of the cells to denature. Normally, the function of a cell’s protein is linked to their structure, thus when denaturation occurs it is followed by a significant functional cell disruption. In very extreme heat such as in burn injury, protein is chemically transformed by combining with oxygen. The product of this transformation is the blackening and charring characteristic of a burned tissue.
- Ionizing radiation
Ionizing radiation is a high-energy radiation that is associated with x-rays and nuclear radioactivity. Very high exposures to ionizing radiation produce temperature elevation in the tissues that can result to burning. Aside from the mentioned information, ionizing injury can also cause injury through the production of free radicals. Free radicals are highly energetic ions that are produced and formed when ionizing radiation strips down the electrons from the cells.
- Mechanical pressure
Mechanical pressure can result to cellular trauma or injury. When cells are faced with increasing pressure, cells are physically overwhelmed and they cannot maintain their structural integrity. In cases where a pressure is applied to a certain body surface or a pressure is created due to the presence of a rapidly expanding tumors adjacent cells are subject to trauma or injury. Even without touching, cells can be injured mechanically. When loud noises are heard high pressures are generated to the fluid of the delicate inner ear that can cause injury.
- Infection
The action of microorganisms can cause not only intoxification or poisoning but also physical trauma. Viral proteins are formed when viral infection takes place. Viral proteins then bind to the cell membrane which results to gap formation that prevents normal cell operation causing cell rupture.
- Immune system defect
Antigen-antibody interactions at cell surfaces can lead to the physical disruption of the cell membrane. This occurs when the newly formed viruses are released from the cell without damaging it and some of their viral proteins are incorporated into the plasma membrane of a normal cell. Specialized cells in the immune system recognize the viral proteins attached to the cell membrane of a normal cell as foreign. The cells of the immune system then attack the foreign substances by binding with the viral proteins which results to membrane injury or damage and cellular death.
Tag :
Pathophysiology,
Deep Vein Thrombosis
Deep Vein Thrombosis (DVT) is a condition wherein a blood clot or thrombus is formed in a deep vein. It can also be called venous thrombosis, thrombophlebitis, phlebothrombosis.
The body is composed of superficial veins, deep veins and perforating veins. Perforating veins are the kind of veins that permit one – way flow of blood from the superficial to the deep vein system. On the other hand, superficial veins are made of thick – walled muscles and lie just beneath the skin. Deep veins however, are made of thin – walled muscle media. Both superficial and deep vein have valves that allows unidirectional flow of blood to and back the heart. The valve is situated along the vein’s base segment and extends into a sinus. With these structural arrangements, the valves readily open and close without coming in contact with the vein walls, it also permits rapid closure when the blood flows backward, preventing regurgitation.
There is generally an unknown etiology regarding how DVT is formed, factors however, like the Virchow’s triad, were attributed to having DVT. The Virchow’s triad are: venous stasis, vessel wall injury and altered blood coagulation. For a DVT to occur, at least two among the triad should be presented by the patient.
Venous stasis happens when there is low blood volume and flow; in conditions like shock or heart failure, vein dilatation, medical therapy effects, decreased skeletal muscle contraction and bed rest, venous stasis is apparent. Vessel wall injury may be precipitated by trauma, fractures, chemical irritation, dislocation, or vein diseases. Sudden stoppage of anti coagulant medications, use of oral contraceptives and blood dyscrasias on the other hand may introduce increased blood coagulability.
The triad would cause inflammation of the vein walls or what we call thrombophlebitis, this would be eventually lead to thrombus formation. In cases where no inflammation occurs, thrombus is formed through phlebothrombosis.
Venous thrombi are accumulation of platelets (in response to the inflammation); and are attached to the vein wall and contains a tail- like attachment made of WBC, RBC and fibrin. This tail can grow or can spread in the direction of blood flow as layers of clot are formed through time. This could be critical since some parts of the clot may break off, travel in the blood stream and occlude other veins.
Development of DVT may cause physical manifestations but are generally non – specific. Deep vein obstruction would present through edema, tenderness (Homan’s sign: pain in the calf after the foot is sharply dorsiflexed) and swelling of the affected extremity. Superficial vein obstruction on the other hand causes pain, tenderness, redness and warmth.
Image by: circulationfoundation.org.uk
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Pathophysiology,
