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,
