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Showing posts with label Anatomy and Physiology. Show all posts
Showing posts with label Anatomy and Physiology. Show all posts

Pathophysiology of Myocardial Infarction

pathophysiologyofMyocardialInfarction thumb Pathophysiology of Myocardial InfarctionIn Myocardial Infarction, inadequate coronary blood flow rapidly results in myocardial ischemia in the affected area. The location and extent of the infarct determine the effects on cardiac function. Ischemia depresses cardiac function and triggers autonomic nervous system responses that exacerbate the imbalance between myocardial oxygen supply and demand. Persistent ischemia results in tissue necrosis and scar tissue formation, with permanent loss of myocardial contractility in the affected area. Cardiogenic shock may develop because of inadequate CO from decreased myocardial contractility and pumping capacity.

Increased Intracranial Pressure

Increased Intracranial Pressure
Intracranial pressure (ICP) is the pressure in the skull that results from the volume of three essential components: cerebrospinal fluid(CSF), intracranial blood volume and central nervous system tissue. The normal intracranial pressure is between 5-15 mmHg. This is slightly lower than the mean systemic arterial pressure but considerably higher than venous pressure.
The intact cranium is essentially inexpandable containing about 1400 grams ofcentral nervous system (CNS) or brain tissue, 75 ml of blood and about 75 ml of cerebrospinal fluid (CSF). These three components of the cranial vault maintain a state of equilibrium. Their pressure and volume determine the condition of balance. According to Monro-Kellie hypothesis, any increase in one of these elements must be balanced or compensated by a proportional constriction either or both of the other two components such as decreasing the volume of cerebral blood flow, shifting CSF flow (into the spinal canal) or increasing CSF absorption. Absence of these compensatory changes results toincreased intracranial pressure. Once ICP reaches around 25 mmHg marked elevation in intracranial pressure will be noted.
CSF is formed from the blood by the choroid plexuses, which are hanging at the roof of the brain’s ventricles. From the point where it is produced, it flows through the aqueduct of Sylvius to the fourth ventricles. Three apertures (opening) are found in the fourth ventricle which serves as passageway going to the subarachnoid spaces in the brain and spinal cord. These openings are Foramina of Magendie (median aperture) and two Foramina of Luschka (lateral apertures). A presence of tumor in choroid plexus may cause an overproduction of CSF. If the passageway of CSF is obstructed or brain tissue damage during surgery occurs, elevated ICP is inevitable.
Normally, a change in CSF and blood volume occurs. For instance, during exhalation a temporary rise in intrathoracic pressure occurs. This impairs cerebral venous drainage and thereby reabsorption of CSF. An increase in ICP might likely occur, unless the blood will be expelled or the brain tissue will shrink (compensatory mechanism). If no compensation will occur, based on Monro-Kellie hypothesis, a slight increase in intracranial pressure will take place. The same process occurs during Valsalva maneuver (forcible exhalation against a closed glottis), sneezing, coughing and straining at stool. This is the main reason why people with increase ICP and at risk for cerebral hemorrhage are instructed to avoid these instances.
Presence of carbon dioxide can also increase ICP. Carbon dioxide is a potent vasodilator that dilates aretrioles (including those in the chorionic plexus in the brain) which elevates cerebral blood volume and ICP.
Etiology
CSF – hydrocephalus
  • Overproduction of CSF
  1. Meningitis
  2. Subarachnoid hemorrhage
  3. Brain tumor
  • Impediment of CSF flow
  1. Narrowed foramina of Magendie and Luschka
  2. Obstruction in the Aqueduct of Sylvius
  3. Arnold-Chiari disorder
  • Interference with CSF absorption
  1. Surgery
CNS tissue
  • Head injury
  • Cerebral edema
Blood
  • Cerebral venous sinus thrombosis
  • Hematoma
  • Increased carbon dioxide partial pressure
Sources:
  1. Medical Surgical Nursing by Smeltzer and Bare
  2. Pathophysiology by Nowak and Handford

Thalassemias

Thalassemias
Definition
Thalassemia is a group of inherited disorders which is associated with hemoglobin defects. The disorder results in excessive destruction of red blood cells leading to anemia.
Types of Thalassemia
There are two main types of Thalassemia based on the chain of hemoglobin it affects. These are the following:
  • Beta Thalassemia or Cooley’s anemia – defect in the beta-chain of hemoglobin is present.
  • Alpha Thalassemia – defect in the alpha-chain of hemoglobin is present.
Forms of Thalassemia
Both the alpha and beta thalassemia include the following forms:
  • Major - threatening disease characterized by severe anemia, hemolysis and ineffective erythropoiesis
  • Minor - a mild form of anemia. The affected individual has only one defective gene and is asymptomatic.
Incidence
Aplha thalassemias occur frequently among Southeast Asians,Middle East Asians, Chinese and Africans.
Beta Thalassemias occur frequently to those of Mediterranean origin and lesser to Chinese, other Asians and African Americans.
Review of Related Anatomy and Physiology
Red blood cells or erythrocytes carry oxygen to the different parts of the body. Different from other cells, RBC’s do not contain a nucleus (anucleated). These small cells are circular and flattened with depressed centers on both sides resembling to that of a doughnut when viewed under a microscope. Their size and shape provides a large surface area for carrying oxygen in relation to their volume. The normal RBC count is 4-6 million/mm3. RBC’s has the life span of 120 days.
Hemoglobin is a form of protein that contains iron which is responsible for transporting oxygen that is carried in blood. Adult hemoglobin contains a beta chain (HBB) while a fetus’ hemoglobin has a gamma chain. Hemoglobin is comprised of four protein (amino acid) components. It has two beta-globin and two alpha-globin. The subunit beta-globin is located inside the RBCs. These amino acids carry an iron-bearing molecule called heme. Heme molecules, which are only found in mature RBC’s, enables the erythrocytes to pick oxygen from the lungs and transport it throughout the body. Once oxygen attaches to hemoglobin it gives the blood its bright red pigment.
The more hemoglobin molecules the RBC contain, a higher amount of oxygen will they be able to carry. If the hemoglobin is defective, the erythrocyte will also malfunction. A red blood cell is just a vessel; the one that performs the oxygen transportation is the hemoglobin. Normal hemoglobin is 13-18 grams/100 ml of blood in males and 12-16 grams in females.
Pathophysiology
Risk Factors
  • Family history
  • Asian, Chinese, Mediterranean or African American ethnicity
Causes
  • Thalassemia is an inherited disorder that follows an autosomal recessive pattern.
Thalassemias are inherited disorders of hemoglobin synthesis that result from a change in globin chain production. Beta-globin normally joins to alpha-globin component of hemoglobin. When beta-protein is lacking, alpha-globin accumulates and causes destructive membrane effects and vice versa. This leads to destruction of red blood cells. Not only that it causes membrane damage and cell destruction but it also suppresses the mitosis in stem cells, thus RBC production falls. The result of impaired hemoglobin synthesis is a microcytic, hypochromic anemia.

Hypocalcemia in Newborns

Hypocalcemia in Newborns
Definition
Hypocalcemia is a disorder where there is a lowered blood calcium levels in newborns. It is defined as a total serum calcium concentration of less than 7 mg/dl. It is divided into early onset which occurs in the first 72 hours of life and late onset at about 5 to 10 days of age.
Incidence
Occurrence of this disorder is about 30% in infants with very low birth weight (<1500 g) and approximately 89% in premature infants. A very high prevalence rate is also noted in infants born with a diabetic mother.
Review of Anatomy and Physiology
Parathyroid glands are masses of glandular tissues found on the posterior surface of the thyroid gland. The parathyroids secrete parathyroid hormone (PTH) or parathormone which regulates the calcium levels in the blood. PTH is called a hypercalcemic hormone as it acts to increase the serum calcium blood levels.
Normal calcium levels in the blood vary with age: (from Saunder’s Foundations of Maternal-Newborn Nursing by Murray and McKinney, 4th Ed)
Cord = 9-11.5 mg/dl
Newborn, 3-24 hours = 9-10.6 mg/dl
Newborn, 24-28 hours = 7-12 mg/dl
Newborn, 4-7 days = 9-10.9 mg/dl
When the calcium levels in the blood drop, the parathyroids release PTH, which stimulates osteoclasts (bone cell destruction) to break down bone matrix and release calcium in the blood. The PTH also stimulates the kidneys and intestine to absorb more calcium. In contrary, the hormone that functions to decrease calcium in the blood (hypocalcemic hormone) is the calcitonin. Calcitonin is produced by the thyroid glands which cause calcium to be deposited in the bones.
Pathophysiology
Causes
Early Onset Hypocalcemia
  • Maternal diabetes (gestational or insulin dependent) related to increased calcium demands of a macrosomic infant. Hypocalcemia tends to accompany the hypoglycemia that occurs in infants of a diabetic mother.
  • Perinatal Asphyxia or stress
Perinatal asphyxia (suffocation) or stress could lead to anoxia. Phosphorous is released with anoxia, thus elevating its level. As phosphorous levels rise, calcium levels drop. This may also be related to renal insufficiency, metabolic acidosis and diminished parathyroid hormone secretion.
  • Prematurity
Preterm babies are at an increased risk of early onset hypocalcemia in the extrauterine life. This may be related to immature parathyroid glands, premature separation of trans-placental supply, diminished responsiveness of target organs to parathyroid hormone, increased calcitonin, poor intake and decreased responsiveness to Vitamin D.
  • Intrauterine growth retardation
Late Onset Hypocalcemia
  • Vitamin D deficiency

This is possible related to malabsorption, renal insufficiency, maternal Vitamin D deficiency or hepatobiliary disease. Vitamin D is needed for the absorption of calcium, without it the body cannot utilize calcium.
  • High phosphate formula
Phosphorous and calcium levels are maintained in an inverse proportion to each other in the bloodstream. If phosphorous levels rise, calcium levels decrease. If calcium levels elevate, phosphorous levels drop.
If an infant is fed with a phosphate-rich formula or cow’s milk tendencies of having a low calcium level in the blood may result. Whole cow’s milk has 7 times more phosphate load than breastmilk.
  • Low magnesium levels or hypomagnesemia
  • Congenital hypoparathyroidism
  • Real disease or insufficiency

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