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NR 507NR507 FINAL EXAM STUDY GUIDE (3) LATEST 2024/2025. The endometrial cycle and ovulation in females. It explains the menstrual cycle, phases of the cycle, and the occurrence of ovulation. It also covers uterine prolapse and polycystic ovary syndrome (PCOS). clinical manifestations, evaluation, and treatment of PCOS. Additionally, it discusses testicular cancer and its risk factors.
Typology: Exams
1 / 102
Diagnosis of PCOS is based on evidence of androgen excess, chronic anovulation, and inappropriate gonadotropin secretion. Tests for impaired glucose tolerance are recommended. As stated, polycystic ovaries do noT have to be present and, conversely, their presence alone does not establish the diagnosis. Goals of treatment include reversing signs and symptoms of androgen excess, instituting cyclic menstruation, restoring fertility, and ameliorating any associated metabolic or endocrine, or both, disturbances.
*Most common cause of anovulation and ovulatory dysfunction in women. *Leading cause of infertility and most common endocrine disturbance. *Mostly common in younger women *Usually has two/three of the following: irregular ovulation, elevated levels of androgens (testosterone), and the appearance of polycystic ovaries on ultrasound. *Polycystic ovaries do not need to be present to dx POS. *Thyroid dysfunction, hyperprolactinemia, and congenital adrenal hyperplasia must be ruled out first. *Associated with metabolic dysfunction, dyslipidemia, insulin resistance, and obesity. *Strong genetic component and possibly differentially inherited. *Difficult to diagnose as symptoms may change over time. *80% of women have one or more of the symptoms with normal ovaries. *More prominent sx as we age. *May be associated with Cushing’s syndrome, acromegaly, premature ovarian failure, obesity, congenital adrenal hyperplasia, thyroid disease and androgen producing adrenal tumors. Pathophysiology: Underlying cause is unknown Genetic involvement suggested because of steroid and androgen biosynthesis. No single factor accounts for abnormalities of pcos. *** A HYPERANDROGENIC STATE IS A CARDINAL GEATURE IN THE PATHOGENSIS OF PCOS -3 X LIKELY TO HAVE INSULIN RESISTENCE. *Insulin stimulates androgen secretion by the ovarian stroma and reduces the serum sex hormone-binding globulin.
Decreased intraovarian receptors for estrogen receptor -a - or insulin like growth factor 1, increased leptin levels, or direct infrared redaction select ovarian cells. *Intrauterine and early child enviroment contribute to childhood development. *Weight gain aggravates symptoms and women will have an increased leptin level. *Leptin levels are increased in thin women as well *Leptin influences the hypothalamic pulsatility of GNRH and interaction with HPO. *Dysfunction in ovarian follicle development results from inappropriate gondatropin secretes and triggers the beginning of anovulation.
*dx is made based on androgen excess, chronic anovulation, and sonographic evidence of polycystic ovaries. *Must have 2 -3 of these. *Impaired glucose tolerance test is recommended
Body’s process for adapting to high hormone levels: Negative-feedback systems are important in maintaining hormone concentrations within physiologic ranges. The lack of negative-feedback inhibition on hormonal release often results in
pathologic conditions. hormonal imbalances and related conditions are caused by excessive hormone production, which is the result of failure to “turn off” the system. High concentrations of hormone decrease the number of receptors, called down-regulation. Thus the cell can adjust its sensitivity to the concentration of the signaling hormone. The receptors on the plasma membrane are continuously synthesized and degraded, so that changes in receptor concentration may occur within hours. Various physiochemical conditions also can affect both the receptor number and the affinity of the hormone for its receptor. Some of these physiochemical conditions are the fluidity and structure of the plasma membrane, pH, temperature, ion concentration, diet, and the presence of other Cushing’s Syndrome : overproduction of anterior pituitary ACTH by a pituitary adenoma; chronic excess cortisol (at any age) With ACTH-dependent hypercortisolism, the excess ACTH stimulates excess production of cortisol and there is loss of feedback control of ACTH secretion. Whatever the cause, two observations consistently apply to individuals with Cushing syndrome : (1) they do not have diurnal or circadian secretion patterns of ACTH and cortisol, and (2) they do not increase ACTH and cortisol secretion in response to a stressor. Exogenous result from administration of glucocorticoids. Endogenous either corticotropin dependent (most common & caused by ACTH-secreting pituitary tumor) or corticotropin independent (usually caused by an adrenal cortical tumor). Clinical features: weight gain in trunk, face, and cervical areas. “truncal obesity, moon face, buffalo hump”. Transient weight gain from sodium and water retention may be present because of the mineralocorticoid effects of cortisol, exhibited when cortisol is present in high levels. Glucose intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver. Protein wasting is caused by the catabolic effects of cortisol on peripheral tissues. Muscle wasting leads to muscle weakness and is especially obvious in the muscles of the extremities with thinning of the limbs. In bone, loss of the protein matrix and increases in bone resorption lead to osteoporosis and can result in pathologic fractures, vertebral compression fractures, bone and back pain, kyphosis, and reduced height. Hypercalciuria may result in renal stones, which are experienced by approximately 20% of individuals with this disease. Loss of collagen also leads to thin, weakened integumentary tissues through which capillaries are more visible; the tissues are easily stretched by adipose deposits.
Hypoparathyroidism CX: low PTH levels. Usually caused by damage to the PT glands during thyroid surgery & anatomic proximity of PT glands to thyroid. Assoc c genetic syndromes, including familial HX & DiGeorge syndrome (velocardiofacial syndrome) & idiopathic or autoimmune form of the disease. Low mag can cause a decrease of PTH secretion & function Lab results point to primary hypothyroidism: caused by a deficient production of TH by the thyroid gland. Primary hypothyroidism the loss of functional thyroid tissue leads to a decreased production of TH. Causes in adults include autoimmune thyroiditis (Hashimoto disease), iatrogenic loss of thyroid tissue after surgical or radioactive treatment for hyperthyroidism, head and neck radiation therapy, medications, and endemic iodine deficiency. Primary hypothyroidism DX: is made by documentation of the clinical symptoms of hypothyroidism, and by measurement of increased levels of TSH and decreased levels of TH (total T3 and both total and free T4). When hypothyroidism is caused by pituitary deficiencies, serum TSH levels are decreased or are inappropriately normal in the face of low levels of TH. Pathophysiology of thyroid storm: (Thyrotoxic Crisis) rare but dangerous worsening of thyrotoxic state. Death within 48hr without treatment. Occurs in individuals who have undiagnosed or partially treated severe hyperthyroidism & subjected to excessive stress. CX: infection, pulmonary/cardiac disorder, trauma, burns, seizures, SX (esp thyroid surgery), OB complications, emotional distress, or dialysis. Symptoms: ↑thyroxine action(T4) & triiodothyronine (T3) exceeding metabolic demands. Signs of thyrotoxicosis : Excessive concentrations of thyroid hormones. Symptoms: ↑metabolic rate, hyperthermia (heat intolerance), tachycardia (esp atrial tachydysrhythmias), high-output HF; agitation or delirium, goiter, reproductive disorders, excessive sweating, nausea, vomiting, diarrhea (n/v/d=fluid volume depletion)
Specific areas of cutaneous (skin) innervation at these spinal cord segments. The dermatomes of various spinal nerves are distributed in a fairly regular pattern, although adjacent regions between dermatomes can be innervated by more than one spinal nerve.
The region between adjacent neurons is called a synapse. Impulses are transmitted across the synapse by chemical and electrical conduction. The conducting substance is called a neurotransmitter and it is often formed in the neuron, transported to the synaptic knobs (boutons) of the presynaptic neuron’s axon, and stored in synaptic vesicles within the knobs. Action potentials in the presynaptic neuron cause the synaptic vesicles to release their neurotransmitter(s) through the plasma membrane into the synaptic cleft (the space between the neurons), where they bind to specific neurotransmitter (protein) receptor sites on the plasma membrane of the postsynaptic neuron
Degenerative process of the vertebral column and associated with soft tissue. Characterized by a structural defect of spine involving lamina or neural arch of vertebra. Most common site affected is the lumbar spine. This defect occurs in the portion of the lamina between the superior and inferior articular facets called the pars interarticularis. Mechanical pressure may cause a forward displacement of the deficient vertebra called spondylolisthesis. Heredity plays a significant role, and spondylolysis is associated with an increased incidence of other congenital spinal defects. As a result of torsional and rotational stress, “microfractures” occur at the affected site and eventually cause dissolution of the pars interarticularis.
The special senses of vision, hearing, touch, smell, and taste are the means by which individuals perceive stimuli that are essential for interacting with the environment. Special sensory receptors are connected to specific areas of the brain through the afferent pathways of the peripheral and central nervous system (CNS). Each of the special senses thus involves a connected system of organs and tissues that receives stimuli and sends sensory messages to areas of the CNS, where they are processed and guide behavior. Patho of cerebral infarction and excitotoxins results when an area of the brain loses supply and becomes ischemic because of vascular occlusion embolic or thrombotic.
Agnosia Impaired/defect of recognition and may be tactile, visual or auditory stimuli. Caused by dysfunction in the primary sensory area or the interpretive areas of the cerebral cortex Accumulation of blood in a subarachnoid hemorrhage (SAH) Hemorrhage from a defective or injured vasculature into the subarachnoid space. The blood is extremely irritating to the meningeal and other neural tissues and so produces an inflammation & impairs circulation of cerebrospinal fluid. Additionally, the blood coats nerve roots, clogs arachnoid granulations (impairing CSF reabsorption), and clogs foramina within the ventricular system (impairing CSF circulation). ICP immediately increases to almost diastolic levels within 10 mins. ICP returns to near baseline in about 10 minutes. Cerebral blood flow and cerebral perfusion pressure (CPP) decrease. The expanding hematoma acts like a space-occupying lesion, compressing and displacing brain tissue. Granulation tissue is formed and scarring of the meninges, with resulting impairment of CSF reabsorption and secondary hydrocephalus, often results. Most common cause of meningitis Meningitis is inflammation of the brain or spinal cord. Infectious meningitis may be caused by bacteria, viruses, fungi, parasites, or toxins. Bacterial & viral meningitis is the most common. Bacterial infection may be due to Neisseria meningitis, Haemophilus influenza, streptococcus pneumoniae, or Escherichia coli. Sometimes, no causative organisms can be found. In most patients, the infections that cause meningitis is secondary to another bacterial infection, such as bacteremia. Respiratory infections increase the risk. It may follow a skull fracture, a penetrating head wound, lumbar puncture, ventricular shunting, or neuro procedure. Viral meningitis aka aseptic viral meningitis may result from a direct infection or secondary to disease such as mumps, herpes, measles, or leukemia. ( Textbook)
Evidence exists that dietary factors play a role in prostate cancer development. The lack of biomarkers for certain nutrients, difficulty measuring and quantifying diet, and limitation of clinical trials all make the understanding of the relationship difficult.
Dietary intake effects the signaling pathways, hormones, oxidative stress, and reactive oxygen species (RDS). Nutrients most associated with cancer are carotenoids, fat, vit E, vit D/calcium, and selenium. Less studied are isoflavones, curcumin, lycopene, zinc, green tea, omega 3 polyunsaturated fats, and sulforaphane. The hypothesis for MEAL is that a change in diet of higher intake of animal products to vegetables and fruits will slow the progression of the indolent to the aggressive form of prostate cancer. As adipose tissue is increasingly being regarded as hormonally active tissue, high body fat and obesity need in- depth exploration to understand the associated risk of prostate problems Obesity has a positive association with aggressive prostate cancer and worse outcomes but a negative association with indolent (slow growing) prostate cancer. Adipose tissue is considered hormonally active tissue. It effects circulating bio-active messengers therefore influences the risk of developing prostate problems.
Benign Prostate Hyperplasia is an enlargement of the prostate gland. As the prostatic tissue enlarges is compresses the urethra, where it passes through the prostate, causing lower urinary tract symptoms. At birth the gland is pea sized and growth is gradual until puberty. Development continues until 3rd^ decade of life. Benign hyperplasia begins around age 40-45 and continues until death.
Bladder outflow obstruction occurs as the hypertrophy continues and the urethra is compressed.
The role of DNA in genetics – Genes are composed of DNA Chromosomes are composed of many genes = basic units of inheritance, carrying information for synthesis of specific proteins. Genes are composed of the chemical deoxyribonucleic acid (DNA). the replication of DNA occurs a finite number of times per chromosome due to the presence of telomeres
= short nt/protein segments on the ends of chromosome arms that protect DNA and prevent chromosome fusions during the cell division cycle. Telomeres gradually erode away with each cell division until DNA unravels and chromosome disintegrates. This is an important way to help eliminate chromosomes (and cells) carrying accumulated undesirable mutations! DNA is the genetic basis of life = the “blueprint of life" Transcription –Transcription is the process by which DNA specifies a sequence of mRNA. RNA is synthesized using DNA as the template via the process of transcription. However, unlike the replication process where an exact copy is made of all the DNA within the nucleus, only small portions of DNA are transcribed at a time to make RNA. Each transcribed segment of DNA corresponds to one of the 1000’s of genes that make up our chromosomes. Several 100-1000 DNA nt comprise a gene = information for synthesis of a specific protein. Effects of genetic mutations – Changes in the DNA can also occur as the result of a mutation = inheritable alteration of genetic material. Mutations can occur either spontaneously or as a result of exposure to external mutagens such as radiation, chemicals, and even certain infectious agents (eg – viruses). Mutations in individual genes can also result in single gene disorders. (e.g. sickle cell anemia, cystic fibrosis, hemophilia) Depending on the location of the mutated gene, and whether or not it is a dominant or recessive allele, disorders are classified as: autosomal dominant, autosomal recessive, sex-linked Most diseases (including diabetes, dementia, cardiovascular conditions, cancer) have a genetic component and are classified as multi-factorial: mutations occur at multiple (polygenic) chromosomal sites that have a cumulative effect to cause disease. Down syndrome/ Trisomy : Trisomy is a type of aneuploidy in which one chromosome is present in three copies in somatic cells. A partial trisomy is one in which only part of a chromosome is present in three copies. Down Syndrome- pg. 146 – aneuploidy in an autosome is trisomy of the 21 chromosome, low nasal bridge, epicanthal folds, protruding tongue, flat low set ears. Down syndrome, a trisomy of chromosome 21, is the most well-known disease caused by a chromosome aberration. It affects 1 in 800 live births and is much more likely to occur in the offspring of women older than 35 years of age.
o The only trisomies frequent in live births are trisomy 13, 18 and 21. Fetuses with other trisomies do not survive to term, trisomy 16 most common trisomy among abortuses. o Partial trisomy: extra portion of a chromosome is present in each cell. o Most well-known example of aneuploidy in an autosome is trisomy 21= Down Syndrome o IQs between 25- Facial appearance: low nasal bridge, epicanthal folds, protruding tongue, flat low-set ears, poor muscle tone. Congenital heart defects are common with inability to fight off respiratory tract infections and increased susceptibility to leukemia. o After age of 40, develop symptoms similar to Alzheimer disease because gene of Alzheimer disease is located on chromosome 21. o 97% of Down Syndrome cases are caused by nondisjunction during the formation of one of the parents games or early embryonic development. Remaining 3% is translocation. 90-95%, nondisjunction occurs in formation of mothers egg cell. o 1% of individuals with ds are known to be mosaics, the effects of the trisomic cells are attenuated and symptoms are less severe. Klinefelter syndrome:
o If the prevalence of the disease in a population is f, the risk for offspring and siblings of probands is approx. square root of f What is multifactorial inheritance?
Ions that initiate muscle contraction : (page 1533) Calcium is the main ion that initiates muscle contraction, 4-step process: excitation, coupling, contraction, and relaxation. Initial contraction process is the excitation-contraction coupling (ECC) series involving the electrical properties of all cells and the movement of ions across the plasma membrane.
Specific intracellular receptors with skeletal muscle sarcoplasmic reticulum, called ryanodine receptors (RyRs) are primary ion channels that control calcium release. RyRs are the largest known channels, allowing rapid movement of calcium. RyRs1 is predominantly found in skeletal muscle. Excitation – the first step of muscle contraction, begins with the spread of an action potential from the nerve terminal to the neuromuscular junction. The rapid depolarization of the membrane initiates an electrical impulse in the muscle fiber membrane called the muscle fiber action potential. The action potential spreads to the T-tubules. An action potential triggers receptors in the T-tubule wall, opening the RyR channels, releasing calcium from the sarcoplasmic reticulum. The second stage, Coupling, consists of the migration of calcium ions to the myofilaments. Calcium affects troponin and tropomyosin, muscle proteins that bind with actin when the muscle is at rest. In the presence of calcium, both of these proteins are attracted to calcium ions, leaving actin free to bind with myosin. Contraction begins as the calcium ions combine with troponin, a reaction that overcomes the inhibitory function of the troponin-tropomyosin system (troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue. In a relaxed muscle, tropomyosin blocks the attachment site for the myosin crossbridge, preventing contraction). The thin filament actin then slides toward the thick filament myosin. The two ends of the myofibril shorten after contraction when the myosin heads attach to the actin molecules, forming a cross- bridge that constitutes an actin-myosin complex. ATP, located on the actin-myosin complex, is released when the cross-bridges attach. *the useful distance of contraction of a skeletal muscle is approximately 25-35% of the muscles length. The last step, Relaxation , begins as the sarcoplasmic reticulum absorbs the calcium molecules, removing them from interaction with troponin. Calcium is pumped back into the sarcoplasmic reticulum by means of an active transport process. The cross-bridges detach, and the sarcomere lengthens. Growth of long bones in children : 1592 Long bones of the body include: clavicles, humeri, radii, ulnae, metacarpals, femurs, tibiae, fibulae, metatarsals, and phalanges. Endochondral formation of bone is the development of new bone from cartilage. First, mesenchymal tissue forms a cartilage anlage , which defines the shape of the bone by 6 weeks of gestation. Blood vessel invasion to inside the anlage brings osteoprogenitor cells leading to primary centers of calcification by 8 weeks. Endochondral bone formation begins in the outer layer of the cartilage model, which consists of a layer of dense connective tissue called perichondrium. The perichondrium contains cells that develop into osteoblasts, forming a collar of bone, termed the periosteal collar , around the cartilage model. Cartilage enclosed within the periosteal collar degenerates, and capillaries from outside the perichondrium invade the degenerating cartilage cells, carrying with them osteoblast precursors from the inner layer of the perichondrium and osteoclast precursors from the blood itself. Endochondral bone formation progresses at the primary center of ossification in the middle of the cartilage model and extends toward either end of the developing bone. At the same time, the periosteal collar thickens and becomes wider toward the epiphyses. By the end of gestation secondary centers of ossification begin to lay down bone at both ends of the cartilage model. Here, too, cartilage within the periosteal collar degenerates, and blood vessels grow inward, delivering bone cell precursors. Once the osteoblasts begin to secrete osteoid, ossification spreads from the secondary centers in all directions until all the cartilage within the model is replaced by bone. Two regions of cartilage remain at the ends of long bones: (1) articular cartilage over the free ends of the bone, and (2) the physeal plate, a layer of cartilage between the metaphysis and epiphysis. The physeal plate retains the ability to form and calcify new cartilage and deposit bone until the skeleton matures approximately 1 year after sexual maturity (11-15 yrs. in females, 15-18 yrs. in males). Bones belonging to the appendicular skeleton : pg. 1519 Appendicular skeleton has 126 bones and supports the appendages of the body. Pectoral Girdle – total of 4 bones Clavicle (2) - braces the shoulder joint against the sternum, it articulates with the scapula Scapula (2) - flat, triangular bones, lateral angle articulates with the head of the humerus and forms the shoulder joint Upper Extremities – total of 60 bones Humerus (2)- only long bone of the arm, articulates at the proximal end with the glenoid cavity of the scapula
Radius (2) – the lateral forearm bone. Proximal end articulates with the capitulum of the humerus, distal end widens and forms primary articulation with proximal carpal bones. Ulna (2) – medial bone of the forearm. Proximal end forms the olecranon process (the point of the elbow) Carpals (16) – (wrist) each bone has a unique shape and name. Metacarpals (10) – (palm) associated with a number starting with the thumb on lateral side Phalanges (28) – (fingers) thumb has two phalanges and each finger has three Pelvic Girdle– total of 2 bones Coxal (hip) bone (2) – results from the fusion of three bones Ilium, Ischium, and Pubis Ilium – large flaring bone that forms the superior part of hip. Upper edge is the iliac crest, crest ends anteriorly in the anterior superior iliac spine (can be felt easily in thin people). Ischium – inferior part of coxal bone. Inferior surface has roughened part called the ischial tuberosity, they are the parts of the hip bones that press against objects you sit on. Pubis – (pubic bone) most anterior part of hip. **the ilium, ischium and pubis together form a deep socket called acetabulum which articulates with the head of the femur Lower Extremities – total of 60 bones Femur (2) – only long bone of the thigh, heaviest and strongest bone in the body. Proximal end has ball like head (greater trochanter) that fits into the acetabulum of the coxal (hip) bone. Patella (2) – (kneecap) small, freestanding bone that rests between the femur and tibia. Femur has a dedicated groove which the kneecap slides. Tibia (2) – (shinbone) is the larger, medial bone of lower leg. Anterior surface forms an anterior border that can be easily felt, distally there is a process called the medial malleolus that forms the inner bulge of the ankle. Fibula (2) – long, slender bone lateral to the tibia. Distal part forms the lateral malleolus (outer part of ankle) Tarsals (14) – 2 notable tarsal bones are the calcaneus (heel bone), and the talus which articulates with the tibia to form hinge- like ankle joint Metatarsals (10) - form the sole of the foot Phalanges (28) – similar to phalanges of hand, great toe, like thumb, has only two phalanges.
How vaccines are performed – A vaccine is a biological preparation that provides active acquired immunity to a particular disease. A vaccine typically contains an agent that resembles a disease-causing microorganism and is often made from weakened or killed forms of the microbe, its toxins, or one of its surface proteins. Vaccines are like a training course for the immune system. They prepare the body to fight disease without exposing it to disease symptoms. When foreign invaders such as bacteria or viruses enter the body, immune cells called lymphocytes respond by producing antibodies, which are protein molecules. Antigens are present in extremely small quantities to elicit an immune response through a vaccine. The most common routes of administration are intravenous, intraperitoneal, subcutaneous, intranasal, and oral. Each route stimulates a different set of lymphocyte-containing tissues and therefore results in the induction of different types of cell-mediated or humoral immune responses. Vaccines are considered nonimmunogenic. P opulations are risk for getting systematic fungal infections and parasitic infections - In immunocompromised individuals, particularly those with diminished levels of neutrophils (neutropenia), fungal infections may occur. Candida is the most common fungal infection in people with cancer (particularly acute leukemia and other hematologic cancers) transplantation (bone marrow and solid organ), and HIV/AIDS. Almost 90% of people with AIDS have candida at least one time (usually thrush or vaginitis) because of their decreased number of neutrophils. Invasive candidiasis may also be secondary to indwelling catheters, intravenous lines, or peritoneal dialysis which provided direct entrance into the blood. Disseminated candidiasis may involve several internal organs, including abscesses in the kidney, brain, liver, and heart. It is characterized by a persistent fever and gram-negative shock like symptoms (hypotension, tachycardia), DIC, and death. The mortality rates of sepsis or disseminated candidiasis are in the range of 30-40%. Parasitic infections are uncommon in the United States, with significant mortality and morbidity of individuals in developing countries. Malaria is most common in Africa. Systematic manifestations of infection – Systematic infection is the term used to describe an infection that is circulating in the blood. This means it affects the entire body. Signs/symptoms of this can be fever, tachycardia, hypotension, septic shock, toxic shock, hypovolemia, respiratory alkalosis, and hyperventilation, neutropenia, thrombocytopenia, and DIC. Alterations in sensorium may occur in severe infection and may cause anxiety, confusion, delirium, stupor, seizures, and coma. Mechanism responsible for the increase in antimicrobial resistance worldwide – Antimicrobial resistance occurs naturally overtime, usually through genetics. However, the misuse and overuse of antimicrobials is accelerating this process. In many places antibiotics are overused and misused. Example of misuse include they are taken by people with viral infections such as the flu. Poor infection control, inadequate sanitary conditions and inappropriate food handling encourage the spread of antimicrobial resistance. Functions of normal body flora The normal microbiome provides protection by inhibiting colonization by pathogens and by releasing chemicals that prevent infection. Each surface including the skin, mucous membranes of the eyes, upper and lower GI, urethra and vagina are all colonized by combo of bacteria (mostly bacteria) and fungi that are unique to the particular location. The relationship between this “good” bacteria and humans is both commensal (to the benefit of one organism without affecting the other) and mutualistic (to the benefit of both). Many of these microorganisms help digest fatty acids, large polysaccharides and other dietary substances. They also produce biotin and Vit K, assist in the absorption of various ions: such as calcium, iron and magnesium. These good bacteria compete with pathogens for nutrients and block attachment to the epithelium. They produce chemicals (ammonia, phenols, and indoles). Treatment with broad spectrum abx can alter this normal flora, decreasing its protective activity, leading to overgrowth of yeast Candida Albicans or C Dif. The good flora trains the adaptive immune system by growth of gut-associated lymphoid tissue (where cells of adaptive immunity reside). Desensitization therapy Also known as allergen Immunotherapy. This is where minute quantities of the allergen are injected in increasing doses over a prolonged period. The therapy may reduce the severity of the allergic reaction in the treated individual. This therapy is associated with a risk of systemic anaphylaxis, which can be life threatening. This approach works best for routine respiratory allergies and biting insect allergies (80-90% rate of desensitization over 5 years of treatment). The mechanisms by which desensitization occurs may be several, one of which is the production of large amounts os so called blocking antibodies, usually circulating IgG. A blocking antibody presumably competes in the tissues or in the circulation for binding with antigenic determinants on the allergen so the allergen is “neutralized” and is unable to bind with IgE on the mast cells. Desensitization
injections may also stimulate the generation of clones of T- regulatory lymphocytes which inhibit hypersensitivity by suppressing the production of IgE and anti-inflammatory cytokines. Cells involved in the “left shift” in the WBC count differential -Neutrophil left shift and white blood cell (WBC) count are routine laboratory tests used to assess neutrophil state, which depends on supply from the bone marrow and consumption in the tissues Early in the response to infection or inflammation, immature forms of neutrophils will be seen. These are call Stab or Band cells. The presence of these immature cells is called a "shift to the left" and can be the earliest sign of a WBC response, even before the WBC becomes elevated. Forms of Immunity -Innate, native- natural immunity (non-specific)- First line - physical, mechanical and biochemical barriers. Epithelial barrier and inflammation confer innate resistance and protection. Skin, mucous membranes, stomach acid, oils on skin (Barriers). Second line - The inflammatory response (redness, swelling, heat and pain). Cells involved in the inflammatory response are Phagocytes (WBC-Leukocytes) and chemical mediators (leukotrienes and prostaglandins).
Process by which a deep pressure ulcer heals: Most significant cause is constant pressure that interrupts arterial and venous blood flow to and from the skin or deeper tissue. Healing requires continued relief of pressure, debridement of dead tissue, wound care products (dressings…), and repair with skin flaps for large/deep ulcers. Antibiotic treatment for infection. Stage I & II pressure ulcers and partial thickness wounds heal by tissue regeneration. Stage III & IV pressure ulcers and full thickness wounds heal by scar formation and contraction Phases of wound healing: Inflammatory-Proliferation-Maturation Inflammatory phase : 0 – 3 days