Intrinsic Mechanisms of GFR RegulationGlomerular filtration rate (GFR) is the total volume of ultrafiltrate formed by the collective kidney nephrons per minute; GFR is closely regulated to balance potentially opposing requirements: – Excess solutes and water needs to be removed from the blood. – The body tissues need nearly constant blood volume and pressure. Intrinsic mechanisms are physiological responses that are initiated by renal structures to modify the hydrostatic capillary pressures; renal autoregulation. They work to maintain nearly constant GFR as long as mean arterial pressure is 80-180 mmHg, which allows for consistent kidney functioning despite changes in blood pressure.During daily activities, cardiac output, and, therefore, arterial blood pressure fluctuates—for example, during exercise it increases and during sleep it decreases.At high blood pressures, autoregulation protects the glomerulus from damage, and, at lower blood pressures, it ensures that the kidneys receive sufficient blood flow to filter wastes. If mean arterial pressure drops below 80 mmHg, such as during hemorrhage, extrinsic mechanisms activate (which we discuss in detail, elsewhere). Myogenic mechanismThe myogenic mechanism relies on inherent properties of the arterioles, themselves.Recall that the arteriole walls comprise smooth muscle, made of vascular smooth muscle cells.When increased renal blood flow exerts increased hydrostatic capillary pressure on the walls, stretch receptors are activated and induce vasoconstriction.This reduces renal blood flow and, therefore, GFR.When renal blood flow is low, the stretch receptors are inactivated, and the arteriole dilates to increase GFR. Tubuloglomerular feedback mechanismThe tubuloglomerular feedback mechanism relies on interaction between the nephron tubule and glomerulus. As renal blood flow increases, so does hydrostatic capillary pressure, and, therefore, GFR increases.As the GFR increases, so does the concentration of salt in the ultrafiltrate, because high flow rate allows less time for tubular reabsorption.The macula densa of distal tuble senses the high salt concentration in the ultrafiltrate as it passes through the distal tubule.In response, it releases vasoconstrictor chemicals (the specifics of which are disputed).Consequently, the nearby afferent arteriole constricts, which, as we saw earlier: Reduces renal blood flow, hydrostatic capillary pressure, and GFR.When renal blood flow decreases, so does the sodium concentration, and eventually the macula densa stops releasing vasoconstrictors, which ultimately allows renal blood flow and GFR to again increase.

What can you do with a kinesiology degree? Health educator, fitness trainer, exercise psychologist, physical therapist, chiropractor, and more.

Discover common rosacea triggers that are to blame for the symptoms of this skin condition. Clear your face redness & flare-ups naturally with Dr. Tara O'Desky!

While for some women it's been a lifesaver, the utility of mammography screening for breast cancer has been a bone of contention since it's unpleasant and can be downright painful. One way to make it more bearable would to give women more control over the procedure – and the FDA recently approved a device to do just that.

Spinothalamic TractDorsal Root & Spinal Cord • The dorsal horn receives sensory innervation. • The dorsal root receives sensory fibers. - The dorsal root ganglion houses the primary sensory neuron. - It is pseudounipolar, meaning it sends fibers both towards the spinal cord and also toward the periphery. • Indicate that where the roots merge, they form the mixed spinal nerve. • The sensory nerve activates a neuron in the dorsal horn (nociception most notably involves neurons of lamina I). • Spinothalamic tract (STT) fibers cross within the spinal cord to the contralateral side. Spinothalamic Projection • Leg fibers synapse within the lumbar spinal cord and then decussate and ascend the anterolateral cord and brainstem to the thalamus. • Arm fibers synapse within the cervical spinal cord, and, also decussate and ascend the anterolateral cord and brainstem to the thalamus. • Trigeminothalamic fibers decussate within the pons and ascend the brainstem, medially, to the thalamus.Thalamocortical Projection • Leg fibers project to the midline region; they terminate in the posterior paracentral gyrus. • Arm fibers project from the lateral thalamus to the upper convexity of the postcentral gyrus, lateral to the leg fibers. • Facial fibers project from the medial thalamus to the lateral cerebral hemisphere.Medial-lateral orientation • Note that medial-lateral orientation of these fibers in the cerebral cortex is opposite of that in the thalamus.Additional Pain Projection Fibers • Pathways, such as the spinoreticular, spinomesencephalic, and spinohypothalamic tracts, and the cervicothalamic tracts all also carry noxious stimuli from their self-named origins and termination sites and synapse in many regions, including the nuclei we addressed with the descending pain modulatory system. Pain is more than simply the detection of a direct noxious stimulus, it is the emotional integration of many different influencing stimuli. • For a detailed understanding of these pathways, as well as the trigeminothalamic tracts, and the correlating neurotransmitters that play a role in pain, review our tutorials on the: Midbrain, Pons, & Medulla.descending pain modulatory system Origins • Originates from numerous regions, including the anterior cingulate gyrus, amygdala, insula, etc... And along its descent innervates the: Periaqueductal gray area • The periaqueductal gray area at the midbrain level. Parabrachial complex • The parabrachial complex in the dorsal pons at the superior cerebellar peduncle, which comprises the "brachium conjunctivum". Rostral ventromedial medulla • The rostral ventromedial medulla. Dorsal horn • The dorsal horn of the spinal cord where they inhibit pain pathways.Clinical Terminology • As a final part of this tutorial, let's learn some key clinical terminology, so we can get a sense of all of the ways that pain can manifest. Pain types: • Neuropathic pain is a broad term, which can refer to pain that stems from any somatosensory nervous system lesion or pathologic process. • Whereas neuralgia is a more specific term, which refers to pain in a nerve distribution (or in the distribution of multiple nerves). • And neuritis specifically refers to inflammatory nerve pain. Abnormal pain responses: • Hyper/hypo-esthesia refers to an increased (hyper) or decreased (hypo) sensitivity to a any sensory stimulus – it's a broad term. • Whereas hyper/hypo-algesia specifically refers to an increased (hyper) or decreased (hypo) pain response to a noxious stimulus. Unexpected pain: • Allodynia refers to pain to a non-noxious stimulus, such as the bed-sheets brushing over your feet. This is especially common in complex regional pain syndrome (aka reflex sympathetic dystrophy). Abnormal sensations: • Dysesthesia, which refers to an unpleasant response and can encompass allodynia or hyperalgesia. • Whereas, paresthesia is a similar term that describes an abnormal sensation but the sensation isn't unpleasant. Absence of pain: • Analgesia refers to the absence of pain to a painful stimulus.

Parametric and Non-parametric tests for comparing two or more groups Statistics: Parametric and non-parametric tests This section covers: Choosing a test Parametric tests Non-parametric tests Choosing a Test

Viral Childhood Exanthems Viral rashes are often caused by immune reactions to the virus and cell damage caused by the virus.A key bacterial cause of rash is Streptococcus pyogenes, which causes Scarlet Fever. Helpful DistinguishersHelpful distinguishers between the viral exanthems:Initial location and pattern of the rash.Three viral exanthems tend to initiate on the face: Measles, rubella, and erythema infectiosum.Face/Scalp & Trunk: ChickenpoxTrunk: Roseola infantum typically first appears on the trunkHand, Foot, and Mouth disease produces rash on the hands and feet, in the mouth. Be aware that these are meant to be helpful generalizations, and may not always hold true; for example, hand, foot, and mouth disease can also produce rash on the buttocks. Rash types:Multiple rash types can exist at once.Macules are flat, colored spots on the skin.Papules are solid, raised areas; larger papules are called nodules.Vesicular rashes comprise raised "pockets" of fluid in the skin.Timing of Rash/Other Signs and Symptoms:The timing of the rash and presence of other symptoms can also help distinguish among the exanthems. For example, some infections are associated with fever, malaise, and respiratory symptoms. Knowing the time lapse between virus introduction and symptom appearance can also help, although the incubation periods of the various viruses often overlap and may include a wide range. Hand, foot, and mouth diseaseUsually caused by Coxsackievirus A.Average incubation period of 3-6 days.Most common in children younger than 5.As its name suggests, hand, foot, and mouth disease is characterized by a rash that can be macular, maculopapular, or vesicular on the hands, feet, and in and around the mouth. Erythema infectiousum, aka, Fifth DiseaseCaused by Parvovirus B19. Average incubation period of 7 days.Tends to affect children 5-15 years old. Initial symptoms can include fever, runny nose, headache; diarrhea is also possible.These flu-like symtpoms are followed by a malar facial rash that spreads to the trunk and extremities. Facial rash takes on a characteristic "slapped cheeks" pattern, whereas the rash on the extremities often comprises maculopapular rash in a "lacy" pattern. Roseola infantum, aka, exanthema subitumMost commonly caused by Human Herpes Virus 6, and sometimes Human Herpes Virus 7. Roseola infantum is also sometimes called "6th disease", because it was the 6th exanthema identified (erythema infectiosum was the fifth). Average incubation period is 9 days.Although disease can occur in a wide range of ages, it most commonly affects children younger than 2 years old.Initial symptoms include a very high fever (exceeding 104 degrees Fahrenheit/40 degrees Celsius). The fever lasts approximately 3 days, which is why Roseola infantum is sometimes called "3-Day Fever".Macular or maculopapular "blanching rash" arises first on the trunk. "Blanching rash" means that when the skin is pressed upon, often with a clear glass, the rash fades from red to pale. Another common finding are red uvulopalatoglossal spots, aka, Nagayama spots.A range of other symptoms, including gastrointestinal, respiratory, ocular, and auditory problems, can occur. Febrile seizures are a common complication in roseola infantum. Chickenpox Caused by Varicella-Zoster virus (aka, Human Herpes Virus-3)Average incubation period is 16 days. Often affects children younger than 5.Prior to rash, patients may experience fever, malaise, sore throat, and low appetite.Rash is characterized by crops of lesions that pass through macular, vesicular, and crusted phases.– Lesions usually first appear on the head/neck, and spread to the rest of the body. Clinical correlation: Shingles is an illness that occurs in adults upon reactivation of the Varicella-Zoster Virus; the reactivated virus is called Herpes-Zoster Virus. Whereas the chickenpox rash is often itchy, the shingles rash can be very painful. Vaccination against Varicella-Zoster virus also prevents shingles. Measles (aka, rubeola)Caused by the Measles virus.Average incubation period is 14 days. Prior to rash, patients often experience Fever and the "Three C's": Cough, Coryza (runny nose), and Conjunctivitis.These symptoms are followed by a maculopapular rash that begins on the face and neck and spreads.Before the body rash, many patients also develop Koplik spots, which are spots along the palate and internal buccal surfaces (these spots are sometimes calked Koplik's sign). Serious complications from measles virus infection include potentially fatal pneumonia and encephalitis; vaccination helps to prevent these and other complications. Rubella (aka, German measles)Caused by Rubella virus.Average incubation period is 14 days. Rubella is characterized by the acute onset of a pink maculopapular rash that begins on the face and spreads. The rash lasts about 3 days, so Rubella is sometimes called "3-Day measles" – careful not to confuse this with Roseola infantum, which is sometimes called "3-Day Fever."Some patients also have swollen lymph nodes in the neck area; systemic symptoms, such as headache, are mild if present. Congenital rubella, which is contracted during fetal development, is associated with severe birth defects; this form of rubella can also be prevented by the rubella vaccine. Additional Images//d1j63owfs0b5j3.cloudfront.net/media/image/8814-1701801884536.png //d1j63owfs0b5j3.cloudfront.net/media/image/1701802080419.png

CRANIAL NERVES ✨ - Mnemonic for CN: "Oh Oh Oh To Touch And Feel A Girls V*gina Ah Heavenly" - Mnemonic for Nerve Fibers: "Some Say Money Matters But My Brother Says Big Brains Matter More" Reference: Tortora, 2010. #CranialNerves #Anatomy #MedicalFacts #Studygram #Medicine

What are proteins ?? Proteins are generally the biomolecules , also called as macromolecules which consists of One or more chains of aminoacid recidues. In a simple way, we can say the building blocks of Aminoacids as a protein. Few Definitions👇 Peptide-sequence of aminoacid recidues. Gene sequence- The sequence or the arrangement of aminoacid recidues in a protein. Cofactors- Protein with non-peptide groups, which are also known as prosthetic groups. Purification of proteins Proteins from different cellular components can be purified by various techniques like •Electrophoresis [Seperates the molecules based on their size, Charge and binding affinity] *Proteins move towards positive Charge* •Chromatography [Separation of a mixture] •Ultra Centrifugation [Separates bio-organelles & Sub-cellular components based on their sedimentation rate. •Precipitation [Formation of a precipitate] Coming to the Nutritional role of proteins We need to understand the types of aminoacid first. There are basically two types of aminoacids. Essential and Non-essential aminoacids. Non-essential aminoacids can be produced in the body or the organism itself . So there is no need to get them through the diet. The name essential aminoacids itself indicates that these aminoacids are essential , so they should be obtained from the diet. Most of the microbes and plants can produce all the aminoacids. Where as animals and human bodies cannot produce all of them. Hence there is a need for obtaining them through diet. Therefore When we consume proteins through diet, they will be broken down into aminoacids which are the building blocks of proteins. These proteins undergoes the denaturation process by the action of acids in the stomach and the hydrolysis process by proteolytic enzymes . So here, the ingested aminoacids will be taken for protein biosynthesis and other Aminoacids gets converted to proteins and then to glucose ( A form of energy or body fuel) through gluconeogenesis or can be fed or stored by the process of kreb's cycle. Therefore this stored energy can be Used during starving conditions . Particularly when the body's main energy source i.e carbohydrates gets depleted, then these protein stores releases proteins (especially from the muscles) in the form of energy and supports the body for surviving. Is this information useful ? Yes or No ?? Please leave a comment :-)

Adrenal insufficiency (AI)Overview:Adrenal insufficiency is associated with high morbidity and mortality, which increase when diagnosis is delayed.We should be suspicious of adrenal crisis in patients who present with acute shock that is refractory to vasopressors and fluid replacement. Adrenal crisis can be fatal.We can broadly classify adrenal insufficiency as primary vs central. Primary adrenal insufficiency (PAI), also called Addison's disease, is rare, and is caused by adrenal gland dysfunction. - All adrenal cortex hormones are potentially affected (cortisol, aldosterone, and androgens). - Primary AI affects slightly more women than men and is typically diagnosed in patients 30-50 years old.Central adrenal insufficiency is more common and is caused by a deficiency in CRH and/or ACTH; thus, it primarily affects cortisol and androgen secretion (recall that aldosterone secretion is primarily directed by the renin-angiotensin-aldosterone system).In chronic AI, adrenal reserves may initially maintain basal hormone levels, but with impaired ACTH stress response. Eventually, however, even basal levels of hormones drop. As we'll see, these nuances in progression of AI can complicate its diagnosis. Treatment for AI includes glucocorticoid, and, in the case of primary AI, mineralocorticoid replacement. - However, we have to beware of overtreatment, especially with glucocorticoids, given that excessive cortisol exposure produces Cushing's syndrome. Primary AI, aka, Addison Disease)Cortisol and aldosterone deficiency are of primary concern. Without the negative feedback effects of cortisol, ACTH levels rise.As a result of elevated ACTH production, patients with Primary AI have characteristic hyperpigmentation of the skin and mucosa; we show this around the gums and in the folds of the hands. - John F Kennedy Jr, the 35th President of the United States, had a famously "bronzed" look due to Addison Disease. Patients are also hypotensive and hyponatremic, with hyperkalemia and metabolic acidosis. Causes of Chronic PAI:Autoimmune diseases: In the United States and other countries where tuberculosis is no longer endemic, autoimmune diseases are the most common causes of primary AI. - In these patients, anti-adrenal antibodies destroy the adrenal cortex.Some important examples of autoimmune disorders resulting in Primary AI are: Autoimmune Polyendocrine Syndrome Type 1 (APS-1): onset is typically in childhood, and the disorder is characterized by adrenal insufficiency, hypoparathyroidism, and mucocutaneous candidiasis. - In children, recurrent mucocutaneous candidiasis is a potential indicator of APS-1 – we show thrush and angular cheilitis, which are common manifestations.Autoimmune Polyendocrine Syndrome Type 2 (APS-2) is associated with adrenal insufficiency, Hashimoto's thyroiditis, and Type I diabetes mellitus. - Be aware that patients with APS are likely to have additional endocrine-related disorders.Infections are another important cause of Primary AI, particularly in countries where TB and/or HIV are endemic. Signs/Symptoms of Chronic PAI:Patients with chronic Primary AI experience symptoms and signs that reflect loss of cortisol and aldosterone: - Weakness, fatigue, weight loss, gastrointestinal problems, and possibly salt cravingsAcute adrenal crisis occurs when patients with adrenal insufficiency face additional stressors, including infections, trauma, surgery, and dehydration. Acute adrenal crisis is a life-threatening situation: look for shock, fever, dehydration, nausea, vomiting, hypoglycemia, apathy, and weakness. To avoid acute adrenal crisis in patients with diagnosed adrenal insufficiency, we provide additional doses of glucocorticoids when stressors, such as surgery, are expected. Patients can also carry medical cards that warn of their condition in the case of accidental trauma, etc. Causes of Acute PAI:Bilateral adrenal hemorrhage: it is thought that the anatomy of the adrenal gland blood supply makes it especially vulnerable to venous congestion and hemorrhaging, so we'll show that each adrenal gland is supplied by three arteries but drained by only one vein.Risk factors for bilateral adrenal hemorrhage include: - Anti-coagulation therapy and disorders that increase the risk of venous blood clots, such as antiphospholipid antibody syndrome and systemic lupus erythematosus. - In children, we watch for the development of Waterhouse-Friderichsen Syndrome, in which adrenal bleeding and dysfunction is caused by septicemia, most often associated with meningococcal or pseudomonas infections. Signs and symptoms of Acute PAI: Fever, nausea, vomiting, tachycardia, cyanosis, and flank and abdominal pain and tenderness. • Additional Causes of PAI: - Adrenoleukodystrophy (X-linked) - Infiltrative disorders (i.e., metastatic, sarcoidosis) - Familial glucocorticoid deficiency - Congential adrenal hypoplasia - Cortisol resistance due to abnormal receptors - Drug effects - Disorders of aldosterone synthesis & action *Central AIBe aware that some authors further divide central into secondary and tertiary, where secondary AI refers to pituitary/ACTH dysfunction and tertiary refers to hypothalamic/CRH dysfunction; however, others lump tertiary in with secondary. Thus, we use "central" to avoid confusion. Central AI is characterized by cortisol and androgen deficiencies due to ACTH deficiency. As mentioned in the introduction, aldosterone secretion is maintained in the absence of ACTH. Central AI (CAI) is more common than Primary AI.Causes of Central AI: Most commonly caused by long-term exogenous steroid use. - Central AI can develop as a result of sudden cessation of the drugs or by the inability of the HPA axis to respond to additional stressors.Central AI may also be caused by dysfunction in the pituitary or hypothalamus, including tumors, infections, and drugs. - Some examples of drugs that interrupt ACTH production include immune checkpoint inhibitors, high-dose progestins, and opioids. - Pituitary and/or hypothalamic dysfunction is often associated with deficiencies of other pituitary hormones. Signs/Symptoms of Central AI: Chronic and nonspecific due to glucocorticoid deficiencies. - Thus, manifestations are similar to what we see in Primary AI, with important exceptions: - There is no hyperpigmentation in central AI, since ACTH is deficient, and, - There is less hypovolemia or hypotension, since aldosterone secretion is normal.We still need to watch for and avoid acute adrenal crisis in these patients. Distinguish between PAI & CAIWhen AI is suspected, we do a rapid ACTH stimulation test, which, in a healthy person, would raise cortisol levels.If the patient has abnormal cortisol levels after the ACTH stimulation test, then we know that the patient has some form of adrenal insufficiency. - If plasma ACTH is high, then the patient has Primary AI; if plasma ACTH is low or normal, then the patient has Central AI. On the other hand, if the ACTH stimulation test results are normal, then we know that the patient does not have primary adrenal insufficiency. - But, we'll need to make sure that the test results aren't simply reflecting decreased ACTH reserves, as we'd see in someone in early stages of central adrenal insufficiency.So, to test for this, we can give the patient metyrapone, which prevents cortisol synthesis, or, we can give an insulin tolerance test, and measure cortisol levels. - If plasma cortisol is normal after the test, we can exclude adrenal insufficiency. - If plasma cortisol is low, then the patient has central adrenal insufficiency, and we'll need to investigate the causes. For references, please see full tutorial.

HypopituitarismHypopituitarism occurs when one or more of the pituitary hormones is deficient. Panhypopituitarism: All 6 anterior pituitary hormones are deficient.Diabetes Insipidus: When the posterior pituitary is affected, ADH is the most apparent loss (i.e., patients have diabetes insipidus).Signs and symptoms: Depend on which hormones are deficient, the extent of the deficiency, and the age of onset.Furthermore, deficiencies tend to develop in this order: Growth hormone, Luteinizing hormone, Follicle stimulating hormone, Thyroid stimulating hormone, ACTH, then Prolactin. Of course, variations occur by etiology.Hypopituitarism is associated with increased mortality, particularly due to cardiovascular and respiratory effects. Diagnosis: Rule out end-organ failure (for example, is TSH deficient or is the thyroid unable to respond to it?). - As part of this process, we can evaluate hormone levels (or use stimulation tests for GH and ACTH), and use brain imaging to look for pituitary tumors, etc. Treatment: Hormone replacement. Anatomy ReviewHypothalamus and pituitary gland. - Hypothalamus, pituitary stalk, and the anterior and posterior pituitary lobes. Hypophyseal portal system, which carries hypothalamic hormones to the anterior pituitary. Primary hypopituitarism: Abnormalities in the pituitary gland that produce pituitary hormone deficiencies. Secondary hypopituitarism: Occurs when there are issues with the hypothalamus or pituitary stalk that precipitate pituitary hormone deficiencies. Causes of HypopituitarismInvasive and compressive anomalies can interfere with hormone production. - Pituitary Adenoma: The most common cause in this category is pituitary adenoma; we show a tumor invading the space around the gland and compressing the anterior lobe where it sits in the sella turcica. - Pituitary apoplexy, which is associated with adenomas, can cause infarction or hemorrhaging, which further impairs hormone production. Pituitary apoplexy can cause headaches, nausea and vomiting, and visual disturbances; can be fatal. - Craniopharyngiomas are a cause of invasive and compressive hypopituitarism in children, in whom we see disturbed growth from the loss of growth hormone.More generally, tumors can interfere with pituitary hormone production. Bear in mind that this includes CNS tumors (meningioma, chordoma, etc.) and metastatic tumors (esp. of the breast and lung).Empty sella syndrome, which is characterized by cerebrospinal fluid leaking into the sella turcica and compressing the pituitary gland. - Risk factors for empty sella syndrome include female sex and hypertension. Traumatic brain injury can damage the pituitary gland – this can be the result of falls (particularly in the elderly), car accidents, and physical violence. Iatrogenic causes include complications of treating brain tumors, etc. with radiation therapy and/or surgery. Sheehan's syndrome is associated with hypotension and pituitary ischemia resulting from severe postpartum hemorrhage. - Hypopituitarism may be evident soon after birth, or later, in the form of low blood pressure, vision deficits, the inability to lactate or menstruate, or other deficiencies. Infiltrative, granulomatous disorders can also affect the pituitary gland. - Two examples include sarcoidosis (neurosarcoidosis, esp. of the pituitary stalk), and Langerhans histiocytosis (which is associated with posterior pituitary involvement and diabetes insipidus).Infectious diseases, particularly tuberculosis meningitis, syphilis, and some fungal infections are known to interfere with pituitary functioning. Immunologic triggers can induce hypophysitis, in which infiltration of lymphocytes and inflammation causes enlargement and malfunctioning of the pituitary gland. - Two examples of this: Lymphocytic hypophysitis, aka, autoimmune hypophysitis, which most often occurs in pregnant females, and, Immune checkpoint inhibitors, such as ipilimumab, that enhance T-cell activation. Since symptoms are generally non-specific, we should monitor the hormones of patients on these treatments. Hemochromatosis, is also associated with hypopituitarism; hemochromatosis, which can be congenital, occurs when excessive GI iron absorption allows for iron overload and damage to tissues, including the pituitary.Other genetic or congenital problems can also cause hypopituitarism. - Combined hormone deficiencies include mutations in POU1F1, PROP-1, HESX1, and PITX2. - Isolated hormonal deficiencies have also been associated with specific mutations (for example, recall that defects in the TRH receptor can lead to TSH deficiencies). Idiopathic: In some cases, no cause can be identified, so we also include "idiopathic" as an etiological category. Signs and Symptoms of Hormone DeficiencyFor a more comprehensive look at these hormonal deficiencies, please see their separate tutorials or the flashcards linked in our notes.Growth Hormone - Deficiencies in children produce slowed growth. - Adults may experience a vague sense of lowered well-being with lethargy and loss of interest; more specific signs include a shift in body composition with decreased muscle mass and increased fat, hyperlipidemia, insulin resistance, and cardiovascular effects including endothelial dysfunction and reduced cardiac output. LH/FSH - Indicate that the effects of reduced luteinizing hormone and follicle stimulating hormone may be particularly subtle, but when the deficiency is extreme, patients can experience amenorrhea, erectile dysfunction, and infertility. - Kallman Syndrome is a genetic absence of GnRH receptors leading to LH/FSH deficiency – this is an example of a genetic etiology for a specific hormonal deficiency. TSH - Lack of thyroid stimulating hormone produces hypothyroidism without the goiter. - Symptoms are usually less severe than in primary hypothyroidism, but still include cold intolerance, fatigue, weight gain, muscle/joint pain, constipation, and bradycardia. ACTH - ACTH deficiency and adrenal insufficiency can cause serious problems due to loss of glucocorticoid actions, including fatigue, hypotension, increased risk of infections, and hypoglycemia. - These effects are usually worse when the patient experiences stress - recall that cortisol is released in response to stress, but is lacking in these patients. - Mineralocorticoid levels (aldosterone) are often preserved, since they are primarily maintained by the renin-angiotensin-aldosterone system. Prolactin - Prolactin deficiency is most obvious when lactation is deficient.ADH - Antidiuretic hormone (aka, vasopressin) can be deficient when the posterior pituitary is involved – recall that ADH deficiency causes diabetes insipidus, in which the kidneys produce large volumes of hypo-osmolar urine. Patients are hypovolemic and dehydrated. • For references, please see the full tutorial on Hypopituitarism.

We often feel redness, heat, swelling and pain at the site of wounds. Actually this is body’s defence mechanism to destroy the pathogen. ...

Hyperparathyroidism OverviewParathyroid hormone increases ECF calcium levels. Regulated by calcium and vitamin D.Parathyroid hormone protects against hypocalcemia by causing calcium release from the bones and reabsorption from the kidneys. Calcium is a vital mineral that participates in various cellular processes, including muscle contraction, nerve conduction, bone and tooth formation, and blood clotting (for a full review of parathyroid hormone and calcium physiology, please see the tutorial on Parathyroid Hormone & Calcium Homeostasis). Physiology Review:Both calcium and phosphate are stored within the hydroxyapatite crystals of bone, and calcium can be retained or excreted in renal and digestive systems, depending on the body's needs. A typical reference blood calcium range is 2.2-2.6 mmol/L (8.6-10.3 mg/dL). Parathyroid gland location: posterior aspect of the thyroid gland.Other key organs that engage in calcium homeostasis: Kidneys, small intestine, particularly the duodenum and, bone. In response to reduced extracellular calcium concentration, the parathyroid glands secrete parathyroid hormone (PTH). Effects of parathyroid hormone on the bones and kidneys: - Prolonged exposure to parathyroid hormone promotes resorption of old bone, and, therefore, the release of calcium and phosphate into extracellular fluid (episodic, transient binding of parathyroid hormone causes an increase in new bone synthesis). - In the kidneys, parathyroid hormone works directly and indirectly to raise extracellular calcium levels:Parathyroid hormone increases calcium reabsorption in the distal convoluted tubule of the nephrons.It also stimulates activation of Vitamin D (activated form = 1,25(OH)2-VD). - Vitamin D acts on the nephron to increase reabsorption of calcium and phosphate. - In the small intestine, Vitamin D increases calcium and phosphate reabsorption. - In the bones, Vitamin D works with parathyroid hormone to facilitate skeletal remodeling, which requires both synthesis and resorption of bone. Thus, the total effect of parathyroid hormone is to elevate extracellular calcium levels. If Vitamin D levels are high, parathyroid hormone secretion is inhibited. Treatment In most cases of hyperparathyroidism, partial or total gland removal is prescribed. Hungry bone syndrome Parathyroid gland removal can lead to "hungry bone syndrome" which manifests as severe and prolonged hypocalcemia after gland removal. Prior to gland removal, the bones were heavily shifted towards resorption and calcium release; it is thought that, after the glands are removed, bones shift towards growth and high calcium uptake. Patients tend to feel tired and weak, or can have more severe responses to the hypocalcemia, which we address in the next section. Primary HyperparathyroidismToo much parathyroid hormone production.Causes:Hyperplasia, adenoma, or carcinoma of the parathyroi glands. Hypercalcemia: Elevated parathyroid hormones stimulate calcium release and retention, resulting in high calcium levels. Signs/Symptoms/Complications:Early and mild cases are often asymptomatic, or present with nonspecific symptoms like fatigue and depression. Because of increased screening for hormone and electrolyte imbalances, most people diagnosed with primary hyperparathyroidism fall into the asymptomatic or mild categories. Chronic and severe hyperparathyroidism experience a variety of signs and symptoms that can be remembered with the expression "stones, bones, abdominal groans, thrones, moans, neuropsychiatric overtones and blood flows." Stones - Renal: Renal effects include kidney stones (from excessive calcium retention), polyuria, and renal insufficiency – this accounts for the "stones and thrones" (thrones meaning the "porcelain throne" that patients spend more time on, thanks to the kidney stones and polyuria)."Bones": Bone pain, fractures, and osteitis fibrosis cystica caused by hyperparathyroidism. In areas where detection of hyperparathyroidism is delayed, osteitis fibrosis cystica is still a classic marker of the disorder. We show three key features of osteitis fibrosis cystica: - "Brown tumor" (shown in a distal phalange). Brown tumors are giant cell lesions caused by excessive bone resorption with fibrovascular tissue replacement and hemorrhaging (hence the reddish-brown color of the lesions and their name). These tumors are most often found in the extremities, clavicles, ribs, mandible, and pelvic girdle. - Subperiosteal resorption of cortical bone (shown on middle phalange) - "Salt and pepper skull" (aka, pepper pot skull) has numerous small but well-defined spots of trabecular bone resorption. Be aware that osteitis fibrosis cystica is also associated with secondary hyperparathyroidism, which we'll address, soon."Abd. Groans" - Gastrointestinal Effects: GI effects include nausea, vomiting, constipation, pancreatitis, and peptic ulcers.The volume depletion caused by renal and gastrointestinal effects of primary hyperparathyroidism (vomiting, polyuria) exacerbates hypercalcemia, so we need to pay attention to fluid loss in these patients."Moans": Muscle weakness is common, and accounts for the "moans.""Neuropsychiatric overtones": Lethargy and confusion; severe cases of hyperparathyroidism can lead to coma. "Blood flows" - Cardiovascular Effects Including hypertension, left ventricular hypertrophy, arrhythmias, calcium valvular deposit, a shortened QT interval, and heart failure. Normocalcemic primary hyperparathyroidism Patients present with primary hyperparathyroidism but have calcium levels within the normal range. In some studies, patients progressed to hypercalcemia over time, leading some authors to wonder if this is merely an early stage of Primary hyperparathyroidism. Secondary Hyperparathyroidism Causes: Chronic kidney disease Vitamin D or calcium deficiency. Chronic kidney disease is a significant cause of secondary hyperparathyroidism in the United States. As a result of diseased, ineffective renal functioning: Phosphate excretion and activation of Vitamin D are both reduced, and calcium reabsorption falls. As a result of low calcium and high phosphate levels, parathyroid hormone is elevated (recall that a key signal for parathyroid hormone release is low extracellular calcium levels). Signs, Symptoms, Complications:Renal osteodystrophy in patients with chronic kidney disease. Similar to patients with primary hyperparathyroidism, patients experience bone pain, increased fractures, and osteitis fibrosa cystica.Calciphylaxis can also occur; indicate that calcium-phosphate products deposit in the blood vessels, fat, and skin, leading to thrombosis and necrosis. Though rare, this is a serious complication of secondary hyperparathyroidism.

In response to The Daily Post’s writing prompt: “Cringe-Worthy.” As we all know, the feeling of “cringe-worthy” is unbecoming. Though it is difficult to articulate, th…

Let’s talk about cravings! How many of you have a pesky craving for sweets...

In the cervix there is a nice transition from the rough and tough squamous epithelial cells of the outside world (vagina) to the squishy secretory columnar epithelial cells of the inside (uterus). …

Plyometrics are often used to bridge the gap between strength and speed, and are a potent training method for enhancing athletic performance.

Learn about the NICABM Experts, including Bessel van der Kolk, Pat Ogden, Peter Levine, Tara Brach, Stephen Porges, and Ruth Buczynski.

Childhood epilepsy is a neurological disorder characterized by recurrent seizures. It is one of the most common neurological disorders

Deep Vein Thrombosis DVT/PE RelationshipDVT is the leading cause of pulmonary embolism.Virchow TriadThe "Virchow Triad" comprises three factors that predispose an individual to deep vein thrombosis; each of the three elements of the Virchow Triad contribute to the formation of clots in the blood vessels.Endothelial injury promotes clotting – endothelial injury can be due to fracture, surgery, trauma, or even previous deep vein thrombosis. • Upon injury, the endothelium responds by triggering the clotting cascade (review of hemostasis). If this process goes unchecked, and the clots are not ultimately dissolved, they can be problematic.Venous stasis is another predisposing factor – venous stasis can be caused by immobility (if a person is bed-ridden or on a long flight, for example), elevated central venous pressure, heart failure, and obesity. • To prevent DVT in hospitalized patients, we use SCD's (sequence compression devices), which prevent venous stasis in the legs. • In select patients, we use prophylactic anticoagulants, which includes low doses of enoxaparin or heparin. • Note that heparin-induced thrombocytopenia is a worrisome complication of anticoagulant, but, overall, in the correct population, prophylactic anticoagulants can be an important way of preventing DVT.Hypercoagulation states are predisposing medical conditions • Pregnancy (which is also associated with inferior vena cava stasis) • The post partum period • Smoking (which is also associated with endothelium damage) • Cancer • Medications, including combined hormonal contraceptives and some hormonal replacement therapies • Coagulation disorders, such as Factor V Leiden disorder. - Be aware that individuals with multiple predisposing factors (i.e., pregnant women who are put on bed rest, for example), are at higher risk for developing deep vein thrombosis.SymptomsWhen present, symptoms of deep vein thrombosis tend to arise unilaterally in the legs, leaving them swollen, tender, and with signs of venous dilation. Deep vein thrombosis can occur in the upper body, too, but this is less common.Post thrombotic syndromePost thrombotic syndrome occurs when the venous valves are damaged. Diagnosis of DVTFor the diagnosis of deep vein thrombosis, we rely on the Wells Score for Deep Vein Thrombosis, which gives points based on several factors including the presence of swelling, edema, and the likelihood of alternative diagnosis.D-dimer level is an important way to try to rule out low-probability DVTs. • If deep vein thrombosis is highly suspected, imaging with contrast venography or venous ultrasonography with compression can verify the presence of thrombus. For references, please see our tutorial on Pulmonary Embolism and Deep Vein Thrombosis

Why Perform A Meta – Analysis Evidence Based Research? Fig 2. Pyramid of evidence-based medicine The Need Of Performing Meta-Analysis: The validity of hypothesis cannot […]

Binary fission involves the cell splitting into two daughter cells while multiple fission involves... read more.

Why are some types of cancer so much more common than others?