Results for "Sweat"

System Interactions in Animals Tools Finish System Interactions in Animals The human body is made of many different organ systems. Each system performs unique functions for the body, but the systems also interact with each other to perform more complex functions. Major Organ Systems Body Systems In humans, cells, tissues, and organs group together to form organ systems. These systems each perform different functions for the human body. The major organ systems and their functions in humans include: The Nervous System — The nervous systems consists of two parts. The central nervous system consists of the brain and spinal cord, while the peripheral nervous system consists of nerves that connect the central nervous system to other parts of the body. The brain plays an important role in interpreting the information picked up by the sensory system. It helps in producing a precise response to the stimuli. It also controls bodily functions such as movements, thoughts, speech, and memory. The brain also controls many processes related to homeostasis in the body. The spinal cord connects to the brain through the brainstem. From the brainstem, the spinal cord extends to all the major nerves in the body. The spinal cord is the origin of spinal nerves that branch out to various body parts. These nerves help in receiving and transmitting signals from various body parts. The spinal cord helps in reflex actions of the body The smallest unit of the nervous system is the nerve cell, or neuron. Neurons communicate with each other and with other cells by producing and releasing electrochemical signals known as nerve impulses. Neurons consist of the cell body, the dendrites, and the axon. The cell body consists of a nucleus and cytoplasm. Dendrites are specialized branch-like structures that help in conducting impulses to and from the various body parts. Axons are long, slender extensions of the neuron. Each neuron possesses just a single axon. Its function is to carry the impulses away from the cell body to other neurons. The Circulatory System — The circulatory (or cardiovascular) system is composed of the heart, arteries, veins, and capillaries. The circulatory system is responsible for transporting blood to and from the lungs so that gas exchange can take place. As the circulatory system pumps blood throughout the body, dissolved nutrients and wastes are also delivered to their destinations. The heart is a muscular organ roughly the size of an adult human's closed fist. It is present behind the breastbone, slightly to the left. It consists of four chambers: right atrium, left atrium, right ventricle, and left ventricle. The heart receives deoxygenated blood from the body and pumps this blood to the lugs, where it is oxygenated. The oxygen-rich blood reenters the heart and is then pumped back through the body. The circulatory system is responsible for transporting blood to and from the lungs so that gas exchange can take place. As the circulatory system pumps blood throughout the body, dissolved nutrients and wastes are also delivered to their destinations. Blood circulation takes place through blood vessels. Blood vessels are tubular structures that form a network within the body and transport blood to each tissue. There are three major types of blood vessels: veins, arteries, and capillaries. Veins carry deoxygenated blood from the body to the heart, except for pulmonary veins, which carry oxygenated blood from the lungs to the heart. Arteries carry oxygenated blood from the heart to different organs, except for the pulmonary artery, which carries deoxygenated blood from the heart to the lungs. The arteries branch out to form capillaries. These capillaries are thin-walled vessels through which nutrients and wastes are exchanged with cells. The Respiratory System — The main structures of the respiratory system are the trachea (windpipe), the lungs, and the diaphragm. When the diaphragm contracts, it creates a vacuum in the lungs that causes them to fill with air. During this inhalation, oxygen diffuses into the circulatory system while carbon dioxide diffuses out into the air that will be exhaled. The trachea branches out into two primary bronchi. Each bronchus is further divided into numerous secondary bronchi. These secondary bronchi further branch into tertiary bronchi. Finally, each tertiary bronchus branches into numerous bronchioles. Each bronchiole terminates into a tiny, sac-like structure known as an alveolus. The walls of each alveolus are thin and contain numerous blood capillaries. The process of gaseous exchange occurs in these alveoli. The diaphragm is a dome-shaped muscle situated at the lower end of the rib cage. It separates the abdominal cavity from the chest cavity. During inhalation, the diaphragm contracts, and the chest cavity enlarges, creating a vacuum that allows air to be drawn in. This causes the alveoli in the lungs to expand with air. During this process, oxygen diffuses into the circulatory system while carbon dioxide diffuses out into the air that will be exhaled. On the other hand, expansion of the diaphragm causes exhalation of air containing carbon dioxide. The Digestive System — The digestive system consists of the mouth, stomach, small intestine, large intestine, and anus. It is responsible for taking in food, digesting it to extract energy and nutrients that cells can use to function, and expelling the remaining waste material. Mechanical and chemical digestion takes place in the mouth and stomach, while absorption of nutrients and water takes place in the intestines. The digestive system begins at the mouth, where food is taken in, and ends at the anus, where waste is expelled. The food taken into the mouth breaks into pieces by the grinding action of the teeth. Carbohydrate digestion starts in the mouth with the breakdown of carbohydrates into simple sugars with the help of salivary enzymes. The chewed food, known as a bolus, enters the stomach through the esophagus. The bolus mixes with acids and enzymes released by the stomach. Protein digestion starts in the stomach as proteins are broken down into peptides. This partially digested food is known as chyme. Chyme enters the small intestine and mixes with bile, a substance secreted by the liver, along with enzymes secreted by the pancreas. The digestion of fats starts in the small intestine as bile and pancreatic enzymes break down fats into fatty acids. The surface of the small intestine consists of hair-like projections known as villi. These villi help in absorbing nutrients from the digested food. The digested food enters the large intestine, or colon, where water and salts are reabsorbed. Any undigested food is expelled out of the body as waste. The Skeletal System — The skeletal system is made up of over 200 bones. It protects the body's internal organs, provides support for the body and gives it shape, and works with the muscular system to move the body. In addition, bones can store calcium and produce red and white blood cells. The Muscular System — The muscular system includes more than 650 tough, elastic pieces of tissue. The primary function of any muscle tissue is movement. This includes the movement of blood through the arteries, the movement of food through the digestive tract, and the movement of arms and legs through space. Skeletal muscles relax and contract to move the bones of the skeletal system. The Excretory System — The excretory system removes excess water, dangerous substances, and wastes from the body. The excretory system also plays an important role in maintaining body equilibrium, or homeostasis. The human excretory system includes the lungs, sweat glands in the skin, and the urinary system (such as the kidneys and the bladder). The body uses oxygen for metabolic processes. Oxygen metabolism results in the production of carbon dioxide, which is a waste matter. The lungs expel carbon dioxide through the mouth and nose. The liver converts toxic metabolic wastes, such as ammonia, into less harmful susbtances. Ammonia is converted to urea, which is then excreted in the urine. The skin also expels urea and small amounts of ammonia through sweat. The skin is embedded with sweat glands. These glands secrete sweat, a solution of water, salt, and wastes. The sweat rises to the skin's surface, where it evaporates. The skin maintains homeostasis by producing sweat in hot environments. Sweat production cools and prevents excessive heating of the body. Each kidney contains about a million tiny structures called nephrons, which filter the blood and collect waste products, such as urea, salts, and excess water that go on to become urine. The Endocrine System — The endocrine system is involved with the control of body processes such as fluid balance, growth, and sexual development. The endocrine system controls these processes through hormones, which are produced by endocrine glands. Some endocrine glands include the pituitary gland, thyroid gland, parathyroid gland, adrenal glands, thymus gland, ovaries in females, and testes in males. The Immune System — The immune system is a network of cells, tissues, and organs that defends the body against foreign invaders. The immune system uses antibodies and specialized cells, such as T-cells, to defend the body from microorganisms that cause disease. The Reproductive System — The reproductive system includes structures, such as the uterus and fallopian tubes in females and the penis and testes in males, that allow humans to produce new offspring. The reproductive system also controls certain hormones in the human body that regulate the development of sexual characteristics and determine when the body is able to reproduce. The Integumentary System — The integumentary system is made up of a person's skin, hair, and nails. The skin acts as a barrier to the outside world by keeping moisture in the body and foreign substances out of the body. Nerves in the skin act as an interface with the outside world, helping to regulate important aspects of homeostasis, such as body temperature. Interacting Organ Systems The organ systems work together to perform complex bodily functions. The functions of regulation, nutrient absorption, defense, and reproduction are only possible because of the interaction of multiple body systems. Regulation All living organisms must maintain homeostasis, a stable internal environment. Organisms maintain homeostasis by monitoring internal conditions and making adjustments to the body systems as necessary. For example, as body temperature increases, skin receptors and receptors in a region of the brain called the hypothalamus sense the change. The change triggers the nervous system to send signals to the integumentary and circulatory systems. These signals cause the skin to sweat and blood vessels close to the surface of the skin to dilate, actions which dispel heat to decrease body temperature. Both the nervous system and the endocrine system are typically involved in the maintenance of homeostasis. The nervous system receives and processes stimuli, and then it sends signals to body structures to coordinate a response. The endocrine system helps regulate the response through the release of hormones, which travel through the circulatory system to their site of action. For example, the endocrine system regulates the level of sugar in the blood by the release of the hormones insulin, which stimulates uptake of glucose by cells, and glucagon, which stimulates the release of glucose by the liver. The nervous and endocrine systems interact with the excretory system in the process of osmoregulation, the homeostatic regulation of water and fluid balance in the body. The excretory system expels excess water, salts, and waste products. The excretion of excessive amounts of water can be harmful to the body because it reduces blood pressure. If the nervous system detects a decrease in blood pressure, it stimulates the endocrine system to release antidiuretic hormone. This hormone decreases the amount of water released by the kidneys to ensure appropriate blood pressure. Appropriate levels of carbon dioxide in the blood are also maintained by homeostatic mechanisms that involve several organ systems. Excess carbon dioxide, a byproduct of cellular respiration, can be harmful to an organism. As blood circulates throughout the body, it picks up carbon dioxide waste from cells and transports it to the lungs, where it is exhaled while fresh oxygen is inhaled. If the concentration of carbon dioxide in the blood increases above a certain threshold, the nervous system directs the lungs to increase their respiration rate to remove the excess carbon dioxide, which ensures that the levels of carbon dioxide in the blood are maintained at appropriate levels. In this way, the circulatory, respiratory, and nervous systems work together to limit the level of carbon dioxide in the blood. Nutrient Absorption To absorb nutrients from food, the nervous, digestive, muscular, excretory, and circulatory systems all interact. The nervous system controls the intake of food and regulates the muscular action of chewing, which mechanically breaks down food. As food travels through the stomach and intestines, the digestive system structures release enzymes to stimulate its chemical breakdown. At the same time, the muscular action, called peristalsis, of the muscles in the wall of the stomach help churn the food and push it through the digestive tract. In the intestines, nutrients from food travel across the surfaces of the villi. The nutrients are then picked up by the blood, and the circulatory system transports the nutrients throughout the cells of the body. The endocrine system releases hormones, such as insulin, that control the rate at which certain body cells use nutrients. Any excess minerals, such as calcium, in the blood are deposited in and stored by the skeletal system. Waste products produced by the use of nutrients, as well as the leftover solid waste from the digestion of food, exit the body through the excretory system. Throughout the process of nutrient absorption, the nervous system controls the muscles involved in digestion, circulation, and excretion. Defense Several body systems interact to defend the body from external threats. The body's first line of defense is the integumentary system, which provide a physical barrier that prevents pathogens from entering the body. The skin of the integumentary system also contains receptors for pain, temperature, and pressure. If an unpleasant stimulus is encountered, these receptors send signals to the central nervous system. In response, the central nervous system sends commands to the muscles to move the body part away from the stimulus. In this way, the integumentary, nervous, and muscular systems interact to prevent damage to the body. In the event of a break in the skin, the nervous, immune, lymphatic, and circulatory systems work together to repair the wound and protect the body from pathogens. When the skin is broken, specialized blood cells called platelets form a clot to stop the bleeding. These platelets also release chemicals that travel through the circulatory system and recruit cells, like immune system cells, to repair the wound. These immune cells, or white blood cells, are transported by the circulatory and lymphatic systems to the site of the wound, where they identify and destroy potentially pathogenic cells to prevent an infection. Some lymphocytes, white blood cells produced by the lymphatic system, also produce antibodies to neutralize specific pathogens. All of the white blood cells involved in the body's response were originally produced in the bone marrow of the skeletal system. If an infection does occur

Spanish - Ordinal Numbers

EL 7 Blood, sweat and seas

Know the relationship between molecular weight and rate of diffusion The rate of diffusion is inversely proportional to the molecular weight Small weight-fast diffusion; heavy weight-slow diffusion Identify RBC’s in various solution and determine tonicity Tonicity - the ability of an extracellular solution to make water move into or out of a cell by osmosis If a cell is placed in a hypertonic solution, there will be a net flow of water out of the cell, and the cell will lose volume (shrink). A solution will be hypertonic to a cell if its solute concentration is higher than that inside the cell, and the solutes cannot cross the membrane. If a cell is placed in a hypotonic solution, there will be a net flow of water into the cell, the cell will gain volume (bigger). If the solute concentration outside the cell is lower than inside the cell, then solutes cannot cross the membrane, then the solution is hypotonic to the cell. If a cell is placed in an isotonic solution, there will be no set flow of water into or out of the cell, and the cell’s volume will remain stable. If the solute concentration outside the cell is the same as inside the cell, and the solutes cannot cross the membrane, the solution is isotonic to the cell. Homeostatic feedback loop for respiratory rate, heart rate and temperature Respiratory Rate: Stimulus : The level of carbon dioxide (CO2) in the blood increases (often due to exercise or hypoventilation) . Receptors: Chemoreceptors in the medulla oblongata, carotid arteries, and aortic arch detect changes in blood pH and CO2 levels Control Center: The medulla oblongata processes this information Effectors: Respiratory muscles (diaphragm and intercostal) adjust breathing rate and depth Response: Increased respiratory rate removes CO2 and increases O2 intake, restoring normal pH and gas levels. Heart Rate: Stimulus : Changes in blood pressure, O2, CO2, or pH levels Receptors: Baroreceptors (detect blood pressure changes) in the carotid sinus and aortic arch; chemoreceptors monitor blood chemistry Control Center: The medulla oblongata (cardiac center) processes signals Effectors : The autonomic nervous system (ANS) adjusts heart rate through the sympathetic nervous system (increases heart rate) or parasympathetic nervous system (decreases heart rate) Response : Heart rate increases during low O2 or low blood pressure (to circulate oxygen) and decreases when homeostasis is restored. Temperature Regulation Stimulus: Changes in body temperature (hyperthermia or hypothermia) Receptors: Thermoreceptors in the skin and hypothalamus detect temperature fluctuations. Control Center: The hypothalamus processes this information and signals effectors Effectors and Responses: If too hot: Blood vessels dilate (vasodilation) to release heat, and sweat glands produce sweat for cooling If too cold: Blood vessels constrict (vasoconstriction) to retain heat, and shivering generates warmth. Steps of a generic homeostatic feedback loop Stimulus : A change in the internal or external environment that disrupts homeostasis (eg. temperature change, pH levels, blood sugar levels) Sensor (Receptor) : Specialized cells or receptors detect the change and send information to the control center. Control Center (Integrator): Often the brain or endocrine glands, this component processes the information from the sensors and determines the appropriate response to restore balance. Effector: This component carries out the response to the stimulus as dictated by the control center. Effectors can be muscles or glands that help to counteract the change. Response: The action taken by the effectors to restore homeostasis. This could involve increasing or decreasing a physiological process (e.g. sweating to cool down or shivering to warm up) Feedback: The results of the response are monitored. If homeostasis is restored, the system maintains its state; if not, the loop may repeat, continuing to adjust until balance is achieved. How to evaluate data to determine the set point, error, and disturbance Identify the set point The set point is the optimal level or range that the system aims to maintain. To determine the set point: Gather baseline data: Collect data over a period to understand the normal range for the variable in question (e.g. body temp., BP, blood glucose levels) Analyze Trends: Look for patterns in the data to identify the average or median value that represents the stable condition of the system. Consult Literature: Reference established physiological norms or previous studies to confirm the typical set point for the variable. Assess Disturbance A disturbance is any factor or event that causes a deviation from the set point. To evaluate disturbances: Identify External and Internal Factors: Analyze the data for any external influences (e.g. environmental changes, dietary habits) or internal changes (e.g. illness, stress) that might have impacted the variable. Quantity Disturbance: Measure the magnitude and duration of the disturbance. This can be done by comparing the data points during the disturbance against the established set point. Monitor Changes: Track how the system responds to disturbances over time to assess their impact on maintaining homeostasis. WBC types and normal distribution values/ abnormal values and what those values indicate (infections/diseases) (Never Let Monkeys Eat Bananas) Neutrophils (50-70%) - First responders to infections, especially bacterial. High levels indicate bacterial infections, inflammation, or stress. Low levels can indicate bone marrow disorders or severe infections. Lymphocytes (20-40%) - Include B cells and T cells, important for immunity. High levels can suggest viral infections or leukemia, while low levels might indicate immune deficiency. Monocytes (2-8%) - Help with cleaning up dead cells and fighting infections. High levels can be linked to chronic infections or autoimmune diseases. Eosinophils (1-4%) - Involved in allergic reactions and fighting parasites. Elevated levels may indicate allergies or parasitic infections. Basophils (0.5-1%) - Release histamine during allergic reactions. High levels might be see in allergic conditions or blood disorders. Normal WBC Count Total WBC Count: 4000-11000 cells per microliter of blood (varies slightly by lab) Leukocytosis (High WBC): Can indicate infection, inflammation, stress, or leukemia Leukopenia (Low WBC): Can result from bone marrow disorders, viral infections, or autoimmune diseases Neutrophils: Banded vs Segmented Neutrophils are the most abundant type of white blood cells and play a crucial role in fighting infections. They exist in different stages of maturation: Banded Neutrophils (“Bands”) - Immature Neutrophils Appearance: Have a curved, unsegmented nucleus (band-shaped) Normal Range: 0-6% of total WBC count (~0-700/uL) Clinical Significance: Increased Bands (Bandemia) -> Indicates an acute bacterial infection or severe stress (e.g. sepsis). The bone marrow releases immature neutrophils in response to infection. Low Bands -> Not clinically significant unless the total WBC count is low, which could suggest bone marrow suppression. Segmented Neutrophils (“Segs”) - Mature Neutrophils Appearance: Have a segmented nucleus with 2-5 lobes Normal Range: 50-70% of total WBC count (~2500-7000/uL) Clinical Significance: High Segs (Neutrophilia) -> Suggests bacterial infections, stress, chronic inflammation, or leukemia Low Segs (Neutropenia) ->Can be caused by viral infections, bone marrow disorders, chemotherapy, or autoimmune diseases. Discuss the stages of cell cycle/mitosis-which stages are longest/shortest The cell cycle is a series of events that cells go through to grow and divide. It consists of two main phases: Interphase (Longest Phase) – Preparation for division Mitosis (Shortest Phase) – Actual cell division Stages of the Cell Cycle Interphase (90% of the Cell Cycle – Longest Phase) Interphase is the period of cell growth and DNA replication. It has three subphases: G1 Phase (Gap 1) The cell grows, produces proteins, and prepares for DNA replication. Longest variable phase; some cells may stay here indefinitely (e.g., neurons in G0 phase). S Phase (Synthesis) DNA replication occurs, ensuring each daughter cell gets a complete genome. Takes about 6-8 hours in human cells. G2 Phase (Gap 2) The cell prepares for mitosis by producing proteins and organelles. Shorter than G1 but still significant in length. Mitosis: Prophase, Metaphase, Anaphase, Telophase Know proportional and inversely proportional relationships Direct (Proportional) Relationship When two quantities increase or decrease together at a constant rate, they are directly proportional. Inversely Proportional When one variable increases, the other decreases proportionally. Know relationship between molecular weight and rate of diffusion The rate of diffusion of a substance is inversely proportional to the square root of its molecular weight. Lighter molecules diffuse faster Heavier molecules diffuse slower due to greater mass. Know relationship between filtration rate and pressure of fluid or weight of fluid Filtration rate is directly proportional to the pressure or weight of the fluid driving the filtration process. Higher pressure → Higher filtration rate Lower pressure → Lower filtration rate Know why men and women blood values are different The differences in blood values between men and women are due to biological, hormonal, and physiological factors

Sputum, BAL, and sweat

BASIC STRUCTURE AND PROMINENT FUNCTIONS OF VERTEBRATE INTEGUMENT INTRODUCTION The integument or the outer cover of the body is commonly referred to as the skin. Together with its derivatives it makes up the integumentary system. It is continuous with the mucous membrane lining the mouth, eyelids, nostrils, rectum and the openings of the urino-genital ducts. The skin functions primarily to cover and protect the tissues lying beneath it. In other words, it forms the external protective covering of an animal. Forms interface between organism and external environment. Part that the predator sees first, and which offers the first line of defense. Abundantly supplied with sensory nerve endings, which are affected by environmental stimuli and play an important role in communication. General metabolism of the body, temperature regulation and water loss. Character of the skin and its derivatives shows variation in different regions of the body, in different individuals, in the same individual as age advances and in different groups of vertebrates. The type of environment whether aquatic or terrestrial is of importance in connection with these variations. The evolution of vertebrate integument is correlated with the transition of vertebrates from an aquatic to a terrestrial environment. Nevertheless, basic similarities exist in the integument of all vertebrates. INTEGUMENT PROPER In Annelids, Arthropods, integument consists of single layer of cells, the EPIDERMIS, together with an outer non-cellular CUTICLE, secreted by the cells. Annelids have a body covered with an external thin collagenous cuticle (never shed or molted). In Arthropods, the chitinous and rigid cuticle makes up the exoskeleton. Periodic shedding of this cuticle is termed Ecdysis. THE VERTEBRATE SKIN DIFFERS FROM INVERTEBRATE SKIN TWO LAYERS – Outer epidermis derived from ectoderm Inner dermis or corium of mesodermal origin. The relative amount of the two layers varies with the environment. EPIDERMIS – the epidermis is made of stratified epithelium (several layers of columnar epithelium cells). These cells are held together tightly by minute intercellular bridges found on the surface of cells. The innermost layer is stratum Malpighii or stratum germinativum placed over a thin basement membrane. These cells divide constantly to produce new cells. Move upwards, tend to become flattened, protoplasm becomes horny (keratinisation). In fishes and amphibians, this keratinised layer forms a cuticle, but in amniotes, it forms stratum corneum, of hard, horny, flat, cornified cells made largely of keratin, which is tough, waterproof and insoluble protein. It affords protection against mechanical injuries, fungal and bacterial attacks and prevents desiccation. In many Tetrapoda, this layer is shed periodically in pieces or all at once. No stratum corneum in cyclostomes and fishes (since they are fully aquatic) here the epidermis has mucous glands, secreting mucus to keep the skin slimy and protects it from bacteria. The epidermis has no blood vessels and is nourished by capillaries in the dermis. The epidermis rests on a thin basement membrane which separates it from the dermis Dermis has an outer loose layer and inner dense layer Made up of dense connective tissue having cells, muscles, blood vessels, lymph vessels, collagen and elastic fibres, and nerves. Amphibians and reptiles -collagen fibres at right angles in three planes Birds and mammals, they have an irregular arrangement. Substances pass by diffusion from the dermis to the epidermis. Skin contains pigment, if present in epidermis, it occurs as a diffuse substance or as granules. If in dermis, then in the form of granules in special branching cells called chromatophores. The pigment can either collect as a central ball making the skin lighter or spread out into all the branches making the skin darker, thus, chromatophores bring about colour variations. Chromatophores are of many kinds, Melanophores that contain brown to black pigment Lipophores or xanthophores which contain yellow red fatty pigments Iridocytes or guanophores contain crystals of guanine which reflect light. Under dermis, the skin has subcutaneous loose areolar tissue which separates the skin from the underlying muscles, it may contain fat and muscles, especially in mammals. Integument of Anamnia shows a decrease in thickness and also a decrease in the degree of ossification. These are of advantage in allowing greater mobility and in amphibians, they permit respiration by the skin. But in Amniota, the skin becomes progressively thicker to prevent loss of water and to retain body heat. STRUCTURE OF INTEGUMENT IN CYCLOSTOMATA Epidermis is multi-layered (stratified) but has no keratin. It has three types of unicellular gland cells: mucus glands (secrete mucus), club cells (scab-forming cells) and granular cells (unknown function). Below epidermis is the cutis formed of collagen and elastin fibres. Star- shaped pigment cells are also present in the cutis. STRUCTURE OF INTEGUMENT IN PISCES The epidermis has several layers of simple and thin cells, but there is no dead stratum corneum. The outermost cells are nucleated and living. The stratum Malpighii replenishes the outer layers of cells which have some keratin. Unicellular goblet or mucous gland cells are found in the epidermis, as in all aquatic animals. The mucous makes the skin slimy reducing friction between the body surface and water, protects the skin from bacteria and fungi and assists in the control of osmosis. Multicellular epidermal glands like poison glands and light producing organs may also be found. The epidermis rests on a delicate basement membrane. The dermis contains connective tissue, smooth muscles, blood vessels, nerves, lymph vessels and collagen fibres. The connective tissue fibres are generally not arranged at right angles but run parallel to the surface. Scales are embedded in the dermis and projected above the epidermal surface. The colours of fishes are due to chromatophores and iridocytes. STRUCTURE OF INTEGUMENT IN AMPHIBIA: The epidermis has several layers of cells, six to eight cells in thickness and is divisible into three layers: stratum corneum, stratum germinativum and a basal portion in contact with the basement membrane. The outermost layer is a stratum corneum, made of flattened, highly keratinised cells. Such a dead layer appears first in amphibians and is best formed in those which spend a considerable time on land. The stratum corneum is an adaptation to terrestrial life (protects body and prevents excessive loss of moisture). In ecdysis, stratum corneum is cast off in fragments or as a whole in some. (moulting / desquamation i.e., removal of unicellular sheet of stratum corneum). The dermis is relatively thin in amphibians, it is made of two layers - upper loose stratum spongiosum and a lower dense and compact stratum compactum. Connective tissue fibres run both vertically and horizontally. Blood vessels, lymph spaces, glands and nerves are abundant in the stratum spongiosum. There are two kinds of glands, multicellular mucous glands and poison glands in the dermis, but they are derivatives of the epidermis. Mucous gland produces mucus (slimy protective covering, helps in respiration). Amphibian skin is an important organ of respiration. Poison glands produce a mild but unpleasant poison which is protective. In the upper part of the dermis are chromatophores. (melanophores and lipophores) Ability of the skin for changing colour to blend with the environment is well developed. INTEGUMENT IN REPTILIA. The integument is thick and dry, it prevents any loss of water, it has almost no glands. The only glands present are scent glands for sexual activity. The epidermis has a well-developed stratum corneum well adapted to terrestrial life. The horny scales of reptiles are derived from this layer. Ecdysis is necessary to remove dead outer layers, hence scales are shed periodically in fragments or cast in a single slough as in snakes and some lizards Scales often form spines or crests. Below the epidermal scales are dermal bony plates or osteoderms in tortoises, crocodiles and some lizards (Heloderma). The dermis is thick and has an upper layer and a lower layer, upper layer has abundance of chromatophores in snakes and lizards. Lower layer has bundles of connective tissue in which collagen fibres lie at right angles. Leather of high commercial value can be prepared from the skin of many reptiles like lizards, snakes and crocodiles. Many lizards and snakes have elaborate colour patterns, they may be for concealment or as warning colours. There is marked colour change in certain lizards such as chameleon, the colour may change with the environment for concealment or it may change in courtship or threat. The ability of chameleons and some other animals to change colour is known as metachrosis. (metachromatism) In Calotes, chromatophores are controlled by the posterior lobe of pituitary whereas in chameleons they are controlled by the Autonomic Nervous System. INTEGUMENT IN BIRDS Thin, loose, dry and devoid of glands. There is only a uropygial gland at the base of the tail, its oil is used for preening (to clean and tidy its feathers with its beak) and waterproofing the feathers (aquatic birds) Epidermis is delicate except on shanks and feet where it is thick and forms epidermal scales. The rest of the body has a protective covering of epidermal feathers. The keratin producing powers of the epidermis are devoted to producing feathers and scales. The dermis is thin and has interlacing connective tissue fibres, abundant muscle fibres for moving feathers, blood vessels and nerves. The dermis has an upper and lower compact layer, between which is a vascular layer, the dermis also contains fat cells. The skin has no chromatophores. Pigment is found only in feathers and scales. Colour patterns in birds are vivid (concealment, recognition and sexual stimulation) Colours are produced partly by pigments and partly by reflection and refraction from the surface of the feathers. INTEGUMENT IN MAMMALS Skin is elastic and waterproof, much thicker than in other animals, especially the dermis is very thick and is used in making leather. Epidermis is thickest in mammals. Outer stratum corneum containing keratin, cells not dead as believed before. Below this is stratum lucidum (barrier layer), chemical called eleidin Below this stratum granulosum, darkly staining granules of keratohyalin Below this is stratum spinosum whose cells are held together by spiny intercellular bridges. Lastly stratum germinativum which rests on a basement membrane Dermis is best developed in mammals. Upper layer is papillary layer made up of elastic and collagen fibres with capillaries in-between, thrown into folds called dermal papillae, especially in areas of friction Greater lower part of dermis is reticular layer, having elastic and collagen fibres. In both layers there are blood vessels, nerves smooth muscles, certain glands tactile corpuscles and connective tissue fibres in all directions. Below dermis the subcutaneous tissue contains a layer of fat cells forming adipose tissue In the lowest layer of epidermis there are pigment granules, no pigment bearing chromatophores in mammaIs (in man, branching dendritic cells or melanoblasts) FUNCTIONS OF THE INTEGUMENT ▪ PROTECTION ▪ TEMPERATURE CONTROL ▪ FOOD STORAGE ▪ SECRETION ▪ EXCRETION ▪ SENSATION ▪ RESPIRATION ▪ LOCOMOTION ▪ DERMAL ENDOSKELETON ▪ SEXUAL SELECTION 1. Protection: The integument forms a covering of the body and is protective. It protects the body against entry of foreign bodies and against mechanical injuries. It protects the tissues against excessive loss of moisture, this is very important because both aquatic and terrestrial animals are dependent upon water in their bodies for various metabolic activities. The integument forms protective derivatives, such as scales, bony plates, layer of fat, feathers and hair which reduce the effect of injurious contacts. In some animals the skin shows protective colouration which makes the animals resemble their environment, thus, making them almost invisible to their enemies. Poison glands of toads, slippery skin of aquatic animals and an armour of spines of some mammals are protective devices of the integument. The skin forms a covering which prevents the passage of water and solutes in one of the following ways: (a) By formation of cuticle in Protochordata and embryos of fishes and amphibians, (b) By secreting a coat of mucus in fishes and aquatic amphibians, and (c) By formation of keratin layers in the epidermis of tetrapoda. Keratin is formed from the cytoplasm of degenerating cells of the epidermis which finally form a layer of horny stratum corneum. 2. Temperature Control: Heat is produced constantly by oxidation of food stuffs in tissues. This heat is distributed evenly by the circulating blood. The body heat is lost constantly with expired breath, with faeces and urine, and from the surface of the skin. The integument regulates heat and maintains a constant temperature in endothermal animals. In birds the heat is regulated by adjustment of feathers which retain a warm blanket of air, when feathers are held close to the body, they remove warm air and body cooled, when feathers are fluffed out, they keep the warm air enclosed. In mammals, constant evaporation of sweat regulates the body heat. In cold weather contraction of skin’s blood capillaries reduces the loss of body heat. In some animals, fat in the skin prevents loss of heat because it is a non-conductor of heat. 3. Food Storage: The skin stores fat in its layers as reserve food material which is used for nourishment in times of need. In whales and seals the fat of the skin forms a thick layer, called blubber which is not only reserve food but also maintains the body temperature. 4. Secretion: The skin acts as an organ of secretion. Glands of the skin are secretory. In aquatic forms there are secretory mucous glands whose secretions keep the skin moist and slippery. In mammals, sebaceous glands secrete oil which lubricates the skin and hairs. Mammary glands produce milk for nourishment of the young. In birds uropygial glands secrete oil for preening the feathers. Odours of scent glands attract the opposite sex. Lacrymal glands’ secretion wash the conjunctiva of eyeball in mammals. Ear wax (cerumen) secreted by the glands of auditory meatus greases the eardrums and avoids insects to enter the canal. 5. Excretion: The integument acts as an organ of excretion. Shedding of the corneal layer during ecdysis removes some waste substances. In mammals metabolic waste (salts, urea and water) is removed from the blood by means of sweat. Chloride secreting cells are found in gills of marine fishes. 6. Sensation: The skin is an important sense organ because it has various kinds of tactile cells and corpuscles which are sensory to touch, temperature changes, heat, cold, pressure and pain. 7. Respiration: In amphibians, the moist skin acts as an organ of respiration, in frogs the respiratory function of the skin is greater than that of the lungs. 8. Locomotion: Derivatives of the integument bring about locomotion in some animals, such as the fins of fishes aid in locomotion in water, the web of skin in the feet of frogs and aquatic birds aid in swimming, feathers of the wings and tail of birds are used for flying, and extensions of the integument forming “wings” of flying lizards, extinct pterodactyls, flying squirrels and bats. 9. Dermal Endoskeleton: The skin contributes to the endoskeleton. It forms the dermal bones of vertebrates and also forms parts of the teeth. Endoskeleton of head protects the brain and sense organs. In the body it protects the soft, tender viscera. 10. Sexual Selection: The skin acts as an organ of sexual selection. It provides the feathers of birds which often have brilliant colours which are for sexual attraction. Some integumentary glands of mammals produce odours far attracting the opposite sex. Antlers of male deer distinguish it from female. Besides the above functions, mammalian skin synthesizes the vitamin D with the help of Sebum of sebaceous glands. Brood pouches beneath skin in some fishes and amphibians protect unhatched eggs. Nasal glands of tetrapods, keep the nostrils free of dirt and water. Skin also has the power of absorption of oils, ointments, etc

Sweat glands

Save Flashcards Learn Test Blocks New Blast Match Worries about Kennedy during 1960 election Shortcut Press Space or click on the card to flip He was too young, inexperienced, and Catholic Track progress 4 / 58 Profile Picture Vera_Klochkova Top creator on Quizlet · Created 5 days ago 0:05 / 0:15 Students also studied Flashcard sets Study guides Practice tests Modern Era Review Teacher 167 terms Profile Picture PhillipsPHS Preview Civil Rights 69 terms Profile Picture apantis7 Preview Lecture Notes (History 5B-01 Final) 83 terms Profile Picture Samuel_Soohoo7 Preview Chapter #26 Quiz 10 terms Profile Picture pixelpirate87 Preview HIST 1302 Exam 3 40 terms Profile Picture jeremy1220045 Preview ap world unit 5 learning objectives & historical developments 11 terms Profile Picture Paul_Espinosa32 Preview history test 6 terms Profile Picture isabel_irwin9 Preview Neolithic Era: Turning Point in History 21 terms Profile Picture artisticallyselena Preview Unit 4 History Study Guide 24 terms Profile Picture crimsontraylor723 Preview ch. 28--29 45 terms Profile Picture leslierodriguez_24 Preview LOUISIANA HISTORY: Chapter 1, Lesson 4 34 terms Profile Picture frcramer Preview Mil History WEEK 1 7 terms Profile Picture SiahQuizzes Preview Ship Designations and Classes 41 terms Profile Picture sayers001 Preview Worldview and the History of Life 56 terms Profile Picture bbene792 Preview Key Events and Concepts of WWII and Human Rights 84 terms Profile Picture kaptsany27 Preview Chapter 16 Terms 20 terms Profile Picture A_ydunx Preview World War I Causes and Impact 38 terms Profile Picture quizlette76576101 Preview Euro 8.2 WW1 9 terms Profile Picture Daniela_Arana-Duenas Preview 9/11 Quiz 25 terms Profile Picture aprilsimmons8 Preview History WWII Test 19 terms Profile Picture vbaseball09 Preview Social Studies 5004 World History 49 terms Profile Picture anna_reimers7 Preview World History : Chapter 19 - 21 Vocab 39 terms Profile Picture aucletic Preview AP World History People 30 terms Profile Picture Allyson_Bell924208 Preview Final Exam for Global World History 56 terms Profile Picture Esme1058 Preview World History 7 terms Profile Picture plehmann2 Preview social studies 13 terms Profile Picture Amanda_Lin57 Preview AP U.S. History - Chapter 12 23 terms Profile Picture Mancan76 Preview Practice questions for this set Learn 1 / 7 Study with Learn Kennedy seemed cool & appealing, spoke to people - Nixon looked sickly, sweaty and uncomfortable Choose matching term 1 Engel v. vitale 2 Robert f. kennedy 3 Baker v. carr 4 Kennedy / Nixon Debate Don't know? Terms in this set (58) Your stats Still learning (58) You've started learning these terms. Keep it up! Select these 58 John F. Kennedy (JFK) 35th President - youngest man ever elected & first Catholic; won election by NARROW margin over Nixon; inspired HOPE in all Americans; assassinated in Dallas, Texas on Nov. 22, 1963 Robert F. Kennedy Attorney General of the US; he was JFK's younger brother and trusted advisor Kennedy / Nixon Debate Kennedy seemed cool & appealing, spoke to people - Nixon looked sickly, sweaty and uncomfortable Worries about Kennedy during 1960 election He was too young, inexperienced, and Catholic Camelot Was the name of a popular Broadway musical about King Arthur who fought to make things right -- "Camelot" came to represent the energetic, idealistic image of the Kennedy White House Why were many of Kennedy's proposals defeated in Congress? He did NOT have a strong mandate to push them through Mandate Public endorsement of a candidate's proposals -Kennedy did NOT have this b/c he won by slim margin; LBJ did have this, he won by a landslide 3 Goals of Kennedy's New Frontier (1) Improve the economy / cut taxes (2) Fight poverty / provide aid to the poor (3) Speed up the space program **He gave Americans HOPE for a better future Strategies JFK used to improve relations between US and developing countries Peace Corp & Alliance for Progress Peace Corps Federal programs established to send AMERICAN VOLUNTEERS to help developing nations around the world to raise their standard of living - would help them resist communism Alliance for Progress Program set up by JFK for the US and cooperating nations to send money to LATIN AMERICA in an attempt to help them resist communism Berlin Crisis Soviet leader Khrushchev tried to bully Kennedy (wants US out of Berlin) - Kennedy responds by building up the US military - Khrushchev responds by building the Berlin Wall Why did USSR build the Berlin Wall? Built by the Soviets in order to prevent the EAST GERMANS from fleeing to West Berlin for freedom Bay of Pigs Invasion - who planned it? Eisenhower - he approved plans for the CIA to train Cuban exiles as guerillas to invade Cuba Bay of Pigs Invasion - what happened? 1,400 Cuban exiles invaded Cuba on April 17, 1961 Bay of Pigs Invasion - goal? To overthrow Fidel Castro, the communist leader of Cuba Bay of Pigs Invasion - outcome? The mission failed miserably - Kennedy's administration humiliated - Cuba gov't turned to USSR for protection from the US Cuban Missile Crisis The confrontation between the US and the USSR that brought them to the brink of a nuclear war What event started the Cuban Missile Crisis? American spy plane discovered Russian missile sites being placed in Cuba 4 options Kennedy had in handling the Cuban Missile Crisis 1) Do nothing & avoid immediate war 2) Attack and destroy missile site 3) Diplomatic pressure to remove missiles 4) Naval blockade (quarantine) How was the Cuban Missile Crisis resolved? Kennedy set up a naval blockade - Soviets backed off - Soviets agreed to remove missiles from Cuba - US agreed not to invade Cuba Results of Cuban Missile Crisis US promised to remove their missiles from Turkey, US & Soviets signed Limited Test Ban Treaty, US & Soviets establish "hot-line" for future crises Nikita Krushchev Soviet leader (1953-1964) during Berlin crisis and the Cuban Missile Crisis. He and JFK signed the Limited Nuclear Test Ban Treaty in 1963, temporarily easing Cold War tensions Hotline Direct telephone line between US & Soviets that was set up after the Cuban missile crisis; direct line of communication between JFK & Khushchev Effect Cold War had on NASA US was losing the space war to the Soviets, US spent a lot of money on NASA and on science & math education in schools JFKs goal for NASA To land a man on the moon before 1970 Limited Test Ban Treaty An agreement between the US & Soviets, and 40 other countries, not to test nuclear weapons above ground; result of Cuban missile crisis November 22, 1963 President Kennedy was shot and killed Why did Kennedy's assassination deeply affect Americans? He represented hope for a better future Magic Bullet Theory Theory by Warren Commission that one bullet caused wounds in both Kennedy and Texas Gov. John Connally, who sat in the front seat of the presidential limousine Lee Harvey Oswald Ex-Marine & communist sympathizer who killed JFK in Dallas, Texas, on November 22, 1963 - he was murdered two days later by Jack Ruby Jack Ruby Night club owner who assassinated Lee Harvey Oswald, he was suspected of having ties to Mafia What was the Warren Commission? A committee that investigated the assassination of President Kennedy Findings of Warren COMMISSION Determined that Oswald acted alone; 3 shots from the book depository Lyndon B. Johnson (LBJ) Vice-president to JFK; became the 36th president after Kennedy's assassination; reelected in 1964; domestic policy called the "Great Society" Great Society Johnson's domestic policy - series of legislative issues that included major poverty relief, education aid, healthcare, voting rights, conservation, urban renewal & economic development (his programs were a continuation of JFKs New Frontier plans) Criticism of the Great Society It spent too much money on the poor and it gave too much authority to Fed. gov't Equal Pay Act of 1963 Law that required both men and women to receive equal pay for equal work Civil Rights Act of 1964 A federal law that made discrimination illegal in voting, public places, schools and jobs VISTA (Volunteers in Service to America) Federal program to send volunteers to help people in poor communities in the U.S.; includes Head Start pre-school program to help kids from low income families Medicare Federal program that provides health insurance for Americans 65 and older Medicaid Federal program that provides health insurance to poor Americans of any age who cannot afford it Immigration Act of 1965 Law that abolished immigration quotas and increased the number of immigrants allowed into the US What is the Warren Court? Supreme Court named after Chief of Justice Earl Warren during JFK's presidency - he overturned many old laws & rulings & established new legal procedures 5 matters supported by the Warren COURT Rights of the accused, voting rights, the poor, civil rights, religious freedom Apportionment Warren Court decision about the way seats in a legislative body are distributed among electoral districts Baker v. Carr Voting districts must be based on population - "one person, one vote" Engel v. Vitale Public schools can't require a school prayer because it defies separation of church and state Mapp v. Ohio Police required to have specific warrants in order to make arrests Miranda v. Arizona Criminal suspects must be informed of their right to consult with an attorney and of their right against self-incrimination Miranda Rule Ruling by the Warren Court that police must inform persons accused of a crime their legal rights Why LBJ won 1964 election by a landslide He ran against Barry Goldwater who threatened to use nuclear weapons (think of Daisy commercial) How did Johnson continue Kennedy's plan to eliminate poverty in the US He pushed to pass JFKs anti-poverty programs, such as the Economic Opportunity Act (including Head Start & VISTA) Relationship between Warren Court & Great Society Both dealt with the rights of the poor & disadvantaged Similarities between the New Frontier (JFK) & the Great Society (LBJ) Both focused on civil rights and helping the poor and elderly (believed federal gov't should help the less fortunate with their economic & social needs) Differences between the New Frontier (JFK) & the Great Society (LBJ) LBJ had a strong mandate in Congress and was able to get laws passed - JFK did not; LBJ focused on domestic policy, JFk more on foreign Panama Canal Zone Controlled by the US since early 1900's; in 1964, nationalist rioted & demanded US give up control - Panama President and LBJ negotiated treaties Invasion of Dominican Repbulic Attacks on Dominican Republic gov't by rebels. LBJ said it was fueled by Communists - sent 22,000 marines. Gov't & marines took control, attack over, provisional US gov't set up in 1965 Add or remove terms You can also click the terms or definitions to blur or reveal them Review with an activity About us About Quizlet How Quizlet works Careers Advertise with us Get the app For students Flashcards Test Learn Solutions Modern Learning Lab Quizlet Plus Study Guides Pomodoro timer For teachers Live Checkpoint Blog Be the Change Quizlet Plus for teachers Resources Help center Honor code Community guidelines Privacy Terms Ads and Cookie Settings Quizlet for Schools Parents Language English (USA) © 2025 Quizlet, Inc. COPPA Safe Harbor Certification seal Home Your library Notifications 2 MUSH Psychology 2023 Fall B Peri... 2023 Fall A Peri... Spanish 2H New folder Start here Flashcards Study Guides Practice Tests Expert Solutions Home

sweat quotes - 12.02.25

Primary adrenal insufficiency = problem at level of adrenal glands Causes? Addison’s disease Pathophys? Autoimmune destruction of the adrenal glands Associated with hyperpigmentation POMC is precursor to both ACTH and MSH PAI → lack of negative feedback → high ACTH Lab findings? ACTH high Aldosterone low Destruction of zona glomerulosa Renin high Hypotension → RAAS activation Electrolytes Na+ low, K+ high CBC Eosinophils high Pathophys? Glucocorticoids → eosinophil apoptosis. Lack of glucocorticoids cause eosinophilia. Dx? Cosyntropin testing → no rise in cortisol Adrenal glands aren’t working, so no response to ACTH. Tx? prednisone/hydrocortisone/dexamethasone + fludrocortisone (mineralocorticoid) Stress-dose steroids for surgery, serious illness, etc. Secondary adrenal insufficiency = problem at level of pituitary, reduced ACTH release Causes? MC is prolonged steroid use → ACTH suppression Sheehan’s syndrome (infarction of pituitary) pregnancy Pituitary tumors (ACTH-producing tumor) Lab findings? ACTH low Anterior pituitary is being inhibited Aldosterone normal Zona glomerulosa under control of RAAS system Renin normal Electrolytes Na+ & K+ unaffected (Aldosterone levels are normal) CBC Neutrophilia due to demargination (if pt was recently taking steroids) Dx? Cosyntropin testing → rise in cortisol Adrenal gland is functional Tx? Glucocorticoids Do not need to replace mineralocorticoids since adrenals are functional and aldosterone is under RAAS control Stress-dose steroids for surgery, serious illness, etc. AI with a history of nuchal rigidity and purpuric skin lesions → Waterhouse-Friedrichson syndrome Pathophys? AI 2/2 hemorrhagic infarction of the adrenal glands in the context of Neisseria meningitidis infection Adrenal synthesis enzymes If the enzyme starts with 1 → HTN (high mineralocorticoids) and hypokalemia If the second # is 1 → virilization (high androgens) E.g. 11-beta hydroxylase deficiency → HTN & virilization E.g. 21 hydroxylase deficiency → virilization only E.g. 17-alpha hydroxylase deficiency → HTN only B12 deficiency Where does B12 come from? Animal products VS folic from plants Physiology R factor in saliva binds to B12 and protects it from acidity in the stomach. R factor protector -B12 travels to the duodenum. Parietal cells produce intrinsic factor, which travels to the duodenum. Pancreatic enzymes cleave B12 from R factor and B12 then binds IF. B12-IF complex is reabsorbed in the terminal ileum Reabsorption where? Terminal ileum Causes of B12 deficiency Extreme vegan Pernicious anemia Pancreatic enzyme deficiency Cystic Fibrosis Can’t cleave B12 from R factor Crohn’s Affects terminal ileum Lab markers Homocysteine HIGH MethlyManoicAcid HIGH Presentation? Megaloblastic anemia Subacute combined degeneration (of dorsal columns + lateral corticospinal tract) Peripheral neuropathy Dx of pernicious anemia? anti-IF Ab Folate deficiency Where does folate come from? Leafy things Causes of folate deficiency Poor diet (e.g. alcoholics, elderly) Phenytoin Lab markers Homocysteine HIGH MMA normal Presentation? Megaloblastic anemia Prophylaxis in HIV+ patients CD4 < 200 → PCP TMP-SMX, inhaled pentamidine, dapsone, atovaquone CD4 < 100 → Toxoplasm Treat: TMP-SMX CD4 < 50 → MAC Treat: Azithromycin If live in endemic area, CD4 < 250 → Coccidioides Immitis E.g. Arizona, Nevada, Texas, California Treat: Itraconazole If live in endemic area, CD4 < 150 → Histoplasma Capsulatum E.g. Kentucky, Ohio, Missouri Treat: Itraconazole Diabetes insipidus Dx? Water deprivation test Measure serum osmolality & urine osmolality Deprive pt of water Remeasure serum osmolality & urine osmolality If urine osmolality doesn’t go up → suspect DI Central DI → deficiency of ADH Pathophys? Supraoptic nucleus not making enough ADH Dx? Give desmopressin → urine osmolality increases significantly Nephrogenic DI → kidneys are not responding to ADH Dx? Give desmopressin → urine osmolality doesn’t change much Tx? Hydrochlorothiazide Unless 2/2 lithium, use amiloride or triametere Causes? Lithium SSRIs Carbamazepine Demeclocycline Tx of normovolemic hypernatremia? D5W to correct free water deficit Divine says NS, but most other resources I found said correct free water deficit Tx of hypovolemic hypernatremia? Give NS first until normal volume, then give D5W Consequence of correcting hypernatremia too rapidly? Cerebral edema Osteoarthritis Presentation? Old person with joint pain that gets worse throughout the day Risk Factr? Obesity vs decreases osteoporosis Imaging findings? Joint space narrowing Subchondral sclerosis Subchondral cysts Osteophytes Arthrocentesis findings? <2000 cells Tx? 1st line acetaminophen 2nd line NSAID (e.g. naproxen) 3rd line joint replacement surgery Returned from a business conference 1 week ago + Fever + Nonproductive cough + Abdominal pain + Hyponatremia → Legionella Dx? Urine antigen Tx? FQ or macrolide MaCroLide mnemonic = Mycoplasma, Chlamydia, Legionella What are the common causes of atypical PNA? Mycoplasma, Legionella, Chlamydia MC cause? Mycoplasma CXR findings? Interstitial infiltrates HY associations C. Psittaci → birds C. Burnetii → cows, goats, sheet Mycoplasma → college student w/ walking pneumonia Midsystolic click heard best at the apex. → mitral valve prolapse “Stenosnap & Proclick” Risk Factor? Connective tissue disease Marfarn Ehlers-Danlos ADPKD bilateral renal masses Classic demographic? Young woman psychiatric Pathophys? Myxomatous degeneration MVP vs aortic dissection: cystic medial necrosis Exam maneuvers Anything that increase amount of blood in LV → murmur softer Increase preload Increase afterload Anything that decreases amount of blood in LV → murmur louder Dx? Echo Scaly, itchy skin with yellowish crusting in the winter. → seborrheic dermatitis Tx? Topical antifungals e.g. ketoconazole or selenium sulfide shampoo Classic disease distribution? Hair → e.g. cradle cap Eyebrows Episodic/intermittent HTN + HA → pheochromocytoma Genetic disease associations MEN2A MEN2B VHL in brain (hemangioma) NF-1 growth in skin Pathophys? Catecholamine-secreting tumor Location? Adrenal medulla Posterior mediastinum Organ of Zuckerkandl (chromaffin cells along the aorta) Dx? 1st step: urine metanephrines If elevated → CT abdomen If nothing found on CT → MIBG scan Tx? Alpha blocker (e.g. phenoxybenzamine, phenotaline) THEN beta blocker Most common cause of a Lower GI Bleed in the elderly → diverticulosis Dx? Colonoscopy or barium enema Recall that you acutely do a CT scan for diverticulitis, then 6 weeks later colonoscopy to r/o cancer Ppx? Eat fiber Megaloblastic anemias Blood smear findings? Hypersegmented neutrophils MCV > 100 Classic patient demographic with folate deficiency? Alcoholics Elderly person with poor nutrition Folate synthesis inhibitors Pt with molar pregnancy → methotrexate Pulmonary issue? Pulmonary fibrosis HIV+ pt with ring-enhancing lesions → pyrimethamine-sulfadiazine Pyrimethamine inhibits DHFR AIDS pt on ppx for toxo → TMP-SMX TMP inhibits DHFR Use of leucovorin? Rescue bone marrow in setting of methotrexate toxicity Mechanism? Folinic acid analog CMV presentations Esophagitis → linear ulcers Colitis → post-transplant pt Retinitis → HIV pt with CD4 < 50 Congenital CMV → periventricular calcifications + hearing loss calcifications elsewhere → toxo Histology? Owl’s eye intranuclear inclusions Tx? Gancicyclovir Resistance? UL97 kinase mutation Tx for resistance? foscarnet CD4 < 200 + severe peripheral edema + frothy urine. → FSGS in HIV pt Variant classic in HIV+ pts? Collapsing variant Tx? Steroids + cyclophosphamide + ACE-I Indinavir AE? Kidney stones triad of fever, rash, and eosinophiluria → acute interstitial nephritis Drugs cause? Penicillins Tx? Stop the drug! Can add steroids if severe Vitamin D metabolism Liver converts Vit D to calcidiol (25OH-Vit D). Calcidiol goes to kidney. Alpha-1 hydroxylase converts calcidiol to calcitriol (1,25-OH Vit D). Common causes of Vitamin D deficiency CKD → 1-alpha hydroxyalse deficiency Liver disease → can’t make calcidiol CF → malabsorption Crohn’s → malabsorption Osteomalacia vs Rickets Osteomalacia in adults Rickets in kids Tx? Calcium + vit D Lab findings? Ca++ low Phos low Low in liver disease High in kidney disease (kidneys can’t get rid of phos) PTH high (2ary hyperpara) vs liver dx PTH low Alk phos Aspiration pneumonia Risk Factor? Alcoholism Dementia Neuromuscular problems (e.g. MG, ALS) Bugs? Anaerobes foul smelling Bacteroides FUsobacterium Peptostreptococcus Klebsiella → currant jelly sputum alcoholic Tx? Clindamycin CURB-65 criteria Purpose? Who to admit Cutoff? 2+ → hospitalize C = confusion U = uremia (BUN > 20) R = RR > 30 B = BP < 90/60 Age > 65 Drugs commonly used in PNA treatment Ceftriaxone Levofloxacin fluoroquinolone Macrolides - great for atypical PNA Pharmacological management of pulmonary arterial HTN Endothelin antagonists Bosentan ambrisentan PDE-5 inhibitors Sildenafil Tadalafil Prostacyclin analogs Iloprost Epoprostenol Treprostinil Causes? Young female → idiopathic PAH Mutation? BMPR2 55 yo F presents with a 5 week history of a rash on her forehead. PE reveals scaly macules with a sandpaper texture. → actinic keratosis Risk Factor? Sun exposure Tx? Topical 5-FU Possible dangerous sequelae? Squamous cell carcinoma Most likely disease sequelae? Resolution 1ary hyperparathyroidism 2ary hyperparathyroidism 3ary hyperparathyroidism Autonomous PTH production Causes? Adenoma Parathyroid hyperplasia PTH high Ca++ high Phos low Low Ca++ → PTH production Causes? CKD PTH high Ca++ low Phos high PTH production despite normalized of Ca++ levels Causes? CKD s/p transplant PTH high Ca++ high Phos low Tx? Parathyroidectomy (remove 3.5 glands) Cinacalcet (CSR modulator) Hypercalcemia Presentation? bones, stones, groans, psychic overtones Tx? 1st step: Normal Saline Hypercalcemia of malignancy → bisphosphonates EKG finding? Shortened QT Periumbilical pain that migrates to the right lower quadrant. → appendicitis PE findings? McBurney’s point tenderness Psoas sign (flex hip pain) Obturator sign (pain with internal rotation of hip) Rovsing’s sign (palpation of LLQ → pain in RLQ) Dx? CT scan Pregnant → US Kid → US Tx? Surgery Classic drug and viral causes of aplastic anemia. Drugs? Carbamazepine Chloramphenicol Viral? Parvovirus B19 (single stranded DNA virus) Fanconi anemia Pathophys? Problems with DNA repair Fanconi anemia vs Fanconi syndrome Fanconi anemia → cytopenias + thumb anomalies + short stature + cafe-au-lait spots Fanconi syndrome → type 2 RTA (proximal) CD4 count of 94 + MRI revealing ring enhancing lesions in the cortex → toxoplasmosis Tx? Pyrimethamine-sulfadiazine Rescue agent for pt who becomes leukopenic with treatment? leucovorin Who should get steroids? Increased ICP For PCP pneumonia: O2 sat < 92 PaO2 < 70 A-a gradient > 35 Ppx? TMP-SMX for CD4 < 100 Congenital toxo Hydrocephalus Chorioretinitis Intracranial calcifications Classic methods of transmission? handling cat litter Lupus nephritis Associated autoantibody? anti-dsDNA Classic “immunologic” description? “Full house” pattern Tx? Steroids + cyclophosphamide Osteoporosis Screening population? women > 65 Screening modality? DEXA scan Dx? T-score < -2.5 Risk Factor? Postmenopauseal Low BMI Smoking Alcohol Preventive strategies? Weight bearing exercise Smoking cessation Reduce alcohol consumption Tx? 1st line: bisphosphonates + Ca/Vit D supplementation Raloxifene (SERM) Agonist in bone Blocker Antagonist in breast Classic locations of osteoporotic fractures Vertebral compression fracture Hip fracture Name the PNA Red currant jelly sputum. → Klebsiella Rust colored sputum. → Strep pneumo PNA in an alcoholic. → Klebsiella Post viral PNA with a cavitary CXR lesion. → Staph aureus PNA in a patient that has chronically been on a ventilator. → Pseudomonas MC cause of Community Acquired Pneumonia. → Strep pneumo Pharmacological management of MRSA. Vancomycin Clindamycin Linezolid Ceftaroline (5th gen cephalosporin) Tigecycline, tertracycline Pharmacological management of Pseudomonas. Ceftazidime (only 3rd gen cephalosporin) Cefepime (4th gen cephalosporin) Pip-tazo Fluoroquinolones Carbapenems Aztreonam Aminoglycosides JVD and exercise intolerance in a patient with a recent history of an URI. → dilated cardiomyopathy 2/2 viral myocarditis MC cause? Coxsackie B VS Coxsackie A: Hand foot mouth dx Drug causes myocarditis Clozapine Anthracyclines Prevention? Dexrazoxane (iron chelator) Trastuzumab reversible tx for breast cancer Classic cause in a patient with recent history of travel to S. America? Chagas T. Cruzi Potential sequelae? Achalasia Dilated cardiomyopathy Megacolon (2/2 degeneration of myenteric plexus) Massive skin sloughing (45% BSA) in a patient that was recently started on a gout medication? TEN Dx? <10% BSA → SJS >30% BSA → TEN Tx? STOP the drug IVF Topical abx to prevention infection Tetany and a prolonged QT interval in a patient with recent surgical treatment of follicular thyroid carcinoma. → hypocalcemia due to removal of parathyroids Recurrent viral infections + QT prolongation + tetany → DiGeorge syndrome Pathophys? Failure of development of 3rd/4th pharyngeal pouches Trousseau and Chvostek signs. Trousseau → inflation of BP cuff causes carpopedal spasm Chvostek → taping on cheek causes facial muscle spasm Hypocalcemia that is refractory to repletion → consider hypomagnesemia Electrolyte/drug causes of prolonged QT intervals Electrolytes? Hypocalcemia Hypomagnesemia Hypokalemia Drugs? Macrolides FloroQunlones Haloperidol Ondensatron Methadone Hypoalbuminemia and Ca balance Hypoalbumenia → decrease in total body Ca++, no change in ionized Ca++ Drop of 1 in albumin → add 0.8 to Ca++ Abdominal pain radiating to the back → acute pancreatitis Causes? #1 = Gallstones #2 = Alcohol Hypertriglyceridemia Hypercalcemia Scorpion sting Handlebar injuries Lab markers? Lipase - most sensitive Amylase Physical exam signs in pancreatitis. Cullen’s sign = periumbilical ecchymosis Grey Turner sign = flank ecchymosis Tx? NPO + IVF + pain control Meperidine is a good agent because it doesn’t cause sphincter of Oddi spasms Management of gallstone pancreatitis Dx? US then ERCP Tx? DELAYED cholecystectomy What if the patient becomes severely hypoxic with a CXR revealing a “white out” lung? ARDS noncardiogenic pulm edema PCWP? <18 mmHg NORMAL 20 yo M with red urine in the morning + hepatic vein thrombosis + CBC findings of hemolytic anemia. → paroxysmal nocturnal hemoglobinuria Pathophys? Defect in GPI anchors, which attach CD55 and CD59 to cell (they prevent complement from destroying RBC) Sleep → hypoventilation → mild respiratory acidosis → activation of complement cascade Gene mutation? PIGA Dx? Flow cytometry Tx? Eculizumab (terminal complement inhibitor) Vaccine required? pnemococal Neisseria meningitidis Chronic diarrhea and malabsorption in a HIV+ patient + detection of acid fast oocysts in stool. → cryptosporidium parvum Acid-fast organisms Cryptosporidium TB MAC Nocardia Dx? Stool O&P Tx? Nitazoxanide Route of transmission? Contaminated water Muddy brown casts on urinalysis in a patient with recent CT contrast administration (or Gentamicin administration for a life threatening gram -ve infection) → Acute Tubular Necrosis Woman with morning joint stiffness > 1 hr → Rhematoid Arthritis. Antibodies? Rheum Factor (IgM against IgG) anti-CCP - more specific HLA? DR4 Pathophys? IgM constant region activates complement → inflammation → formation of pannus (hypertrophied synovium) → damage to cartilage and bone Caplan syndrome = RA + pneumoconiosis Felty syndrome = RA + neutropenia + splenomegaly (“RANS”) Classic hand/finger findings/distribution? MCP & PIP joints of hands (DIP joints spared) Imaging findings? Symmetric joint space narrowing Tx? Methotrexate (DMARDs) If no response → TNF alpha inhibitor (e.g. infliximab) Required testing prior to starting methotrexate? PFTs Required testing prior to starting infliximab? TB Hep B/Hep C Differentiating Strep pharyngitis from Infectious Mononucleosis LND distribution Anterior cervical → Strep Posterior cervical → Mono Disease onset Acute → Strep Over weeks → Mono Organ involvement Splenomegaly → Mono Pt with sore throat takes amoxicillin and gets rash → mono NOT allergic rxn! CENTOR criteria C = absence of Cough E = tonsillar Exudates N = nodes/anterior cervical lymphadenopathy T = temp (fever) OR <15 → +1 >=45 → -1 Using CENTOR score 0/1 → don’t test, don’t treat 2/3 → rapid antigen test Positive → treat Negative → throat culture 4/5 → treat empirically Tx of Strep pharyngitis? Amoxillcin If PCN allergic → azithromycin Potential sequelae of Strep pharyngitis RF - preventable with abx PSGN Endocarditis MC cause of endocarditis? IVDU Bug? Staph aureus Valve? tricuspid Prosthetic valve endocarditis Bug? Staph epidermidis Endocarditis after dental procedure? Viridans group streptococci Strep viridans, Strep mitis, Strep mutans, Strep sanguineous Patient with malar rash and echo showing vegetations on both sides of the mitral valve → Libman-Sacks endocarditis Presentation? Fever + night sweats + new murmur Splinter hemorrhages Roth spots (retinal hemorrhages) Painless Janeway lesions + painful Osler nodes (immune phenomenon) Dx? 1st step: blood cultures TEE Tx? Abx that include Staph aureus coverage (e.g. vancomycin) for WEEKS Bugs implicated in culture negative endocarditis HACEK H = haemophilus A = actinobacillus C = cardiobacterium E = eikenella K = kingella Coxiella burnetii Blood cultures in a patient with endocarditis reveal S. Bovis (or S. Gallolyticus bacteremia). NBS? Colonoscopy Who needs antibiotic prophylaxis? Hx endocarditis Prosthetic valve Unrepaired cyanotic congenital dz Heart transplant with valve dysfunction Erythematous salmon colored patch with silvery scale on the elbows and knees. → psoriasis Tx? Topical steroids If this patient presents with joint pain (especially in the fingers)? Psoriatic arthritis Imaging? Pencil-and-cup deformity Tx? NSAIDs T of 104 + tachycardia + new onset Afib in a patient with a history of Graves disease. → thyroid storm Lab findings? TSH low T3/T4 high Tx? 1st step: propranolol 2nd step: PTU Then: Prednisone Potassium iodide (Lugul’s solution) Wolff-Chaikoff effect → large amounts of iodine inhibit thyroid hormone synthesis Biopsy revealing tennis racket shaped structures in cells of immune origin. → Langerhans cell histiocytosis Electron microscopy? Birbeck granules (tennis rackets) Marker? S100 Small bowel obstruction in a HIV patient with purple macules on the face, arms, and lower extremities. → Kaposi’s sarcoma Bug? HHV8 Tx? HAART Pathophys of vascular lesions? Overexpression of VEGF Fever + rash + eosinophiluria 10 days after a patient started an antistaphylococcal penicillin. → acute interstitial nephritis Tx? STOP drug + steroids SLE SOAP BRAIN MD S = serositis O = oral ulcers A = arthritis P = photosensitivity B = blood disorders (cytopenias) R = renal A = ANA/anti-dsDNA I = immunologic N = neurologic findings M = malar rash D = discoid rash Type 2 vs 3 HSRs in lupus Type 2 → cytopenias Type 3 → all other manifestations Lupus Ab? ANA anti-dsDNA anti-Smith Lupus nephritis → full house pattern on IF Antiphospholipid antibody syndrome → recurrent pregnancy losses Pathophys? Thrombosis of the uteroplacental arteries. MC cause of death in lupus patients? What I’ve read recently: CV disease Per Divine: Treated → infection Untreated → renal dz Also 40x risk MI Endocarditis in lupus pt? Libman-Sacks endocarditis Neonatal 3rd degree heart block → neonatal lupus Maternal autoimmune dz? Sjogren’s SLE Ab? anti-SSA/anti-Ro anti-SSB/anti-La Tx? Steroids Cyclophosphamide Hydroxychloroquine → good for skin lesions Pulmonary abscesses Bugs? Staph Anaerobes Klebsiella RF? Alcoholism Elderly Post-viral pneumonia MC location of aspiration pneumonia? Superior segment of RLL Chest pain worsened by deep inspiration and relieved by sitting up in a patient with a recent MI or elevated creatinine or URI or RA/SLE. → pericarditis EKG findings? Diffuse ST elevations + PR depression PE finding? Friction rub (“scratchy sound on auscultation”) A few days after MI → fibrinous pericarditis Weeks after MI → Dressler’s Tx? NSAIDS Consider adding on colchicine Cardiac tamponade Beck’s triad = hypotension + JVD + muffled heart sounds EKG findings? Electrical alternans Type of shock? Obstructive cardiogenic (Amboss) CO low SVR high PCWP high Tx? Pericardiocentesis or pericardial Pearly lesion with telangiectasias on the ear in a farmer. → Basal Cell Carcinoma MC type skin cancer Location? Upper lip Dx? Biopsy Tx? Mohs surgery Cold intolerance in a 35 yo white F → hypothyroidism MC cause? Hashimoto’s Histology? lymphoid follicles w/ active germinal centers Lab findings? TSH high T3/T4 low Ab? anti-TPO Anti-thyroglobulin HLA? DR3/DR5 Tx? Levothyroxine Future complication? thyroid lymphoma Massive hematemesis in a patient with a history of chronic liver disease. → ruptured varices Pathophys? L gastric vein has anastomosis with azygos veins. Increased portal pressure → backward flow from L gastric veins to azygous vein (which empties into SVC). Acute tx? IVF + octreotide + ceftriaxone/cipro + EGD w/ ligation/banding Do NOT give a beta blocker for acute tx Prophalaxsis? Beta blocker + spironolactone Other manifestations of elevated portal pressures Caput medusa Internal hemorrhoids Tx for cirrhotic coagulopathies? FFP If uremia → give desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Hemophilia A Pathophys? deficiency of factor 8 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH b/c clotting problem PT normal Hemophilia B Pathophys? deficiency of factor 9 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH PT normal Hemophilia C Pathophys? deficiency of factor 11 Inheritance? AR Coag labs? Bleeding time normal PTT HIGH PT normal Bernard Soulier Syndrome Pathophys? Deficiency of GpIb Coag labs? Bleeding time HIGH PTT normal PT normal Glanzmann Thrombasthenia Pathophys? Deficiency of GpIIbIIIa Coag labs? Bleeding time HIGH PTT normal PT normal Von Willebrand’s disease Pathophys? Deficiency of vWF Inheritance? AD Coag labs? Bleeding time HIGH PTT HIGH vWF is a protecting group for factor 8 PT normal ITP Pathophys? Ab against GpIIbIIIa Classic pt? Pt with SLE Tx? Observation Steroids IVIG Splenectomy TTP Pathophys? Deficiency in ADAMTS13 enzyme → cannot cleave vWF multimers → activation of platelets → thrombosis → thrombocytopenia Presentation? microangiopathic hemolytic anemia + thrombocytopenia + renal failure + fever + neurologic problems Tx? Plasma exchange transfusion****** HUS Bugs? Shigella or E. coli O157:H7 Presentation? Fever+ microangiopathic hemolytic anemia + thrombocytopenia + renal failure + neurologic Platelet deficiency vs coagulation factor bleeds Platelet deficiency → mucosal bleeds, petechiae, heavy menses Coag factor deficiency bleeds → hemarthrosis Why do patients with CKD develop coagulopathy? Uremia → platelet dysfunction Tx? Desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Exercising caution with transfusion in patients with Bernard Soulier syndrome Do NOT give transfusion that includes platelets They can have an anaphylactic rxn to GpIb (since they don’t have GpIb) Oropharyngeal candidiasis. RF? HIV Chronic ICS use TNF inhibitor Micro finding? Germ tubes at 37 C Tx oral candidiasis? Nystatin swish-and-swallow Tx invasive candidiasis? Amphotericin B Prevention of Amphotericin B toxicity? Liposomal formulation Pleural effusions Light’s criteria (must meet all 3 to be considered transudative!) LDH < 2/3 ULN LOW Pleural LDH/serum LDH < 0.6 LOW Pleural protein/serum protein < 0.5 LOW Causes of transudative effusion CHF Cirrhosis Nephrotic syndrome Note: Per UW 2021: Mechanism of transudate effusion? Decreased pulmonary artery oncotic pressure, e.g. hypoalbuminemia in nephrotic syndrome Increased pulmonary capillary hydrostatic pressure, e.g. volume overload in heart failure Causes of exudative effusion Malignancy Cancer Parapneumonic effusion Tb Note: Per UW 2021: Mechanism of exudate effusion? Inflammatory increased in vascular permeability of membrane (increased flow of interstitial edema into pleural space) Unique cause of both transudative & exudative effusions? PE Classic Pleural Effusion findings? Decreased breath sounds Dullness to percussion Decreased tactile fremitus Tx? Chest tube Chylothorax = lymph in the pleural space Pathophys? Obstruction of thoracic duct or injury to the thoracic duct Pleural fluid findings? High Triglycerides Holosystolic murmur heard best at the apex with radiation to the axilla in a patient with a recent MI. → mitral regurg 2/2 papillary muscle rupture Dx? Echo Why widely split S2? Aortic valve is closing earlier (LV is emptying into both aorta & LA) Maneuvers that increase intensity Increase preload (putting more blood in that can be regurgitated) Increase afterload Decubitus ulcers RF? Elderly Paraplegic Fecal/urinary incontinence Poor nutrition Staging Stage 1 = non-blanchable erythema Tx? Repositioning q2hrs Stage 2 = loss of epidermis + partial loss of dermis Tx? Occlusive dressing superficial Stage 3 = involves entire dermis, extending to subQ fat Does NOT extend past fascia Tx? Surgical debridement Stage 4 = muscle/tendon/bose exposed Tx? Surgical debridement General tx strategies? Repositioning + good nutritional support Marjolin’s ulcer = non-healing wound that is actually squamous cell carcinoma T1DM Pathophys? Autoimmune destruction of pancreas Ab? anti-GAD 65 (glutamic acid decarboxylase) anti-IA2 (islet tyrosine phosphatase 2) Islet cell autoantibodies Insulin autoantibodies Dx? A1c > 6.5% (twice) Fasting BG >= 126 (twice) Oral glucose tolerance test >= 200 (twice) Sxs of DM + random glucose > 200 Tx? Long-acting insulin + mealtime insulin Long-acting Glargine Detemir Rapid-acting Lispro Aspart Glulisine 3 HY complications Nephropathy Retinopathy & cataracts Neuropathy Chronic DM care A1c q3 months Foot exam annually Eye exam annually Microalbumin:Cr ratio annually Nephroprotection in DM? ACE-I GI bleed algorithm 1st step: ABCs + 2 large-bore IVs + IVFs 2nd step: NG lavage Clear fluid → go deeper Blood → UGIB → upper endoscopy Bilious fluid → have ruled out UGIB → proceed to colonoscopy See source → intervene as needed See nothing → CT angiography for large bleed Tagged RBC scan for smaller bleed Antiplatelet Pharmacology Aspirin Mechanism? Irreversibly inhibits COX-1 and COX-2 Clopidogrel/ticlopidine = P2Y12 (ADP receptor) blockers Mechanism? Inhibit platelet activation Abciximab/eptifibatide/tirofiban = GpIIbIIIa receptor blockers Mechanism? Inhibit platelet aggregation Ristocetin cofactor assay Issues with adhesion step → abnormal result Abnormal ristocetin cofactor assays: Von Willebrand disease Bernard Soulier disease Normal ristocetin cofactor assay: Glanzmann Thrombasthenia Von Willebrand disease effects on PTT? Increased Pathophys? vWF is a protecting group for Factor 8. Treatment of VWD? Desmopressin Mechanism? Increases release of vWF from Weibel-Palade bodies of endothelial cells Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH HSV1 vs HSV2. Oral herpes → HSV1 Genital herpes → HSV2 Dx? PCR (most up-to-date) Tzanck smear (outdated, not very sensitive, nonspecific) → intranuclear inclusions Brain area affected by HSV encephalitis? Temporal lobes CSF findings in HSV encephalitis? RBCs******* Tx herpes encephalitis? Acyclovir AE? Crystal nephropathy Can’t see, can’t pee, can’t climb a tree. → reactive arthritis HLA? B27 Classic bug? Chlamydia Tx? steroids Need abx? Only if ongoing infection Can’t see, can’t pee, can’t hear a bee → Alport syndrome Inheritance? X-linked dominant Tx of NG & CT NG → treat empirically for both → ceftriaxone + azithro/doxy CT → azithro/doxy Hypovolemic Septic Neurogenic Cardiogenic CO low PCWP low SVR high*** CO high PCWP normal SVR low Tx? norepi CO low SVR low CO low PCWP high*** SVR high*** Tx anaphylactic shock? epinephrine Melanomas ABCDE A = asymmetry B = irregular borders C = color variation D = diameter > 6 mm E = evolving Dx? Full-thickness biopsy Excisional for small lesions Punch for larger lesions Most important prognostic factor → Breslow depth DM pharmacology Lactic acidosis → metformin Decreases hepatic gluconeogenesis → metformin Hold before CT w/ contrast → metformin Weight gain → sulfonylureas & TZDs (-glitizones) Diarrhea → acarbose & migliton Inhibits disaccharidases (can’t reabsorb disaccharides) Recurrent UTIs → SGLT-2 inhibitors Weight loss → GLP-1 agonists (e.g. liraglutide, exenatide) & DPP4 inhibitors (-gliptins) Contraindicated in pt with HF → TZDs PPAR-gamma receptor found in kidney → water retention Contraindication in pt with MTC → GLP-1 agonists Biggest risk of hypoglycemia? Sulfonylureas RF esophageal adenocarcinoma Barrett’s esophagus RF esophageal squamous cell carcinoma Smoking Drinking Achalasia Location esophageal adenocarcinoma? Lower 1/3 Location esophageal squamous cell carcinoma? Upper 2/3 MC US? Adenocarcinoma MC worldwide? Squamous cell carcinoma Presentation? Dysphagia to solids → dysphagia to liquids Dx? EGD Staging? CT scan or esophageal US Factor V Leiden Pathophys? Resistance to protein C Dx? Activated Protein C resistance assay Patient needs super large doses of heparin to record any changes in PTT → AT-III deficiency Recall that heparin is a AT-III activator 35 yo with a hypercoagulable disorder that does not correct with mixing studies. → antiphospholipid antibody disorder Anaphylaxis in a patient with a long history of Hemophilia A → Ab against factor 8 that cause type 1 HSR with transfusion Hx of hemophilia, diagnosed 5 years ago. Before you would give them factor 8 concentrate and PTT would normalize. Now they’re requirizing larger doses of factor 8 to normalize PTT. → inhibitor formation (antibodies against clotting factors) Skin necrosis with Warfarin → protein C/S deficiency Prothrombin G20210 mutation → overproduction of factor II Rash in dermatomal distribution → VZV infection Contraindications to VZV vaccination? Pregnant woman Kid < 1 year Severe immunosuppression (e.g. HIV with CD4 < 200) Tx? Acyclovir If resistant, foscarnet Tzanck smear findings? Intranuclear inclusions Shingles vaccination guidelines? Adults over 60 #1 cause of ESRD in the US → DM nephropathy Histology? Kimmelsteil-Wilson nodules #2 cause of ESRD in the US → hypertensive nephropathy Pt with BP 240/150. How fast should you lower BP? 25% in first 24 hrs Drugs for hypertensive emergencies? Nicardipine Clevidipine Nitroprusside AE? Cyanide poisoning Tx? Amyl nitrate + thiosulfate OR hydroxocobalamin Labelol Renal protective medications in patients with DKD or hypertensive nephropathy? ACE-I Anemia + Cranial Nerve deficits + Thick bones + Carbonic Anhydrase 2 deficiency + Increased TRAP + Increased Alkaline Phosphatase. → osteopetrosis Pathophys? Carbonic anhydrase is defective → osteoclasts cannot produce acid to resorb bone Tx? IFN-gamma Osteoclasts are a specialized macrophage IFN-gamma is an activator of macrophages Clinical diagnostic criteria for Chronic Bronchitis Diagnostic criteria? 2 years 3 months/year of chronic cough PFT findings FEV1 low FEV1/FVC ratio low RV high TLC high Which PFT market can differentiate CB from emphysema? DLCO DLCO normal → CB DLCO low → emphysema ****** Tx acute exacerbation? Abx + bronchodilators + corticosteroids (“ABCs”) Prevention? Stop smoking! Afib #1 RF? Mitral stenosis #1 RF MS? Rheumatic fever #1 RF CAD and AAA: smoking #1 RF stroke and aortic dissection: HTN MC arrhythmia in hyperthyroidism → Afib MC site of ectopic foci in Afib → pulmonary veins EKG findings? “Irregularly irregular” + no P waves Location of emboli formation? LA appendage Who should be cardioverted back to sinus rhythm? New onset (<48 hrs) Afib Anticoagulated for 3 weeks + TEE negative for clot Afib that’s refractory to medical therapy Afib & HDUS Q on T phenomenon? Depolarization during T wave (repolarization) can cause QT prolongation → Torsades → death Prevention? SYNCHRONIZED cardioversion Tx? Rate control Beta blockers ND-CCB (e.g. verapamil, diltiazem) Rhythmic control Amiodarone Reducing stroke risk in Afib? Anticoagulation for CHA2DS2VASc score >= 2 Anticoagulation options Valvular cause (e.g. MS) → warfarin Any other cause → warfarin or NOAC (apixiban) Reversal of AC Warfarin → Vit K, four-factor PCC Heparin → protamine sulfate Dabigatran → idarucizumab Crusty, scaly, ulcerating lesion with heaped up borders → squamous cell carcinoma Classic location? Below Lower lip Precursor lesion? Actinic keratosis What if it arises in a scar or chronic wound? Marjolin ulcer Hypothermia + hypercapnia + non pitting edema + hyponatremia + HR of 35 + hypotension in a patient with a history of papillary thyroid cancer → myxedema coma Tx? Levothyroxine + steroids Lab findings? TSH high T3/T4 low LDL high Acute onset “dermatologic” breakout in a patient with a recent history of weight loss and epigastric pain. → Leser–Trélat sign associated with visceral malignancy pancreatic cancer Lymph node associations Supraclavicular → Virchow’s node Periumbilical → Sister Mary Joseph What are mets to the ovaries called? Kruckenberg tumor Classic bug associated with gastric cancer? H. pylori (MALToma) Classic histological finding in the diffuse type of gastric cancer? Signet ring cells RBCs without central pallor + elevated MCHC + anemia. → hereditary spherocytosis Inheritance? AD Pathophys? Deficiency of spectrin, ankyrin, or band 3.2 Intravascular or extravascular hemolysis? Extravascular (RBCs bound by IgG, attacked by splenic macrophages) Dx? Osmotic fragility test Eosin-5-maleimide Acidified glycerol lysis test Tx? Splenectomy Post-splenectomy preventative care? Strep pneumo Hinflue vaccine Neisseria Septic shock Hemodynamic parameters CO high SVR low PCWP normal MvO2 high Tx? IVF + norepi + broad-spectrum abx (cover MRSA + Pseudomonas) E.g. vanc + pip-tazo E.g

sweat critical quotes - 12.02.25

Chapter 3 - Tissues 1. Introduction Main tissue types: Epithelial, Connective, Muscle, Nervous Functions: Protection, secretion, absorption, connection, movement, information processing Tissue membranes: Epithelial membranes: Mucous, Serous, Cutaneous Connective tissue membranes: Synovial membranes (joints) 2. Types of Tissues Four categories: Epithelial: Covers surfaces, lines cavities Connective: Supports, connects, transports Muscle: Enables movement Nervous: Sends and receives signals Embryonic origin: Derived from ectoderm, mesoderm, endoderm 3. Epithelial Tissue Characteristics: Closely packed cells, avascular, polarity (apical/basal surfaces), rapid regeneration Cell Junctions: Tight junctions: Barrier function (e.g., intestines) Anchoring junctions: Stability (e.g., skin) Gap junctions: Communication (e.g., heart) Types: Simple (one layer) vs Stratified (multiple layers) Shapes: Squamous (flat), Cuboidal (cube-shaped), Columnar (tall) Specialized types: Pseudostratified: Appears layered but isn’t Transitional: Stretchable (e.g., bladder) Glands: Endocrine (ductless, secretes hormones into bloodstream) Exocrine (ducts, secretes onto surfaces) Modes of secretion: Merocrine: Exocytosis (e.g., sweat glands) Apocrine: Pinched off portion of cell (e.g., mammary glands) Holocrine: Entire cell disintegrates (e.g., sebaceous glands) 4. Connective Tissue Structure: Cells dispersed in extracellular matrix (ground substance + protein fibers) Fiber types: Collagen (strong, flexible) Elastic (stretchy) Reticular (supportive framework) Categories: Proper: Loose (Areolar, Adipose, Reticular) Dense (Regular, Irregular, Elastic) Supportive: Cartilage (hyaline, elastic, fibrocartilage) Bone (osteocytes in lacunae, vascularized) Fluid: Blood (RBCs, WBCs, plasma) Lymph (immune function) Functions: Structural support, transport, immune defense, energy storage 5. Muscle Tissue Properties: Excitable, contractile Types: Skeletal: Striated, voluntary, attached to bones Cardiac: Striated, involuntary, heart muscle (intercalated discs) Smooth: Non-striated, involuntary (digestive, respiratory, reproductive systems) 6. Nervous Tissue Function: Conducts electrical impulses, processes information Cell types: Neurons: Transmit signals (axon, dendrites) Neuroglia: Support, protect, nourish neurons 7

. The last experimental. So this is going to involve the event relationship to between more variables. And do much changing on manipulating one of the variables theries as you already talked about both designs. And then we record or collect data, what obser the change in the dependent variable that result from our manipulation of the. That's what we're looking at. We're moving and sh and manipulating one and seeing if it causes an effects or change in the other. That's what we're looking for. So have experimental research, we are looking for causation not just correlation. We're not just looking to see due to variables moved together. No, we're actually looking to see if we make a change in one variable, do we see a subsequent change in the other word? If we make another change in that variable, we shift it more, we change it fast. We take it away. Do we need a consequential change in the independent variableag yet, okay, you're able to shift and manipulate the independent variable and consistently see a change of the dependent variables, then you know you have causation, a change in one causes a change in the other. They've already kind of gone over this multiple things, so I will just briefly say this again, but you've got the independent variable dependent variable, the independent ones you what we're going to manipulate and change, whatever. that looks like. um at a very simple level of experimental research, you can have one level of your independent variable, and then nothing, right? You can have your experimental group and your controller. The group that gets the treatment, that group that does not. So that is your very basic experimental research where you just have two groups and one of them is to control groups. But even still, you should see a change in the depependent variable to the group that is receiving treatment and you should see no change for the group that is not receiving treatment, right? That would be causation. Now, of course, you can have multiple levels of the independent variable, we're not gonna get too much into that. In this course, um, but two is kind of the minimal, right? treatment, no truth, and then you can move beyond that. The dependent variable is the one that is being measured. It is hopefully changing. If you see no change in the dependent variable when you're making changes to the independent variable, you've got a big problem, right? That means that your independent variable that you manipulating actually has nothing to do with the behavior that you're trying to observe. It doesn't impact it at all, and you're going to have no results, no adjacent. It's very disappointing. It does happen. and it's disappointing, but not happen. Um, so it is the uh the outcome orependent measure. Now, something I briefly mentioned that I have gone too much into depth, yet are the confounding variables, so the confounding or they're also called you probably heard them called extraneous variables. These are other variables, other than your independent variables. So anything that is not your independent variable can be a confounding variable, and it can cause and change in the dependent variable if you have not accounted for and controls something that has to be at and avoid it at all costs. Let's say let's say we're doing a study and we are trying to decrease the amount of smoking individuals engage. Hi, so we're trying to help them. We're trying to decrease their smoking paper. And our treatment is going to be some sort of meditation and relaxation techniques that they can learn because of that is based on the research that people smoke war when they're experiencing higher levels of stress. So how can we decrease their stress? Let's teach them various coping mechanisms, deb breathing techniques, meditation techniques, other things that they can do to decrease their stress and hopefully have a decrease in theopy behavior. Okay, great. So we implement our treatment. But what if we forgot to ask participants? if any of them had gotten pug onto to the doctor recently and had some maybe vac about their health, if they received some not so great news about their health, could that be a variable that is intacting how much they decide to smoke after that document? Absute, right? The doctors that said, hey, you' lungs are not looking for good, or you've got something precursors to cancer, we're gonna have to run some tests. That type of news could certainly impact someone who's smoking and could result in a change in their smoking behavior, they might leave that doctor's office and go, okay, wow, I really need to stop smoking. But if we didn't ask them that, we don't know. We don't have that information. So, we've moved forward, we implement our procedure and our treatment, and theyreased their smoking and we go, wow, our treatment works really great. Look at all these people that stop smoking. But in fact, all those people went to the doctor got not so great, there was a decided to not smoke, regardless of whether or not you taught them had a meditate break, right? That is a confounding variable that will throw your data because you did not account for it. Whenever we're doing a study like that, on any type of addictive behaviors for illness, if you're doing a medication study, you have to ask all of those questions. You have to get all of that information up front, because those are come down in variables that can change the behavior that you did not account for and you are not manipulating or control. So now we can't make the claim that if we um, you know, give individuals, um different mechanisms to decrease their stress, it will decrease their snow people. We can't make that claim anymore because that's not what caused the meaning. Or at least we don't know for sure that that's what we're doing. So confoundingles are a big bump. we run into these a lot, and I will tell you that when we are designing a research study um when you're working in a lab and you're working with researchers, it is intimidating to bring a research project to the lab. I mean, I did it a lot inad school. We were required to do this. You have to do this when you're doing research, but you bring your research question and your proposal for how you're gonna run your study to the lab. you put it up there and literally everyone in the room writs it apart. Everyone sits there for an hour or two and says, what about this confounding birdle? What about this? Well, this one's gonna throw your data. Well, this one's not gonna work. Well, you have an accountant for this, they rip it apart. It doesn't feel great in the moment. However, that is how you identify all of the compounding variables and you find a way to account. so that you have good data in the end. It's very important piece of research and experimental research specifically. We do want to avoid them at all costs. Okay, so here's another example. Let's say a researcher investigate whether giving students more time to study, reduces their tests anxiety. Okay. What is going to be the dependent variable here? What are we measuring? What are we looking at? We wouldn't want to take it again. Test anxiety. levels of anxiety when you're taking a test, right? That's what we're measure. We're trying to change that, okay? So that's gonna be the behavior that we're looking at. What is the independent variable here? Time to set, the amount of time that you're set, whatever that may be, okay? So the DV is test anxiety or levels of anxiety will take the test whatever you will word that, that's what we're measuring. Am amount of study time is what we're looking at for the independent version. Now, when you're taking a test, there are multiple things that happen that have nothing to do, maybe, with the amount of time you study. Can we reduce test anxiety by making sure that you study at least a minimum amount of time? Yes, we can reduce your test anxiety a little bit. But there are also other factors that if we if I was running this study as an experimental research, not just as like the naturalistic observation in a classroom, like let's just see if we can help. If I was actually running an experimental res research that many things that I have to account for. I need to account for type of tests. What if I get half of my participants, the tests is the morning and half of my participants the test in the afternoon? That's the I founding variable. Maybe the students in the morning are more stressed out because they didn't have time to relax in the morning and get ready for this test that I'm about to do them yet. Right? They're getting ready, they're in traffic, they're driving here, trying to park and so and so forth. Yes, we might run into that in the afternoon, but you still have got more time in the day. to get ready for it. So that's a confounding marriage, time of test. Another confounding variable would be temperature in the room. If it's too cold or too hot, you've got one room that's hotter, one room that's colder. That can impact someone's test anxiety. When you're feeling anxious, if I'm sure everyone has felt that feeling at one point in their life, it doesn't feel great to then also be hot and sweat. It usually makes that anxiety a little bit worse. You start to feel kind ofustrophobic and you're like, I don't know what's going on. I'm getting really hot. I don't feel good, I'm getting kind of dizzy, like, and your anxiety skyrock. right? So, I wanna make sure that the temperature in my room every time participants are taking the test, it has to be exactly the same, or usually within a couple degrees of the temperature. Okay, so these are just a few examples I can go on and on about all of the things that would impact you while you're having an exam that would impact your test anxiety. I need to help for all of those things, and every participant in all of my different groups would all have to have the same things so that I can truly say it was the amount of set. and it wasn't possibly due to during the room, time of the test, the room that they're in, how close they're sitting to each other and so on. and and that and that's part of the roofing unit ofart process, right? If I came to my lab and just said, oh, I'm gonna do this. They're like, well, what else, what else are you controlling for? I'm like, nothing, you know,'ll be fine. They're gonna rivet apart, right? All of those confounding variables that we need to account for. Um, a study involved investigating how manipulating the accuracy with which feedback is delivered, affects a number of work tasks that can be completed by college. So this is essentially, say, a student is doing a work task, and if I give you no feedback on that, as to whether you're doing it track, if I give you feedback that is correct and it matches, I say, yes, that's correct. or if I give you wrong feedbacks. So that's what we're talking about when we were saying a different type of feedback on your ability to complete a task. So, what is the independent variable here? What are we manipulating? Yeah, that's hypo feedback, right? We're gonna change that. It's gonna be different. What's the dependent variable that we're measured? It's the behavior we're looking at here? Yeah. Uh, number of work task. Correct, yes. How many workops did they actually complete? Do they get more done when they're getting positive feedback? Do they get more done when they're getting no feedback at all? You probably don't get more done when they're getting negative. You back would probably be my hypothesis, but we're gonna look at them, right? We're gonna count how many tasks they get done based on the type of feedback that they are given. And then we see how this impact that dependent varies. How does that impact the behavior that they're engaging? So, there will be questions like this on these things. This is like a perfect example. It will be this exact one, I'll change the words I'll change a thing. And I'll ask you these questions. What is the independent? What is the dependent variable? And sometimes I'll put a confounding variable in there and I'll say like, identify the confounding variable. and you'll hopulate pick one of the choices. So very similar to what I've test questions would look like for something like that. But the good to be able to look at examples and pull these things up about. If you're in any type of research class, statistics class, you need to be able to have this very uh, you guys could go over these ones.. I'm not gonna keep going, but you get you get this. All right. So experiments typically involve two groups at a minimum, which I talked about already, but you're gonna have atom minimum, your control group, and your experimental. The control group is a group of participants that does not receive the treatment. No treatment. Okay. Um, you don't change it. You essentially just measure their behavior, but you don't expose them to anything. Um, so work tasks with the feedback, that would be the control group is no feedback, okay? So we just allow the students to complete tasks as they normally would, we do not interject, we do not give the feedback one way or another. We just sort of let them carry on with their day as they normally would and we count how many works how they could. Versus, the experimental group are the ones that are going to receive some type of treatment. Now, as I've said before, minimally, you've got one experiment group and your control but you can have multiple experimental groups and a controll. And so you can have two or three different types of feedback. Those would be your experimental groups, and you can still have a group that received no feedback. if we're looking at study fine with students, you can look at, you know, two hours, four hours, six hours a week. Those are your experimental groups. the other students, you would sort of just allow them to either or you would prevent them from studying at all, or you just would not manipulate the study time for them, you would allow them to study however long they normally do and have them report on. So you would just basically specify that this group did not have a controlled set amount of set, and then they would report on how many hours they affected. versus the other three experimental groups would have a set amount by the time that you're controlled. Okay. Here's a question, a clinical psychologist conducts a study that involves ten people. He thinks he can cure depression by giving his science a particular type of drug. So he prescribes the drugs and finds his 60 days later, all clients show fewer signs of depression, as the psychologist includes he has cured depression. So what's the problem? There's a lot of problems here, but like, what's the main simple problem with what we understand in this particular research research? What has not been done? Yes.... doesn't describe. There is no controller, right? Every single person got the drug. There's no control group. So how do you know that that drug improved their depression? If you do not have a control group, you have no comparison to make, the whole point of having a control group, the whole reason we do it is so that if the drug does work, let's say that the psychologist is correct, this drug works, it cures depression. If you have a controlled group, we have a group of participants who didn't get the dress, what should happen for them? is someone over here? I take a guy? What should happen for people who are naked? Is it control with this? What do you expect? Yes. Yes, they should save the same, right? They're not getting the drugs. So they shouldn't get better. And then the people in the experimental group who are getting the drug if the drug works, they should get better. And you have that comparison. You now you can definitively say, okay, look at all these people that did not get the drug in my control group, they didn't get any better. The symptoms of depression persisted. But look at all of my participants, my experimental your, we saw a significant improvement in depression symptoms. Okay, now maybe you have a plane. But if you give the drugs to every single person, you have nothing to compare. How do you know what your drug is not something else that you're their depression? Maybe a bunch of people were unemployed and during that time that they were given the drug, they got a job. Back didn't improve someone's levels of depression, especially if it's a situational depression. course, there's a depression that is biologically, you know, that's a different type of depression, but there's also situational depression. And if you have an accountant for every single situation that person is in, those are confounding variables that can impact in this case, levels of depression. Do you know how control group, you have nothing to compare. You cannot make this. big problem. can't rule out any other expavation. So that's why minimally we always have to have at least a control group and an experimental group. And as I said, you can have more than that, but the bare minimum requirement, no treatment, treatment, control group, experiment. So when we use, um control groups and experimental groups, individuals are randomly assigned to each group, and I've kind of talked about this a little bit that the need for this in order to make sure that the participants in each group represents the larger population. That's the, right? You're never going to be able to access the entire population. You're not going to be able to access every single person who's ever experienced depression or has symptoms of depression in a drug site. You're going to have to randomly assign participants to certain groups and hope that they represent the larger population of people that experience symptoms of depression, right? So that is the point of random assignment to different conditions. Usually, the experimenter, I mean, ideally, the experimenter doesn't even know who's in which group, in a drug study that is ideal. We call it a double blind assignment where the participant doesn't know if they're getting a drug or not and the experiments or also does't know if they're getting the drug or not. Why? Because bias can be introduced? If they're participant thinks they're getting the drug, um, they can have sort of placebo effects, right? If you've ever heard of that, the placebo effects, or they think they're getting better because they're underlyression, they're getting the drug. researchers can also treat participants differently based on if they know who is getting the drug and who's not, and that will impact the data that they're collecting on that person's behavior. So, ideally, like the perfect scenario, nobody knows what's going on. There's a lab that assigns the drug and puts it in an envelope and assigns names, randomly and they give the envelope to their researcher and there's a red pill and there's a blue pill, but the researcher doesn't know which one is which. One could be trained it, one could be placebo, we don't know, and that's very important, but kind of nobody knows what's going on. until the end. And that's how you get the best data. out of something like this. Now, group should be comparable to each other. um, they should be assigned to the group based on Chancel, essentially. Um, usually we use some sort of computer programming to randomly assign numbers, two people and then randomly assign those numbers into the groups that were trying to produce. This can be very difficult to do. The smaller your participant pool, in fact, the more impossible this gets. So that's why a lot of research studies try to get so many participants and absorbid an amount of participants, um or why you need to run several studies to build your participant pool, before you can make any sort of claim about your data. because the smaller you participant pool gets, the less representative of the population they will be. because you do need to think about things like, um intelligence or um education level personality type socioeconomic status, ethnicity, um, their income, there's so many things that you have to think about and a smaller you participant will gets, the less representative of all of these things it will be. And then we run into the problem that your participants didn't actually represent the larger population, and your data really only applies to that very small group, and it cannot be applied to the larger group, which is always the goal. The goal of research is to collect data with a smaller amount of people, but you hope that you can go and apply those kinds and those results to the larger population. If you are looking for a drug that cares depression, you want those results to be good and to be representative of the larger population so that you can then produce a drug that can be distributed to people who have symptoms of depression and it cures them, right? You don't only want that drug to work for 60 people that you ran the side with, and that's it. and it doesn't work for anyone else. So, random assignment does help with this, but also large participant groups are going to make sure or ensure that you have a representative family of the larger published. Okay. yeah. So some other important things we have to considerable we're running research. and just terms that you should be aware of, so a confederate is someone who is employed by the researcher or is a researcher themselves that is going to participate in the study and pretend to be a participant. So they're gonna essentially take part in the study. um, the participants will not know that that person is a confederate, obviously it's a secret, so this involves some level of deception, usually in the study that we have to present to our review board and make sure that all of that is okay. But when you use a confederate, it's usually because you are conducting a study that people know they're being observed, they're going to change their behavior. So that's why we have confederates. When I was in grad school, a a grad friend of mine, she was in a different lab, and I was helping with her study. She ran this really interesting study on graphic Ed, so people would eat very, very fast. And I'm not just talking like, you know, kind of fast. We're talking like a burrit that big, is gone in one minute or less, like gone. And so, like barely chewing their food, like, wrap it, rapid, you. And as you can expect, there is a lot of health concerns that come first. We had some children who were rabbit eaters in that study. um there was significant choking hazards that had already occurred with some of those personents because they're eating much too fast, too large in bites. Um, but before we could run our study with children, we had to make sure that it was safe and it was not going to impact them too greatly, so we ran it with college students here on campus. Um and when we first started running it, you realized very quickly that they knew they were being observed, and so they were slowing down their eating. They were still eating fast, but it wasn't quite as fast as they had reported in their interviews when we were trying to pull participants. So what did we do? We got conf better. So we had a sticker researcher in there. and we left, so we who were identified as the researchers, we were like, hey, um, we're gonna be back a little later, and we're just we're gonna ask for your report on how fast you ate, but we gotta go. We'll be back later. Maybe pizza in the middle of the room, help yourselves. And then we actually had another researcher in there who was a participant, but she was a confederate. And she had to eat with them, which was difficult because she had to eat very, very quickly, so that they didn't know that she was a confederate. But that is an example of what we would do. Now, she had a time where she had different time on her too, that she was like collecting data for certain people in different sessions, so we could get a truer representation of how fast those people ate and their behavior was a different because they didn't know that they were being observed. So that is a perfect example when we could use the compatory. Um, replication and I've already sort of talked about this before, but we always wanna ask if we can rep replicate the results that have been found. This is extremely important. Scientific understanding is based on the accumulation of knowledge. The more knowledge we have, the more data we have on a on a body of research, the greater our scientific understanding is of that res research, of that behavior, of that phenomenon or theory, or whatever it is that we're investigated, the more research we have, the better we understand it. Replication is foundational to science moving forward. If we adjust did research for the heck of it, just to entertain ourselves to stimulate our reins or whatever research we just want to do, it doesn't help science, it doesn't move us forward at all. We have to publish it and then other scientists, other researchers have to replicate it and move the science forward. It's an extremely important part of research and without it, it really would kind of be pointless to do research at all. The point is to accumulate the knowledge and move the science forward. I've gonna talk about briefly about significant outcomes. If you take a statistical course, they get into this in great detail. But whenever we're looking at data, we're looking for what is called significant outcomes, statistically significant differences. We're not just looking for minimal differences between our groups, between our control group and our experimentsal groups, or even between our different experimental groups, we're looking for significant changes. big changes, changes that make a difference in people's lives. and a difference in their behavior changes, not just very small minuscule differences that maybe we can kind of say, well, there's a slight change. No, there must be a statistically significant dip. Now, of course, that is determined by the statistical analysis that are run. um, or if you're doing a study that's sort of based on kind of like a real world problem, um, things like when we work with children with autism and things like that, um, or any individual with a developmental disability, we're looking for um learning outcomes, so do they make significant jumps in their learning outcomes or their development? E cognitive or physical development, right? So they need to be meaningful differences as, you know, we're not just looking for tinyunicule changes, we're looking for meaningful, statistically significant differences between our groups. Experimental bias is something we always have to be aware of, these are going to be factors that could impact your dependent variable, a bias from the researcher, a bias from the in from the first incipant. Those can impact the data that you get in the way that they be hidden um any expectations that you are the persistent have can surely impact how they are behaving. We always need to account for that and make sure that we're, you know, making sure that doesn't do. Well is a false treatment. I've already kind of mentioned this before, but we typically see this with any sort of drug study um, but it's just the no treatment. They're given a pill that doesn't have any chemical properties to it, so it shouldn't impact their um system.? So if it impacts them in any way? That's what we need when we say alpha seat. And then finally, I've also talked about this already, but double blind means both the experimenter and the person do not know who's receiving treatment and who's not. That is the ideal standard to lose a another one in experiment, nobody knows. And it prevents

SPUTUM, BAL, SWEAT

Systolic pressure within the arteries when the heart beats; systole is the contraction phase of the cardiac cycle. Diaphoretic excessively sweaty. Commonly caused by exertion or a medical problem such as heart attack or shock. Baseline vital signs first set of vital signs obtained on a patient. Capillary refill time it takes for the capillaries to refill after being blanched. Normal capillary refill time is 2 seconds or less. Trending act of comparing three or more sets of signs and symptoms over time to determine if the patient’s condition is worsening, improving, or remaining the same. Symptom something the patient complains of or describes during the secondary assessment. OPQRST assessment tool mnemonic used as a reminder during a secondary assessment to help assess the patient’s chief complaint; the letters stand for onset, provocation, quality, region/radiate, severity, and time. Vital signs six most common signs used to evaluate a patient’s condition (respirations, pulse, blood pressure, skin, pupils, and mental status). Stethoscope device used to auscultate sounds within the body; commonly used to obtain blood pressure. SAMPLE history tool acronym used as a reminder in obtaining a patient history during the secondary assessment; SAMPLE stands for signs/symptoms, allergies, medications, past pertinent medical history, last oral intake, and events leading to the problem today. Sign something that can be observed or measured when assessing a patient. Pulse pulsation of the arteries felt with each heartbeat. Cyanotic describes bluish coloration of the skin caused by an inadequate supply of oxygen. Typically seen at the mucous membranes and nail beds. Blood pressure measurement of the pressure inside the arteries, during and between contractions of the heart. Jaundice medical condition that causes yellowing of the skin and whites of the eyes. Typically caused by liver failure or obstruction of the bile duct. Mental status general condition of a patient’s level of consciousness and awareness. Diastolic pressure within the arteries when the heart is at rest; diastole is the resting phase of the cardiac cycle. Auscultation listening to internal sounds of the body, typically with a stethoscope. Palpation using one’s hands to touch or feel the body. Medical history previous medical conditions and events for a patient. Hypertension high blood pressure

Introduction to Tissues A. Histology=the study of tissues. B. Although studying tissues can be accomplished using a light microscope, studying cell parts often requires an electron microscope and the study of atoms and molecules can only be examined through special imaging techniques and experimental procedures. Types of Tissues A. Despite the fact the body is composed of trillions of cells, there are only about 200 different cell types. These cells in turn produce only four principle tissue types: 1. Epithelial tissues=covers exposed surfaces; lines internal passageways; and produces glandular secretions. 2. Connective tissues=fills internal spaces; provides structural support, and stores energy 3. Muscle tissues=contracts to produce active movements 4. Nervous tissue=conducts electrical impulses; detects, interprets, and responds to stimuli B. Relative contribution of the four tissue types to the overall weight of the adult body. C. Embryonic origins: There are three types of embryonic tissues from which all adult tissues are derived. a. Endoderm=gives rise to the functional linings of the digestive and respiratory tracts as well as to the associated accessory glands and organs (i.e. liver, stomach, pancreas, etc.) b. Mesoderm= gives rise to the components of the skeletal, muscular, and circulatory systems c. Ectoderm= gives rise to the epidermis of skin and all of the components of the nervous system D. Tissue Membranes 1. Mucous Membranes=composed of epithelial tissues. These membranes line body cavities that open to the exterior environment such as those of the digestive tract, respiratory tract, or urogenital tract. In all cases, these are "wet" or moist membranes because of the secretion of mucous. The moisture helps reduce friction and in many cases, facilitates absorption or secretion activities. 2. Serous Membranes=consists of a mesothelium supported by areolar tissue. These are never exposed or connected to the exterior. Serous membranes secrete transudate, or serous fluid. There are three serous membranes that line the ventral body cavity: a. Pleura=lines the chest cavity and surrounds the lungs. b. Pericardium=lines the pericardial cavity and surrounds the heart c. Peritoneum=lines the peritoneal cavity and lines the surfaces of the visceral organs 3. Cutaneous Membranes=made of stratified squamous and areolar tissue reinforced by dense irregular connective tissue. In contrast to mucous and serous membranes, cutaneous membranes are dry, relatively thick, and waterproof. 4. Synovial Membranes=line mobile joint cavities but do not cover the opposing joint surfaces. Secretes synovial fluid. Although the covering of the synovial membrane is often called an epithelium, it differs from true epithelia in four respects: it develops within a connective tissue, no basal lamina is present, gaps of up to 1 mm may separate adjacent cells, and the synovial fluid and capillaries in the underlying connective tissue are continuously exchanging fluid and solutes. Epithelial Tissues A. Functions of Epithelial Tissues 1. Epithelia provide physical protection. Epithelial tissues protect exposed and internal surfaces from abrasion, dehydration, and destruction by chemical or biological agents. 2. Epithelia control permeability. Any substance that enters or leaves the body has to cross an epithelial tissue. Some epithelia are relatively impermeable, whereas others are permeable to compounds as large as proteins. Most are capable of selective absorption or secretion. The epithelial barrier can be regulated and modified in response to various stimuli. For example, a callus forms on your hands when you do rough work for an extended period of time. 3. Epithelia provide sensation. Sensory nerves extensively innervate most epithelia. Specialize epithelial cells can detect changes in the environment and convey information about such changes to the nervous system. 4. Epithelial cells that produce secretions are called glands. Individual gland cells are often scattered among other cell types in an epithelium that may have many other functions. B. Location of Epithelial Tissues 1. Epithelia=forms sheets or layers of cells that line the body tubes, cavities, or coverings of the body surfaces. 2. Glands=formed of epithelial cells with secretory functions. Two types of glands are found in the human body: a. Endocrine glands=secrete hormones (or hormonal precursors) into the interstitial fluid or bloodstream. These glands are ductless. b. Exocrine glands=secretes non-hormonal substances (milk, wax, enzymes, oil, acids, etc.) onto external surfaces or internal passageways (ducts) that connect to the exterior. C. Characteristics of Epithelial Tissues 1. Polarity=epithelial cells possess two structurally and functionally different surfaces: a. Apical surface=free edge which faces the exterior of the body or the lumen of an internal space. b. Basal surface=attached surface which anchors the cells to adjacent tissues. 2. Supported by a basal lamina=also known as the basement membrane, is a complex structure produced by the basal surface of the epithelial cells and the underlying connective tissue. The underlying connective tissue is composed of two things: 3. Cellularity=epithelial cells are extensively interconnected so that they create an effective barrier that behaves as if it were a single cell. a. Occluding junctions=form a barrier that isolates the basolateral surfaces and deeper tissues from the contents of the lumen. At an occluding junction, the attachment is so tight that it prevents the passage of water and solutes between the cells. b. Adhesion belt=locks together the terminal webs of neighboring cells, strengthening the apical region and preventing distortion and leakage at the occluding junctions. It forms a continuous band that encircles cells and binds them together. c. Gap junctions=permits chemical communication that coordinates the activities of adjacent cells. At a gap junction, two cells are held together by interlocking junctional proteins called connexons which serve as channels that form a narrow passageway to let small molecules and ions to pass from cell to cell. d. Desmosomes=provides firm attachment between neighboring cells by interlocking their cytoskeletons. At a desmosome, the opposing plasma membranes are very strong and resist stretching and twisting. Hemidesmosomes attach the basal surface to the basement membrane. e. CAM=cell adhesion molecules; present in the adhesion belt and desmosomes; transmembrane proteins that bind to each other and to extracellular materials. 4. Avascular=epithelial tissues lack blood vessels; all nutrient and waste exchange occurs as a result of diffusion and osmosis from underlying tissues. 5. Highly innervated=epithelial tissues are supplied with many nerve endings 6. Regenerate rapidly=although the exact rate varies from one type of epithelia to another, most epithelial tissues regenerate within days (rather than weeks or years). D. Naming Epithelial Tissues 1. Almost all epithelial tissues possess a two part name where the first part of their name indicates their arrangement (number of layers) while the second part of their name indicates the shape of the cells. 2. Arrangement of epithelial tissues a. Simple=only one layer thick b. Stratified=more than one layer thick c. Pseudostratified= “false layers”; it looks like more than one layer but in fact its only one layer thick 3. Shape of epithelial cells a. Squamous=thin, flat, and somewhat irregular in shape. From the surface, they look like fried eggs lay side by side. In a sectional view, they look like a pancake with a pat of butter (indicating the nucleus). b. Cuboidal=are about as wide as they are tall; resemble hexagonal boxes with the spherical nucleus located in the center of each cell. c. Columnar=are taller than they are wide; resemble rectangles with the elongated nuclei tend to crowd into a narrow band close to the basal lamina. E. Diversity of Epithelial Tissues 1. Simple squamous epithelium a. Description: single layer of flattened cells with a disc-shaped central nuclei and sparse cytoplasm. b. Function: allows passage of materials by diffusion and filtration in sites where protection is not important. Also secretes lubricant. c. Locations: Kidney glomeruli, air sacs of lungs, capillaries, linings of heart and lymphatic system. 2. Stratified squamous epithelium a. Description: thick layers of flattened cells; often keratinized layer and a mitotic layer. b. Function: protects underlying tissues in areas subject to abrasion c. Location: non-keratinized type lines the mouth and vagina; keratinized type forms the epidermis of skin. 3. Simple cuboidal epithelium a. Description: single layer of cube-like cells with large spherical centrally located nuclei. b. Function: secretion and absorption c. Locations: Kidney tubules, ducts and secretory portions of glands, ovary surface 4. Stratified cuboidal epithelium a. Relatively rare in the human body. b. Most common along the ducts of sweat glands, mammary glands, and other exocrine glands. c. DO NOT NEED TO KNOW FOR THE LAB PRACTICAL!! 5. Simple columnar epithelium a. Description: single layer of tall cells with round to oval nuclei; some cells bear cilia; may contain goblet cells that produce mucus; may contain microvilli. b. Function: absorption; secretion of mucus and enzymes; cilia propel substances. c. Location: non-ciliated type lines digestive tract, gallbladder, and ducts from glands; ciliated type lines small bronchi, uterine tubes, and uterus. 6. Stratified columnar epithelium a. Relatively rare in the human body. b. Most often found lining large ducts such as those of the salivary glands and pancreas. c. DO NOT NEED TO KNOW FOR THE LAB PRACTICAL!! 7. Pseudostratified columnar epithelium a. Description: single layer of cells of differing heights so that nuclei are a differing levels; may contain goblet cells and bear cilia. b. Function: secretion, propulsion by ciliary action. c. Location: non-ciliated type lines male reproductive ducts; ciliated type lines much of respiratory tract. 8. Transitional epithelium a. Description: resembles both stratified squamous and stratified cuboidal. Basal cells are cuboidal or columnar; surface cells are dome shaped. b. Function: stretches readily and permits distension. c. Location: Lines uterus, bladder, and urethra F. Glandular Epithelia are Specialized for Secretion 1. Endocrine glands= “ductless” glands that produce hormones. Secrete directly into interstitial fluids or bloodstream. Examples: pituitary gland, adrenal gland, thyroid gland, etc. 2. Exocrine glands=glands possessing ducts. Exocrine glands secret their substance either on the body surfaces or within ducts. They general demonstrates one of two different modes secretion: a. Merocrine=secrete products from secretory vesicles by exocytosis. Most common type. Example: salivary glands of the oral cavity b. Holocrine=accumulate products until the cell ruptures. Destroys the cell and must be replaced by cell division. Example: sebaceous glands of the skin c. Apocrine=products accumulate within the cells then the apex of the cell pinches off packets that contain the secretion. Example: mammary gland of the breast 3. Exocrine glands are unicellular or multicellular. a. Unicellular=goblet cells that produce mucin which mixes with water to form mucus. b. Multicellular=two structural classes: i. Simple=a single duct that does not branch on its way to the secretory cells (examples: gastric glands, sebaceous glands) ii. Compound= duct divides one or more times on its way to the secretory cells (examples: duodenal glands, mammary glands and salivary glands) Connective Tissues: Supports and Protects A. Location of Connective Tissues 1. Most abundant tissue in the body. 2. Never exposed to the outside environment. B. Characteristics of Connective Tissues 1. All types of connective tissue originate from mesenchyme. 2. Connective tissues vary widely in appearance and function but all forms share three basic components: a. Specialized cells=the cells present in each type of connective tissue helps to distinguish the various types from one another. A few of the cells are listed here: i. Fibroblast cells=produce connective tissue proper ii. Chondrocytes=produce cartilage iii. Osteocytes=produce bone iv. Hemocytoblast cells=produce blood b. Extracellular proteins fibers=three primary fibers are produced in connective tissues i. Elastic fibers=slender, straight, and very stretchy. They recoil to their original length after stretching or distortion. ii. Collagen fibers=thick, straight or wavy, and often forms bundles. They are very strong and resist stretching. iii. Reticular fibers=strong fibers that form a branching network or scaffolding c. Ground substance=material that fills the space between cells and surrounds the extracellular fibers. In some connective tissues the ground substance is gel-like while in others it is liquid based and in others it is rigid or calcified. Ground substance and extracellular fibers make up the matrix of connective tissues. 3. Many types of connective tissue are highly vascular and contain sensory receptors that detect pain, pressure, temperature, and other stimuli. C. Functions of Connective Tissues 1. Establish a structural framework for the body. 2. Transport fluids and dissolved materials. 3. Protect delicate organs. 4. Support, surround, and interconnect other types of tissue. 5. Store energy reserves, especially in the form of triglycerides. 6. Defend the body from invading microorganisms. D. Diversity of Connective Tissues 1. Connective Tissue Proper=includes connective tissues with many types of cells and extracellular fibers in a gel-like ground substance. a. Loose Connective Tissues – fibers created a loose, open framework i. Areolar tissue=most common form of connective tissue proper in adults. It is the general packing material in the body. Attaches skin to underlying body parts and is sometimes called the superficial fascia. All of the cell types found in other forms of connective tissue proper can be found in areolar. ii. Adipose tissue=found deep to the skin, especially at the flanks, buttocks, and breasts. It also forms a layer that provides padding within the orbit of the eyes, in the abdominopelvic cavity, and around the kidneys. The distinction between areolar tissue and adipose is the larger number of adipocytes (fat cells). iii. Reticular tissue=found in the liver, kidney, spleen, lymph nodes, and bone marrow, where it forms a tough, flexible network that provides support and resists distortion. In reticular tissue, reticular fibers create a complex supporting network known as a stroma. Fixed macrophages and fibroblasts are present but these cells are seldom visible. DO NOT NEED TO KNOW FOR THE LAB PRACTICAL!! b. Dense Connective Tissues – fibers are densely packed together i. Dense regular=all collagen fibers are oriented parallel to each other providing strength along the axis of the collagen fibers. Found in cords (such as tendons) or sheets (ligaments). Tendons connect muscle to bones. Ligaments connect bones to bones. ii. Dense irregular=collagen fibers are non-parallel forming an interwoven network. These tissues provide strength in many directions and are particularly important in areas subjected to stress from many directions such as the dermis of the skin. iii. Elastic=when elastic fibers outnumber collagen fibers, the tissue has a springy, resilient nature that allows it to tolerate cycles of extension and recoil. This elastic tissue is bound between the vertebrae of the spinal column and the erectile tissues of the penis. DO NOT NEED TO KNOW FOR THE LAB PRACTICAL!! 2. Fluid Connective Tissues=have distinctive populations of cells suspended in a watery matrix that contains dissolved proteins. NOT ON LAB PRACTICAL! a. Blood – flows within the cardiovascular system 3. Supporting Connective Tissues=differ from connective tissue proper in have a less diverse cell population and a matrix containing much more densely packed fibers. Supporting connective tissues protect soft tissues and support the weight of part or all of the body. a. Cartilage – solid, rubbery matrix containing chondrocytes. All cartilage is surrounded by a membrane of connective tissue called the perichondrium. i. Hyaline cartilage=found connecting the ribs to the sternum, covering the articular surfaces of long bones, supporting the respiratory passageways such as the trachea, and forming the tip of the nose and part of the nasal septum. Has an amorphous matrix with few visible fibers. It provides stiff but somewhat flexible support and reduces friction between bony surfaces. ii. Elastic cartilage=found in the ear and epiglottis. Has many more elastic fibers within the matrix and is therefore more flexible. iii. Fibrous cartilage=found within the intervertebral discs, the meniscus of the knee, and pubic symphysis. Has many more collagen fibers within its matrix and is therefore very strong. b. Bone – solid, crystalline matrix containing osteocytes. All bone is surrounded by a membrane of connective tissue called the periosteum. NOT ON LAB PRACTICAL! c. Comparison of cartilage and bone. Muscle Tissue in Motion (discussed in detail in Chapter 10-11) NOT ON LAB PRACTICAL! A. Highly vascularized muscular tissue is comprised of elongated cells (called fibers) containing myofilaments (actin and myosin proteins). 
 B

Unidad 3 - Verbos

„ INTRODUCTION Medulla is the inner part of adrenal gland and it forms 20% of the mass of adrenal gland. It is made up of interlacing cords of cells known as chromaffin cells. Chromaffin cells are also called pheochrome cells or chromophil cells. These cells contain fine granules which are stained brown by potassium dichromate. Types of chromaffin cells Adrenal medulla is formed by two types of chromaffin cells: 1. Adrenaline-secreting cells (90%) 2. Noradrenaline-secreting cells (10%). „ HORMONES OF ADRENAL MEDULLA Adrenal medullary hormones are the amines derived from catechol and so these hormones are called catecholamines. Catecholamines secreted by adrenal medulla 1. Adrenaline or epinephrine 2. Noradrenaline or norepinephrine 3. Dopamine. „ PLASMA LEVEL OF CATECHOLAMINES 1. Adrenaline : 3 μg/dL 2. Noradrenaline : 30 μg/dL 3. Dopamine : 3.5 μg/dL „ HALF-LIFE OF CATECHOLAMINES Half-life of catecholamines is about 2 minutes. „ SYNTHESIS OF CATECHOLAMINES Catecholamines are synthesized from the amino acid tyrosine in the chromaffin cells of adrenal medulla (Fig. 71.1). These hormones are formed from phenylalanine also. But phenylalanine has to be converted into tyrosine. Stages of Synthesis of Catecholamines 1. Formation of tyrosine from phenylalanine in the presence of enzyme phenylalanine hydroxylase 2. Uptake of tyrosine from blood into the chromaffin cells of adrenal medulla by active transport 3. Conversion of tyrosine into dihydroxyphenylalanine (DOPA) by hydroxylation in the presence of tyrosine hydroxylase 440 Section 6tEndocrinology FIGURE 71.1: Synthesis of catecholamines. DOPA = Di- hydroxyphenylalanine, PNMT = Phenylethanolamine-N- methyltransferase. 4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase 5. Entry of dopamine into granules of chromaffin cells 6. Hydroxylation of dopamine into noradrenaline by the enzyme dopamine beta-hydroxylase 7. Release of noradrenaline from granules into the cytoplasm 8. Methylation of noradrenaline into adrenaline by the most important enzyme called phenylethanolamine- N-methyltransferase (PNMT). PNMT is present in chromaffin cells. „ METABOLISM OF CATECHOLAMINES Eighty five percent of noradrenaline is taken up by the sympathetic adrenergic neurons. Remaining 15% of noradrenaline and adrenaline are degraded (Fig. 71.2). FIGURE 71.2: Metabolism of catecholamines. COMT = Catechol-O-methyltransferase, MAO = Monoamine oxidase. Stages of Metabolism of Catecholamines 1. Methoxylation of adrenaline into meta-adrenaline and noradrenaline into metanoradrenaline in the presence of ‘catechol-O-methyltransferase’ (COMT). Meta-adrenaline and meta-noradrenaline are together called metanephrines 2. Oxidation of metanephrines into vanillylmandelic acid (VMA) by monoamine oxidase (MAO) Removal of Catecholamines Catecholamines are removed from body through urine in three forms: i. 15% as free adrenaline and free noradrenaline ii. 50% as free or conjugated meta-adrenaline and meta-noradrenaline iii. 35% as vanillylmandelic acid (VMA). „ ACTIONS OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline stimulate the nervous system. Adrenaline has significant effects on metabolic functions and both adrenaline and noradrenaline have significant effects on cardiovascular system. „ MODE OF ACTION OF ADRENALINE AND NORADRENALINE – ADRENERGIC RECEPTORS Actions of adrenaline and noradrenaline are executed by binding with receptors called adrenergic receptors, which are present in the target organs. Chapter 71tAdrenal Medulla 441 Adrenergic receptors are of two types: 1. Alpha-adrenergic receptors, which are subdivided into alpha-1 and alpha-2 receptors 2. Beta-adrenergic receptors, which are subdivided into beta-1 and beta-2 receptors. Refer Table 71.1 for the mode of action of these receptors. „ ACTIONS Circulating adrenaline and noradrenaline have similar effect of sympathetic stimulation. But, the effect of adrenal hormones is prolonged 10 times more than that of sympathetic stimulation. It is because of the slow inactivation, slow degradation and slow removal of these hormones. Effects of adrenaline and noradrenaline on various target organs depend upon the type of receptors present in the cells of the organs. Adrenaline acts through both alpha and beta receptors equally. Noradrenaline acts mainly through alpha receptors and occasionally through beta receptors. 1. On Metabolism (via Alpha and Beta Receptors) Adrenaline influences the metabolic functions more than noradrenaline. i. General metabolism: Adrenaline increases oxygen consumption and carbon dioxide removal. It increases basal metabolic rate. So, it is said to be a calorigenic hormone ii. Carbohydrate metabolism: Adrenaline increases the blood glucose level by increasing the glycogenolysis in liver and muscle. So, a large quantity of glucose enters the circulation iii. Fat metabolism: Adrenaline causes mobilization of free fatty acids from adipose tissues. Catecholamines need the presence of glucocorticoids for this action. 2. On Blood (via Beta Receptors) Adrenaline decreases blood coagulation time. It increases RBC count in blood by contracting smooth muscles of splenic capsule and releasing RBCs from spleen into circulation. 3. On Heart (via Beta Receptors) Adrenaline has stronger effects on heart than nor- adrenaline. It increases overall activity of the heart, i.e. i. Heart rate (chronotropic effect) ii. Force of contraction (inotropic effect) iii. Excitability of heart muscle (bathmotropic effect) iv. Conductivity in heart muscle (dromotropic effect). 4. On Blood Vessels (via Alpha and Beta-2 Receptors) Noradrenaline has strong effects on blood vessels. It causes constriction of blood vessels throughout the body via alpha receptors. So it is called ‘general vasoconstrictor’. Vasoconstrictor effect of noradrena- line increases total peripheral resistance. Adrenaline also causes constriction of blood vessels. However, it causes dilatation of blood vessels in skeletal muscle, liver and heart through beta-2 receptors. So, the total peripheral resistance is decreased by adrenaline. Catecholamines need the presence of glucocor- ticoids, for these vascular effects. 5. On Blood Pressure (via Alpha and Beta Receptors) Adrenaline increases systolic blood pressure by increasing the force of contraction of the heart and cardiac output. But, it decreases diastolic blood pressure by reducing the total peripheral resistance. Noradrenaline increases diastolic pressure due to general vasoconstrictor effect by increasing the total peripheral resistance. It also increases the systolic blood pressure to a slight extent by its actions on heart. The action of catecholamines on blood pressure needs the presence of glucocorticoids. TABLE 71.1: Adrenergic receptors Receptor Mode of action Response Alpha-1 receptor Activates IP3 through phospholipase C Mediates more of noradrenaline actions than adrenaline actions Alpha-2 receptor Inhibits adenyl cyclase and cAMP Beta-1 receptor Activates adenyl cyclase and cAMP Mediates actions of adrenaline and noradrenaline equally Beta-2 receptor Activates adenyl cyclase and cAMP Mediates more of adrenaline actions than noradrenaline actions IP3 = Inositol triphosphate 442 Section 6tEndocrinology Thus, hypersecretion of catecholamines leads to hypertension. 6. On Respiration (via Beta-2 Receptors) Adrenaline increases rate and force of respiration. Adrenaline injection produces apnea, which is known as adrenaline apnea. It also causes bronchodilation. 7. On Skin (via Alpha and Beta-2 Receptors) Adrenaline causes contraction of arrector pili. It also increases the secretion of sweat. 8. On Skeletal Muscle (via Alpha and Beta-2 Receptors) Adrenaline causes severe contraction and quick fatigue of skeletal muscle. It increases glycogenolysis and release of glucose from muscle into blood. It also causes vasodilatation in skeletal muscles. 9. On Smooth Muscle (via Alpha and Beta Receptors) Catecholamines cause contraction of smooth muscles in the following organs: i. Splenic capsule ii. Sphincters of gastrointestinal (GI) tract iii. Arrector pili of skin iv. Gallbladder v. Uterus vi. Dilator pupillae of iris vii. Nictitating membrane of cat. Catecholamines cause relaxation of smooth muscles in the following organs: i. Non-sphincteric part of GI tract (esophagus, stomach and intestine) ii. Bronchioles iii. Urinary bladder. 10. On Central Nervous System (via Beta Receptors) Adrenaline increases the activity of brain. Adrenaline secretion increases during ‘fight or flight reactions’ after exposure to stress. It enhances the cortical arousal and other facilitatory functions of central nervous system. 11. Other Effects of Catecholamines i. On salivary glands (via alpha and beta-2 receptors): Cause vasoconstriction in salivary gland, leading to mild increase in salivary secretion ii. On sweat glands (via beta-2 receptors): Increase the secretion of apocrine sweat glands iii. On lacrimal glands (via alpha receptors): Increase the secretion of tears iv. On ACTH secretion (via alpha receptors): Adrenaline increases ACTH secretion v. On nerve fibers (via alpha receptors): Adrenaline decreases the latency of action potential in the nerve fibers, i.e. electrical activity is accelerated vi. On renin secretion (via beta receptors): Increase the rennin secretion from juxtaglomerular apparatus of the kidney. „ REGULATION OF SECRETION OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline are secreted from adrenal medulla in small quantities even during rest. During stress conditions, due to sympathoadrenal discharge, a large quantity of catecholamines is secreted. These hormones prepare the body for fight or flight reactions. Catecholamine secretion increases during exposure to cold and hypoglycemia also. „ DOPAMINE Dopamine is secreted by adrenal medulla. Type of cells secreting this hormone is not known. Dopamine is also secreted by dopaminergic neurons in some areas of brain, particularly basal ganglia. In brain, this hormone acts as a neurotransmitter. Injected dopamine produces the following effects: 1. Vasoconstriction by releasing norepinephrine 2. Vasodilatation in mesentery 3. Increase in heart rate via beta receptors 4. Increase in systolic blood pressure. Dopamine does not affect diastolic blood pressure. Deficiency of dopamine in basal ganglia produces nervous disorder called parkinsonism (Chapter 151). „ APPLIED PHYSIOLOGY – PHEOCHROMOCYTOMA Pheochromocytoma is a condition characterized by hypersecretion of catecholamines. Cause Pheochromocytoma is caused by tumor of chromophil cells in adrenal medulla. It is also caused rarely by tumor of sympathetic ganglia (extra-adrenal pheochromocytoma). Chapter 71tAdrenal Medulla 443 Signs and Symptoms Characteristic feature of pheochromocytoma is hyper- tension. This type of hypertension is known as endocrine or secondary hypertension. Other features: 1. Anxiety 2. Chest pain 3. Fever 4. Headache 5. Hyperglycemia 6. Metabolic disorders 7. Nausea and vomiting 8. Palpitation 9. Polyuria and glucosuria 10. Sweating and flushing 11. Tachycardia 12. Weight loss. Tests for Pheochromocytoma Pheochromocytoma is detected by measuring meta- nephrines and vanillylmandelic acid in urine and Cathecolamines in olasma

CLINMIC LEC SWEAT AND STOOL

Urine, Sweat, Saliva