Lecture Exam 1- Endocrine and Lymphatic Flashcards
Lecture topics and Desicriptions
General comparisons and differences of nervous and endocrine system
both specialize in coordination and communication. Nervous communicates using neurotransmitters, endocrine uses hormones
four principal mechanisms of communication
gap junctions, neurotransmitters, hormones, and paracrines
gap junctions
pores in cell membrane, joining smooth & cardiac muscle, and epithelial. Enable cells to pass nutrients, electrolytes, and signaling molecules from cytoplasm to cytoplasm
neurotransmitter
released by neuron through synaptic cleft
paracrine
secreted by one cell, diffuse to nearby cells in same tissue throughout organs
hormones
chemical messengers transported by bloodstream and stimulate some type of response in cells and organ tissues pretty far away by traveling through blood with more widespread effects to multiple organs.
Speed and persistence of response in nervous vs. endocrine
Nervous: reacts quickly (ms timescale), stops immediately
Endocrine: reacts slowly (seconds or days), effect may continue for days or longer
Adaptation to long-term stimuli in nervous vs. endocrine
Nervous: response declines (adapts quickly)
Endocrine: response persists (adapts slowly)
Area of effect in nervous vs. endocrine
Nervous: targeted and specific (one organ)
Endocrine: general, widespread effects (many organs)
Comparing Communication by the Nervous and endocrine System
sometimes use the same hormones/neurotransmitter (norepinephrine, dopamine, and antidiuretic hormone), or have the same effect (hormone secretion stimulate or inhibit neurons). Has specialized receptors that only receive signal in that area of the body or that organ (target neuron/target organ)
Neuroendocrine glands
act like neurons in many respects, but release secretions (ex. oxytocin) into bloodstream
Physiology of Hypothalamus-
Regulates primitive functions from water balance and thermoregulation to sex drive and childbirth functions carried out by pituitary gland. Produce 8 hormones, six regulate the anterior pituitary and two are released into capillaries in the posterior pituitary stored until released into the blood
6 hormones Secreted by Hypothalamus and travel to Anterior Pituitary:
Hint: all of the releasing and inhibiting hormones that pituitary ends up secreting!
Gonadotropin-releasing hormone (↑FSH & LH), thyrotropin-releasing hormone (↑TSH and prolactin), corticotropin-releasing hormone (↑ACTH), prolactin-releasing hormone, prolactin-inhibiting hormone (ḻ prolactin), growth hormone- releasing hormone (↑GH), and somatostatin (growth hormone inhibiting hormone ḻ GH & TSH)
Secreted by Anterior Pituitary that is under control of hypothalamus
follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone (thyrotropin), Adrenocorticotropic hormone, prolactin, and growth hormone
Hormones released by posterior pituitary
two Hormones made in hypothalamus but stored and released by posterior pituitary anti-diuretic hormone & oxytocin
FSH
follicle stimulating hormone secreted by anterior pituitary. women-stimulates secretion of ovarian sex hormones (estrogen) and egg follicles, men- stimulates sperm production
LH
luteinizing hormone secreted by anterior pituitary. women-stimulates ovulation (release of egg) and secretion of progesterone by corpus luteum, men- stimulates testes to secrete testosterone
TSH
thyroid stimulating hormone/thyrotopin. Secreted by anterior pituitary stimulates growth of thyroid gland and secretion of thyroid hormone (impacts metabolic rate, body temperature etc.)
ACTH
adrenocorticotropic hormones/corticotropin. Secreted by anterior pituitary stimulates adrenocortex to secrete glucocorticoids (cortisol impacting glucose, protein, and fat metabolism stress response)
PRL
prolactin secreted by anterior pituitary after birth stimulates mammary glands to synthesizing milk
GH
growth hormone/somatotropin secreted by anterior pituitary most numerous stimulating mitosis and cellular differentiation. GH has widespread effects on the body tissues including bones, muscle, fats, ligaments but also induces liver to produce growth stimulants
ADH
antidiuretic hormone secreted by posterior pituitary affects kidneys increasing water retention by decrease urine volume preventing dehydration. Also a neurotransmitter aka vasopressin causing vasoconstriction
OT
oxytocin secreted by posterior pituitary affecting uterus and mammary glands leading to uterine/labor contractions, milk release, sexual arousal and orgasm, and bonding mother to child and sexual satisfaction
Control of Anterior Pituitary Secretions w/ examples:
Hypothalamic control allows brain to monitor conditions w/in and outside body based on feedback and stimulate or inhibit release of anterior lobe caused Negative feedback—increased target organ hormone levels inhibit release of hypothalamic and/or pituitary hormones. Ex. stress cause ACTH secretion for tissue repair, pregnancy prolactin for after birth.
Control of Posterior Pituitary Secretions w/ examples
Posterior pituitary controlled by neuroendocrine reflexes, based on the release of hormones in response to nerve signals. Ex. Dehydration raises osmolarity of blood detected by osmoreceptors triggering ADH causing water conservation decreasing blood osmolarity; high BP cause stretch receptors in heart to secrete natriuretic causes reflex that inhibits ADH release increasing urine output. Ex. infant succling or crying sends signal to hypothalamus to respond and release oxytocin. Stress disrupt ovulation, menstrual cycle, and fertility
negative feedback of hypothalamus and examples
increased target organ hormone levels inhibit release of hypothalamic and/or pituitary hormones. Example: thyroid hormone final hormone inhibits release of TRH by hypothalamus and of TSH by anterior pituitary
positive feedback of hypothalamus and examples
Positive feedback can also occur
Stretching of uterus increases OT release, causes contractions, causing more stretching of uterus, etc. until delivery
Insulin-like growth factors
prolong the action of GH. GH affect is only 6-20 minutes. IGF-I: has a 20 hour half life, which leads to protein synthesis, lipid metabolism (protein sparing), carbohydrate metabolism (glucose-sparing effect for brain) using fatty acids reducing cells need for glucose, increasing glucose synthesis, and electrolyte balance retention of sodium, potassium and chlorine by kidneys, and Calcium retention by small intestine, potassium absorption in kidneys & tissues
GH affects in children, and adults
Bone growth, thickening, and remodeling influenced, especially during childhood and adolescence
Secretion high during first 2 hours of sleep.
Can peak in response to vigorous exercise, trauma, physical or emotional stress, hypoglycemia. Causes hunger by ghrelin hormone in stomach negative beeback for GHRH.
GH levels decline gradually with age wrinkling of skin, loss of muscle mass and strength
Pineal Gland Structure and Function
pine cone shape attached to roof of third ventricle beneath the posterior end of corpus callosum.
Function: synchronizes w/ 24 hour circadian rhythms, releasing melatonin from serotonin at night. Also fluctuates seasonally w/ day length
Pineal gland in children
After age 7, it undergoes involution(shrinkage)
Down 75% by end of puberty
Tiny mass of shrunken tissue in adults
Pineal gland may influence timing of puberty in humans
seasonal affective disorder
influenced by the pineal gland and typically found in winter or northern climates includes depression, sleepiness, irritability, and carb cravings relieved w/ 2-3 hours of bright light decreasing the symptoms of the disorder.
Thymus systems it affects, structure, function, and affect w/ age
plays a role in three systems: endocrine, lymphatic, immune
made of two lobes that split. Involution as we age turns to fat more as you get older just fat. Located behind the sternal manubrium superior to the heart. Secretes hormones (thymopoietin, thymosin, and thymulin) that stimulate development of other lymphatic organs and regulate development & activity of T lymphocytes, site where they mature
Thyroid gland functions
Release thyroid hormone (thyroxine/T4/tetraiodothyronine) or 10% is T3 (triiodothyronine). TH increase metabolic rate (breakdown of carbs, fat, and protein for fuel), raising oxygen consumption (therefore increasing heat production), raise respiratory rate, heart rate, and strength of heartbeat, stimulating appetite, promote alertness & quicker reflexes. Stimulates growth hormone for bones, hair, skin, nails and teeth.
thyroid effects in children
Contains special parafollicular cells (C cells) periphery of follicles respond to rising blood Ca releasing calcitonin antagonizing PTH stimulating osteoblast promoting calcium deposision and formation mostly affecting children.
Parathyroid Gland function:
Secrete parathyroid hormone, which regulates blood calcium (when low: reabsorption of calcium from bones, decreasing loss in urine; when high increase urinary excretion, bone formation). Not directly regulated by pituitary monitor blood calcium
Medulla is classified as ? and what is its function in times of stress
endocrine gland and ganglion of SNS, will atrophy w/out stimulation w/out stimulation of cortisol. In times of fear, pain, or stress release signal originates in medulla leading to cortex to secrete corticosteroids as well as catecholamine (raise heart rate, blood pressure, circulation to muscles, pulmonary airflow, and metabolic rate, inhibit urine production) release epinephrine (glucose-sparing effect inhbitting secretion of insulin so organs consume less glucose change to alternative fuels allowing brain for glucose) , norepinephrine, and dopamine increasing alertness, prepare for physical activity, high energy fuels (lactate, fatty, acids, and glucose) boosts glycogenesis (hydrolysis of glycogen to glucose) and glucogenesis (conversion of fats, amino acids and noncarbs to glucose).
Cortex location, function, kinds and general functions of hormones
- surrounding medulla, produces corticosteroids are all made from cholesterol three kinds: mineralocorticoid (regulate body’s electrolyte balance), glucocorticoid (regulate metabolism of glucose and other fuels), and sex steroids (controlling developmental and reproductive functions)
Aldosterone kind and function
mineralocorticoid, uses renin-angiotensin-aldosterone system (baroreceptors cause angiotensin II then aldosterone) stimulates sodium retention in kidneys w/ water maintaining blood volume and pressure.
Cortisol kind and function
-glucocorticoid responding to ACTH stimulate fat and protein catabolism, gluconeogenesis, release of fatty acids and glucose into blood allowing body to adapt to stress and repair tissue. Additional Anti-inflammatory effect
Androgen kind and function
primary adrenal sex steroids regulated by ACTH, induce growth of pubic and axillary hair and apocrine scent glands, stimulate libido throughout life and prenatal male development
Estradiol kind and function
sex steroids and a kind of adrenal estrogen important after menopause, fat converts androgen to estrogen which promote adolescent skeletal growth maintaining adult bone mass
glucagon function
secreted by alpha cells between meals affecting liver when blood glucose concentrations are falling causing 1) glycogenolysis or the breakdown of glycogen into glucose and 2) Gluconeogenesis synthesis of glucose from fats and proteins. These two stimulates release of glucose into circulation, raising levels. In adipose- stimulates fatty catabolism release of free fatty acids. Secreted in response to rising amino acids promoting absorption creating raw material for gluconeogenesis.
Insulin function
secreted by beta cells during and immediately after a mean affecting liver, muscles, and adipose causing to absorb flucose, fatty acids, and amino acids for storage and metabolism lowering the levels in blood. Promoting synthesis of glycogen (in liver), fat, and protein enhancing cellular growth and differentiation. ad alaready stored fuels brain liver kidneys w/out sinuslin but others reuqite it without its diabetes.
Somatostatin function
secreted by D cells, which works suppresses secretion of insulin and glucagon, prolonging absorption of nutrients by inhibiting it.
Gonads classification, timing, and function
endocrine and exocrine (whole cells-eggs and sperm). Only active puberty and on.
secretes egg, sperm, estradiol, progesterone, and inihibin, and testosterone
Ovaries main hormones’ location and function
found in woman secrete estradiol (made by outer cells of egg follicle), progesterone (secrete by the remains of follicle after rupture aka corpus luteum), and inhibin (secreted by follicle and corpus luteum suppresses FSH by negative feedback). Estradiol and progesterone- development of reproductive system and feminine physique, adolescent bone growth, regulate menstrual cycle, sustain pregnancy, prepare mammary for lactation.
Testes main hormones’ location and function
found in men secrete testosterone (between tubules stimulates development of male reproductive system in fetus and adolescent, masculine physique, sex drive, sustains sperm production and sexual instinct throughout adult), inhibins (seminiferous tubules limiting FSH secretion regulating sperm production), and weaker androgens and estrogens.
skin endocrine function
Keratinocytes convert a cholesterol-like steroid into cholecalciferol using UV from sun to calcitriol regulating calcium.
Liver endocrine function
involved in the production of at least five hormones. 1) cholecalciferol into calcidiol for calcitriol. 2) angiotensinogen converts to angiotensin regulating BP. 3) erythropoietin stimulates red bone marrow to produce red blood cells increasing carrying capacity of oxygen. 4) IGF-I- mediates growth hormone. 5) hepcidin- controls iron homeostasis inhibitting
Kidneys main hormones’ function
play role in production of three hormones 1) convert calcidiol into calcitriol (vitamin d), raising blood concentration of calcium by promoting intestinal absorption inhibiting its loss in urine. 2) renin-converts angiotensinogen to angiotensin converted further constricting blood vessels and raising BP. 3) 85% of erythropoietin- bone marrow to produce RBCs renal failure causing anemia
Heart endocrine function
- rising blood pressure stimulates muscle to secrete natriuretic peptides increasing sodium excretion and urine output, decreasing blood volume opposing angiotensin II, lowering blood pressure
Stomach and small intestines general endocrine function
secrete at least 10 enteric hormones secreted by enteroendocrine cells coordinate different regions and gland of system w/ each other stimulating hypothalamus influence hunger and satiety. Ex. Gastrin-upon arrival of food to stomach to release HCl and Ghrelin- secreted when stomach is empty stimulating appetite and GHRH
Adipose tissue endocrine function and hormone
fat cells secrete leptin- appetite regulation w/ low level indicating deficiency of body fat, increases appetite and food intake, high leptin blunts appetite, signals onset of puberty, which can be delayed by low body fat.
Osseous tissue endocrine function
osteoblasts secrete osteocalcin, inhibit weight gain, onset of type 2 diabetes, iincrease B cells, increase insulin secretion, insulin sensitivity to tissues, reduce fat deposition
Placenta endocrine function
Secretes estrogen, progesterone, and others regulate pregnancy development of fetus and mammary glands.
Hormone Chemistry: three chemical classes,
steroids, monoamines, and peptides
examples of each class
steroids- derived from cholesterol ex. Sex steroids, corticosteroids only produced in adrenal and gonads
peptides- synthesized in same way as any protein ex. Oxytocin, ADH, insulin hypothalamus hormones besides doapmine.
Monoamines ex. catecholamines: Dopamine, epinephrine, norepinephrine;, melatonin (synthesized from the amino acid tryptophan), and thyroid (two tyrosine and an iodine)
Other monoamines come from the amino acid tyrosine
How are hormones transported, how are they conserved?
Most monoamines and peptides are hydrophilic
Steroids and thyroid hormone are hydrophobic bind to transport proteins (albumin and globulin made in liver) to get from one place to another. Longer half life protected from liver enzymes and kidney filtration lasting for hours and weeks, unbound hormones leave capillary to go to target cells broken down in minutes.
Thyroid hormone binds to three transport proteins in the plasma
Steroid hormones bind to globulins
Transcortin: the transport protein for cortisol
Aldosterone0 short half life unbound and would bind to albumin
hormone receptors and modes of action
hormones stimulate only cells that have receptors for them including proteins or glycoproteins in plasma membrane, cytoplasm, or nucleus specifically binding only that receptor w/ a saturation limit that no more hormones can affect.
Peptide & catecholamine hormones receptors and mode of action
hydrophilic so Cannot penetrate target cell
Bind to surface receptors (protein or glycoprotein molecules act like switches tunrning on metabolic pathways when hormones bind to them) and activate intracellular processes through second messengers. ex. cAMP or DAG. Specificity for each hormone and saturation where all occupied. relatively quickly because no synthesis necessary
Steroid hormones receptor’s and mode of action
Estrogen binds to cells in nucleus gene for progesterone and binds to same receptors for synthesizing enzymes one hormone released causing another then to own receptor causing something to happen w/ multi-step.
Penetrate plasma membrane and bind to internal receptors (usually in nucleus)
Influence expression of genes of target cell
Take several hours to days to show effect due to lag for protein synthesis
Steroids and Thyroid Hormone receptor means of action
estrogen binds to nuclear receptors in cells of uterus impacting the activation or inhibition of transcription of gene w/ easy diffusion through plasma membrane. Thyroid hormone enters target cell by means of an ATP- dependent transport protein converting to T3 binding to chromatin NA-K ATPase, activating norepinephrine receptor, and myosin production accounting for the responsiveness of cardiac muscle, sympathetic stimulation and increasing strength of heartbeat.
Signal Amplification and modulation of target-cell sensitivity in response
hormones are potent chemicals w/ one hormone triggering many enzyme molecules aka small stimulus w/ large effect. Tend to be low in hormone concentrations can have big effect if amplifying overtime. Receptors for hormones therefore can change on the cell surface depending upon the regulation of the hormone (w/ increased receptors allowing for it to be more sensitive to hormones, down regulation fewer receptors and cell sensitivity decreases or high hormone levels. Or tolerance.
Hormone Interactions why do they occur? synergistic? permissive?antagonistic?
more than one hormone for one receptor but multiple receptors for different hormones per cell. synergistic effects-work together to produce an effect that is greater than the sum of their separate effects. FSH and testosterone together increasing sperm production, permissive- one hormone enhances target organ’s response to later hormone ex. estrogen preparing uterus for progesterone in event of pregnancy, antagonistic- one hormone opposes action of other blood lowering glucose w/ insulin and glycogen raising it.
Hormone Clearance how does it work how can it be measured
Hormone signals, must be turned off when they have served their purpose. Most hormones are taken up and degraded by liver and kidney excreted in bile and urine, or degraded by target cells. Metabolic clearance rate (MCR) faster MCF shorter the half life.
What is stress? when does it occur?
Stress—any kind of situation that upsets homeostasis and threatens one’s physical or emotional well-being
Injury, surgery, infection, intense exercise, pain, grief, depression, anger, etc.
General adaptation syndrome (GAS) and its three stages
Consistent way the body reacts to stress; typically involves elevated levels of epinephrine and glucocorticoids (especially cortisol)
Occurs in three stages: alarm reaction, stage of resistance, and exhaustion
Alarm reaction
initial response to stress mediated by norepinephrine of SNS (fight flight or freeze) and epinephrine from adrenal medulla. Stored glycogen consumed, stimulate aldosterone and angiotensin raising BP, sodium and water conservation offsetting possible sweating and bleeding.
Stage of resistance
- few hours, glycogen reserves gone, need glucose, w/ stress dominated by cortisol. hypothalamus secrete CRH > pituitary ACTH to release cortisol and glucocorticoids, which convert fat and protein to fatty and amino acids lactate to feed glucose providing liver w/ gluconeogenesis materials. Adverse effects suppresses sex hormones disturbing fertility and sexual function, depressing immune system, susceptible to ulcer infections & cancer, wounds heal poorly.
Stage of exhaustion
stress levels and fat reserves (can carry for months) gone homeostasis is overwhelmed rapid decline of individual ending in death. Protein breakdown contributing to wasting of muscle. Adrenocortex stops producing glucocorticoids not managing glucose well, hypertension from retaining to much water, conserved sodium increased elimination of potassium and hydrogen creating hypokalemia and alkalosis, w/ nervous and muscular dysfunction to heart failure from overwork, kidney failure, or infection leading to death
Paracrine signaling and its three major examples
—chemical messengers that diffuse short distances and stimulate nearby cells.
ex. Histamine- released by mast cells along blood vessels diffusing to smooth muscle relaxing it),
Nitric oxide-endotheltium of blood vessels
Catecholamines- epinephrine from adrenal medulla to cortex stimulating corticosterone secretion. act as neurotransmitters and similar to effect on system
Anti-inflammatory Drugs:
cortisol and corticosterone, aspirin, ibuprofen, and celecoxib (celebrex)
nonsteroidal anti-inflammatory drugs
(NSAIDs). Cortisol and corticosteroids and nsaids anti inflammatory- inhibit inflammation by blocking arachidonic acids from plasma membrane inhibiting certain chemical messengers. No steroid
COX Inhibitory
since block cyclooxygenase, do not affect lipoxygenase or leukotriene. Treat fever and thrombosis because of inhibiting prostaglandin synthesis and antithrombotic effect by inhibiting thromboxane.
Hyposecretion and examples
—inadequate hormone release resulting from Tumors or lesions destroying glands or anything that interferes w/ communication to that area. Ex. fractured sphenoid severs the hypothalamo-hypophyseal tract preventing transport to posterior pituitary can cause diabetes insipidus. Diabetes mellitus as a result from antibodies attacking own endocrine cells
Hypersecretion and examples
—hormone release. Tumors can cause overgrowth of tissue ex. Tumor on adrenal medulla secretes excessive amounts of epinephrine and norepinephrine causing random bouts of sympatheitc nervous system, severe headaches, uncontrollable sweating. Toxic goiter autoantibodies mimic TSH causing TH hypersecretion
Congenital hypothyroidism description and symptoms
present from birth hallmark of decreased TH, causes swelling, treatable. Stunted physical development, thickened facial features, low body temp., lethargy, brain damage
Myxedema
description and symptoms
due to severe or prolonged adult hypothyroidism or graves decreased TH. characterized by low metabolic rate, sluggishness and sleepiness, weight gain, constipation, dry skin and hair, abnormal sensitivity to cold, hypertension, and tissue swelling
Hypoparathyroidism description and symptoms
result of surgery removing glands causing rapid decline of blood calcium causing suffocating spasm of muscle of laryx.
Hyperparathyroidism description and symptoms
excess PTH secretion caused by tumor bones become soft, deformed, and fragile raising calcium and phosphate levels, renal calculi (kidney stone formation)
Goiter description and symptoms
- results from deficiency of dietary iodine not allowing gland to synthesize TH producing more and more thyroglobulin swelling the neck depending on geographic and population all tend to have that random release of hormones.
Cushing syndrome description and symptoms
excessive cortisol because of ACTH hypersecretion, ACTH-secreting tumors, hyperactivity of adrenal cortex. Disrupts cab and protein metabolism, causing hyperglycemia, hypertension, muscular weakness, and edema. Muscle and bone loss as protein catabolized w/ abnormal fat deposition between shoulders creating bufallo humped or in face moon face. Treatable w/ hydrocortisone therapy
Adrenogenital syndrome (AGS) description and symptoms
hypersecretion of adrenal androgens, accompanies cushing often. Cause enlargement of sexual gonads and earlier puberty, masculinization of women w/ increased body hair, deepening of voice and ear growth
Diabetes Mellitus description and symptoms
disruption of carb, fat, and protein metabolism from hyposecretion or inaction of insulin. First presentation: three polys- polyuria (excessive urine output), polydipsia (thirst), and polyphage (hunger) confirming hyperglycemia (high glucose), glycosuria & kenonuria (glucose and ketone in the urine)
Type 1 diabetes causes and treatmen
- heredity genetically susceptible individual infected by viruses destroy pancreatic beta cells require insulin daily w/ meal planning, exercise, and self-monitoring
Type 2 diabetes causes and treatments
- insulin resistance unresponsiveness to the hormone. w/ age, obesity, and sedentary lifestyle along w/ certain populations, and hereditary genes w/ muscle mass important and helpful to regulating glucose. More body fat less efficient glucose uptake w/ weight loss.
Diabetes Pathogenesis
cells cannot absorb glucose, must rely on fat and proteins for energy needs, thus weight loss and weakness. Leading cause of adult blindness, renal failure, gangrene, limb amputations.
Fat catabolism effects from diabetes
Fat catabolism increases free fatty acids and ketones in blood
Ketonuria promotes osmotic diuresis, loss of Na+and K+, irregular heartbeat, abdominal pain, vomiting, and neurological issues
Ketoacidosis occurs as ketones decrease blood pH- Deep, gasping breathing and diabetic coma are terminal result
Chronic pathology (chronic hyperglycemia)
Leads to neuropathy and cardiovascular damage from atherosclerosis and microvascular disease w/ poor wound healing w/ minor injury causing ulceration, infection, and gangrene.
Arterial damage in retina and kidneys (common in type 1), atherosclerosis leads to heart failure blood. Thicken basement membrane of blood vessels interfering w/ delivery of nutrients to tissues and removal of waste w/ tissue degeneration of organs.
lymphatic system-
collection of tissues and organs connected to nearly every tissue producing immune cells including lymph nodes, spleen, thymus, tonsils, and red bone marrow
why do we need an immune system and what does ours do?
In the HUMAN BODY there are bacterial cells in it that beneficial and some that are not. System or cell population defends body from invading pathogens and bad bacteria is lymphatic system. Made up of organs and vein-like vessels in body that inspects body for different disease agents, active immune response, and return fluid back to circulatory system.
three functions of immune system
fluid recovery
immunity
lipid absorption
Fluid recovery-
circulatory system filters through blood capillaries reabsorbing 85% of fluid, lymph absorbs rest Including 50% of water and half of plasma proteins before returning to blood. We would Die w/in hours if water and protein were not returned to bloodstream, lymphatic system responsible for reabsorbing excess and return it too blood. Partial interference with lymphatic drainage can lead to severe lymphedema
Immunity-
as lymphatic system recovers tissue fluid, it picks up foreign cells and chemicals from tissues. Before returning to blood, fluid passes through lymph nodes, where immune cells stand guard against foreign matter. If they detect anything potentially harmful, they activate a protective immune response
Lipid absorption-
in the small intestine, special lymphatic vessels called lacteals absorb dietary lipids that are not absorbed my blood capillaries
Lymph
The recovered fluid, clear w/ less protein structure different per area and time
describe lymphatic pathway
lymphatic capillaries →collecting vessels → six lymphatic trunks → two collecting ducts → subclavian veins.
Lymph vessels
Transport the lymph everywhere but cartilage, bone, bone marrow, and cornea have valves pushing fluid forward w/ overlapping cells. w/ tunica interna (endothelial and valves), tunica media (elastic fibers and smooth muscle), tunica externa
Lymphatic capillaries
converge to form collecting vessels, traveling alongside veins and arteries and sharing tissue sheath with them. w/ collecting vessels converging to form larger lymphatic trunks, which drains major portions of the body. trunks converge to form two collecting ducts, the largest of the lymphatic vessels.
Lymphatic Flow describe its flow. how is the lymph moved
In response to different forces similar to veins but w/out a pump. Flows at low pressure and slower speed than venous. Moved by: Contractions of lymphatic vessels themselves-Rhythmic contractions of vessels move it w/ valves help push in proper direction aided by skeletal muscle pump. Arterial pulses squeeze lymph through vessels, thoracic valve as well as respirations promoting flow of lymph from abdominal to thoracic in inhalation. Rapidly flowing blood in subclavian veins pulling blood in and exercise helps lymphatic return and exchange
Lymphatic tissues what are they made of? where are they found? where arent they found? structure? function?
composed of aggregates of lymphocytes and macrophages that populate many organs in the body. absent from CNS bone and bone marrow. Have capillary walls made of endothelial cells that are closed at one end surrounding the tissue w/ protein filaments allowing bacteria to enter. Forms nodules- where lymphocytes and macrophages congregate come and go as pathogens invade. Endothelial has flaps when fluid pressure high and low. Larger three layers tunica interna, media (smooth muscle), and externa converting into larger and larger thickness. organization changed based on Purpose, theme and location
Lymphatic Cells:
Natural killer (NK) cells T lymphocytes (T cells) B lymphocytes (B cells) Macrophages Dendritic Reticular
Natural killer (NK) cells
- large lymphocytes attack and kill tissue, attacks cancer, and foreign cells
T lymphocytes (T cells)
mature cells from thymus
B lymphocytes (B cells)
from bone marrow differentiate to plasma cells, which produce antibodies
Macrophages
-large phagocyttotic cells of connective tissue from monocytes eat tissue debris, dead neutrophils foreign matter, bacteria showing antigens to t cells
Dendritic
- branched mobile antigen of lymphatic organs. Located in epidermis, mucous membranes, and lymphatic organs. Alert immune system to pathogen on surface engulfing via endocytosis then migrating to nearby lymph node
Reticular-
antigen cells contribute to connective tissue framework of lymphatic organs
Lymphatic Organs what are their functions
connective tissue castles w/ a connective tissue capsule that adds another layer of protection to organ from neighboring tissue
- Defense cells are especially concentrated in these organs
Materials diffuse through lymphatic tissue, which are scattered body passages open to exterior world
Red bone marrow-
Primary lymphatic organ where B and T lymphocytes become immunocompetent they grow in endosteum and as blood cells they develop push through reticular to sinusoid and flow away in blood stream.
Thymus
primary organ where T cells & B cells form are housed and secreted from. Degenerates w/ age. Made of lobes cortex (cortical epithelial surround capillaries forming blood-thymus barrier isolating lymphocytes) and medulla (T lymphocytes come from cortex for longest time). Secretions: thymosin, thymopoietin, thymulin, interleukins, and interferon governing T cell creation
Secondary organs
Lymph nodes (most numerous cleanse lymph and activating T and B cells), Tonsil and, Spleen–T and B cells migrate to these organs neuro competent cells
Lymph Nodes what is it? what is its function? what is its downfall? how does lymph travel through this?
lymph fluid and tissue congregating in response to pathogens in response to some type of invader.
All over body- great travel route for bad things if lymphatic system doesn’t pick up in time. Cleans lymph, site of T and B cell activation, enclosed in fibrous capsule w/ trabeculae dividing into compartments w/ sinus containing-reticular fibers, macrophages, and dendritic cells. w/in cortex and germinal centers in medulla are where B cells multiply and differentiate into plasma cells. Lymph travels by afferent fibers into node throughout sinuses where it is bottlenecked slowing to filter and leave via efferent vessels in hilum to cortex surface. Have blood contact surfaces where lymphocytes enter lymph nodes in the deep cortex near junction w/ medulla, mostly T cells.
When a lymph node is under challenge by an antigen
Lymphadenitis:
swollen, painful node responding to foreign antigen
Lymphadenopathy-
collective term for all lymph node diseases
Areas of Lymph Node Concentration-
Lymph nodes in different areas cervical abdominal, intestinal, lingual, mass concentrations of lymph nodes.
Lymph Nodes and Metastatic Cancer-
Metastatic cancer where cancer cells break free from original place traveling through lymphatic and enter easily lodging in first one they encounter multiplying and can destroy node are swollen but firm and painless. Sometimes cancer can be caught in original and you can stop it there by removing it and nearby lymph not but can spread quickly. Treatment of breast cancer- mastectomy and of nearby nodes in case small cells remove to be safe.
Metastasis
—cancerous cells break free from original tumor, travel to other sites in the body, and establish new tumors
Tonsils-
patches of lymphatic tissue in entrance of pharynx guarding against ingested and inhaled pathogens covered by epithelium, w/ deep pits called tonsillar crypts that pathogens, food debris, antigenic chemicals, and dead leukocytes get into and encounter lymphocytes. Patches of lymphatic tissue located in different areas in entrance to pharynx
Tonsilitis when swollen will get removed.
Three major set.
Palatine- posterior part of oral cavity most often infection largest and most often infected, Lingual-root of tongue. Pharyngeal-adenoids- single tonsil on wall of nasopharynx Deep crypts.
Spleen-
Biggest lymphatic organ-fits between diaphragm, stomach, and kidney medial hilum w/ splenic vessels. Parancehemia red: red pulp- sinuses filled w/ erythrocytes and white pulp- lymphocytes and macrophages that surrounding splenic artery, w/ permeable blood capillaries allowing RBCs to leave. Function is to hold healthy red blood cells storing them or graveyard for red blood cells. Fetus- blood cell production occurs and in severely anemic adults. White pulp-monitors blood for foreign antigens monocytes ready for release in case of invade in body. Stabilizing blood volume by transferring excess plasma into lymphatic. Highly vascular and to trauma and infection will bleed out quickly splenectomy- can live w/out leaving person more vulnerable to infection
Innate immunity-
defenses we are born w/. First and second lines of defense. Local- ward off pathogen point of invasion w/ little effect elsewhere, nonspecific- works on broad spectrum, lacks memory w/ protective protein (keratin, interferons, and complement); protective cells (neutrophils and macrophages, and protective processes (fever and inflammation).
Adaptive immunity
- third line of defense based on memory adapting body to presence of environmental pathogen becoming less vulnerable to illness Specific immunity each pathogen warding off more easily different barrier lines of defense against different pathogens.
Skin
physical barriers to microbial invasion composed of: tough keratin difficult to penetrate, too dry not a lot of nutrient or bacterial growth, acid mantle- thin film of lactic and fatty acid peptide against microbes, and dermcidin, defensin, and cathelicidins on skin
mucous membranes
- lining digestive tract, urinary, and respiratory acts as protective barrier against invading trapping microbes in mucus moved via cilia to pharynx and swallowed, mucus, tears, and saliva have lysozymes destroying bacterial cell wall. Below is Subepithelial areolar tissue- barrier to tissue makes hyaluronic acid viscous cant pass through Pathogens have hyaluronidase- in snake venom bacterial toxin breaking down layer to be penetrated
Pathogens
—agents capable of producing disease
Include viruses, bacteria, and fungi
Three lines of defenses against pathogens
First line of defense: epithelial barriers skin and mucous membranes impenetrable
Second line of defense: several nonspecific defense mechanisms
Leukocytes and macrophages, antimicrobial proteins, natural killer cells, inflammation, and fever
Third line of defense: adaptive immunity the immune system
Defeats a pathogen, and leaves the body with a “memory” of it so it can defeat it faster in the future
THREE External Barriers
- skin, mucous membranes, subepithelial areolar tissue
Leukocytes:
phagocytes- cells that engulf foreign matter. Neutrophils Eosinophils BASOPHILS lymphocytes monocytes
Neutrophils
(cells that wander throughout connective tissue killing bacteria by phagocytosis and emitting cloud of bactericidal chemicals by discharging lysosomes aka degranulate and exchange causing respiratory burst around bacteria killing everything around it)
Eosinophils
- in mucous membranes guard against parasites, allergens (also found at inflammation), and other pathogens. Killing tapeworms and roundworms, by hydrogen peroxide, superoxide, and proteins such as neurotoxin. Promote Basal cells and mast cells. Phagocyteiz antigen antibody complexes, stop antihistamine.
Basophils
- secrete chemicals that aid mobility of other leukocytes. Ex. leukotienes (activate and attract neutrophils and eosinophils), histamine (increse blood flow), heparin (inhibits blood clots impeding leykocyte) also by mast cells.
Lymphocytes
- Circulating t cells, B cells, K cells destroying foreign material breaching human body.
Monocytes
-from blood to tissue become macrophages phagocytize bad cells have two kinds
Macrophage system-all the body’s avidly phagocytic cells, except leukocytes including dendritic cells
Wandering macrophages:
actively seek pathogens throughout connective tissue
Fixed macrophages:
reticular cells phagocytize only pathogens that come to them found in alveolar, hepatic, microglia
Antimicrobial Proteins what do they do and what are the two families?
Proteins that inhibit microbial reproduction and provide short-term, nonspecific resistance to pathogenic bacteria and viruses. Help lymphatic and immune.
Two families of antimicrobial proteins: interferons, complement cells
Interferons
certain cells (leukocytes) infected w/ viruses secrete this dying words alerting neighbors protecting from becoming infection by causing anti-viral proteins against their genes and activate NK cells and macrophages (to break down before virus released) and destroy cancer.
Complement cells-
30+ globulins powerful proteins to nonspecific resistance and adaptive immunity synthesized by liver activated by presence of pathogen responding by four methods inflammation, immune clearance, phagocytosis, and cytosis
complement system Pathways:
Classical
Alternative
Lectin-
Classical complement system pathway
requires antibody molecules, adaptive immunity, bind to surface of system forming antigen antibody complex exposing pairs of complement binding sites and fixation chain of complement proteins attaching to pathway amplifying process
Alternative
-binds directly to target tumor, bacterial, virus, yeast. Autocatalytic affect production of more of itself. Nonspecific no antibodies specific targets.
Lectin-
plasma proteins binding to sugars setting of more cascades of C3 production
Mechanism of action of complement proteins
Inflammation
Immune clearance-
Phagocytosis-
Inflammation
- mast cells stimulates basal cells to secrete histamine and other inflammatory molecules. Activates neutrophils and macrophages to destruction
Immune clearance-
c3 binds antigen and antibody to RBCs when circulated circulating through spleen and liver stripping complex making the RBCs unharmed clearing from blood stream
Phagocytosis-
bacteria and viruses easy to phagocytize. But can’t phagocytize naked pathogens, C3 opsonization coats microbial cells and serve as binding sites for attachment by macrophages and neutrophils to destroy cells
Cytolysis and what is the Membrane Attack complex
- C3 split complement and they all bind forming membrane attack complexes, which makes hole in target cells w/ electrolytes out water in and cell ruptures
- complement proteins form ring in plasma membrane of target cell causing cytolysis
Course of a Fever-
Elevation of body temperature from trauma, infection, drug reactions. Adaptive defense mechanism moderation but more good than harm if too long or high detrimental effects for shorter periods promotes interferon activity, inhibits reproduction of bacteria and viruses, and elevates metabolic rate, which accelerates tissue repair
Antipyretic-
reduce fever by inhibiting prostaglandin synthesis.
Fever is triggered by
exogenesis glycolipids on bacterial, w/ pyrogens secreted by neutrophils and macrophages raises hypothalamic setpoint. Neurons in exterior hypothalamus secrete prostaglandin raises set point.
what are the three stages of a fever describe them
Three stages: Onset (shivers to generate heat w/ cutaneous arteries constrict decreasing heat loss rising temperatures feeling cold and clammy), stadium (temperature oscillates around higher set point as long as pathogen present enhancing interferons), and defervescence (pyrogen secretion ceases cutaneous vasodilation and sweating warm and flush) w/ higher over 105 causing discoordination and disfunction deliria and brain damage.
Reye syndrome
children younger than 15 w/ acute viral infection chickenpox or influenza cause swelling of brain neurons fatty infiltration of liver and viscera. Neurons die from hypoxia and pressure from swelling brain symptoms include: nausea, vomiting, disorientation, seizures and can put kid into coma 30% die or suffer from mental retardation too much aspirin can’t give to children w/ flu or
Inflammation-
local defensive response to tissue injury, including trauma and infection by limiting spread of pathogens, remove debris of damaged tissue, initiate tissue repair. Four cardinal signs of inflammation: redness, swelling, heat, and pain.
Cytokines-
small proteins regulate inflammation and immunity secreted by leukocytes altered physiology of neighboring cells via paracrine effect, autocrine effect, endocrine effect including interferons, interleukin, tumor necrosis factors,.
Three major processes of inflammation.
Most immediate requirement leukocytes to site to defend area. Damaged tissue release cytokines to bring neutrophils to area from bone marrow, cells secrete vasoactive chemicals (histamine, leukotrienes, and other cytokines secreted by basophils, mast cells, and cells damaged by pathogen) dilating blood vessels and contract widening gaps between them increasing capillary permeability and allowing leukocytes to enter injury site causing hyperemia- vasodilation rapid delivery of leukocytes and washes toxins and wastes from area quickly. VasoChemical Widen gap between cells increasing liquidsand everything leave bloodstream more area.
Describe the causes for the four cardinal signs of infection?
Heat-hyperemia, redness-hyperemia extravasated erythrocytes, swelling-increased fluid filtration from capillaries, pain-direct injury or pressure on nerve from edema stimulation of pain receptors by prostaglandin, bacterial toxins, and bradykinin
margination-
cell adhesion help to recruit leukocytes to adhere to vessel wall by selecting they then crawl through gaps to fluid, diapedesis or emigration
margination-
cell adhesion help to recruit leukocytes to adhere to vessel wall by selecting they then crawl through gaps to fluid, diapedesis or emigration
Containment and Destruction of Pathogens
- Second step, prevent pathogen spread, fibrinogen filters into tissue fluid clotting in area adjacent to injury sticky mesh walling off bacteria and microbes
Heparin
- anticoagulant prevents clotting trapping pathogens in fluid pocket around clot
Neutrophils-
within an hour to fight off pathogen chemotaxis- attraction to chemicals bradykinin and leukotrienes guiding to injury site. As encounter bacteria phagocytosis respiratory bursts & recruiting macrophages. Use cytokines colony- stimulating factors promoting production of leukocytes raising WBC count.
Bacterial infection
- high neutrophil
Eosinophils
- parasitic infections
Tissue Cleanup and Repair
- Monocytes-8-12 hours turning into macrophages destroy bacteria, dead dying neutrophils, damaged host cells, and antigen-presenting cells for memory.
Edema-
contributes to tissue cleanup swelling compresses veins reducing drainage opening lymphatic to allow to drain better than blood.
Pus-
abscess dead cells, tissue debris, and fluid form yellowish fluid
Hyperemia
- delivers oxygen, amino acids, and other necessities for protein synthesis w/ heat of tissue increasing metabolic rate and speed of mitosis and tissue repair
Platelet-derived growth factor
is secreted by blood platelets and endothelial cells in injured area stimulates fibroblasts to multiply and synthesize collegagen, fibrin clot scaffold for reconstruction.
Pain- makes us limit use of whatever injured rest heal and repair damage.
Three characteristics distinguish adaptive immunity from nonspecific resistance state and describe them
systemic effect (when adaptive response mounted against particular threat such as bacterial infection acting throughout body to defeat pathogen wherever found)
specificity (immunity directed against a particular pathogen)
memory (when re-exposed the same pathogen, the body reacts so quickly that there is no noticeable illness)
Different forms of adaptive immunity:
cellular and humoral can work and act together:
Cellular adaptive immunity
cell mediated lymphocytes directly attack and rid body of pathogens or diseased cells where inaccessible to antibodies all of the targets that are intracellular.
Humoral adaptive immunity
use antibodies to tag for destruction effective against extracellular pathogens.
Natural active immunity
Production of one’s own antibodies or T cells as a result of infection or natural exposure to antigen
Artificial active immunity
Production of one’s own antibodies or T cells as a result of vaccination against disease
Vaccine:consists of dead or attenuated (weakened) pathogens that stimulate the immune response without causing the disease ex. botulism, rabies, or tetanus
Booster shots: periodic immunizations to stimulate immune memory to maintain a high level of protection
Natural passive immunity
- 2-3 week window
Fetus acquires antibodies from mother through placenta, milk.
Artificial passive immunity - 2-3 week window
Temporal immunity
from other human or animal w/ the antibodies. Treatment for snakebite, botulism, rabies, tetanus, and other diseases
Antigens
any molecule that triggers an immune response ex. Toxins, venoms, cell walls, part of membrane but w/ most having large molecular weight, w/ complex molecule having unique antigen that enables body to distinguish self from foreign
•Haptens-
too small to be antigenic in themselves but trigger immune response by host macromolecule making unique complex that is then classified as foreign. Ex. penicillin is a hapten binding to host proteins in allergic individuals creating complex binding to mast cells triggering histamine etc.
•Epitopes(
antigenic determinants)—certain regions of an antigen molecule that stimulate immune responses,
Antibody what cells are they located in?
integral proteins in plasma membrane of basophils and mast cells (innate), adaptive immunity (membrane proteins of B lymphocytes) or soluble in a variety of tissues
Lymphocytes THREE KINDS
- major cells of adaptive immune: natural killer cells, T lymphocytes, and B lymphocytes
T Lymphocytes (T cells): three stages in life of T cell
–Born in bone marrow by hematopoietic stem cells
–Educated in thymus (reticular endothelial cells stimulate maturing T cells antigen receptors capable of recognizing antigens present to them tstT cells by doing cells if unable to recognize other multiple times, ones that failed eliminated by macrophages and apoptosis. Negative selection-elimination or conversion of self-reactive T cells w/self tolerance restraining attacking one’s tissues (only 2% pass) medulla- tested against one’s own cells to different antigens immunocompetent cells passed test by positive selection being immunocompetent deployed as naïve pool to thymus and elsewhere body
–Deployed to various organs especially deep cortex of lymph nodes to carry out immune function
B lymphocytes (B cells)
B cells develop in bone
B cells that react to self-antigens undergo either apoptosis or clonal deletion, same as T cell selection
Self-tolerant B cells synthesize antigen surface receptors, divide rapidly, produce immunocompetent clones just like t cells colonize lymphatic organs and tissues as T cells.
Antigen-Presenting Cells:
•T cells cannot recognize antigens on their own. Antigen-presenting cells (APCs) are required when they encounter antigens they internalized by endocytosis digesting and displaying fragments.
Wandering t cells-
inspect for displayed antigen of only self disregards, if foreign immune attack mobilize immune cells against antigen chemical messengers to coordinate interleukins.
Dendritic cells, macrophages, reticular cells, and B cells function as APCs
Function of APCs depends on
major histocompatibility (MHC) complex proteins Act as cell “identification tags” that label every cell of your body as belonging to you Structurally unique for each individual, except for identical twins
Cellular Immunity
Cell-mediated where T lymphocyte directly attack and destroy foreign & diseased cells remembering the antigens to prevent later disease
Cytotoxic T (TC) cells:
killer T cells (T8, CD8, or CD8+)
“Effectors”of cellular immunity; carry out attack on enemy cells. Only T cells that do
Helper T (TH) cells
Help promote T cell roles in humoral and adaptive immunity; cellular and humoral
Regulatory T (TR) cells: T-regs
Inhibit multiplication and cytokine secretion by other T cells; limit immune response after infection over to protect body. Cellular immunity
Memory T (TM) cells
Descend from the cytotoxic T cells
Responsible for memory in cellular immunity vigilant w/out damage
Recognize step from cellular immunity describe pathway
Recognize- when an APC encounters and processes antigen migrating to nearest lymph node displaying to T cell. Cytotoxic or helper T cell bind to APC and recognize that it is binding to an antigen bind to another protein related to interleukins, costimulation check twice to see if boud to foreign antigen ensuring immune system launch attack in absence of enemy.
Lack of costimulation drives T cells into anergy, inactivity and ineffectiveness, successful costimulation triggers repeated mitosis giving rise to clone cells against the same epitope becoming effector cells, carrying out attack or memory T cells.
React step from cellular immunity describe pathway
React-Attack occurs w/ helper and cytotoxic t cells. Helper t cells recognize Ag-MHC secretes interleukins Attracting neutrophils and natural killer cells; attract macrophages stimulate phagocytic activity and inhibit form leaving area; stimulate t and b cells maturation. Cytotoxic- docks on antigen complex delivering lethal hit of chemicals (perforin and granzymes kill target cell same as NK, interferons- inhibit viral replication and recruit macrophages to kill whole cell before burst, tumor necrosis macrophage activation and kills cancer cells.) Once chemicals released by cytotoxic search enemy cell still
Remember
Immune memory follows primary response in cellular immunity
Following clonal selection, some TC and TH cells become memory cells
Long-lived
More numerous than naive T cells
Fewer steps to be activated, so they respond more rapidly
T cells call response same things later in life so no noticeable illness occurs
Remember step from cellular immunity describe pathway
Immune memory follows primary response in cellular immunity
Following clonal selection, some TC and TH cells become memory cells
Long-lived
More numerous than naive T cells
Fewer steps to be activated, so they respond more rapidly
T cells call response same things later in life so no noticeable illness occurs
Humoral Immunity
-more indirect method of defense than cellular immunity
B lymphocytes of humoral immunity
produce antibodies that bind to antigens and tag them for destruction by other means
Cellular immunity attacks the enemy cells directly
Works in three stages like cellular immunity
Recognition step of humoral immunity
immunocompetent B cell antigen binds to several of same receptors, which links them together and then is taken into cell by endocytosis (not antigenic if can’t link multiple receptors together) B cell digests antigen w/ epitopes linked to MHC proteins displaying. w/ helper t cell binding to complex secreting interleukins activating B cell triggering clonal selection against that antigen into plasma cells in germinal centers of lymph nodules of nodes producing antibodies
react step of humoral immunity
neutralization- masking of critical regions of antigen by antibody around only pathogenic parts,; fixation- antibodies bind complement proteins to enemy cell igM and IgG and complement lead to inflammation, phagocytosis, immune clearance, and cytolysis opsonizing bacteria making easier to destroy; agglutination- clumping of enemy cells by antibodies sticking multiple problem cells together preventing spread phagocytizing efficiently; precipitation- antigen molecules clumped by adhesion to antibodies removed by immune clearance.
memory step of humoral immunity
Primary immune response—immune reaction brought about by the first exposure to an antigen. Primary response leaves one with an immune memory of the antigen Primary –delayed for 3-6cells while differentiate to plasma cells produce antibodies titer rising as produced leaves one w/ immune memory of antigen and clonal selection germinal centers of lymph nodes w/ secondary response
Secondary(anamnestic) response—if exposed to the same antigen plasma cells w/in hours no noticeable effect in body so no invader noted, long lasting protection weak to years lasts longer in cellular.
variability in antibodies
Human immune system capable of as many as 1 trillion different antibodies
But there are as few as 20,000 genes in the human genome, so the variety of proteins must be accomplished by: Bind to antibody and destroy, go to memory. IG-antibody defensive globulin body secretion. Antibody monomer-
Somatic recombination
DNA segments shuffled and form new combinations of base sequences to produce antibody genes
Somatic Hypermutation
B cells in lymph nodules rapidly mutate creating new sequences
Immune system disorders
Immune response may be: Too vigorous (hypersensitivity) , Too weak(immunodeficient, Misdirected against wrong targets (autoimmune_
Hypersensitivity what it is and what does it include
allergies excessive reaction of environmental antigens occur w/ certain types of medication. an excessive immune reaction against antigens that most people tolerate. Types based on type of immune agents involve\
alloimmunity
autoimmunity
allergies
Alloimmunity:
reaction to transplanted tissue from another person
Autoimmunity:
abnormal reactions to one’s own tissues
Allergies:
reactions to environmental antigens (allergens)—dust, mold, pollen, vaccines, bee and wasp venom, poison ivy and other plants; foods such as nuts, milk, eggs, and shellfish; drugs such as penicillin, tetracycline, and insulin
Anaphylaxis
hypersensitivity
Immediate, severe type I reaction
Local anaphylaxis can be relieved with antihistamines
Anaphylactic shock
hypersensitivity
Severe, widespread acute hypersensitivity that occurs when an allergen is introduced into the bloodstream or when certain foods are ingested by an allergic individual
Characterized by bronchoconstriction, dyspnea (labored breathing), widespread vasodilation, circulatory shock, and sometimes death
Antihistamines Are inadequate by themselves
Epinephrinerelieves the symptoms by dilating bronchioles, increasing cardiac output, and restoring blood pressure
Fluid therapy and respiratory support are sometimes required
vasodilation and cardiac shock leading to death epi help relieve system respiratory therapy and supprt.
asthma
hypersensitivity
Effects
Bronchospasms within minutes
Severe coughing, wheezing, and sometimes fatal suffocation
Second respiratory crisis often occurs 6 to 8 hours later
Interleukins attract eosinophils to bronchial tissue
Secrete proteins that paralyze respiratory cilia
Severely damage epithelium leading to scarring and long-term damage to lungs
Bronchioles become edematous and plugged with thick, sticky mucus
Treatment
Epinephrine and other β-adrenergic stimulants to dilate airway and restore breathing, and with inhaled corticosteroids to minimize inflammation and long-term damage
autoimmune diseases
Autoimmune diseases—failures of self-tolerance
Immune system does not correctly distinguish self-antigens from foreign ones
Producesautoantibodies that attack body’s own tissues
Three reasons for failure of self-tolerance: cross-reactivity, abnormal exposure to self-antigens, changes in self-antigens
Cross-reactivity
abnormal exposure of self-antigens in blood
changes in structure of self-antigens
Cross-reactivity
Some antibodies against foreign antigens react to similar self-antigens
Rheumatic fever—streptococcus antibodies also react with heart valves
Abnormal exposure of self-antigens in the blood
Some of our native antigens are not normally exposed to blood
Blood–testes barrier isolates sperm from blood
Changes in structure of self-antigens
Viruses and drugs may change the structure of self-antigens or cause the immune system to perceive them as foreign
Self-reactive T cells
Not all are eliminated in thymus and are normally kept in check by regulatory T (TR) cells
Immunodeficiency diseases
•Immune system fails to react vigorously enough
Severe combined immunodeficiency disease (SCID)
Hereditary lack of T and B cells
Vulnerability to opportunistic infection and must live in protective enclosures
Acquired immunodeficiency syndrome (AIDS)
Nonhereditary diseases contracted after birth
Group of conditions that severely depress the immune response
AIDS is caused by infection with the human immunodeficiency virus (HIV)
Invades helper T cells, macrophages, and dendritic cells by “tricking” them to internalize via endocytosis viruses by receptor-mediated endocytosis
By destroying THcells, HIV strikes at the central coordinating agent of nonspecific defense, humoral immunity, and cellular immunity
Incubation period ranges from several months to 12 years
signs and symptoms of AIDS
Early symptoms: flu-like symptoms of chills and fever
Progresses to night sweats, fatigue, headache, extreme weight loss, lymphadenitis
Normal THcount is 600 to 1,200 cells/mL of blood, but in AIDS it is less than 200 cells/mL
Person susceptible to opportunistic infections (Toxoplasma,Pneumocystis,herpes simplex virus, cytomegalovirus, or tuberculosis)
Candida (thrush): white patches on mucous membranes
Kaposi sarcoma: cancer originates in endothelial cells of blood vessels; causes purple lesions in skin
transmission of AIDS
HIV is transmitted through blood, semen, vaginal secretions, breast milk, or across the placenta
Most common means of transmission
Sexual intercourse (vaginal, anal, oral)
Contaminated blood products
Contaminated needles
Not transmitted by casual contact
Undamaged latex condom is an effective barrier to HIV
strategies to combat AIDS
Strategies to combat AIDS
Prevent binding to CD4 proteins of THcells
Disrupt reverse transcriptase to inhibit assembly of new viruses or their release from host cells
Medications for AIDS
None can eliminate HIV, all have serious side effects
HIV develops drug resistance
Medicines used in combination
Azidothymidine(AZT)
First anti-HIV drug: inhibits virus from cells.
Protease inhibitors
Inhibit enzymes HIV needs to replicate
Now more than 24 anti-HIV drugs on the market
