Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
134 Cards in this Set
- Front
- Back
|
7 Functions of water in biology |
1. maintaining homeostasis 2. solvent in many metabolic reactions 3. medium to transport nutrients in/waste out of cells 4. transports enzymes in digestive system 5. transports blood components 6. Facilitates joint movements 7. body water composition |
|
|
Name one very important way water maintains homeostasis in body |
Hydrostatic/hydraulic pressure of the IVC to maintain blood flow, BP and allow concentration gradients (high to low) |
|
|
Body water compositions |
-Infants: high water % but get dehydrated more due to frequent N/V and undeveloped kidneys -Elderly and obese: have less body water % and thus get dehydrated quicker
|
|
|
2 main reasons for Dehydration |
1. Hypotension 2. Acid-base imbalances |
|
|
Fluid compartments and whats in them? |
-Intracellular compartment - Everything inside cell, majority of water here, ICF -Extracelluar compartment - everything outside cell, ECF |
|
|
Tell me about the Intravascular Fluid (IVF) |
-blood, where labs are drawn from to see patients electrolyte levels - wall composed of epithelial cells controlled by passive difussion: Arteriole side - hydrostatic pressure high, pushing oxygen and nutrients into ISF Venual side - hydrostatic pressure much less, ISF can then be sucked back into vein to take waste away from cell
|
|
|
Tell me about 3 other fluids |
ISF - interstitial fluid: bathes cells CSF - Cerebrospinal fluid Transcellular fluid: around paricarial and joints |
|
|
Getting from ISF to ICF requires: |
1. most things require active transport using ATP as energy 2. Other things may bind to receptor - energy not used by still regulated 3. Water gets free ride - this can be bad if there is an electrolyte or protein embalance |
|
|
Osmosis |
-no energy required -flow of water from high concentration of water to low concentration of water. Aka it moves in the direction of higher concentration of salt where there is higher "osmolarity" |
|
|
The 3 major forces involved in flow shifts and an example. |
1. Hydrostatic pressure - "push" ex) arterial BP pushes blood out of IVF into ISF 2. Osmotic pressure - "pull" or "sucking" to bring fluid toward ex) Na+, chemical mediators, albumin keep fluid in IVF 3. Permeability - ability of fluid to get through a membrane |
|
|
Controllers of fluid balance |
1. Thirst mechanism in the hypothalamus - osmoreceptors in high salt concentration 2. Antidiuretic hormone (ADH) 3. Low BP causes kidneys to secrete renin, which then stimulates adrenal gland to secrete aldosterone. |
|
|
What is ADH and what does it do? |
Antidiuretic hormone: stimulates the kidneys to reabsorb more "pure water" and causes vasoconstriction so more water stays in ISF |
|
|
What is aldosterone? |
hormone secreted by the adrenal gland that signals kidneys to increase reabsorption of Na+ (and thus more water too because water follows Na+) |
|
|
What is Edema and what does it cause? |
Definition: excessive amount of fluid in the ISC and ICC (can cause cells to swell and burst). Signs: swelling, enlargement of tissues, usually localized by can be all over (anasarca), visible/invisible, pitting/non-pitting |
|
|
Dependent Edema |
Dependent on gravity -feet fine int he morning but swollen by the evening |
|
|
Causes of Edema (4) |
1. Increased capillary hydrostatic pressure - aka HTN, swollen ankles one of first signs, fluid stays in ISC and is not picked up by venuals. 2. Loss of Albumin - less osmotic pressure - so H2O stays in cells. 3. Obstruction of the lymphatic system - "Lymph edema", increased hydrostatic pressure, damaged lymph node causes waste to collect in ISC 4. Increased capillary permeability - inflammation |
|
|
Effects of Edema |
-swelling -pitting -increased weight (check in congestive heart failure patients) -functional impairments (espeically joints) -Pain -Impaired arterial circulation - slows healing |
|
|
Definition of Dehydration and what populations are most susceptible and why? |
Def: insufficient body fluid due to excessive loss, inadequate intake or combination of both. -infants, obese and elderly more susceptible due to less fluid reserves and inability to conserve fluid quickly under stress. |
|
|
Causes of Dehydration (8) |
1. Vomitting - H20 and hydrochloric acid loss - body becoming more basic (alkalosis) 2. Diarrhea - cholera and dysentery 3.excessive sweating 4. Diabetic ketoacidosis (DKA) 5. Insensible loss - fever/heavy breathing 6. Polyuria 7. insufficient water intake 8. Third-spacing - nonfunctional collection of water where its not being used by vascular system (this occurs in burn patients) |
|
|
11 Signs and symptoms of Dehydration |
1. dry mucous membranes 2. skin turgor 3. low BP/tachycardia - 4. weak pulse 5. fatigue 6. increased HCT (hematocrit) - blood becomes concentrated 7. Metabolic acidosis 8. Polydipsia 9. Oliguria 10. Pale/blue skin 11. Confusion/LOC - water pulled into blood from cells thus decreasing their fucntion |
|
|
What is usually the first symptom of Dehydration? |
Low BP with Tachycardia (high HR) |
|
|
Metabolic acidosis |
Lack of glucose in circulation causes cells to anaerobically metabolize ATP producing lactic acid |
|
|
Polydipsia |
excessive thirst |
|
|
Oliguria |
lack of urine due to kidneys pulling water back into body due to excessive ADN and renin/aldosterone secreation |
|
|
What are the big three electrolytes? |
1. Na+: maintains extracellular fluid volume (osmotic pressure), Na-K pump action potential 2. K+: Na-K pump action potential, contraction of cardiac tissue, influenced by insulin and acid-base balance 3. Ca++: "calms" skeletal muscle, strengthens cardiac muscle contraction and strengthens bones |
|
|
What are the three smaller electrolytes? |
1. Mg+ : 2. PO4- : opposite of Ca++ 3. Cl-: |
|
|
Sodium (Na+) |
-135-145 meq/L -Cation in extracellular (90%) fluid that maintains vascular volume. High in blood, low inside cells (constantly pumped out via active transport). -Allows for osmosis between IVC and ISC -Regulated by the renin angiotensin aldosterone system -Sources: food, drinks, IV fluids -loss: perspiration, urine, poop |
|
|
Adrenal insufficiency |
-when there is not enough aldosterone in body and we loose too much Na+ |
|
|
Na+ Functions (3). |
1. Volume Control 2. nerve conduction 3. muscle contraction |
|
|
Hyponatremia (level, causes, effects, treatment) |
-<135 mEq/L Causes: sweating, V/D, Diuretics, hormone imbalance (Addison's disease, SIADH) Effects: impaired nerve function, to much Na+ in cells, decreased osmotic pressure in ECF resulting in hypovolemia and hypotension, Cerebral edema due to increased Na+ in cell, confusion, coma, seizure, death Treatment: Hypertonic IV fluid |
|
|
Hypernatremia (level, causes, effects, treatment) |
->145mEq/L Causes: insufficient ADH (kidneys secreting too much H20), loss of thirst mechanism, watery diarrhea, insensible loss (rapid respiration). Effects: increased osmotic pressure in IVC - fluid pulled/sucked out of cells, cell crenation, decreased brain cell function, impaired nerve function, confusion/LOC, weakness, agitation, polydipsia, rough mucous memranes, oliguira Treatment: Dilute Na+ IV in blood (hypotonic or isotonic) slowely |
|
|
Addison's disease |
lack of aldosterone |
|
|
SIADH |
true disease and paraneoplastic syndromes - inappropriate amounts of ADN in body thus diluting the bloodstream with too much water |
|
|
Potassium (K+) |
-intercellular cation (blood levels low b/c K+ in cell) -Sources: food (banana legumes, nuts), kidney resorption |
|
|
K+ functions (2) |
1.Nerve conduction/action potential via Na-K pump 2.Cardiac cycle |
|
|
Hypokalemia (Levels, causes, effects, treatment) |
-<3.5 mEg/L -Causes: diarrhea, K+ wasting loop diuretics, too much aldosterone and glucocorticoids, decreased diet intake, rapid DKA treatment -Effects: cardiac dysrythmias, flat T-wave, skeletal muscle weakness, shallow breaths, fatigue, paresthesias, decreased digestive motility (nausea) and kidney function (polyuria) Treatment: Give K+ PO or IV - slowly (max 10 mEq/Hr) |
|
|
parethesias |
feeling of pins and needles |
|
|
Hyperkalemia (Levels, causes, effects, treatment) |
->5 mEq/L -Causes: Renal failure (acute or chronic), severe acidosis, Aldactone, Addison's disease, massive trauma, DKA Effects: cardiac dysrhythmias, Peaked T-waves, muscle weakness -> paralysis/asystole, fatigue Treatment: lower K+ in blood and push back in cell by giving NaHCO3 |
|
|
Aldactone |
K+ sparing diuretic that is an aldosterone blocker |
|
|
NaHCO3 |
Insulin, Glucose, Bicarbonate mixture given for Hyperkalemia to push K+ from blood into cell |
|
|
Calcium (Ca++) |
-9-10.5 mg/dL -important extracellular cation -Source: food, bone, blood -Control: PTH, CAL -Influenced by: Vit D, phosphate (inversely related) -Functions: bone strength, metabolism, nerve tissue stability, calms skeletal fibers, strengthens cardiac tissue |
|
|
Parathyroid hormone (PTH) |
stimulates GI absorption and bone breakdown to raise blood Ca++ levels |
|
|
Calcitonin (CAL) |
stimulates bone building to lower blood Ca++ levels |
|
|
Hypocalcemia (level, causes, effects, treatment) |
-<9.0 mg/dL -Causes: hyperparathyroidism, malabsorption, low albumin, alkalosis, hyperphosphatemia Effects: increased skeletal nerve excitation, twitching, hyperactive refelxes, carpopedal spasms (Chvostek/Trousseau sign), tetany, decreased cardiac strength Treatment: Give Ca++ salts |
|
|
Chvostek and Trousseau signs and what are they used to test for? |
- Hypocalcemia diagnostic tool where the nurse to rub the cheek or arm to check for twitches |
|
|
What is Tetany and what can it be a sign of? |
sustained muscle contraction during hypocalcemia |
|
|
Hypercalcemia (levels, causes, effects, treament) |
-> 10.5 mg/dL Causes: too much Ca released from bone (possibly due to neoplasm), hyperthyroidism, immobility, increased intake of Ca, Milk-Alkali syndrome Effects: muscle weakness, decreased muscle tone, bone destruction, lethargy, stupor, personality change, anorexia, N, increased cardiac function Treatment: phosphate salts |
|
|
What is Milk Alkali syndrome and what other problem can it cause? |
Syndrome where kidney's can't excrete Ca thus causing hypercalcemia |
|
|
when there is increased cardiac function what can this do? (3 main things) |
1. arrhythmias 2. high BP 3. high pulse |
|
|
What are the 3 crystalloids |
1. Isotonic 2. Hypotonic 3. Hypertonic |
|
|
Isotonic fluid osmotic pressure and the 3 types of solutions |
-same osmotic pressure as our own ECF so no fluid shifts 1. Normal saline 2. lactated ringers 3. D5W (starts isotonic then becomes hypotonic) |
|
|
Hypotonic fluid osmotic pressure and the type of solution |
-lower osmotic pressure than our own ECF so pushes fluid into ICF -1/2 Normal saline (increases edema) |
|
|
Hypertonic fluid osmotic pressure and the type of solutions |
-higher osmotic pressure than our of ECF so pulls fluid toward IVC -All dextrose solutions (except D5W) - decreases edema but increases BP |
|
|
Colloids (2) |
-large molecules in hypertonic solution 1. Mannitol - large sugar for cerebral edema 2. Albumin - large protein, good for cellular edema |
|
|
What is our normal ph? |
7.35-7.45 |
|
|
When does cellular death occur due to ph? (2) |
<6.8 (acidosis) >7.8 (alkalosis) |
|
|
H+ in reguards to blood gas |
High H+ = low pH = Acidosis Low H+ = high pH = Alkalosis |
|
|
Bodies buffer systems (2) to dispose of CO2 |
- CO2 enters blood -> Blood binds to CO2 thus creating a Carbonic Acid (H2CO3) -> body can dispose of carbonic acid in 2 ways: 1. Respiration - lungs blow off CO2 and H2O (insensible loss) 2. Metabolic - Kidneys reabsorb HCO3- and excrete H+ |
|
|
Respiration buffer unable to function well in those with which 3 conditions and why is this a problem? |
COPD, respiratory failure, lung disease -Acidosis: increased respiratory rate - blows off CO2 -> increasing pH (GOOD!) Alkalosis - decreased resp rate - retains CO2 -> decreasing pH (BAD) |
|
|
Metabolic buffer unable to function well in those with which conditions and why is this a problem? |
acute/chronic renal disease patients -Acidosis: kidneys excrete H+ and return bicarb to blood (GOOD!) -Alkalosis: decreased H+ cleaving, retain more H+ (BAD) |
|
|
Decompensation |
when body is unable to return pH to normal range |
|
|
Respiratory Acidosis (levels, causes, effects, compensation) |
-pH less than 7.35 Causes: Pneumonia, airway obstruction, opioids, COPD, emphysema, chronic bronchitis Effects: HA, lethargy, drowsiness, confusion, CNS depression, coma/death Compensation: acidic urine |
|
|
Metaboilc Acidosis (levels, causes, effects, compensation) |
-pH less than 7.35 Causes: loss of bicarb ions in diarrhea, dehydration, internal bleeding, DKA, Renal disease Effects: HA, lethargy, drowsiness, confusion, CNS depression, coma/death Compensation: increased RR |
|
|
Respiratory Alkalosis (levels, causes, effects, compensation) |
-pH > 7.45 Causes: hyperventilation caused by anxiety, fever, ASA OD, brainstem disease, brain injury Effects: CNS irritability, restlessness, twitching, tingling, numbness of fingers, tetany, seizure coma Compensation: bicarb exretion |
|
|
Metabolic Alkalosis (levels, causes, effects, compensation) |
-pH > 7.45 Causes: early vomiting, NG suction, iatrogenically (overcorrection of acidosis) Effects: CNS irritablity, restlessness, muscle twitching, numbness, tetany, seizure, coma Compensation: decreased RR |
|
|
What is pCO2 and what should its normal range be, and when in acidosis and alkolosis? |
-Acid controlled by respiratory -35-45 -above 45 = acidosis -below 35 = alkalosis |
|
|
What is HCO3 and what should its normal range be and when is acidosis and alkolosis? |
-Base controlled by metabolic -22-26 -above 26 = alkalosis -below 22 = acidosis |
|
|
Uncompensated pH |
-pH is abnormal but pCO2 and HCO3 are normal |
|
|
Completely compensated |
-pH is normal but pCO2 and HCO3 are abnormal |
|
|
Partially compensated |
-pH is abnormal but pCO2 and HCO3 are abnormal |
|
|
Most common thing to cause hormonal abnormalities? |
benign tumors aka an adenoma |
|
|
Relative deficit |
when a endocrine disorder is due to target cell receptors either becoming resistant or insensitive to hormone |
|
|
Where is insulin secreted from? |
Beta cell of islets of Langerhans in pancreas |
|
|
Roles of insulin (5) |
1. Anabolic hormone - builds complex substances from simple molecules 2. transports glucose out of blood and into cells 3. synthesizes glycogen for energy storage 4. inhibits glucagon 5. needed for proper skeletal muscle contraction -Brain and GI tract do not require insulin |
|
|
What does glucagon do? |
catabolic hormone that breaks down glycogen in fat and muscles to increase blood glucose - usually in response to stress |
|
|
Type I Diabetes Mellitus |
Action: autoimmune reaction that completely stops insulin production in pancreas Onset: Acute, patients usually in a state of DKA at diagnosis Patient: younger, thin frame Treatment: insulin replacement |
|
|
Type II Diabetes Mellitus |
Action: insulin resistance Onset: insidious taking years Patient: middle age usually, high BMI, high glucose diet. higher rate in black, latino, American Indian populations. Treatment: diet, exercise, oral drugs, insulin replacement |
|
|
Gestational Diabetes |
-form of Type II during pregnancy -pregnancy protects against hypoglycemia -precursor for Type II later in life |
|
|
8 Signs and Symptoms of Diabetes |
1. decreased transport of glucose into cell 2. hyperglycemia 3. Glucosuria 4. Polydipsia 5. Polyphagia 6. weight gain 7. nocturia 8. elevated HgB A1C (should be below 11) |
|
|
Glucouria |
sweet pee due to Kidneys being unable to fliter all glucose out of filtrate, this leads to polyuria, which then leads to dehydration, eventually leading to anaerobic metabolism creating acidosis |
|
|
Polyphagia |
excessive hunger from lack of nutrients in cells |
|
|
4 Long term Diabetes complications |
1. Microangiopathy 2. Macroangiopathy 3. Neuropathy 4. Cataracts |
|
|
What is Mircoangiopathy and what can it lead to? |
Diabetes complication causing thickened capillary basement membrane resulting in tissue necrosis Leads to: diabetic nephropahty, retinopathy, peripheral neuropathy
|
|
|
What is macroangiopathy and what can it lead to? |
Diabetes complication causing thickening of large artery basement membrane resulting in tissue necrosis Leads to: CAD, CAV, MI, ulcers |
|
|
What is neuropathy and what does it lead to? |
ischemia causing degeneration of nerve fibers leads to: numbness, tingling, muscle weakness/wasting, autonomic damage, impotence |
|
|
What are cataracts and what is it from? |
Clouding of eye due to the abnormal metabolism of glucose causing the accumulation or sorbitol and water in lens |
|
|
Diabetic KetoAcidosis (who, from, problem) |
Who: usually type 1 Results from: prolonged insulin deficit initiated by stress, infection or overindulgence in carbs Whats the problem: lack of glucose in cells leads to catabolism of fats and proteins for energy resulting in lots of nasty byproducts |
|
|
Byproducts of DKA |
-Fatty Acids and ketones - both of these lead to decreased pH leading to KetoAcidosis *glucouria -> decreased bicarb reabsorption -> metabolic acidosis -> lactic acid *Electrolyte imbalance = HyperKalemia |
|
|
Signs and symptoms of DKA |
-N/V, abdominal pain, lethargy, weakness -dehydration, polydipsia, dry mouth, warm/dry skin, low pulse/BP, eventually oliguira -metabolic acidosis |
|
|
Compensation signs of DKA |
Respiratory compensation b/c kidneys don't have no water at this point: 1. Kassmaul respirations - deep/rapid breathing to get rid of CO2 2. Fruity breath - from ketones 3. decreased responsiveness 4. decreased LOC 5. respiratory depression 6. HyperKalemia |
|
|
Treatment for DKA |
Hydration, insulin drip, dicarb, K+ monitoring/replacement |
|
|
HyperOsmolar Hyperglycemic (other name, who, from, problem) |
name: NonKetotic Coma who: elderly type II from: infection, overindulgence in carbs Problem: prolonged TPN resulting in dehydration but different from DKA in that there is no catabolism (so no FFA/ketones) therefore there is no major metabolic acidosis, blood gas should look fine |
|
|
Signs and symptoms of HyperOsmolar Hyperglycemia and treatment |
1. dehydration 2. hypernatremia 3. neurological deficits 4. abnormal reflexes 5. muscle weakness 6. difficulty speaking 7. coma/death Treatment: insulin and fluids |
|
|
Hypoglycemia (other name, s&s, nurse imp) |
Name: insulin shock Neurological s&s: confusion, slurred speech, unsteady gait, sz Sympathetic: tachycardia, diaphoresis, anxiety, tremors Nurse imp: beta blockers may block this alarm system |
|
|
Hypoparathyroidism (causes, s&s) |
Causes: congenital deficiency, surgery/radiation in neck, autoimmune disease S&S: hypocalcemia |
|
|
Hyperparathyroidism (causes, s&s, treatment) |
Causes: adenoma, hyperplasia of organ, secondary to renal failure S&S: hypercalcemia treatment: calcitonin |
|
|
ADH (what is it and what are its actions) |
-secreated by posterior pituitary during hypoveolemia or hypotension -also known as Vasopressin Actions: stimulates water reabsorption in kidneys, increases BP |
|
|
Diabetes insipidus (what, causes, s&s, treatment) |
What: low ADH Causes: head injury, brain surgery, kidneys unrepsonsive to ADH S&S: polyuria, polydipsia, dehydration, hypotension from hypovolemia, hypernatremia treatment: desmopressin |
|
|
What is "low specific gravity" urine? |
diluted urine resulting from polyuria |
|
|
SIADH (what, causes, s&s, treatment) |
what: high ADH causes: stress, water intox, brochogenic carcinoma s&s: oliguria, hyponatremia, cerebral edema treatment: diuretics and sodium tablets |
|
|
What is "high specific gravity" urine? |
concentrated urine |
|
|
Where is thyroid hormone secreted from? |
The thyroid gland which is stimulated by the pituitary release of TSH |
|
|
What are the 2 functions of TSH? |
1. stimulates the thyroid gland to release thyroid hormones 2. stimulates the thyroid gland to grow and produce more T3/T4 hormones |
|
|
Names and functions of thyroid gland hormones? |
T3: Trilodothryronine T4: Thyroxine Functions: increase metabolic rate, increase heat production, increase HR |
|
|
Thyroid goiters (what, cause, s&s, complications) |
What: increase TSH secretion due to inability to produce thyroid hormones Cause: used to be caused by iodine deficiency, now due to goitrogens S&S: hyperplasia of thyroid gland Complications: compression of trachea/esophagus |
|
|
Giotrogens |
Cabbage, turnips, lithium, fluoride |
|
|
Toxic Goiter |
from hyperactivity of thyroid gland causing them to be in a hyperthyroid crisis causing thyroid storm |
|
|
The 2 types of Thyroid disease |
Hypothyroidism and Hyperthyroidism |
|
|
Hypothyroidism (other name, labs, causes, s&s, treatment) |
name: Myxedema labs: high TSH and low t3/t4 causes: hashimoto's thyroiditis (autoimmune) and cretinism (congenital) s&s: cold intolerance, periorbital edema (eye swelling) treatment: thyroid hormone - thyroixine |
|
|
Hyperthyroidism (other name, labs, causes, s&s, treatment) |
name: grave's disease Labs: low TSH, high T3/T4 Causes: autoimmune factor, thyroid tumor, common in women under 30 s&s: heat intolerance, increases SNS, expothalmos (eye protrusion), thyroid storm/crisis Treatment: radioactive iodine, surgery, SSKI |
|
|
Where is the adrenal gland and what are its two parts and the types of hormones produced |
Where: on top of kidneys parts: Medulla - catecholamines cortex - corticoids, androgens |
|
|
Adrenal Medula (what hormones do they secrete and what do they do) |
-Catecholamines = stress hormones aka they increase O2 levels, circulation and metabolism -Epinephrine: vasconstriction, tachycardia, increased cortisol - increased blood glucose -Norepinephrine: vasoconstriction with not as much heart affct |
|
|
Adrengergic medications |
increase the secretion of catecholamines |
|
|
Adrenal cortex (what hormones secreted and what do they do?) |
-corticoids and androgens (sex hormones) -Derived by cholesterol and activated by ACTH -Mineralicoricoid is Aldosterone - effects electrolyte retention regulated by angiotensin II and K+ -Glucocortidoid is cortisol - activated by catecholamines to elevate blood glucose/BP
|
|
|
Pheochromoytoma |
benign tumor of adrenal medulla increasing catecholamine secretion treatment: surgery |
|
|
HyperCortisolim (other name, what, causes, s&s) |
Name: Cushing's syndrom What: excessive amounts of gluccocortiboids from cortisol Causes: tumors, steroids s&s: muscle wasting, hirsutism, retention of Na+ and water, immune supression, increased erythrocyte, emotional lability, moon face, gynecomastia |
|
|
What is cushings "like" syndrome from and who might get it? |
-taking too much hydrocortisone or prednisone -seen with chronic COPD patients |
|
|
Adrenocortical insufficiency |
Name: addison's disease what: complete deficiency of adrenocortical hormones cause: autoimmune, tumor s&s: low cortisol, infections, fatigue, wight loss, low serum Na+/high K+, decreased body hair, hyperpigentation, anemia, Addisonian crisis: lethargy, delirium, fever Treatment: hormone replacement, hydrocortisone
|
|
|
Hans Salye's general adaptation syndrome |
systematic response to a stressor that plays a huge role in disease development and exacerbation |
|
|
Distress |
when body is unable to restore homestasis and stessor becomes harmful |
|
|
3 stages of GAS |
1. Alarm - activation of hypothalamus, SNS, adrenal glands 2. Resistant - elevated hormone levels, organs at peak performance 3. exhaustion - body is unable to return to homeostasis or continued peak response |
|
|
Adrenergics hormones |
hormones of action for the SNS aka bodies "fight or flight" response |
|
|
Cholinergic/muscarinic hormones and 3 functions |
hormones of the Parasympathetic nervous system aka our bodies "flex and digest" response 1. increase acetylcholine at neuromuscular junction to increase muscle contraction/tone and GI motility 2. increase salivation secretions 3. bradycardia through intervention of vagus nerve |
|
|
Somatic pain |
sharp pain conducted through nerve fibers |
|
|
Visceral pain |
dull pain originating from organs and travels through sympathetic fibers |
|
|
Dermatome |
specific area of skin from which spinal nerves conduct signals |
|
|
Reflex response |
protective involuntary muscle contraction that involves no CNS involvement - action initiated by dorsal root ganglion before brain is made aware aka Reflex Arc |
|
|
Spinothalmic tracts and what are the 2 types |
-Conduct pain to the brain Paleospinothalmic: slow, dull, chronic pain Neospinothalmic: fast, sharp, acute pain |
|
|
The Reticular activating system (RAS) |
arousal state in pons and medulla influences brains pain awareness. Many drugs target this system thus dulling pain |
|
|
Somatosensory cortex |
helps identify location of pain |
|
|
Thalmus |
sensory relay center stimulates the: Limbic system: emotional response to pain Hypothalamus: stress response to pain |
|
|
The Pain process: |
1. stimulus 2. spinothalmic tracts 3. RAS 4. thalmus 5. somatosensory cortex (locate pain) 6. Limbic system and Hypothalamus |
|
|
Gate control theory |
Pain blocking using stimulus overload creating spinothalmic "traffic jam" |
|
|
Pathway blockage |
meds blocking a pain pathway or its transmitter |
