• criticical in maintainig homeostasis
• solvent of metabolic reactions
• transport nutrients and wasts from cells
• transport enzymes in the digestive system
• transport blood 
• facilitates joint movement

• High water content
• More susceptible to effects of dehydration
• vomiting and diarrhea
• 70% Body Water Composition

Everything outside of the cell!

This includes IVF, ISF, CSF, and Transcellular Fluid

1. Major cellular membrane: between ISF and ICF (Active Transport). ATP Used

2. IVF (blood) and ISF/Cells: free flow of nutrients/wastes (Gradient) Example: Osmosis

1) Hydrostatic Pressure

2) Osmotic Pressure

3) Permeability

Hydrostatic Pressure

"Push" pressure to take fluid out from...

ex: Arterial blood pressure (pushes blood out of vascular and into interstitial fluid)

Pulling or Sucking pressure to bring fluid toward 

Ex: Chemicla mediators of inflammation, Blood Proteins (Albuming) keep fluid in Vascular compartment.

Thirst mechanism in the hypothalamus: osmoreceptors in high salt concentration: Ex: ADH - Antidiuretic hormone stimulate reabsorption of "Pure Water"

- Low BP: kidneys secrete renin to stimulare adrenal gland secretion. * Aldosterone signals kidney increase in reabsorption  of Na+ and H2O

Excessive amount of fluid in interstitial compartment

• swelling or enlargement of tissue
• localized and generalized as anasarca
• highly visible and relatively invisible
• pitting or non-pitting

Cause of Edema:

Increased capillary hydrostatic pressure (HTN) - Increased hydrostatic pressure

Loss of Albumin (low osmotic pressure)

Obstruction of the lymph system (Increased hydrostatic pressure) "backup"

Increased capillary permeability (Inflammation)

Effects of Edema:

• swelling
• pitting
• increased body weight from retention (Rationlae for daily weight check in CHF and Renal Dz)
• Functional impairment, joints
• Pain
• Impaired arterial circulation (delayed healing)

Insufficiency from either excessive loss, inadequate intake, or both

*More serious in infants and elderly

decrease in fluid reserves

decrease in ability to conserve fluid quickly under stress

Electrolytes significantly effect fluid balance, especially Sodium Na+

1. Vomiting and Diarrhea
2. Excessive Sweating
3. Diabetic Ketoacidosis (insensible loss, polyuria)
4. Insufficient water intake
5. Insensible loss: respiration, metabolism (fever)
6. Third Spacing: "nonfunctional" collection of fluid

• Dry Mucous Membranes
• Decreased skin turgor
• Low BP
• weak, thready pulse
• fatigue
• Increase Hct (blook becomes concentrated)
• Metabolic acidosis (lack of glucose circulation)
• Polydipsia-excessive thirst, Oliguria - small amounts of urine (ADH, renin/Aldosterone secretion)
• Tachycardia constricting cutaneous blood vessels (pale, cool skin)
• Water pulled to blood, so cells lose water, decreasing function (mental confusion, LOC)

1. Sodium
2. Potassium
3. Calcium

• (135-145 mEq/L)
• Major Cation on in the ECF (high in intravascular/low in intracellular)
• Allows for diffusion of fluid between vascular and interstitial compartments (osmosis) 
• Controlled by the Na-K pump (active transport)
• 90% of solutes in ECF
• Maintains nerve conduction

Causes of

Hyponatremia (<135 mEq/L)

• Sweating/Vomiting/Diarrhea
• Many diuretics
• Hormonal Imbalances
• Low Aldosterone
• Addison's Dz
• SIADH: True disease and paraneoplastic syndrome

• Impaired nerve function
• fluid imbalance
• Decreased osmotic pressure in ECF
• Hypovelemia-decrease in blood volume, Hypotension
• Brain cells may swell (more Na in cells)
• Cerebral Edema - confusion, coma, sz, or death
• Treatment: give Na+ Usually hypertonic fluid

• Insufficient ADH (excessive loss of "pure" water)
• Loss of thirst mechanism (hypth & pituitary
• Watery diarrhea (more water loss than salt)
• Insensible loss: prolonged period of rapid respiration (thyroid storm)

• Increased Osmotic pressure of IVC
• Fluid pulle/sucked out of cells
• Cell crenation - cells "dry up" - water follows blood
• Decreased cell function, including decreased LOC
• Weakness/agitation
• Increased thirst, dry, rough mucous membranes
• Decreased urine output (ADH secreted)
• Increased urine output * ONLY if diabetes insipidus - No ADH
• TREATMENT:Dilute blood NA+ Hypotonic or Isotonic IV fluids

• Major Intracellular Cation: Serum levels are LOW
• Major control is over the RENAL system
• Controlled by the Na-K pump (active transport)
• Affected by acid-base balance

Acidosis shifts K+ out of cells = increased blood K+ 

Regulated by Insulin

*No Insulin function = Altered K+ Transport (Elevated blood K+)

Food- bananas, legumes, nuts

kidney reabsorption

Vomiting/Diarrhea

Kidney excretion through diuretics

• Important in nerve conduction/action potential (Na-K pump)
• Critical in cardiac cycle
• Abnormal levels: High or Low, adversely affect the cardiac cycle

• Severe diarrhea
• K+ wasting diuretics (loops)
• Excessive Aldosterone (spares Na+ and wasts K+
• Excessive glucocorticoids
• Decreased dietary intake
• Rapid treatment of DKA (insulin infusion, acid correction)

• LETHAL: Cardiac dysrythmias
• EKG changes: Flattened T-wave
• Skeletal muscle weakness 
• Shallow resp
• Fatigue
• Parathesis - "pins and needles"
• Decreased digestive tract motility = nausea
• Decreased kidney function
• Decreased Urine concentration - polyuria
• Treatment: give K+ (po or IV) IV=SLOWLY!! (max 10 mEq/hr)

• Renal failure (Acute or Chronic)
• Severe Acidosis - displaced froms cells by H+
• K+ - sparing diuretics (Aldosterone blockers, Decreased Na+
• Aldosterone deficit (Addison's Disease) Low Na+= High K
• Massive Trauma: leakage of intracellular K+ into IVC
• DKA: Acidosis shifts K+ into blood and Decrease insulin function

• LETHAL: Cardiac Dysrythmias
• EKG changes: Peaked T-waves
• Muscle weakness (leads to paralysis/Asystole)
• Fatigue
• Nauasea
• Parasthesias - "pins and needles"
• Treatment: Lower K+
• Insulin, Glucose, Sodium Bicarb * Insulin and Base = push K+ back into the cell and out of blood

Calcium: Ca++ (9-10.5 mg/dL)

• Food
• Bone (stored in bone and blood)
• Excreted in Urine and Feces

• Parathyroid Hormone (PTH): stimulates GI absorption & Bone Breakdown (High Ca++)
• Calcitonin (CAL):stimulates Bone building (Ca++ storage) and lowers blood Ca++

• Vitamin D (cofactor in Ca++ absorption and usage)
• Phosphate: Inversely related to Ca++ (Values go in opposite directions)
• Alkalosis: limits Ca++ ioization (active form); includes hypocalcemia

• Bone Strength
• Metabolic Processes (coenzyme)
• Nerve Tissue stability: Calcium - Ca-lms skeletal muscle fibers
• Cardiac tissue strength: Ca-lcium strengthens Ca-rdiac contractions
• *Ca calms contractions of skeletal muscles, but strengthens contractions of cardiac tissue

• Hypoparathyroidism
• Malabsorption or diet deficiency
• Serum Albumin Deficiency (bound to protein)
• Alkalosis (increased pH): cannot ionize/activate
• Hyperphosphatemia - abnormally high levels of phosphate, lowers Ca++ levels in blood

• Increased skeletal nerve excitation
• Muscle twitching, hyperactive reflexes
• Capopedal spasms, Chvostek's, Trousseau's
• Tetany; sustained muscle contraction
• Decreased Cardiac strength - conduction delays, arrythmias, Low BP
• TREATMENT: give calcium salts

Realse of Ca++ from bones (neoplasms)

Hyperparathyroidism (excess bone demineralization)

Immobility: leads to bone demineralization

Increased intake of Ca++

Milk-Alkali Syndrome (Ca++/Base)

• Depression of skeletal contraction
• Muscle weakness, Decreased muscle tone
• Letargy, Stupor, personality changes
• Anorexia, nausea
• Increased cardiac functions - Arrythmias possibe
• If Excess PTH cause: bone destructions and Fx's
• TREATMENT: phosphate salts

0.9% NS -- 308 mOsm/L

Ringer's Lactate -- 275 mOsm/L

About 300 = Isotonic

** Dextrose 5% water D5W starts Isotonic; then becomes hypotonic

3% Sodium Chloride (3% NS) -- 1026 mOsm/L

5% Sodium Chloride (5% NS) --1710 mOsm/L

10% Dextrose in Water (D10W) -- 505 mOsm/L

D5NS (406) D5 1/2 NS (406), D5NS (560) D5LR (525)

**All Dextrose solutions (except D5W) are hypertonic. D5W is isotonic, then hypotonic

Contain large molecules which are hypertonic - shifts fluid out of ICF into ECF/IVF 

Ex: Mannitol (large sugar) Albumin (large protein) *Good for cellular edema

Cellular enzymes/metabolism can only function in a narrow pH 

* Optimal pH for cellular meatbolism is 7.35-7.45

Cellular death at <6.8 (acidosis) or >7.8 (alkalosis)

Logarithmic calculation of amt of acid (H+ = Acid)

Logarithmic= inversely related 

So, High H+ = LOW pH (Acidosis) Acidic

Low H+ = High pH (Alkalosis) Basic

All cellular metabolism creates Acidotic by-products

One major by-product of cellular respiration is Carbon Dioxide (CO2), which is Acidic

Acidosis: Increased Respiratory Rate (Blows off CO2, decreasing blood pH)

*FASTEST compensation process w/ significant changes in Minutes!!

HC203 to H2O + CO2

Unable to function in: COPD, Resp Failure, Lung Dz

• Acidosis: Kidneys cleave and excrete H+ 
• Return Bicarb base (HCO3-) to blood
• Alkalosis: Decrease H+ cleaving; retain more H+
• ** SLOW compensation process hours to days for response but most potent/effective (still slow)
• H2CO3 to HCO3- + H+
• Unable to function in: Renal Dz (acute or chronic)

Recall Homeostasis, body makes changes...

Body then compensates or reacts to keep pH within normal range (7.35 -7.45).

So, if Respiratory flawed (COPD, pneumonia) Increasing CO2, kidneys MUST compensate

Acidosis (pH less than 7.35)

Respiratory

• Pneumonia
• Airway obstruction (aspiration or asthma)
• Medications depressing respiratory center
• Chronic Respiratory acidosis (COPD - CO2)

Acidosis (pH less than 7.35)

Metabolic

• Loss of Bicarb ions
• Diarrhea (HCO3 stored in gut)
• Dehydration (anaerobic respiration)
• Internal Bleeding
• Diabetic Ketoacidosis
• Renal Dz

• Headache
• Lethargy
• Drowsiness
• Confusion
• CNS depression
• Coma/Death
• Compensation: Increased RR, acidic urine

Alkalosis (pH greater than 7.35)

Respiratory

• Hyperventilation
• Anxiety
• Fever
• ASA OD
• Brainstem Dz
• Brain Injury

• Early vomiting (removes H + Cl before dehydration)
• NG suction
• Iatrogenic (overcorrection of Acidosis)

• CNS Irritability
• Restlessness
• Muscle Twitching
• Tingling
• Numbness of fingers
• Tetany
• Sz
• Coma
• Compensation: Decreased RR, Bicarb excretion through kidneys

Normal range: 7.35 to 7.45

Low = Acidosis

High = Alkalosis

Normal Range: 35-45

Low = Alkalosis

High = Acidosis

normal range: 22-26

low: acidosis

high: alkalosis

Healthy Endocrine system: hormones 

*Opposition system: Opposite Hormones

Hypothalamus stimulates Pituitary Hormone Release.

Specific hormones stimulate specific organs into certain processes

Response from organs offers negative feedback to satisfy hypothalamus

Manifestations are dependent on which specific hormone is in excess or deficit

Most common cause of endocrine pathophysiology is BENIGN TUMORS adenomas

Resistance/Insensitivity of target cell receptors can create "relative deficit"

• Glucose Tolerance Test: Glucose tests to assess organ response
• 24-hr Urine: assess catecholamine amount (epinephrine and norephinephrine)
• CT/MRI
• Biopsy of Endocrine Organ

If organ doing it's job- hormone is normal in blood

If NOT hormone release is high

perform blood test!!!

Deficits: treat with missing hormone

excess: treat by removing tumor and can be treated with radiation or "shock" meds

ex:SSKI - shrinks thyroid gland and reduces hormones being produced

 A deficit of insulin secretion from beta-cells if islets of Langerhans in the Pancreas

*The lack of response by the cells to the insulin = insulin resistance

• Anabolic Hormone - builds complex substances from simple molecules)
• Transports glucose - out of blood and into cells for metabolism
• Synthesizes glycogen - for energy storage when glucose abundant
• Inhibits glucagon: catabolic hormone breaks down glycogen and increases blood glucose

Skeletal Muscles

*Without cells metabolize fats and proteins and creates fatty acids

• Usually, complete cessation of insulin production
• Acute onset: Ketoacidosis frequent complication of diagnosis (or infection)
• Usualy thin frame, younger onset (often auto-immune reaction)

• Develops as a result of insulin resistance from tissues
• Insidious onset: takes years to develop. Ketoacidosis NOT likely
• Usually high BMI, middle-aged, high-glucose diet

Diabetes Type 1: 

Age of Onset: Children/young adults

Onset: Acute

Etiology: Autoimmune destruction/Family History

Body Weight: Thin

Plasma Insulin level: Low

Treatment: Insulin replacement

Occurrence of hypoglycemia or ketoacidosis: Frequent

• Older Adults
• Onset: Gradual
• Etiology: Familial, lifestyle, environmental factors (diet)
• Body Weight: Obese
• Plasma Insulin level: decreased or normal
• Tx: diet, exercise, oral hypoglycemia agents or insulin replacements
• Ketoacidosis: less common

9% of the population of adults 20 + 

* Higher incidence in Afro Am., Latinos, and Native Am.

Form of Type 2

Pregnancy hormone protect against hypoglycemia

Often precursor for Type 2 DM later in life.

Form of Type 2

Pregnancy hormone protect against hypoglycemia

Often precursor for Type 2 DM later in life.

• Decreased transportation and cell usage of glucose
• Blood glucose levels begin to rise (hyperglycemia)
• Kidneys are unable to filter all glucose out of filtrate = glucosuria
• glucosuria leads to polyuria
• Dehydration leads to anearobic metabolism
• Dehydration leads to thirst (polydipsia)
• Lack of nutrients in the cells stimulates appetite (polyphagia)

• Weight gain
• Abdominal Girth
• Nocturia
• Weight Loss
• Lethargy
• Polydipsia
• Fatigue
• Elevated A1C
• Dry Mouth

1. Polyuria
2. Polydipsia
3. Polyphagia

Microangiopathy: thickened capillary basement membrane; tissue necrosis - diabetic nephropathy(CKD), retinopathy, peripheral neruopathy

Macroangiopathy: Large Arteries affected

- CAD, CVA, MI, Ulcers (infection and gangrene of wounds)

Neuropathy: Ischemia/ altered metabolism, degeneration of nerve fibers - numbness, tingling, impaired sensation, muscle weakness/wasting and Autonomic damage (bladder, impotence)

Cataracts: clouding of eye lens - abnormal metabolism of glucose; accumulation of sorbitol and water in lens 

Lack of glucose in the cells results in catabolism of fats/proteins for energy

Byproduct of catabolism: fatty acids (FFA) and ketones

• Nausea, vomiting, abdominal pain, lethargy, weakness
• Dehydration (from polyuria) Results in anaerobic metabolism (more acids)
• Thirst, dry mucous membranes, warm dry skin, rapid weak pulse, low BP, oliguria

results in decreased renal GFR (decreased bicarb)

Also, decreased ability to clear acid (H+) from blood and worsens 

metabolic acidosis = kussmaul respirations

• Na/K pump insulin-dependent (K+ unable to be moved into cell)
• Metabolic Acidosis: H+ in cell "pushes K+ out" into bloodstream and results in hyperkalemia
• *As acidosis/insulin def. is corrected, K+ will move back in and lower K+

Related to Dehydration:

Neurologic deficits

abnormal reflexes

muscle weakness

diffiulty speaking

*If not corrected, coma and death may result (Hypernatremia = neuro)

Related to Dehydration:

Neurologic deficits

abnormal reflexes

muscle weakness

diffiulty speaking

*If not corrected, coma and death may result (Hypernatremia = neuro)

• Low Simple CHO's (low glycemic index) Minimize insulin surge
• low cholesterol/Lipids
• manage weight (Higher BMI/abd girth increases DM risk

• Increase insulin uptake of muscles/cells
• Increase insulin receptor sensitivity (opposite of resistance)
• Assists with weight management
• Reduce stress (glucocorticoids increase glucose levels)

1) Stimulate Beta Cells of pancreas to secrete more insulin

• Glyburide, repaglinide

2) Reduce insulin resistance at cellular insulin recptor site

Metformin (Glucophage)

3) Increase receptor sensitivity to insulin at cellular level

• Avandia

Neurologic: confusion, slurred speech, unsteady gait, SZ

Sympathetic: Tachycardia, Diaphoresis, Anxiety, Tremors

*Beta-blockers may block this alarm*

Bone demineralization

Elevate blood Ca++

Calcium regulation

Tells GI tract to make Vit E to move Ca++ back into blood stream

• Congenital deficiency
• Surgery/Radiation to neck
• Autoimmune Dz

• HYPOCALCEMIA, leading to...
• Skeletal Muscle: Increased excitatin of nerves
• Twitching/spasms (tetany)
• Chvostek (cheek twitch)
• Trousseau (forearm flap)
• Cardiac Muscle
• Weakened cardiac contractions
• Hypotension
• Arrythmias

Adenoma

Hyperplasia of Organ

Secondary renal failure

HYPERcalcemia which leads to...

Skeletal Muscle:

Flaccid muscle tone, weakness

Cardiac Muscle:

Forceful cardiac contractions

Bones:

Osteoporosis/Pathological Fx's

Renal:

Urolithasis (Ca++stones), polyuria

Treatment: Calcitonin (Moves Ca++ into bone)

Secreted by Posterior Pituitary during hypovolemia or hypotension

*Also known as Vasopressin

*Kidneys: stimulates water reabsorption (concentrates urine)

*Cardiovascular: Increases peripheral vascular resistance (increase BP)

Head Injury or Surgery

Nephrogenic: kidneys don't respond to ADH

Polyuria: low SG in urine (dilute)

Polydipsia: thirst

Dehydration

Hypostension from hypovolemia

Hypernatremia: Confusion, change in LOC

Treatment: Desmopressin (Form of ADH)

Stress/overconsumption of water

Paraneoplastic: Bronchogenic Carcinoma

Oliguria: high SG in urine (Concentrated)

Hyponatremia: Fluid shifts INTO cells

Cerebral Edema: Mental confusion, irritability, sz, coma, death

Treatment: Diuretics & Sodium tablets

Secreted by thyroid gland

stimulated by pituitary release of TSH

1) Stimulates thyroid hormone to release thryroid hormones *Monitored to evaluate Thyroid function

2) Stimulates thyroid to grow (hypertrophy) and produce more T3/T4 *Goiter

1) T-3 - Triiodothyronine

2) T4 - Thyroixine - bound to protein and inactive

Increased Metabolic Rate

Increased Heat production

Increased HR

Increased Metabolic Rate

Increased Heat production

Increased HR

Goitrogens: cabbage, turnips, Lithium, Floride

(Block T3/T4 production and increase TSH release)

Thyroid gland growth: Goiter

Results from hyperactivity of thyroid gland

Hyperthyroid Crisis/Thyroid Storm can result

Myxedema

Hashimoto's Thyroiditis: Autoimmune

Cretinism:congenital hypothyroid

• Cold intolerance
• Weight gain
• Tingling/numbness of extremeties
• Lethargy/Fatigue
• Depression
• PeriOrbital Edema (eye swelling)
• Myxedema: puffy face and thick tongue
• Myxedema Coma: hypotension, coma
• Treatment: Thyroid Hormone, usually Thyroxine

HYPERthyroidism: Grave's Disease 

Labs: low TSH & High T3 & T4

Causes of hyperthyroidism?

Autoimmune factor

thyroid tumor

more common in women under 30 

HYPERthyroidism: Grave's Disease 

Labs: low TSH & High T3 & T4

Causes of hyperthyroidism?

Autoimmune factor

thyroid tumor

more common in women under 30 

heat intolerance

increased SNS stimulation: 

ex. palpitations, nervousness

Exopthalmos:

eye protrusion

Thyroid storm/Crisis:

Hyperthermia, Tachycardia, CHF, Delierium

Treatment: Radioactive Iodine, surgery, SSKI

Ad - Above, -renal - kidey: glands on top of kidneys

 2 parts: Adrenal Medulla 

Adrenal Cortex 

HA

Tachy

Heart Palp

Diaphoresis

Anxiety Attack

Treatment: usually surgery to remove tumor

Cholesterol

Activated by ACTH (adrenocorticotropin Hormone)

Aldosterone (Regulated by Angiotensin II and K+)

Primary function: Sodium retention, Water retention

Cortisol: activated by stress response, catecholamines

Primary Function: Elevation of blood glucose, blood pressure

Adrenal adenoma

Pituitary adenoma

Ectopic Adenoma

Iatrogenic (steroid admin)

Catabolic Effect: Muscle wasting

Metabolic Changes: Hirsutism (body hair)

Retention of Sodium and Water

(mineralicorticoid activity)

Immune suppression (increased infection and decrease healing)

Erythrocyte production (stress response)

Emotional Iability

Moon Faces: Round, swollen faces

Autoimmune Reactions (Type III Hypersensitivity)

Tumors

Decreased/labile glucose levels (low cortisol)

Poor stress response (frequent infections)

Fatigue & Weight loss

Low Serum Na+ (BP lability)

Hyperkalemia (No Aldosterone)

Decreased body hair: decreased androgen activity

Hyperpigmentation: (ACTH hypersecretion -- MSH)

Cardiac arrhythmias and failure

Anemia (decreased erhythrocyte production)

Treatment: hormone replacement (Hydrocortisone)

Addisonian Crisis: lethargy, dilirium, fever

• K+ 
• Ca++
• Fever
• Muscle Pain

• Blood Sugar
• Na+
• Blood Pressure
• Immunity

Systemic response to a stressor (change in homeostasis) 

** Plays enormous role in disease development and exacerbation

Physical, Psychological, or both

Real or anticipated

Short-term or long-term

If the body is unable to restore homeostasis

1) the stressor becomes harmful

2) Age, illness, and attitude affect stress response

1) alarm: activation of hypothalamus, SNS, Adrenal glands (Epi, Norepi, Cortisol)

2) Resistant: Hormone levels elevated (Adrenals), Organs at peak performance

3) Exhaustion: Body is unable to return to homeostasis OR continue peak response

Increase BP

Increase HR

CNS Arousal

Increase glucose levels

Bronchodilation

Increased Ventiliation

Decreased Inflammatory/Immune

Increased O2 level

Increased Circulation

Increased Metabolism

Enhances Cognition

Enhances memory

Endorphins (pain)

Disruption of intellectual function

Disruption of memory

Acute Renal Failure

Stress Ulcers

Infection

Slow healing

PTSD (nightmares, depression)

Sympathetic Nervous System

1. Increase availability of acetylcholine at NMJ (increased muscle contraction)
2. Increase secretions (GI, lacrimation, salivation
3. Decreased heart rate (Vagus nerve) - Bradycardia (decreased cardiac output)

Adequate Rest

Healthy diet 

etc

Adequate Rest

Healthy diet 

etc

1. Increase availability of acetylcholine at NMJ (increased muscle contraction)
2. Increase secretions (GI, lacrimation, salivation
3. Decreased heart rate (Vagus nerve) - Bradycardia (decreased cardiac output)

What are nociceptors?

Adequate Rest

Healthy diet 

etc

Occurs with tissue ischemia or damage from:

Inflammation, infection, stretch, ischemia, tissue necrosis, burns

What are nociceptors?

Occurs with tissue ischemia or damage from:

Inflammation, infection, stretch, ischemia, tissue necrosis, burns

occurs as a result of sudden pain - is protective

*causes involuntary muscle contraction/movement without brain involvement

*Action is initiated at dorsal root ganglion in spine before the brain is aware

Pain - Dorsal Root - Immediate efferent (motor) response

*Occurs without CNS involvement "No upper management"

Reticular Activating System

Pain-Spinothalamic Tracts - RAS- Thalamus-Somatosensory Cortex - Hypothalamus (stress response) - Limbic System (emotional)

1) paleospinothalamic tract - slow, dull, chronic pain impulses

2) Neospinothalamic tract: fast, sharp, acute pain impulses

Arousal state of RAS in pons and medulla influence brain awareness

* MAny drugs are the target of Reticular activating system, dulling pain

Analgesics

Sedatives and antianxiety meds (anxiolytics)

Anesthesia (local, regional, and general)

Gate-control theory

Pathway Blockage