Patho Exam 3
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jcolombini on March 11, 2012
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349 terms
Terms | Definitions |
|---|---|
 Visceral Pain | diffuse, difficult to locate and often reffered to a distant, superficial, structure |
| somatic pain | stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fascia, and muscles, dull aching, poorly localized |
| Pain Threshold | standard among peoplle when the pain is bother some |
| Decrease pain theshold | anxiety, tired, anger, fear, depression, isolation |
| raised pain threshold | sllep, rest, diversion, empathy, medications |
| pain tolerance | amount of pain a person is willing to tolerate varies a lot in one individual |
| pain transduction | whatever stimulus is changes to action potential |
| conduction | passage of energy to neruons |
| transmission | relay of signals across synapses |
| perception | get to area of the brain to allow it to happen, relates to pain |
| modulation | how to stop the pain by blocking specific place or turning brain off, if in controlled by individual usually give less, have to give more if pain is extreme |
| nociception | free nerve ending located throughout the body, receptro, neurone, to spinal cord, to brain, same pathway every time |
| noxious stimuli | provoking such as chemical, ligand, thermal, mechanical |
| mediators of nociception | released by injury, released during inflammation, |
| Transmission of pain | receptor to dorsal horn to spinal cord to brain |
| C-fiber | unmylenated, free nerve ending, slow, projections in brain stem to alert hypothalamus that something bad has happen, follow by level of pain, usually noxious, not very well localized, cross at spinal cord |
| A-Delta | mylenated, faster, less synapses, sharp localized pain, does not cross |
| touch receptors | can over ride the sensation of pain synapse in same areas of cord, gate control theory where over rise and inhibits A and C receptros decreasing amount of pain that goes across |
| Neuropeptides | excitatory and inhibitory of actions of pain |
| Dermatomes | follow vertebraw location of where nerve innervates specific area where most pain occurs |
| RAS | has to get pass here if blockes at the level will no reach perception |
| Thalamus | relay station for pain signlas in the brain |
| primary sensory cortex | pain on one side stimulated on opposite side of the brain, homunculus |
| cortical association area | how to place story on pain |
| limbic structures | memory of pain, learn what's painful what's not and what to avoid |
| nociceptor modulation | directly at area of pain, cold, massage, drugs |
| spinal cord modulation | endogenous endorphins peptides made by sepcific neurons that bind to opiods receptors giving same analgesic effects as narcotics drugs devices (TENS) directed at gate control theory Massage |
| Modulation of pain at brain | endogenoug endorphins, peptides drugs biofeedback, yoga |
| Gate controk theory | spinal cor contains a neurological gate that either block pain signals or allows them to continue on to the brain, can decrease the perception of pain by rubbing the area to reduce intensity of pain |
| Acute pain | nociceptor activity SNA response:L hear, respiratory, BP, diaphoresis, short term |
| Chronic pain | uncertain etiology, little to no SNS response, adaptation, long term |
| Neuropathic/neuralgia | not generated at receptro, typically can not see, disease or unknown causes |
| Trigeminal | compression syndromes, pain in face |
| post herpetic pain | after shingles, pain syndrome still going on |
| Diabetese | number one cause of neuropathic pain |
| Referred pain | pain on surface usually caused from visceral issues, consistent from person to person, pain receptors that come from visceral cavities enter the spinal cord and have cross talking with other receptros in same area |
| cardiac ischemia | pain that occurs in the left arm and or neck |
| coliosistitis | pain can occur in right shoulder |
| lower bowel | pain can occur in the low back |
| kidney | pain can occur in the low back |
| Opiod Receptors | g protein linked inhibitory want agonist for pain relief, body will down regulate receptors and can cause issue with own endoorphines cause dependence changed physiology of receptors = withdrawl and tolerance |
| Respiratory depression | Mu, Kappa, Delta receptors |
| Euphoria | Mu receptors |
| Mu and Kappa Receptors | Constipation sedation pupil constriction Analgesia |
| Mu and Delta receptors | Dependence nausea/vomitting |
| equal analgesics charts | if switching from route such as IV to oral gives you equivalaent doses of medications so that gets effects that are desired |
| Naloxone | opion antagonist used to counter effect overdose specifically used to counteract depression of CNS and respiratory system |
| Opiod Partial Agonist | Used in OB less often used low potential for abuse less analgesic effect and respiratory depression can initiate withdrawal in agonist dependant patient |
| Opioids | act in the brain and spinal cord wherever receptors are to modulate pain used for mild to severe pain absoprtion is rapid from GI and nasal cross placenta and BB |
| Agonist-antagonist | bind to receptor and block endogenous system, little pain relief |
| antagonist | block Mu and Kappa, reversible to block narcotic for people who have OD |
| Pure Opiod Agonist | for mild to moderate pain: codeine for moderate to severe pain: morphine |
| Agonist Opiods ADR | tolerance dependece caused by negative effects on receptor stimulation hypersensitivity reaction venodialtor: reduces work load of heart vasodialator: respiratory and CNS depression |
| opiod antagonist | competitive inhibitors for Mu and Kappa reverse respiratory depression acute withdrawl |
| Morphine, Oxycodone, Fentanyl | opiod agonist, severe pain, high abuse rate |
| hydrocodone + acetominophen | vicodin agonist treats moderate pain lasts longer |
| Oxycodne + Aspirin | percodan helps relieve severe pain longer kidney toxicity |
| Oxycodone + acetaminophen | Percocet severe pain relieved longer liver toxicity |
| Meperidine | demerol agonist acute pain after surgery have high ADR such as seizures |
| Codeine | opiod agonist similar to morphine less effective has ceiling effect moderate pain |
| Hydromorphine | diluadid morphine like but safe in patients with renal failure more potent than morphine |
| Methadone | opiod agoinist detox treatment chronic pain |
| Benzodiazepines | block anxiety, induce sleep, sedative Bind to GABAa receptors and enhance GABA action damps down brain transmission wide spread activity over brain depression of neurotransmission unsafe additive effects with other depressants |
| Sleep agents (Hypnotics) | non bensodiazepine agents different MOA generally less CNS depression less abuse potential worry that sleep is not restorative |
| Barbituates | anxiety, sedation, seizure control high ADR Long acting, phenobarbital Bind GABAa to enhance GABA action to damp down brain transmission P450 enzyme inducer increasing metabolic activity numerous drug interactions |
| GABAa receptor | chloride channel ion, open and inhibits neuronal depolarization, damps down brain transmission |
| P450 | in barabituates this enzyme makes more ER increasing metabolic acitivity metabolizing everything else they are on a lot faster cause numerous drug interactiion |
| Amphetamines | CNS stimulants dependence stimulating one part of the brain can calm down other parts of the brain benefit of the drug outweighs the risk |
| Amphetamine apartate | increase release of norepinephrine used for ADHD |
| Atomoxetime | Norepinephrine reuptake inhibitor |
| Caffeine | inhibit cAMP degradation is an amphetamine |
| Serotonin Agonists | ends in triptan increase heart rate and vasoconstriction |
| Presynaptic receptor Alpha 2 agonist | decrease NE activity with negative feedback loop |
| Na driven carrier | Na goes down electrochemical gradient giving power to take up NE back into cell |
| COMT | once Na gets out of the synapse this in the synapse and extra cellular space degrades catelcholamines |
| NE and serotonin | products can get into vesicle and be recycled to use again or can go to another enzyme works in mitochondria and gets broken down at this location |
| Tricyclic | antidepressants, NE, dopamine, serotonin reuptake inhibition high side effects |
| MOAI | put MAO back into vesicles increasing amounts available high side effects high side effects |
| Selective serotonin reuptake inhibitor | not very good efficacy low side effects anxiety, depression antidepressants |
| Serotonin/NE reuptake inhibitors (SNRI) | leave dopamine alone low side effects |
| Lithium | antipsychotic ion that competes with Na and iodine difficult to mannage used for bipolar |
| Conventional agents | antipsychotics dopamine receptor antagonists |
| Newer agents | antipsychotic better ADT profile atypical dopamine antagonist |
| Anti seizure agents | some used for neuropathic pain and psychiatric disorders MOA: affect ion channels and inhibit AP initiation and conduction |
| Anterolateral | crosses immediately in the cord sensation poorly localized itch, pain, temperature when coming down crosses |
| Dorsal column | ipsilateral until medulla than crosses over sensation well localized fine touch, vibration, pressure when coming down doesn't cross |
| Corticospinal (pyramidal) | crosses at medulla innervates distal muscles fine motor control innervate muscles on opposite side of the body distal muscles, fine motor, voluntary |
| Extrapyramidal | does not cross at medulla innervates proximal muscles involuntary reflexes balance, posture, gross motor |
| Upper neuron injury | Hyperreflexia babinski plasticity hyperexcitable muscles when stretched late atrophy of muscles happens in CNS |
| Lower neuron injury | happens in last neuron in pathway innervates muscle directly hyporeflexia no reflexes flaccidity paralysis early atrophy of muscles |
| Upper motor neurons | motor neurons that originate in the motor region of the cerebral cortes or the brain stem and carry motor information down to the final common pathway, not directly responsible for stimulating target muscles |
| Lower motor neurons | motor neurons connecting the brainstem and spinal cord to muscle fibers, bring nerve impulses from upper out to muscles, axon terminate on a muscle |
| Triptans | important for treating migranes if the only happen so often |
| Peripheral neuropathies | damage to nerves in hands and feet can cause numbness or pain |
| Secondary Brain injury | mechanical trauma causes |
| Irreversible ischemia | brain injury that is caused by necorsis such as a stoke |
| Primary brain injury | causes are CNS infections or CSF obstruction |
| Evaluation of acute brain injury | Airway, Breathing, Circulation neurological exam CT scan Surgical solution |
| Coup (focal) | TBI primary injury very localized direct hit |
| Coup-contra coup (polar) | TBI primary injury head is in motion and suddenly stops affects 2 different poles of the brain |
| Diffuse | TBI primary injury due to major trauma bad outcome |
| Contussion | brain bruise |
| Post concussive syndrome | brain swelling or repeated trauma may have brain problems further down the road |
| Concussion | can be graded 1(less that 15), 2 (longer than 15), or 3 (loss of consciousness) |
| Epidural hematoma | between skull and dura, location where all the large arteries are, causes due to arterial bleeding |
| subdural hematoma | bridging of veins between dura and pia slower acccumlation of blood |
| Hematoma | collections of blood in the brain |
| Ischemic process | stoke or CPR may cause poor flow to an area of the brain |
| Hypoxia | Ischemic process cells down streeam not getting O2 supply no ATP made |
| Ca | accumulates in the cell triggers intracellular cascade causing cell death ischemic process |
| Mitochondira | try to help during Ca overload which can lead to cell death |
| Glutamate | increased due to stress or trauma, normally taken back up by reuptake requires energy with ischemic reuptake fails causing constant activation of Ca channels |
| Free radical | production increases during ischemic process |
| Repurfusion | if this happens during ischemic process brings back O2 into the system because of period of low O2 can cause increase free radical and immunse cells causing inflammation (secondary injury) |
| Normal ICP | less than 15 mm HG |
| space occupying components of ICP | Blood Brain tissue CSF/ventricles |
| Mono-Kellie hypothesis | body's compensatory efforts for increase ICP if one increases another one has to be reduced to keep ICP in range compatible with life |
| Blood | contributors to elevated ICP right heart failure, increased abdominal/thoracic pressure, hypoxia, increased CO2, acidosis |
| Brain tissue | contributes to elevated ICP tumor, hematoma, infection, ischemia, catonic, cerberbal edema, lack of energy to pump K and NA |
| CSF | contributes to elevated ICP hydrocephalus |
| Brain compliance | if ICP increases: has an area of high compliance for awhile to keep pressure from going up chang in LOC indicator of change in ICP don't wake up pressure can keep going blown pupil |
| Glasgo coma scale | gives a number to evaluate things such as respiration, pupils, awareness, key in increased ICP |
| Cushing response | emergency intense increased in ICP elevated systolic pressure widening pulse pressure decreased heart rate |
| Herniation | potential ultimate result of increase ICP, brain pushes through bony structures, blood supply cut off the area where occurs |
| Osmotic diuretics | interventions for increased ICP fake sugar filtered into kidney |
| Barbituate coma | intervention for increased ICP allow brain to heal |
| Decompression Surgery | Intervention for increased ICP drains off excess CSF |
| Mannitol | diuretic that is a fake sugar that is filtered into kidneys used when ICP increases |
| Thormbotic Stoke | type of stoke that is 80% of ischemic stokes blood clot has formed on an atheroscelortic plague often effects whole brain atheroscleoriss with thrombus formation |
| Transient Ischemic Attack | precedes stoke, some symptoms of stokes that resolve quickly |
| Embolic Stoke | 20% of ischemic stokes clot comes from somewhere else other than brain atrial fibirlation valvular disease hypercoagulation states |
| Hemorrhagic stoke | 12% of all stokes strucutral abnormalities such as aneurysm or AVM where artery feeds into vein with no capilarry hypertension arterial wall rupture |
| Ischemia | when blood flow is less than 20 ml/100g stroke |
| Infarction | when blood flow is less than 12ml/100g |
| Secondary injury | in a stoke occurs because of inflammation and apoptosis |
| Dementia | syndrome of deterioration of memory and cognition, occurs when lose enough neurons and when connection in the brain no longer work |
| Vascular dementia | loss of neurons from ischemia |
| Alzheimer | clear symptoms of significant dementia |
| Mild cognitive impairment | stage of alzheimer in decline of mental function without compromising independence |
| preclinical | stage of alzheimer of no symptoms but recoginizable atrophic brain changes |
| Apo-E-gene (E4) | involved in alzheimer if inherit 2 you are at much higher risk to develop alzheimer |
| Presenilin gene | defects in this gene can cause early onset of alzheimers |
| Amyloid Plagues | may only be a marker for alzheimer, degredation of neurons, intracellular, between neurons |
| neurofibrillary tangles | around plagues inside neurons, when collapse sign of neuronal death, pathology of alzheimers |
| Cerebral atrophy and large ventricles | if something is shrinking something else has to get better, pathology of alzheimers |
| Alzheimer Brain abnormalities | Defeciency of Ach secretion serotonin neuronal dysfunction glutamate neuronal dysfunction increased brain cholesterol lessions of amyloids and neurofibrillary tangels |
| Diagnosis | stage of alzheimer use CT scan and neruological/psychological testing |
| Acetylcholinesterase inhibitors | inhibits Ach enzymes that inhibit Ach called donepezil used to treat alzheimers |
| Glutamate inhibitors | inhibiting Ca coming into cells may inhibit apoptosis, Namenda, treats alzheimer |
| Parkinson | starts out lateral than goes bilater, once diagnosed usually in late stages |
| Degranulates neurons | in parkinson's low dopamine level in basal gnaglia cause this |
| Dopamine suppressed | in parkinson this happens with excessive action of Ach |
| Early onset | parkin gene and a-synuclein gene can cause this for parkinson disease |
| D2 | inhibits activation of GABA produces over activity of neurons in next pathway starts domino effect of inhibition and activity over time, in parkinson |
| D1 | in parkinson's causes loss of dopamine |
| Parkinsons | in this disease have excessive involuntary movement and less voluntary movement because of different neurons being inhibited and over activated |
| Dopamine deficiency | in parkinson disrupts normal release of other inhibitory and excitatory neurons in the basal ganglia and cerbral cortex |
| Classic triad | in parkinsons has akinesia, rigidity, resting tremor |
| Assocaited symptoms | in parmkinson's has poor speech, demential, propulsive gair, drooling, expressionless |
| Onset | occurs in parkinson's when 70-80% of striatal dopamine neurons are lost |
| Antiepileptic drugs | individualized single or combination monitor ADR serum level monitored taper off |
| Acquired seizure disorder | caused by head injury, birth trauma, may be on medications even if there are no signs |
| Epileptogenic focus | pathogenesis of seizure in area of cerebral cortex responsible for causing seizures |
| Stimulus | if these are present may trigger a seizure |
| EEG | this used to diagnose a seizure |
| Status epileptics | seizure that goes on for a long period of time |
| Absence | generalized epileptic seizure of sudden onset and termination, impaired consciousness |
| Myoclonic | brief no voluntary twitching of muscles, type of seizures |
| Atonic | brief lapse in muscle tone, type of seizure |
| tonic/clonic | seizure that affects entire brain, gran mal |
| Aura | perception of a strange light, an unpleasant smell or confusing thoughts or experiences, can be a tell for seizure or migrane |
| Postical period | period of being wiped out for hours or days after a seizure |
| Simple | partial/focal seizure no alter to consciousness |
| complex | partial/focal seizure alter to consciousness |
| focal | secondarily generalized seizure start out this and than march across brain to other hemisphere |
| Termination of seizure | if seizure goes on for a long period of time, fast acting benzodiazepines used in IV to increase GABA acitivity and settle down brain, follow with Dilantin |
| Brown-Sequard syndrome | loss of damage to one side of the spinal cord resting in ipsilateral hemi paraplegia and less of muscle and joint sensation contral lateral hemianesthesia |
| Trigeminal nerve | responsible for causing migraines |
| clusters | multiple headaches in a row, severe episodes, eyes tear, seasonal, more men than women, hypothalamus |
| Tension | constant, no throbbing, activity can cause |
| Meningitis | Bacterial Headache Fever Stiff neck meningeal irritation CSF high in protein and WBC low glucose |
| Steroids and antibiotics | used to treat acute bacterial meningitis |
| Duchenne Muscular Dystrophy | x-linked disorders, males affected absent dystrophin protein symmetric proximal weakness no pain, or muslce tenderness, or loss of sensation |
| Myalgia | muscle pain |
| Transient | type of myalgia caused by overuse, injury, viral, strain |
| Chronic | type of myalgia drug related, cholesterol lowering agents (statins) can cause |
| Fibromyalgia | wide spread muslce pain, very localized, chronic |
| Polymylagia rheumatacia | pain in many muscles, chronic |
| poliomyletiis | inflammation in many muscles, chronic |
| Dematomyositis | diffuse, patchy inflammation of muscles, chronic |
| Acute | type of myalgia muscle damage/breakdown |
| Rhabdomyolysis | acute, release of myoglobin into blood can damage kidneys, flush system, NSAID used to treat |
| Systemic Lupus Erythematosus | autoimmune, immune complex circulating around gets a lot of tissue cause systematic issues, chronic inflammation of connective tissues, drug indices |
| Clinical manifestation of lupus | fatigue, fever, orgain failure, butterfly rask, pain in joints, alopecia |
| Anti-nuclear Antibodies | lab test done for these to see if some one does not have lupus |
| Rheumatoid Arthritis | chronic systemic, autoimmune, inflammatory symmetrical of joints tendons and ligaments involved effects proximal joints |
| Rheumatoid factor | elevated erythrocyte sedimentation rate, x-ray changes, in rheumatoid arthritis |
| Antibodies | used to diagnosis Rheumatoid arthritis |
| Osteoarthritis | prgressive, slow, not related to immune response distal joints localized wear and tear crepitus joint space become narrow not systemic |
| Osteoporosis | lower than second standar deviation bone demineralization, brittle bones |
| Osteopenia | lower than first standard deviation, bone demineralization, brittle bones |
| Parathyroid hormone | removes Ca from body can cause osteoporsis |
| Chronic kidney disease | causes low vitamin D lead to osteoporisis |
| Causes of osteopenia/osteoporsis | smoking postmenopausal ethnicity corticosteroid therapy thyroid therapy |
| Bisphosphonates | fake phosphate, stay in bone longer term increasing bone density |
| teriparatide | parathyroid hormone therapy giving high dose changes activity to stop reabsorption |
| Selective estrogen receptor modulators | estorgen like modified to only react with certain receptors will not interact with breast tissues |
| Risk for fracture | trauma, stress fractures (incomplete), pathological |
| Pathological fractures | spontaneous usually in spine, osteoporosis, plasma cell myleoma |
| Compound | open fracture |
| Closed fracture | simple fracure |
| Avulsion | tendons that are hooked into bone pull it innto seperate direction have to be reattached to blood supply can be disrupted can become necrotic |
| Healing of bone fracture | hematoma in area activation of clotting cascade (early) clot reabsorbed osteocyte acitivty fills in with protein and cartilage bony bump forms, bone over shoots Remodiling, callus is reabsorbed bone goes back to normal |
| Nonunion | end pieces fail to grow together properly, steroids or malnutrition or infection |
| delayed untion | more than 3 months for healing of a fracture |
| Malunion | misaligned healing, traction, casting |
| Osteomyletis | infection of bone caused by fracure difficult to treat smell bad inflammatory respnse antimicrobial therapy very long time bed rest debridement, bone grafts, implants |
| Fat Embolism | fat breakage from inside bone usually long and pelvic bones pressure and trauma force release fat droplets into venous system can cause pulmonary embolism need stabilization of fractures |
| Comparment syndrome | acute arterial occlusion distal to injury cast, wsellin can cause check sirculation, sensation, and movement treatment: splitting, cut open fascia pain, pulseless, pale, cold |
| Tetraplegia/quadriplegia | spinal cord injury that is high cervical affects arms and legs seperated from the brain |
| paraplegia | spinal cord injury of the lower extremeties |
| Complete | total resection of spinal cord |
| Secondary Spinal Inury | post inflammation, bleeding, function may return when goes away |
| Primary injury trauma, hyperflexion, hyperextension, compression, cause spinal injury | trauma, hyperflexion, hyperextension, compression, cause spinal injury |
| Spinal shock | hat happens first after an injury loss of function below level of injury loss of all sensory function skeletal muscle flaccidity atonic bowel and bladder |
| Incomplete spinal shock | mixed deficits |
| complete spinal shock | no sensation and plasticity below level of injury |
| Neurogena shock | high injuries vasogenic SNS and PSNS run up type of shock below injury positional sitting up cause baroreceptors not to compensate loss of SNS outflow hypotension bradycardia hypothermia unable to vaoconstict when upright need lower extremety compression slow position change |
| Autoimmune dysreflexia | vasoconstriction below injury vasodialation above injury baroreceptor do no respond reflex activation of SNS neurons below level of injury stimulus induced rapid response removing stimulus can help settle it down hypertension bradycardia headache flush above injury, seating pallor, cool below injury sight |
| MS | autoimmune viral trigger with genetic predisposition Immune injury to myleniated neurons highly variable fatigue weakness bowel/bladder dysfunction |
| Sceloritc plagues | lessions and demylenization noted on MRI part of inflammation and immune attack |
| Demylenization | MS disturbs neuron conduction, neuron axon is injured severing causing degeneration |
| Corticosteroids | for acute exacberation of MS, anti-inflmmatory |
| Interferon 1B, Beta interferon 1a | protect other cells from gettingi nfection, MS treatment |
| Peripheral Neuropathy | affects peripheral nerve diabetes deficient receptors sensory changes autonomic changes motor changes |
| anti-cholinesterase | used for treatment of peripheral neuropathy, allows for more ACTH to help with movement |
| Myasthenia Gravis | gradual harmful onset autoimmune Antibodies bind Ach receptors in NM junction and block activity progressive weakness of muscles |
| Acetylcholine esterase inhibitors | used to treat and diagnose myasthenia gravis |
| Myasthenic crisis | not enough motor acitivty to run respiration, not enough drug given, myasthenia gravis |
| Cholinergic crisis | to much acetylcholine activity causing over stimulatin, to much drug, myasthenia gravis |
| arthritis | painful joint condition |
| Hypothalamus | synthesis/secretion of CRH, GHRH, somatostatin, TRH Synthesis of vasopressin/ADH and oxytocin control what pituitary does |
| portal system | from hypothalamus capillary bed to pituitary capillary bed |
| Anterior Pituitary | synthesis and secretion of trophic hormones TSH, ACTH, GH, PRL, gonandotropins |
| Posterior pituitary | neuron like, secretes vasopressin/ADH and oxytocin |
| Medulla | core of adrenal gland, epinephrine |
| Growth hormone | main target in the liver |
| Trophic | if take away organ gland will under go apoptosis |
| Prolactin | breast tissue, milk production, second most prevelant in anterior pituitary |
| Negative feedback control | can determine if problem with gland or target gland |
| Growth hormone | works with the liver to release insulin growth factor 1, if a person has a lot will make them tall and bulky |
| ACTH | cortisol is released from this |
| TSH | T3 and T4 stimulate |
| Serum osmolarity | water content of the blood stimulates ADH, if to high make more ADH if to low turn off ADH |
| RAAS | aldosterone decreased renal perfusion increased blood volume and BP fluid retention vasoconstriction |
| Parathyroid hormone | increased serum Ca can pull from bones and Kidney GI turns off as Ca levels go up |
| Insulin | decrease serum glucose so as glucose goes up secretion of this goes up |
| Primary disorder | due to dysfunction of the target gland/organ |
| Secondary disorder | due to dysfunction of the pituitary gland or other sources, causes target gland to malfunction |
| Hyperfunction | can be caused from Tumor, Autoimmune, to much replacement therapy, steroid use is treated with removal can later cause hypo function |
| Hypofunction | gland destruction/absence, autoimmune inhibition, nonsecreting tumors, medically caused from removal, cutting blood supply need hormone replacement therapy |
| Target tissue resistance | in hypofunction gland secreting hormone is normal but tarfet tissue ressits, Type 2 diabetes does this, defective receptor for hormone |
| Hyperpituitarism | hyper secreting tumor of 1 or more cell types, bad outcome can lead to increased ICP and have S/S of too much hormone, prolactin most affected, can affect GH, ACTH, TSH |
| Transphenodial pituitary adenectomy | surgically removal of pituitary when overactive |
| Hypopituitarism | non secreting tumor or significant pituitary damage or absent low TSH, ACTH, or GH use target hormone replacement |
| Increase Blood glucose | GH Catecholamines (stress) glucagon Thyroid (overactive increase insulin demands) Glucocorticoids (significant difference) |
| Decrease Blood glucose | Insulin Amylin Gut hormones |
| type 2 diabetes | beta cell dysfunction and insulin resistance produce hyperglycemia High insulin levels and c-peptide present look at plasma osmolality |
| Type 1 Diabetes | beta cell destruction lack of insulin no insulin or c-peptide present look at ketones |
| Progression of Type 1 | Genetic predisposition precipitating event/environment antibodies glucose normal progressive loss of insulin overt diabetes C-peptide present than absent |
| Type 2 progression | slow Stage 1: initial period of pancreas putting out high levels of insulin Stage 2: insulin resistance increases, a lot of insulin but unable to get glucose into cells Stage 3: further increase in insulin resistance, hepatic glucose production impaired |
| Metabolic syndrome | occurs in type 2 Abdominal obesity LDL and triglycerides up, HDL low hypertension insulin resistance of glucose intolerance increase fibrinogen caused by adipsoe c-reactive protein elevated fatty liver disease increased skin tags |
| Diagnosis of Diabetes | FBS > 126 mg 2 hour post-prandial BS > 200 mg Random BS > 200 mg + S/S A1C > 6.5% |
| Diabetic Ketoacidosis | insulin not being made to transport glucose into cells, very high glucose, buring fat instead of glucose, free fatty acids formed, ketones formed, dehydration |
| Diabetic Ketoacidosis | infection may cause omission of insulin undertreatment with insulin undiagnosed diabetes insulin pump poor compliance |
| Hyperosmolar Hyperglycemic State | impaired mental status elevated plasma osmomlarity extreme hyperglycemia severe dehydration renal dysfunction may go into coma and die |
| Neurogenic hypoglycemia | sensation of BS dropping, may not be low |
| Neuroglycopenic | actual lowering of BS |
| Sulfonylureas | stimulate pancreas to produce insulin, increase Basal and meal stimulated insulin action squirt out insulin to lower fasting BS pancreas may wear out if allergic to sulfa do not use avoid alcohol |
| Meglitinides | squirt out insul to lower BS in response to food increase glucose stumulated insulin secretion dose may be omitted if meal skipped |
| Biguanides | improves insulin sensitivity aid weight loss improves plasma lipids can develop lactic acidosis |
| Thiazolineodiones | black box warning good for type 2 act of target tissue to increase insulin sensitivity maximum glucose lowering effects = 12 weeks increase HDL |
| Alpha glycosidase inhibitors | good for postprandial BS slow GI emptying of food so don't get increase BS when eat inhibit membrane bound a-glycosidase enzyme in small intestines decrese glucose absorption |
| GLP-1 | stimulates insulin secretion after eat supress glucagon slows GI emptying so don't eat as much improves sensitivity |
| Exenatide | injectable for type 2 slows GI empting, suppress glucagon, improves sensitivity given with insulin take 60 min within eating |
| Liraglutide | Like GLP-1 given 1 a day long lasting not to be given with insulin |
| DPP-4 inhibitors | block GLP from working satisifies needs |
| Amylin | for type 1 made at the same time of insulin helps replace insulin, acts like GLP-1 |
| Macrovascular complications | myocardial infarction, stoke, peripheral vascular disease |
| Microvascular complications | nephropathy, retinopathy, neuropathy, higher A1C |
| Bolus insulin | mimics insulin produced in response to food, short acting o: 30-60 min p: 2-4 hours d: 6-10 hours fast acting is quicker EX: Regular, can be given in IV, reduce post-prandail hyperglycemia |
| Basal Insulin | mimics continuous insulin, supresses glucose production between meals NPH D: 10-20 hours, can last longer |
| Homonymous Hemianopsia | loss of vision contra lateral to effected side |
| Homonopsia | loss of vision of both sides |
| Antipsychotics | cause rapid bilateral onset of parkinson |
| CO2 | is to low vessels constrict if to high vessels dialate |
| Levodopa/Carbidopa | increase brain levels of fopamine available, used for treatment of parkinson's |
| Encephalitis | caused by viral infection or own body's immune system, brain swelling |
| Hormone solubility | affects how a hormone interacts with the cells |
| Water soluble | hormones that interact on cell surface insulin, GH, prolactin, peptides, Catecholamines |
| Lipid soluble | hormones that interact within the cell steroid and thyroid, dopamine |
| T3 | small amount, crosses directly into target cells, stimulates TSH, receptor had higher affinity for this, does more work |
| T4 | large amout, needs cellular enzymes to activate it into form, helps TSH, usually turns into T3, used prmarily for hypothyroidism treatment |
| T3/T4 | helps with bone maturation CNS maturation Heat production Increase metabolism inhibits TSH Increase cardica output |
| Goiter | this can develop if have hyperthyroid, hypothyroid, euthyroid enlarged thyroid |
| Laboratory Evaluation of Hypothyroidism | T3, T4 may be initiall normal or low TSH is a better indicator for primary which will be elevated in this primary disorder |
| Graves Disease | autoimmune association with HLA, D3, B8 more women affected IgG antibodies bind to stimulate TSH receptors on Thyroid bulging eyes hypersecretion of TSH antibody acts like TSH |
| Exopthalmous | in graves disease due to autoimmune inflammation of tissues behind the eye, more white |
| Increase release of GH | decreased glucose, decreased FFA, fasting, exercise, stress, sleep, adolescence if have to much of this giagantism as an adult can have diabetes, acromegaly |
| Decreased GH | increase glucose, increased FFA, obesity, can lead to short stature in children (Dwarfisim) |
| IGF 1 | liver releases this and glucose in response to GH makes lean body mass, negative feedback for GH |
| Giantism | in children when has excess GH tall stature, usually in early childhood because Epiphiseal plate haven't closed |
| Decreased GH | if this happens in adults can lead to decreased bone and muscle mass |
| Acromegaly | syndrome in adults that have increased GH secretion over time, secreting tumor, S/S of space occupying lesions in brain, stature puts on bulk, person gets thick, hyperglycemia |
| Tretment of GH excess | removal of pituitary, radiation, GH antagonist, synthetic analog of somatostatin |
| Treatment of GH defeciency | replacement therapy in children but not adults, make sure no thyroid or cortical problems |
| Primary Hypothyroidism | Hashimoto's thyroiditis (autoimmune inflmmation) surgery, treatment for hyper iodine deficiency, Elevated TSH low T4 |
| Secondary Hypothyrodism | pituitary failure |
| Hypothyroidism | weight gain, fatigue, cold intolerance, dry skin, low HR/BP, edema around eyes |
| Myxedema Coma | hard edema not fluid filled, worst case scenerio for hypothyroidism stress, cold, narcotics hypothermia, hypotension, bradycardia, caused by low thyroid hormones, high mortality rate if not treated with IV thyroid drugs |
| Primary Hyperthyroidism | elevated T4 low TSH, used also for diagnosis and to monitor Grave's Disease Thyroid Tumore viral inflammation of thyroid, releasing to much thyroid hormone that has been stored |
| Secondary Hyperthyrodism | pituitary adenoma |
| Hyperthyroidism | weight loss, increased appetite, heat intolerance, nervousness, palpation, warm skin, thin hair, increased HR/BP, enlarge thyroid |
| Thyroid Storm | in hyperthyroidism that is life threatening, metabolic activity is to high triggered by stress, hyperrythemia, MI, N/V/D, agitation |
| RAI | intervention for hyperthyroidism that causes radioactive damage to gland cause shrinkage and apoptosis |
| PTU | drug therapy for primary hyperthyroidism that block absorption of thyroid hormone |
| Cushing Disease | caused by to much steroid use, cortisol problem, hyper active adrenal gland, pituitary making to much ACTH, rare, wean off drugs if on |
| Addison disease | caused by to little drug use, not enough cortisol, hypo active adrenal gland |
| Cortisol | carb/fat/protein metabolism, raise BS, protect against inflammation/immune response during stress, enhance Na and H2O retention |
| Gluccocorticoids | can cause shrinkage of adrenal gland because of suppression of ACTH have to lean off so don't get under active adrenal gland |
| Hypercortisolism | over active adrenal gland |
| Cushing syndrome | in over active adrenal gland can be caused by adrenal adenoma, adrenal carcinoma, cancer, gluccocorticoid use |
| Hypercorticolism symptoms | weight gain, fatigue, weakness, hyperglycemia, muscle waisting, centeral obeseity |
| Primary adrenal insufficiency | not enough cortisol addison disease congenital enzymes with defective gene in cortisol pathway (lots of testerone) infarction |
| Secondary adrenal insuffieciency | pituitary failure steroid withdrawl |
| Manifestations of adrenocorticoid insufficiency | May be asymptomatic weakness weight loss hyperpigmentation tachycardia hypotension |
| Hyperpigmentation | involved in adrenocortical insufficiency, ACTH has mylenosights, to much ACTH action cause this |
| Addisonian crisis | worst case scenerio if not enough cortisol, may have hypertensive shock, give gluccocorticoids to treat |
| Acute cortisol replacement therapy | hydrocortison: raise BP fluid replacement |
| chronic cortisol replacement therapy | use steroids to mimick, dosing periodically thoughout day |
| Aldosterone | under the contol of Angiostension II |
| Primary hyperaldosteronism | adrenal pathway only aldosterone pathway in effected |
| Secondary hyperaldosterone | RAAS stimulation for condition related to poor renal perfusion, usual caused by cardiac issues |
| Hyperaldosterone | hypertension, hypervolemia Tx: diuretics to block aldosterone action on kidney |
| Pheochromocytoma | CNS contol catecholamines secreting tumor in adrenal medulla intermittent fight/flight response to much NE and epinephrine released surgery to treat |
| Diabetic insipidus | ADH defeciency damage to hypothalamus or posterior pituitary lack of ADH receptors polyuria, polydipsia, nocturia, weight loss, thirst, seizure/coma/death |
| SIADH | to much ADH cancer related, lung tumore to much water for Na in body not peeing off what should weight gain seizure/coma/death |
| Increased PTH | increase Ca parathyroid tumor PTH release from cancers need sugical removal, diuretic NM depression |
| Decreased PTH | Decreased Ca, post thyroid removal/congenital Acute: IV Ca Chronic: vitamin D/Ca, phosphate restriction NM overreactive |
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