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Syndrome of inappropriate antidiuretic hormone (SIADH) secretion
- Posterior pituitary
- secretion of ADH, pxytocin
- water retention
- hyponatremia
- hyperoosmolarity
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Diabetes Insipidus
- posterior pituitary
- insufficient ADH
- polyuria, polydipsia
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Hypopituitarism
pituitary infarction (Sheehan syndrome, hemorrhage, shock)
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Premenstrual syndrome
- cyclic physical/behavioral changes that impair interpersonal relationships or interfere with usual activities
- luteal phase
- abnormal nervous, immunologic, vascular, GI, etc.
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Dysfunctional uterine bleeding
- heavy/irregular bleeding without disease
- perimenopause
- changes in hormonal levels
- ovaries don't release egg
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polycystic ovary syndrome
- oligo-ovulation/anovulation
- elevated androgens
- infertility
- multifactorial (hyperinsulinism)
- dysfunction of follicle development
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Primary Dysmenorrhea
painful menstruation associated with prostaglandin release in ovulatory cycles
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Endometriosis
- -functioning endometrial tissue or implants outside uterus
- -In endometriosis, displaced endometrial tissue continues to act as it normally would — -it thickens, breaks down and bleeds with each menstrual cycle
- responds to hormone fluctuations of menstrual cycle
- -Causes: retrograde menstruation
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Infertility
- inability to conceive after 1 yr
- structural/hormonal
- adhesions from pelvic inflammation cause obstruction
- hormones disrupt ovulation.
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Benign prostatic Hyperplasia
- enlargement of prostate gland
- urethral compression
- aging
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Follicular cysts
This type can form when ovulation doesn't occur, and a follicle doesn't rupture or release its egg but instead grows until it becomes a cyst, or when a mature follicle involutes (collapses on itself
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corpus luteum cysts
- low LH and pogesterone
- inadequate development of corpus luteum
- fluid accumulates inside the follicle, causing the corpus luteum to expand into a cyst
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corpus albican cyst
- regressed form of the corpus luteum
- As the corpus luteum is being broken down by macrophages, fibroblasts lay down type I collagen, forming the corpus albicans.
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Benign cysts
- increase risk when hormonal imbalances are common (puberty or menopause)
- common
- causes: corpus luteum cysts and follicular cysts.
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Hypersecretion of growth hormone
- acromegaly (during adulthood): cardiac hypertrophy, hypertension, atherosclerosis, type 2 diabetes, coronary heart disease. enlargement of facial bones and hands and feet, kyphosis
- giagantism (children/adolescents)
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Panhypotituitarism
- ACTH-cortisol
- TSH-decreased metabolic rate
- FSH/LH-amenorrhea, atrophic vagina, breast, uterus
- GH-dwarfism
- ...all deficiencies.
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hypersecretion of prolactin
- female: amenorrhea, osteopenia
- males: erectile dysfunction, impaired libido, hypogonadism
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Thyrotoxicosis
- hyperthyroidism; increased TH
- graves goiter, thyroid cancer, increased TSH
- increased metabolic rate, increased tissue sensitivity to sympathetic stimulation, goiter, bruit over thyroid
- primary: excess TH by thyroid gland
- secondary: by TSH secreting pituitary (pathway)
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Graves Disease
- hyperthyroidism
- autoimmune
- groiter, opthalmopathy, dermopathy
- pretibial myxedema (subQ swelling on anterior of legs and indurated and erythemous skin.
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Hypothyroidism
- not enough TRH and TSH
- hashimoto disease
- decreased metabolism, reduced heat production
- myxedema (nonpitting, boggy edema)- pronounced around eyes, feed, hands, tongue thickens and pharynx=slurred speech
iodine deficiency
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Hyperparathyroidism/hypo
- hypercalciuria
- alakaline urine
- hyperphosphaturia-kidney stones
secondary: renal failure
- hypo: opposite- low calcium, high phosphate
- low calcium leads to muscle spasms
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Diabetes type 1
- pancreatic atrophy, loss beta cells
- macrophages, T and B lymphocytes, NKC
- autoimmune
- genetic, environmental
- hyperglycemia
- polydipsia, polyuria, polyphagia, weight loss, fatigue
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Diabetes type 2
- metabolic syndrome
- reoccurring infections, vision, neuropathy
- insulin resistance
- decreased beta cell response with abnormal glucagon secretion
- islet dysfunction due to decreased beta cell mass
- hypoglycemia, diabetic ketoacidosis
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Diabetic ketoacidosis
- absolute or relative deficiency of insuline
- type 1 diaetes
- decreased insulin=fat metabolism=release fatty acids (stimulate gluconeogenesis and ketogenesis)
- by product of fat metabolism: ketones
- vomit, dehydration, kussmal respiration, coma.
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Somogyi effect
- hypoglycemia followed by hyperglycemia
- type 1 diabetes
- glucose high in morning due to stimulation of glucose conteregulation (epinephrine, GH, cortisol, glucagon release) gluconeogenesis from other sights at night- peripheral glucose use is inhibited.
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Dawn Phenomenon
- early morning rise in glucose
- noncturnal elevations of GH=increase glucose
- via fat and muscle metabolism
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Cushing disease/syndrome
- excessive ACTH (disease), cortisol (syndrome)
- adrenal cortex
- rapid weight gain, moon face, glucose intolerant, bone, muscle wasting, immunosuppression, hyperpigmentation
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Addisons Disease
- primary adrenal insufficiency
- autoimmune
- elevated ACTH, inadequate corticosteroid synthesis
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Hyperaldosteronism
increased sodium retention, increased extracellular fluid=increased blood pressure=decreased renin, increased potassium
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Ferminization
hypersecretion of estrogen=development of female sex characteristics
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Virilization
- hypersecretion of androgens
- male sex characteristics.
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Pituitary Gland: posterior and anterior
- posterior: ADH and oxytocin
- anterior: prolactin, LH, FSH, TSH,GH
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Benign vs malignant
Benign: slow growth, well defined, encapsulated, not invasive, well differentiated, low mitotic index, not metastized
malignant: fast growth, undefined, non ecapsulated, invasive, poorly differentiated, high mitotic index, metastize
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Carcinoma in situ (CIS)
- epithelial malignant tumors
- have not broken through basement layer
- preinvasive
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Anaplasia
absence of differentiation
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Stem cells characteristics
- self renew
- multipotent (differentiate into different cell types)
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Oncogenes
- mutant genes
- direct protein synthesis/cell growth
- "gas"
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Tumor suppressor genes
- encode genes proliferation
- "breaks"
if mutation=unregulated cell growth
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Mutations
- stop tumor suppressor genes
- loss of heterozygosity (unmask mutations)
- gene silencing (shut off regions)
- decrease apotosis
in all...cause cancer
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caretaker genes
- protein repair damaged DNA
- if inhibit=increase cancer risk
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Angiogensis
- growth of new vessels
- feed cancer cells
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telomere
- end of chromosome for protection (with each division gets shorter)
- in cancer: production enzyme rebuild telomere
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epigenetics
- heritable changes in gene expression
- lifestyle modifications and pharm
- methylation: silence tumor suppressing gene
- histone modification: chromatin altered
- micro RNA: stimulate gene expression
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Inflammation and cancer
- cytokine stimulate enzyme cox-2= cancer
- free radicals= mutations
- decreased response to DNA damage
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Bacterial/virus-cancer
- helicobacter pylori
- peptic ulcer, stomach carcinoma, lyphomas
virus: hep b and c, HPV
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Metastasis
spread to distant site via lymph, blood
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cancer clinical manifestations
- pain, fatigue, anemia, infection
- cachexia: severe malnutrition (anorexia, early satiety, weight loss, anemia)
- leukopenia: decresed WBC
- thrombocytopenia: decreased platelets
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cachexia
severe malnutrition (anorexia, early satiety, weight loss, anemia)
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xenobiotics
- toxic, mutagenic, carinogenic
- diet
- phase I activation enzyme=stimulate
- phase II detox enzyme= inhibit
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Obesity and Cancer
- BMI
- adipose tissue stimulates endocrine=release free fatty acids, increase insulin resistance=hyperinsulinemia
- plus inflammatory factors
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childhood vs adult cancer
child: <1% of cancers, nonepithelial/messendyrmal, short latency, ecogentic, few prevention, detect on accident, metastized at dx, responsive to tx, long term consequences of tx, >70% cure
adult: >99% of cancers, organs, carcinomas, long latency, environmental/lifestyle, 80% preventable, screen (early detection), local at dx, not responsive to tx, few long term consequences to tx, <60% cure
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Mesodermal germ layer
- origin of most childhood cancers
- give rise to connective tissue, bone, cartilage, etc
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Etiology of cancer in children
- genetic; oncogenes, tumor suppressor genes, chromosomal
- environementa: prenatal, parental age incrased, childhood exposures.
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Gate control theory
- complexities of pain. chronic
- pain transmission to spinal cord via fibers
- inhibit interneurons=stimulate CNS=close pain gate
leads to diminished pain perception.
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Types of pain fibers
- A-delta: fast, thick myelinated
- Type C: small, unmyelinated throbbing, chronic pain
- A-Beta: large, non-nociceptice (pain receptors)
- inhibt a-delta and type c
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neurotransmitters
- pain excitatory: aspartame, glutamate
- pain inhibitory: serotonin, GABA, endorphin
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pain threshold
point at which a stimulus is perceived as pain
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perceptual dominance
pain in one location may decrease threshold in another location
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pain tolerance
- duration of time and intensity of pain that person endures
- cultural, physical/mental health
- decreased with repeated pain, fatigue, anger, bored, sleep deprived
- increased with alcohol, warmth, faith
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nociceptive pain
- normal tissue
- somatic(body)/visceral (organ)
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non nociceptive pain
- neurpathic, pain receptors
- chronic
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Chronic pain
- can be nociceptive but long term (3 months)
- decreased endorphins
- c neuron stimulated
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Neuropathic pain
- is pain caused by damage or disease that affects the somatosensory system
- chronic
- PNS: diabetes, cancer, HIV
- CNS: spinal cord, MS, tumors
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Temperature regulation
- via thermoregulators in hypothalamus
- radiation, conduction, convection, vasodialation, decreased muscle tone, evaporation, incrased respirations
infants: increased surface area, thin subQ layer
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Fever
- adjust heat production, conservation, maintain core temperature
- stimulate sweat, decreased muscle tone, flushed skin, peripheral vasodilation
- benefits: kill microorganisms, lysosomal breakdown, phagocytosis, decrease zing, iron, copper, autodestructing, lymphocytes
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hyperthermia
- 41 degrees: nerve damage
- 43 degrees: death
- heat cramps (loss sodium),
- heat exhaustion (dehydrate, dec plasma vol., hypotension=weak, N&V, dizzy),
- heat stroke (cardio and thermoreg. may cease=increased temperature=cerebral edema, degeneration of CNS, swollen dendrites)
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Malignant hypothermia
- inherited muscle disorder
- increased calcium release or decreased calcium uptake by muscles for contraction
- increased oxygen consumption and lactic acid production
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hypothermia
- 35 degrees
- decreased viscosity of blood, decreased chemical reactions
- accidental
- therapeutic: ischemia is risk
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Sleep
- multiphase process
- restorative and memory consolidation
- REM (20%) (rapid eye movement)
- and NREM (majority 70%)
peds 16-17 hs of sleep, most in REM
with age: decreased total sleep, longer to fall asleep, aware more often, decrased stage 4
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sleep disorders breathing
- upper airway resistance:
- obstructive sleep apnea: obesity: blockage
- obesity hypoventilation syndrome: obese short thick neck, impaired resp mechanism
- leptin
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parasomnias
awake from REM or arousal NREM
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somnambulism
sleep walking
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oculocephalic test
- dolls eyes
- abnormal: don't turn in conjugate
- absent: eyes don't turn as heat position changes
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arousal vs awareness
arousal: awake, alteration. assess: LOC, pupil, motor, oculomotor
awareness: cognitive functions, aware of self, environment, mood.
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oculovestibular test
- caloric ice water test
- abnormal: asymmetric eye movement
- absent: no eye movement (brain dead)
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Brain death
- brain stem death: irreversible
- cant maintain homeostasis
- criteria: unresponsive coma (motor/reflex), apnea, no cephalic reflexes, isoelectric EEG, completion of all app therapeutic procedures, signs present for 1 hr and 6 hrs after onset.
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Cerebral death
- irreversible coma
- no behavioral/environmental response
- body continues with normal respirations, cardio, temp control, GI
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Vegetative state
- wake from unconscious state
- period of eye opening
- potential response to physio stimulus
- occasional eye movement with tracking
- sleep/wake cycles
- normal respirations/GI function
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generalized seizure
- no local (focal) onset, form deep brain, neurons bilaterally
- result from cellular, biochem, structural abnormalities
- consciousness always impaired/ lost
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Partial seizure
- focal
- neurons unilaterally
- consciousness may be maintained.
may go into secondary generalized
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secondary genalized seizure
- partial seizure become generalized
- involves neurons from other hemisphere
- consciousness lost
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static epilepticus
state of continuous seizures lasting more than 5 minutes or rapidly reoccurring before person fully regain consciousness from previous
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seizure consequences on body
- increase ATP
- increased oxygen consumption
- increased cerebral blood flow
- glucose and oxygen depleted
-
agnosia
- cant recognize objects
- pattern recognition
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aphasia
- loss of total comprehension or production of language
- stroke
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dysphasia
- impaired comprehension or production of language
- expressive: cant get words out
- transcortical: cant understand
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dementia
- progressive failure of cerebral functions, not caused by LOC
- mental abilities impaired, decreased memory, language, altered behavior, orientation
alzheimers
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Alzheimer's
- form of dementia
- genetic. early and late onset (non hereditary)
- forgetfulness, emotional upset, disorientation, confused, lack of concentration
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increased intracranial pressure
5-15 mmHg is normal
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suprotentoral hernia: uncal
- most common
- uncus from hippocampal gyrus shift from middle fossa through tentorial notch-posterior fossa
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suprotentoral hernia: central
downward shift of diencephalon through tentorial notch
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suprotentoral hernia: cingulate
gyrus shift under falx cerebri
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hypotonia/hypertonia
decrease/increase muscle tone
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Huntington Disease
- chorea
- heridetary
- severe degeneration of basal ganglia and frontal cortex (GABA reduced)
- disrupt thought process
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Parkinsons Disease
- hypokenesia
- severe degeneration of basal ganglia
- rigidity, bradykinesia, termor, posture abnormal, depression, disorientation, confusion, momroy loss
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hypokinesia
- decreased movement
- akinesia
- bradykinesia
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Basilar skull fracture
- base of skull (face)
- temporal bone, occipital bone, sphenoid bone, ethmoid bone
- raccoon eyes
- battle sign (ecchymosis)
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Diffuse axonal injury (DAI) 1/3
- shaking
- rotation acceleration/deceleration
- sheer, tear and stretch of nerve fibers
- disabled
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Focal injury (2/3)
- contusions
- extra dural hematoma: in temperal fossa. artery bleeding
- subdural hematoma: skull fractures, below dura
- intracerebral hematoma: 3-10 days, increase ICP and compression leads to edema. decreaed LOC
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Mild concussion
- temporary. increase in ICP
- attention/memory deficits
- 1(confusion/disorientation), 2 (momentary confusion with retrograde amnesia) 3 (with amenia retrograde/ anterograde)
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classical concussion
- grade 4
- physio/neuro dysfunction
- LOC less than 6 hrs
- retrograde and anterograde amensia
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Cerebral vascular accidents
- thrombotic stoke: arterial occlusion by thromby (transient ischemic attacks)
- embolic stroke: fragment breaks from thrombus formed outside braine
- Hemorrhagic stoke: rupture in aneurysm
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Multiple sclerosis
- autoimmune
- progressive, inflammation, demylination
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