most prevelent way that a brain trauma occurs?

1. falls(28%)

2. MVA (20%)

physical

intellectual

emotional

social

vocational changes

aka closed trauma, non-missile

most common

head strikes surface

rapidly moving object strikes the head

dura remains intact; brain tissue not exposed to the environment

causes focal (local) or diffuse (general) brain injuries

penetrating

or diffuse

aka penetrating or missile trauma

injury breaks dura

exposes cranial contents

results in primary focal injuries

bullets

sharp projectiles

open risk of infections

are most traumatic brain injuries "severe"?

and

what is the definition of "severe"

NO---- 75-90% are not severe

"severe"  loss of consciousness for six or more hours

discuss focal brain injury

impact causes contusions, bleeding

can progress to edema, ICP

coup-object strikes front of head

injury directly belowpoint of impact

contrecoup-object strikes back of head

injury on opposite site of impact

discuss difference between coup and contrecoup injuries

coup- object strikes front of head

injury is directly below point of impact

contrecoup-object strikes back of head injury on opposite site of impact

in focal brain injury force of impact produces ?

contusion-more severe can lead to bleeding, it is a bruise

concussion-A concussion is a traumatic brain injury (TBI) that may result in a bad headache, altered levels of alertness, or unconsciousness.

located between the skull and the dura

usually due to an arterial tear

pressure on the brain causes coma causes death

symptoms may not appear immediately

may have periods of lucidity with progressive loc

medical emergency-evacuate the hematoma, or ligate the bleeder

there is more bleeding with this type of hematoma-b/c of the arterial involvement

extradural(epidural hematoma or hemmorage)

subdural

intracerebral

most common cause is an MVA

common in older adults and boxers

often (50%) associated with a skull fracture

can be chronic in the elderly

usually due to a vein rupture

blood collects in the space between the dura and the arachnoid layer

syptoms slow to develop, nonspecific, but progress as hematoma develops

acute

develops in 48 hrs-headache, drowsiness, restlessness, headache, slow cognition or confusion

often located on the top of skull

symptoms can be worse, loc, resp. pattern changes- this is due to the involvement of the RAS in the brain

chronic

develops over weeks or months

common in older adults and ETOH abuse

80% complain of chronic headache

tenderness at site of injury

intracerebral hematoma

ventricals

associated with an MVA or a fall

creates an expanding mass from the hemorrgage and hematoma

causes increase ICP

causes compression of brain tissues with resuletant edema

clincal manifestation :decrease LOC

diffuse brain injury/diffuse axonal injury

"shaken baby syndrome"

results from shaking

accelleration/deceleration

axonal damage-shearing, tearing, stretching of nerve fibers

severity corresponds to the amt of shearing force applied to the brain and brainstem

can be mild mod or severe

immediate onset with time of injury

confusion

disorientation

varying degrees of amnesia

requires close observation

post-concussive syndrome

headaches, nervousness, anxiety, irritability, forgetfullness, fatigability

discuss mild cerebral concussion

class 1-3, temporary anoxal damage

causes attention and memory deficits

no loss of consciousness

clinical manifestations: immediate onset with time of injury, transitory, confusion, disorientation, varying degrees of amnesia

grade 4 (the worst)

disconnect of cerebral and brainstem ras

physiologic and neurologic dysfunction

immediate loc (<6hrs)

retrograde and anterograde amnesia

uncomplicated (no focal injury) or complicatied (focal injury)

can happen with any concussion, occurs in 50% of individuals, manifests as

headache

cognitive imparement

psychologic complaint

somatic complaint

cranial nerve signs and symptoms

tx

reassurance and relief of sypmtoms, observation for 24hrs.

injury to vertebral and neural tissues (compression, pulling, shearing forces)

affects most mobile vertebrae (C1-2, C4-7, T1-L2)

vertebral injuries- simple fractures, compressed fractures, comminuted fracture, dislocation

lack continuous nervous discharges from the brain

clinical manifestation: complete loss of reflex function in skeletal, bladder, bowel, sexual function, autonomic control, altered thermal control, vasodilation, hypotensions, bradycardia, hypothermia

may last 7-20 days or 3 months

may develop neurogenic shock!

loss of sypathetic outflow

release of toxic excitatory amino acids, accumulation of endogenous opiates, lipid hydrolysis with production of active metabolites, and local free radical release

what is the key with spinal chord damage

within 4 hrs vs 24 hrs how much necrosis?

prompt treatment!

4 hrs-40%

24 hrs_75%

paraplegia

vs.

quadriplegia

para-paralysis lower half of the body; both legs

quadriplegia-all four extremities

syndrom that occurs after spinal shock

life threatening condition;requires immediate tx

common with lesions at T6 and above

onset associated with distended bladder or rectum

sensory receptors belwo lesions are stimulated but efferent impulses cannot pass

clinical manifestations:  sudden elevated BP(above 300)

punding headache

blurred vision

sweating, flushing

followed by bradycardia (30-40)

common in those >30, withor without pain

spondylolysis-structural defect of lamina or neural arch of vertebrae, common in lumbar area

spondylosisthesis- vertebrae slide forward

spinal stenosis- narrowing of the spinal chord, congenital or acquired, pain numbness, tingling in legs, may require surgical decompression

risk factors-repeating lifting, occupations with vibrating equipment

improper body mechanics-health care workers!

management-bedrest, analgesics, exercise, PT, massage, heat

surgery-diskectomy, spinal fusion

disk material outside of the disk space, compresses nerve root, men to women 2:1

risks:smoking, wt. bearing sports, repetitive liftiing,

clinical manifestations-pain buttocks, calf or ankle , radiates along sciatic nerve, occurs with straining, coughing, lifting, straight leg raise, symptoms subside in 6 wks. persistant pain may require surgery

thrombotic stroke

embolic stroke

hemorrhagic stroke

lacunar stroke

cerebral infarction

cerebral hemorrage

clinical manifestations  of cerebrovascular disease

contralateral weakness-face, arms, legs (hemiparesis)

sensory defects

ischemia

necrosis

discuss occlusive cerebrovascular disease

cerebral thormbosis and cerebral embolism

results in ischemia-infarction-necrosis

atherosclerotic disease(thrombis or embolism) is the leading cause

gradual onset as the vessel is occluded over time

more rapid onset resulting form ischemic infarction in the brain from an embplus dislodged from an atherosclerotic plaque-not really a thrombotic event but embolic

usually occur at bifurcations of vessels

TIA- mini strokes

stroke lasting a few minsto less than an hour

neurologic deficits resolve

usually caused by narrowing of blood vessel or spasm

any cerebral artery may be involved

cerebral aneurysm

and types

outpouching of arterial wall

several types

saccular-berry

fusiform -giant

mycotic-caused by bacteria

traumatic-dissecting

capillary telangiectasis

venous angioma

cappillary telangiectasis- dilated capillaries

venous angioma-bundle of embyolic viens feeding a central vein; rarely hemmoragic

arteries feed directly into veins and are easy to hemmorage...

see in heart defects and

an av is man made fro dialysis

what is a subarachnoid hemmorage

and risk factors

blood escapes from defective or injured vessel into the subarachnid space

risks: familial tendancy-first degree relatives

alcohol, hypertension, smoking, anticoagulants, oral contraceptions

headache

change in mental status

changes of loc

nausea and vomiting

visual/speech disturbance

also see kernig sign and brudzinki sign

sitting, raise leg elicits pain in back and neck

see with subacachnoid hemorrage

passive neck flex produces pain and rigidity

see with subarachnoid hemorrage

cluster headaches

referred to as trigeminal autonomic cephalagia

several attacks can occur diring the day for days

followed by long period of spontaneous remission

largest group-men between 20-50

cranial tumors can be what 2 types?

gliomas or secondary (metastatic)

gliomas- primary cranial tumors

astrocytoma-  poor prognosis-5yr survival

oligodendroglioma- slow growing; more favorable prognosis

ependymoma- more favorable prognosis

treatments: surgery, radiation, chemotherapy

extracerebral tumor

• arise from the meninges
• most are benign
• located in midline impinging from the outside the cerebral hemisphere
• more common in women>70
• usually grow and compress surrounding tissue
• syptoms include seizure, headache, visual impairment, hemiparesis, aphasia
• prognosis depends on site
• can be surgically removed  with an excellent prognosis

relatively rare

intramedullary tumors

extramedullary tumors(intradural or extradural)

manifestations-comressive syndrome, irritative syndrome

bacteria-originates in another area (ex. nasopharynx)

aseptic-(viral, nonpurulent, lymphoctic)-usually limited to meningitis

ex.mumps, herpes simplex, various forms of encephalitis

fungal-chronic, much less common (ex. lyme disease)

tubercular (TB) -most common and serious

acute febrile illness

usually viral origin that affects nervous system

most common forms caused by mosquito born or herpes simplex virus

causes widespread nerve cell degeneration

cerebral abscess

bacterial infection- tick (Borrelia burgdorferi)

initial tick bite then incubates 3-32 days

migrates to skin, lymph nodes, and other body systems

clinical manifestations

stage 1- bulls eye rash

stage 2- cardiac and neurological

stage 3 neurological problems;arthritis, encephalitis, neuropathy

several classes

affects muscle strength, muscle tone and muscle bulk

reflexes may be altered

associated with other disease states-for example diabetes

focal or multifocal neuropathies

radiculitis

inflamation of the spinal nerve roots

causes radicular pain in distribution of nerve

(nerve groups out of IVF)

corticosteroids

immunosuppressive agents

interferon

up and out

aquired inflammatory disease causing demyelination of the peripheral nerves with relative sparing of axons

triggered by preceeding bacterial or iral infection

acute onset, ascending motor paralysis

respiratory muscle weakness-need for ventilatory support

amyotrophic lateral sclerosis (ALS)

Lou Gehrig's disease

affects upper and lower motor neurons of cerebral cortex, brainstem, and spinal chord

progressive weakness which leads to paralysis, resp. failure and death

person has normal intellectual and sensory funtion until death

chronic autoimmune disease

affects neuromuscular junction

antibodies produced against self; block binding of acetylcholine

clincal manifestations:  weakness, fatigue of eye and throat muscles, diplopia, difficulty swallowing, chewing and talking

myathenia crisis

compare with

cholinergic crisis

myasthenia crisis-severe muscle weakness, resp. insufficiency, potential resp. arrest

cholinergic crisis- occurs 30-60 min. after anticholinergic drug o.d., similar to myasthenia crisis 

term coined by eugene bleuler-1911

describes a collection if illnesses characterized by thought disorder

affects 1% pf population

emerges in young adults

slightly earlier onset in males than female

psychotic episode

genetic predisposition

mono-twins-30 to50

dizygotic- 15%

enlargement of lateral and 3rd ventricles; widening frontal cortical fissures and sulci

neurotransmitter alterations:  alters dopamine pathways

clinical manifestations of

schizophrenia

hallucinations

delusions

disorganized behavior

(speech and behavior)

neg. symptom-affective flattening

hallucinations- sensory experiences that aren't there, isolated, auditory sounds

delusions are more patterns of long activity that reoccur over time.  conversation with non-existing things, religion

20-30% of persons with unipolar depression have an altered HPT system

increased CSF levels of Thyrotropin-releasing hormone (TRH)

Blunted Thyroptropin stimulating hormone (TSH) response to TRH challenge

decreased normal rise in TSH

meds-antidepressants

psychotherapy

combination of both

3 major classes of antidepressants

and how they work?

monoamine oxidase inhibitors (MAOis)

Tricyclic antidepressants (TCA's),

Selective seratonin reuptake inhibitors (SSRI's)

all increase monoamine neurotransmitter levels within the synapse

excessive and persistant worries

norepinephrine and seratonin abnormalities

GABA-BZ receptor alterations

exposure to terrifying, life-threatening trauma, prevalence (lifetime) 7-8%

adults: smaller hippocampus, brain structure susceptible to damaging effects of the stress hormone corisol and excitatitory amino acids

peds:  studies reveal generalized effect of trauma on reducing total brain volume

obsessive-compulsive disorder

OCD

repetative intrusive thoughts and or compulsions

obsessions: involve a preoccupation woth contamination, doubting, religious, sexual themes or beliefs that a negative outcome will occur if a specific act is not performed. 

compulsions: physical and mental ritualized acts

circulate bound to a carrier

easily diffuse across the plasma membrane

-bind to cytoplasmic or nuclear receptors

Activate

RNA polymerase

DNA transcription and translation

ex: steroid hormones

Androgens, estrogens, progestins, glucocorticoids, mineralocorticoids, thyroid

high molecular wt.

circulate free and unbound form

cannot diffuse across the plasma membrane-need carrier

first messenger

signal transduction

second messenger molecules

Calcium

Cyclic amp

Cyclic GMP

to respond to an alteration in cellular environment

and to maintain regulated level of certain substances or other hormones

regulated by chemical, hormonal, or neural factors.  the secretion is based on specific rates and rhythms

diurinal, pulsatile, cyclic: all have patterns  depending on circulating substance

up- low concentrations of hormone increase the number of receptors per cell

down-high concentrations of hormone decrease the number of receptors per cell.

this is over time.......

2 structural parts of the pituitary gland

anterior pituitary-Adenohypophysis

posterior pituitary- neurohypopysis(neuro tract)

name all of the Anterior Pituitary Hormones

and these hormones generally do what

Adrenocorticotropic Hormone

Melanocyte-stimulating Hormone

Growth Hormone

Prolactin

Thyroid-stimulating Hormone

Luteinizing hormone

Follicle-stimulating hormone

(B-lipotropin

B-endorphins)

regulate body functions and regulate the secretions of other endocrine glands

hypopituitarism can result in?

anc causes are are?

result in hemmorrhage, shock

causes:  head trauma, infections, and tumors

absence of all hormones

ACTH, TSH, FSH, LH, GH

commonly associated with pituitary adenoma, which is a benign, slow growing tumor

clinically manifests as hyper or hypo hormone secretion

with tumor growth: headache, fatigue, visual changes

with hyposecretion: impairment of anterior pituitary hormones

hyper-acromegaly-giant state

hypo-dwarfism

relatively uncommon

hypersecretion of GH during adulthood

slow progression

often associated with heart disease due to hypertension and diabetes, malignancies are common

clinically: related to proliferationof connective tissues,

enlarged tongue

interstitial edema

enlarged sebaceous glandsand sweat glands

coarse skin and body hair,

bony proliferations, lg. joint arthropathy, kyphosis, enlarged facial bones, protrusion of lower jaw, enlarged hands and feet, wear large shoes, hats, gloves, rings (extra big!)

most common pituitary tumor

pituitary tumor that secretes prolactin

thus it suppresses GnRH)

females:amenorrhea, galactorrhea(milk production), hirsutism-(excessive hair), osteohenia

males-hypogonadism, erectile dysfunction, impaired libedo, diminished ejaculate volume.

discuss ADH.

synthesized by ?

Controls?

target organ?

main action?

adh-keeps water, less concentrated, decreases osmolality

regulates BP

synthesized by hypothalmic neurons

released by the post. pituitary

target-kidneys

action-acts on vasopressin2 receptors of the renal tubular cells controlling plasma osmolality-inc water absorbtion

contracts the uterus

ejects milk in lactating women

secreted by  the hypothalmic neurons

released by the post. pituitary

syndrome of inappropriate antidiuretic hormone-  High levels of ADH without normal stimuli for its release

often associated w CA

can occur with brain injury, trauma

common after surgery, persists fro 5-7 days post-op

may be associated with psychiatric disease and drugs

these pts have normal adrenal and thyroid function

everything normal, but ADH, secretes when shouldn't H2O intoxication

clinical problems that manifest from SIADH

water intoxication

results from enhanced renal water retension

results form increase in total body water

can lead to hyponatremia and hypo-osmolality

toooooomuch water!!!

partial to total inability to concentrate urine

insufficient ADH causes immediate excretion of lg. volumes of dilute urine-will look light, like lemonade

thirst, polydipsia

this is related to ADH

affects growth and maturation of tissues, cell metabulation, heat production, and oxygen consumption

hypo-low energy

hyper-high energy

primary are related to

dysfunction or disease or thyroid gland

thyroid hormone production

hyper or hypothyroidism

thyrotoxic crisis-rare

secondary-alteration of pituitary TSH production

• hyperthyroidism
• most common cause of thyrotoxicosis
• result form stimulation of thyroid with antibodies against TSH receptors
• results in diffuse thyroid enlargement (goiter)
• more common in women

hypothyroidism

reasons

1.congenital defects

2.defective hormone synthesis

• autoimmune thyroiditis(hashimoto disease)
• endemic iodine deficiency

3. iatrogenic

• loss of thyroid tissue after surgical procedure
• radioactive procedure

clinical manifestations of hypothyroidism

myxedema

dermis altered

seperation of connective tissue fibers

binds water causing non-pitting boggy

edema of eyes, hands, feet

discuss parathyroid glands

behind upper and lower poles of thyroid gland

produce PTH

regulate serrum calcium

antagonist of calcitonin

(affects magnesium and phosphate levels as well)

difference

primary hyperparathyroidism

secondary hyperparathyroidism

primary-  excess secretion of PTH form one or more parathyroid gland

85% caused by parathyroid adenomas

more common in females

secondary- increase in PTH secondary to chronic hypocalcemia as a result of renal failure or dietary deficiency of vit. D and inability to achieve normal calcium levels

hypercalcemia

kidney stones

hypophoshatemia

hyperchloremia

increased urinary calcium

hypoparathyroidism

clinical manifestations

abnormally low PTH

therefore-

depressed serum calcium levels-hypocalcemia

lowers threshold of nerve and muscle excitation

muscle spasms hyperreflexia, tonic-clonic convulsions, laryngeal spasms, death from asphyxiation

increased serum phosphate levels-hyperphoshpatemia

***usually caused by parathyroid damage in thyroid surgery

answer: 

hyperparathyroidism is associated with

1.  Pathologic fractures

2. increased osteoblast activity

3.  hyperphosphatemia

4.  acidic urine

functions as an endocrine gland

produces hormones-glucagon, insulin

functions as an exocrine gland-produces digestive enzymes

islets of langerhans

secrete glucagon and insulin

alpha cells-glucagon

beta cells-insulin

delta cells-somatostatin and gastrin

F cells- pancreatic polypeptide

insulin antagonist

secreted with decreased blood glucose levels

stimulates glycogenolysis, gluconeogenesis, and lipolysis

acts on the liver

alpha cells

produced by delta cells of pancreas

little known hormone

in animal studies-regulates alpha and beta cells

may prevent excess secretion of insulin

delta cell

likely to control secretion of glucagon

stimulates GH secretion

controls appetite

regulates insulin sensitivity

• regulated by chemical, hormonal, and neural mechanisms.
• synthesized from proinsulin
• secreted in response to increased blood glucose levels
• facilitates the uptake of glucose into the cells and intracellular export of potassium(beta cells)
• sensitivity of insulin receptor is key component in maintaining normal cellular function(insulin resistance)
• anabolic hormone-synthesis of protein, lipids, and nucleic acids

Type 1 diabetes

clinical manifestations

hyperglycemia

autoimmune destruction of beta cells

strongest gene marker in HLA region chromosome 6

Polyuria-frequent urinating

Polydipsia-frequent thirst

Polyphagia- frequent eating

Wt. loss

affects adults and children

gene-environment interaction

treatment-exercise, wt. loss, medication

clinical manifestations: recurrent medications

vision problems

neuropathy

see microvascular problems

answer with the correct choice

insulin

1.  promotes catabolism if proteins

2.  is particularly required by the brain for glucose uptake

3.  facilitates uptake of glucose by cells

4.  release is stimulated by decreased concentration of glucose

answer 3. facilitates uptake of glucose by cells

aka insulin shock or insulin reaction

symptoms related to decreased blood glucose (40-60)

pallor, tremor, anxiety, tachycardia

palpitations, diaphoresis, headaches

treatment-glucose sources

acute complications of type 1 diabetes

deficiency of insulin

increase in catecholamines, cortisol, glucagon, GH,

fat is mobilized

usually associated with type 1

Illness, trauma, surgery, emotions

total body (not serum) potassium deficiency

cerebral edema, especially in children

hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)

relatively uncommon

usually associated with Type 2 diabetes

poor glucose control

results in excessively high glucose levels (more than 500)

severe dehydration

low blood volume, low perfusion

early morning rise in blood glucose concentration

no hypoglycemia during night

related to nocturnal levels of GH

have problems onlyduring the day

most common cause of neuropathy

result from metabolic and vascular factors related to hyperglycemia

most often see with end stage renal disease

injury to glomeruli by protein denaturation

microalbuminuria is first manifestation (see this in the urine)

related to retinal ishemia

blurred vision

decreased vision form macular edema

on top of kidneys, if you take kidneys they go too.

cortex-lg.est part

zona glomerulosa

zona fasciculata

zona reticuaris

medully-innervated by the sympathetic and parasympathetic  nervous system

ACTH

glucocorticoids

• effects carb. metabolism
• has anti-inflammatory, growth suppressing effect
• influences awareness and sleep  habits
• cortisol-most potent naturally occuring

answer question:

glucocorticoids act to:

1.  reduce syrum glucose concentration

2  increase immune response to microorganisms

3.  reduce appetite

4.  stimulate protein catabolism

answer 4.  sptimulate protein catabolism

(it decreases the immune response, not increases it)

directly affect ion export causing Na retention and K, H loss

aldosterone-regulated by the renning-angiotensis-aldosterone system

cortisal release-excessive levels in body

Excessive ant. pituitary secretion of ACTH

more common in adults

more common in women

Wt. gain

Truncal obesity

Moon Face

Buffalo Hump

conn disease

clinical manifestation:

hypertension

renal K wasting

hypokalemia

neuromuscular mainifestations.

feminization-hypersecretion of adrenal estrogens

development of female sex characteristics(this happens to boys)

virilization-hypersecretion of adrenal androgens, development of male sex characteristics

"primary adrenal insufficiency"

adrenocortical hypofunction

autoimmune (organ) specific

hypocortisolism! 

chromaffin cells=  pheochomocytes

secrete catacholamines

mostly epinephrine

some norepinepherine

catacholamines-involved in fight or flight response and promote hyperglycemia

adrenal medulla hyperfunction

tumors derived from the chromaffin cells

secrete catacholamines continuously

answer:

hormone release is regulated by:

1.  hormone excretion rate

2.  the concentration of hormone receptors

3.  emergency demands

4.  chemical factors

answer:

sensitivity of a target cell is down regulated when

1. level of hormone that binds with the receptor is high

2.  number of receptors for the hormone is high

3.  direct effects of the hormone are detected

4.  permissive effects of the hormone are detected

answer:

antidiuretic hormone

1. released by the anterior pituitary

2. released in response to decreased Na.

3.  regulated by the osmoreceptors in the hypothalamus

4. regulated by the chromophils of the anterior pituitary

answer3.  post. pituitary

answer

Calcitonin

1. increases serum Ca concentration

2.  activates osteoclasts

3.  suppresses osteoblasts.

4.  reduces serum calcium concentrations

answer :

aperson is admitted to the ICU with lung CA and syndrome of inappropriate ADH.  the nurse expects the person to have;

1. dilute urine

2. a hyper-osmolor state

3. hypernatremia

4.  reduced extracellular volume

answer 2

answer Graves disease is caused by

1.  Increased secretion of TSH

2.  Reduced production of TH

3.  Autoimmune response

4.  Reduced secretion of TSH

answer:

in a person with diabetes, exercise

1. increases serum glucose concentrations

2.  increases the insulin need

3.  lowers triglyceride levels

4.  reduces HDL cholesterol

answer

a diabetic arrives at the ER after an abrupt decrease in loc.  he is tachycardic, diaphoretic, irritable, with tremors and confusion.  the nurse suspects

1.  inadequate insulin levels

2. hyperglycemia

3. hypoglycemia

4.  diabetic ketoacidosis

answer: diabetes is associated with micro and macrovasular complications that include

1.  Coronary Artery Disease

2.  Graves disease

3.  hyperpigmentation of the skin

4.  venous atherosclerosis

answer

elevated cortisol levels

1. increase corticotropin releasing hormone

2.  increase ACTH

e.  reduce serum glucose

4.  reduce corticotropin releasing hormone