Patho Exam 4

Cheyne Stokes Respiration

alternating Periods of hyperventilation followed by apnea

Central neurogenic hyperventilation

sustained hyperventilation caused by a lesion in the central pons

Ataxic Respirations

irregular respirations with prolonged periods of apnea associated with damage to the medulla

Ischemia/hypoxia

Results in dilated, fixed pupils

Hypothermia

Results in fixed pupils

Sedatives

Causes pupils that are midposition, moderately dilated, unequal, fixed to light, and coma

central neural mechanism

vomiting without nauseau indicates involvement of what mechanism

Brain death

inability of body to maintain homeostasis

Cerebral death

irreversible coma, no environmental or behavioral responses, but normal respiratory and CV functions, temp control, and metabolism occur

Dementia

Progressive failure of cerebral functions caused by neuron degeneration, atherosclerosis of cerebral vasculature, and genetic predispositions

impairment of intellectual function, memory, language, and alterations in behavior

Dementia manifestations

Alzheimers

Degeneration of basal forebrain cholinergic neurons (loss of acetylcholine) that manifests as mild short term memory deficits and culminates in a total loss of cognition and executive function

age, family history

Alzheimers risk factors

Stage 1 ICP

vasoconstriction and external compression

Stage 2 ICP

continued expansion of intracranial content

Stage 3 ICP

brain hypoxia and hypercapnia; auto regulation lost

Stage 4 ICP

brain herniates, several herniation syndromes

confusion, restlessness, drowsiness; slight pupil and breathing changes

clinical manifestations of ICP (5)

vasogenic cerebral edema

Influx of fluid into the interstitial space

Cytotoxic cerebral edema

Influx of fluid inside the brain cells

Interstitial cerebral edema

volume of fluid increases around the ventricles

Hydrocephalus

excess fluid accumulates within the cerebral ventricles, subarachnoid space, or both; caused by decreased reabsorption of CSF, increased fluid production, or obstruction in the ventricular system

Paresis

weakness, partial paralysis

Diplegia

paralysis of both upper or lower extremities

paraparesis or paraplegia

paralysis or paresis of lower extremities only

quadriparesis or quadriplegia

paresis or paralysis of all 4 extremities

flaccid paresis of paralysis

hyporeflexia or areflexia

spasticity

hypertonia with hyper excitability of stretch reflexes

dystonia

hypertonia with increased involuntary muscle contraction

Rigidity

hypertonia with firm and tense muscles

akinesia

absence of voluntary movement

chorea

wandering, tremors at rest, postural tremors

paroxysmal dyskinesias

abnormal involuntary movements that occur as spasms

tardive dyskinesia

rapid, repetitive, stereotypic movement with slow onset, often from antipsychotic agents

Parkinsons disease

severe degeneration of basal ganglia with loss of DA producing neurons

Rigidity, bradykinesia, resting tremor, postural abnormalities, dementia

symptoms of parkinsons (5)

Huntingtons Disease

Genetic disorder caused by short arm on chromosome 4; characterized by severe degeneration of striatum and basal ganglia resulting in depletion of GABA

abnormal movements, emotional lability, dementia

symptoms of huntingtons (3)

nystagmus, diplopia, blurred vision, dysarthria, dysphagia, urinary retention with spastic bladder, constipation, weakness/paralysis, muscle spasticity, ataxia, vertigo

Symptoms of MS: 3 vision, 2 related to mouth, 3 related to GI/GU, 3 related to movement, +1

Guillain Barre

rapidly ascending progressive limb weakness and loss of tendon reflexes- produces symmetric flaccid paralysis, paresthesia, numbness

Myasthenia Gravis

IgG produced against acetylcholine Rs on post synaptic membrane- results in exertional fatigue and weakness that improves with rest; may cause diplopia, difficulty talking/swallowing/chewing, respiratory distress

Focal TBI

affects one area of brain

Coup injury

injury at site of impact (focal)

contrecoup injury

injury from brain rebounding and hitting opposite side of skull (focal)

Diffuse injury

affects more than one area of brain

decorticate posturing

results from lesions of cerebral hemisphere

decerebrate posturing

results from lesions to midbrain and upper brain stem

closed (blunt) trauma

dura remains intact, brain tissues are not exposed to environment

open (penetrating) trauma

injury breaks the dura and exposes cranial contents to environment

diffuse brain injury

rotational and twisting movements or acceleration-deceleration forces leading to damage to widespread areas of brain

Concussion

diffuse head injury caused from mechanical force to brain- typically acceleration/deceleration

loss of consciousness, headache, N/V, irritability, insomnia, trouble with concentration and memory

concussion symptoms (8 but 2 are combined)

Glasgow coma scale

measures eye response, motor response, verbal response

Severe brain injury

loss of consciousness for 6 or more hours

Degenerative disk disease

dehydration of disc, diminished blood supply, altered disc structure and function

Spondylolysis

degenerative process of vertebral column and associated soft tissue- hereditary aspects

Spondylolisthesis

vertebra slides forward in relation to vertebra below

Seizure

sudden transient disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons

Convulsion

tonic-clonic movements associated with some seizures

Focal (partial) seizures

abnormal discharge from specific area of one hemisphere- localized symptoms

generalized seizures

abnormal discharge from both cerebral hemispheres- bilateral symmetrical symptoms with various seizure types

Prodromal

early clinical symptoms of seizures (malaise, depression- may occur hours or days before)

tonic

excessive muscle contraction

clonic

alternating muscle contraction with excessive muscle tone

Ischemic Stroke

sudden onset of one sided symptoms, weakness of face and arm (occasionally legs), numbness, vision changes, dysphagia and dysphasia, ataxia, and data processing deficits

Hemorrhagic stroke

results in focal neurologic deficits, altered consciousness, headache

Vascular malformation

arteriovenous malformation where arteries feed directly into veins through vascular tangle

Meningitis

Inflammation of brain or spinal cord

Encephalitis

acute febrile illness, usually of viral origin with NS involvement

anaplasia

poor differentiation of cells

Carcinoma in Situ

abnormal cells that are non-malignant but can become malignant (or not)- may also spontaneously regress and disappear

Initiation

exposure to carcinogen- initial mutation occurs

Promotion

unregulated and accelerated growth of cancerous cells

Progression

cancer cells acquire malignant phenotypic properties

Contact inhibition

anti growth messages sent out to stop cell growth when two cells come in contact- process of normal cells that cancerous cells dont obey

Anchorage dependence

normal cells will die if they break free from their site of origin

Telomeres

what are lengthened by cancer cells to activate continued division

angiogenesis

growth of new vessels to feed tumor; angiogenic factors secreted by tumor are VEGF

Proteases

enzymes that digest ec matrix and basement membranes to create pathways through which cells can move

Paraneoplastic syndromes

caused by inappropriate release of hormones by cancer cells

T1

lesion <2cm in size

T2

lesion 2-5cm

T3

skin and/or chest wall involved by invasion

N1

mobile nodes involved

N2

fixed nodes involved

M1

demonstrable metastases

M2

suspected metastasis