Patho Review Test 4

88 flashcardsby Madiruth2
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1
How does cancer spread?
spreads by multiple mutations
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What is cancer spread dependent on?
spread is dependent on how fast it mutates
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Histologic
microscopic aspect of cancer
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Anaplasia
loss of cellular differentiation
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Pleomorphic
variability in size, shape, and replication
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Metastasis
ability to spread far beyond the tissue
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Metaplastic
one cell turns into a nother cell type
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Microscopic analysis of cancer
Stage 1: no metastasis
Stage 2: local invasion
Stage 3: regional structures
Stage 4: distant metastasis
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World Health Org's TNM
T: tumor
N: nodule
M: metastasize
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Dysplasia
tissue appears disorderly but is not cancer
abnormal changes in size, shape, and organization of mature cells
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IN SITU
it has not moved from original place
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Metastatic Process
1st step = invasion (local spread)
2nd step = spread to distant places causes cancer to metastasize
3rd step = metastasis leads to epithelial-mesenchymal transition
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What are tumor markers?
biochemical markers are produced by cancer cells:
hormones
enzymes
genes
antigens
antibodies
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What is the purpose tumor markers?
to find individuals at high risk for cancer
diagnosis specific types of tumors and observe clinical course of cancer
PROBLEM: false positives and false negatives
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Benign Tumors
named by tissue arises from
encapsulated
grows slowly
not invasive
low mitotic index
well differentiation
do not metastasize
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Malignant Tumors
named by cell arises from
not encapsulated
rapidly grows
invasive
high mitotic index
poorly differentiated
metastasized
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Lipoma
fat cells
benign
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Leiomyoma
smooth muscle of uterus
benign
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Meningioma
meninges
benign
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Carcinoma
epithelial tissue
malignant
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Adenocarcinoma
ductal and glandular tissue
malignant
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Sarcoma
mesenchymal tissue
malignant
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Lymphoma
lymphatic tissue
malignant
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Leukemia
blood-forming cells
malignant
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Chief Clinical Sign of Cancer
fatigue
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Biggest risk factor associated with Cancer
tobacco use
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Glioma
primary brain (intracerebral) tumor
malignant
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Rhabdomyosarcoma
tumor of striated muscle
malignant
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Parkinson's
degenerative disorder of basal ganglia function
progressive destruction of nigrostriatal pathway
reduction striatal concentration of dopamine
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What is the first visible sign of Parkinson's Disease?
tremor
rhythmic, alternating flexion and contraction of movements, pill rolling
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Rigidity of Parkinson's
resistance to movement throughout full ROM
most evident during passive joint movement
- jerky, cog wheel
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Key Manifestations of Parkinson's Disease
uncontrolled sweating (ANS involvement) salvation
shuffling gait; short steps; stooped posture
dementia occurs 20%
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Hemiparesis
weakness on one side of the body
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Hemiplegia
paralysis on one side of the body
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Diplegia
paralysis of both upper OR lower extremities
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Paraplegia
paralysis of lower extremities
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Quadriplegia
paralysis of all four extremities
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THE Major clinical sign of hydrocephalus
headaches
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Clinical signs of Hydrocephalus
unsteady, broad-based gait
history of falls
apathy, inattentiveness, indifference to self family and environment
infancy (large head)
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What is hydrocephalus?
excessive fluid in the cranial vault, subarachnoid space, or both
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Stage 1 Alzheimer's
2-4 years
Memory loss
subtle personality changes
disorientation of time and place
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Stage 2 Alzheimer's
confusion stage; lasts several years
impaired cognition, restlessness, agitation
wandering; sundowners
repetitive behavior
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Stage 3 Alzheimer's
terminal stage; lasts 1-2 years
emaciation
inability to communicate
bowel and bladder incontinence
seizures
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Prefocal/Aura Seizures
partial seizure preceding onset of generalization seizure
gustatory (taste), visual or auditory
dizziness, numbness, "funny feeling"
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Prodroma Seizures
early clinical signs and symptoms
malaise (mix of tired and fatigue), headache
sense of depression hours or days before onset or seizure
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Postictal Seizures
time period immediately following the cessation of seizures
feel very drained or tired
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Tonic
state of muscle contraction with excessive tone (prolonged)
stays contracting
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Clonic
state of alternating contraction with relaxation of muscles (usually rapid)
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Locked-in Syndrome
condition in which a patient is aware and awake but cannot move or communicate verbally
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Fully Conscious
15 on glasgow scale
state of awareness and oneself in the environment
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Partially Conscious
not fully aware
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Confusion
loss of ability to think rapidly and clearly
impaired judgement and decision making
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Disorientation
beginning loss of consciousness
disorientation to time followed by disorientation to place and impaired memory
lost last is recognition of self
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Lethargy
limited spontaneous movement or speech
easy arousal with normal speech or touch
may or may not be oriented to time, place, or person
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Obtundation
mild to moderate reduction in arousal (awakeness) with limited response to the environment
falls asleep unless stimulated verbally or tactilely
answers questions with minimum response
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Stupor
a condition of deep sleep or unresponsiveness from which the person may be aroused or caused to open eyes only by vigorous and repeated stimulation
response is often withdrawal or grabbing at stimulus
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Coma
no verbal response to the external environment or to any stimuli, noxious stimuli such as deep pain or suctioning do not yield motor movement
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Types of Coma
light = purposeful movement on stimulation
coma = nonpurposeful movement only on stimulation
deep = unresponsiveness or no response to any stimulus
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Brain Herniation
herniation address how brain matter shifts based on initial cause
several types
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Severe head trauma with high blood pressure?
autoregulation?????
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Autoregulation
body's attempt to go back to homeostasis
compensates by altering intracranial blood vessels' diameter to maintain blood flow during changes in cerebral perfusion pressure
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How do we determine brain death?
get EEG done and if there's any wriggles for 6-12 hours = brain death
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Glasgow Coma Sacle
3/15 = brain death
15/15 = normal/fully conscious
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Deletions
broken chromosomes, one chromosome is there and one is missing
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Duplications
two of something
less serious than deletions
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Inversions
piece of genetic material gets flipped around
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Translocations
should be on one side but flipped around otherside
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Fragile X Syndrome
chromatin fails to condense during mitosis
males>females
2nd most common cause of MR
69
Clinical Manifestations of Fragile X Syndrome
MR
long face, large mandible, and large everted ears
hyperextensible joints, high-arched palate
mitral valve prolapse
macroorchidism
70
Klinefelter Syndrome
47, XXY (extra chromosome)
Karyotype
small testes = underdeveloped
excessive breast tissue
limbs are very long
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Turners Syndrome
monosomy 45, X (one X is missing)
underdeveloped sex
thick neck = webbed neck
wide set nipples
thickened legs
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Downs Syndrome
trisomy 21 (95%)
risk increases with maternal age
AT RISK FOR Alzheimer's Disease
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Euploidy
normal number of chromosomes = 46
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Polyploidy
more than diploid number = over 46
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Triploidy
zygote had 3 copies of chromosome instead of 2
incompatible with postnatal survival
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Tetraploidy
euploid cells have 92 chromosomes
incompatible with postnatal survival
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Aneuploid
does not contain 23 chromosomes
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Trisomy
three copies of one chromosome
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Monosomy
one copy of a chromosome
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Increased Intracranial Pressure (IICP)
best measure of level of consciousness
pressure in the brain builds
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Decorticate Posturing
arms drawn to core
very rigid
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Decerebrate Posturing
everything is straight and stretched out
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Hypotonia
decreased muscle tone
passive muscle movement there is little or no resistance
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Apraxia
disorder of learned skilled movements with difficulty planning and executing coordinated motor movements
interchangeable with dyspraxia
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Tardive dyskinesia
involuntary movement of the face, lips, tongue, trunk, and extremities
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Fasciculations
muscle ripping or quivering under the skin
happens with paralysis
87
Dystonia
sustained involuntary muscle contraction with twisting movement
88
Agnosia
defect of pattern recognition
failure to recognize the form and nature of objects
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