Patho 3 Flashcards
Sorry it's not in order on the list !!
Meningitis
- define
- infection of connective tissue covering brain
- includes CSF
Meningitis - extent of infection
- usually include entire subarachnoid space around brain and spinal cord (dt CSF circulation)
- brain itself (encephalitis)
- blood vessels (vasculitis)
- ventricular system (ventriculitis)
Etiology of meningitis
- bacterial
- viral
- fungal
- protozoa
How treat bacterial meningitis
- hospital admission with strong IV abx
How treat viral meningitis
- Usually self limiting, no real treatment
- aseptic meningitis
True or false - the different types of meningitis present differently
FALSE
- all types are similar in presentation, only way to really differentiate is via lumbar puncture
When considering meningitis, what should the presence of focal neurological signs make you think?
- NOT infectious etiology
- more likely a stroke
Delirium
- describe
- temporary condition of confusion usually associated with reversible cause
- Tx by treating underlying issue
causes of delirium
- hypoglycemia
- hypoxia
- thiamine deficiency
- hypovolemia
- hyponatremia
- chem/drug toxicty
How to treat delirium other than tx underlying issue
- Rally pack or banana bag and O2
- except for hyponatremia and chem/drug tox
Rally pack contents
1 L over 4-8 hrs:
- thiamine
- folic acid
- Multivitamin
- magnesium sulfate
Dementia
- progressive, irreversible process with periods of lucidity
- may be indolent
- interspersed with loss of cognitive ability
Two types of Dementia
- Alzheimers (most common type)
- Multi-infarct
Alzheimers
- onset
- sx
- slow onset (but can be fast and early onset too)
- behavior changes
- anxiety, depression, visual hallucinations, paranoia
- don’t sleep at night, nap during the day
what is an early sx of Alzheimers
Discalculia: lose concept of money
Two histologic characteristics found on pathologic exam of brain
- plaques
- tangles
Also
- shrunken gyre and exaggerated sulci
- What looks like enlarged ventricles but is actually just loss of cortical mass called hydrocephalus ex-vacuo
Multi-infarct dementia
- recurrent minor strokes
- seen in pts with cerebral vascular disease
- many small hemorrhages that accumulate and result in reduced function
Huntington’s Chorea
- etiology
- main sx
- autosomal dominant
- involuntary muscle movements
- facial grimaces
- personality changes
- emotional disturbances
- dementia
- occurs mid-life
Huntington’s Chorea
- genetic problem
- increased triplet nucleotide repeats in DNA
- causes protein to misfold = loss of gaba neurons
- caudate nucleus degenerates
- more and more repeats in subsequent generations so disease is expressed earlier
What is the main neurotransmitter to be lost in:
- Huntingtons
- Parkinsons
- Huntingtons: gaba
- Parkinsons: dopamine
Parkinsons
- cause
- degenerative destruction of substantia nigra = loss of dopaminergic neurons going to forebrain structures (like caudate)
Parkinsons sx
- pill rolling
- postural changes
- poor balance
- shuffling gate
- flat affect
- 20-50% develop dementia
- bradykinesia which progresses to rigidity
Cause of Parkinson’s
- elusive
- neurotoxins (MPTP) can cause immediate onset bc they selectively target the substantia nigra
What are the two demyleninating disease
- ALS
- MS (more common)
what are the two diseases that cause loss of neuron cell bodies
- Huntingon’s
- Parkinson’s
Amyotrophic lateral sclerosis (ALS)
- aka
- describe
- Lou Gehrig’s
- degenerative disease with gradual progressive motor weakness leading to respiratory failure in 3-5 years
- maintain complete awareness/consciousness but lose motor function
What degenerate in ALS
- upper motoneurons (cerebral cortical cells)
- lower motor neurons in SC and brain stem
ALS etiology
- familial
- sporadic
Multiple Sclerosis
- etiology
- when does it usually occur
- autoimmune reaction against oligodendrocytes, triggered by viral infection
- around age 30 (females more often_
Common first presenting complaint of MS
optic neuritis
What is diagnoses of MS on a CT?
plaques involving white matter (where myelin is!)
How to diagnose MS
Diagnosis of exclusion unless plaques on the CT
MS
- progression
- subtle sx like urinary incontinence
- sx progress to blindness, incontinence, ataxia, paraplegia
- episodic exacerbations and remissions
Acute idiopathic polyneuritis
- aka
- describe
- Guillain-Barre Syndrome
- ascending motor paralysis affecting both spinal and cranial nerves (get to C4 affects diaphragm = ventilator)
- post-infectious autoimmune disorder
Two common triggers for Acute idiopathic polyneuritis
- campylobacter jejuni
- vaccinations
Acute idiopathic polyneuritis
- recovery
- gradual
- w/o residual defect
- recover from top down
Acute idiopathic polyneuritis tx
- admit to hospital
- often tx with steroids to reduce inflammation
Inborn errors of metabolism
- gene prevents normal enzymatic pathway
- often related to low IQ, developmental issues
- usually die young
Two metabolic diseases
- Tay-Sachs
- Riemann-Pick disease
Tay-Sachs
- describe
- inheritance pattern
- common in what population
- deficit of ganglioside lipids important in cellular membranes, esp. in nervous tissue in brain
- autosomal recessive
- Ashkenazi jews
neoplastic disease of the CNS
- clinical manifestations
Depend on both
- local effects: irritative, compressive, destructive
- generalized effects: increased pressure, edema, hemorrhage, etc.
neoplastic disease of the CNS
- metastasis
- all are potentially malignant but extra neural metastasis is rare (usually don’t live long enough for mets to occur)
neoplastic disease of the CNS
- how does age affect risk?
- risk increases with age
BUT also - second most common group of childhood tumors
Astrocytoma
- where in brain
- when in life
- sx
- prognosis
- white matter
- 3rd and 4th decades peak risk
- seizures, ICP, motor deficits, mental changes
- slow growing, lots of time to get it out
Glioblastoma
- where in brain
- when in life
- how common
- sx
- usually frontal or temporal lobes
- 5th or 6th decade
- most common type of brain tumor in adults
- same sx as other astrocytomas but more rapid progression/deterioration
Glioblastoma
- life expectancy
- untreated 14 weeks
- treated 10-11 months
Metastatic tumors of the brain
- how common
- sx
- where in brain
- 15-30% intracranial tumors
- HA, seizure, motor deficits, mental change - all due to local expansion/edema
- usually in cortex at gray-white junction
5 most common primary sites that cause brain mets in order of most frequent
Lung Breast Melanoma Kidney GI
Muscle diseases
- how related to neuro
- caused by lesions of anterior horn, peripheral axons, neuromuscular junction
Most common type of muscle disease related to neuro
- muscular dystrophies
- Duchenne is most common
Muscular dystrophy
- describe
- genetic
- regressive alterations in muscle fibers = weakness
Duchenne type muscular dystrophy
- degeneration of muscles, have extreme weakness
- usually of trunk/pelvis
- classic description of kid who gets off teh floor with arms, not “normal” way
Duchenne type muscular dystrophy
life expectancy
- not great
- usually die in 20-30s
- commonly dt pulmonary complications
Duchenne type muscular dystrophy
- gastrocnemius
- may appear enlarged dt pseudohypertorphy (fatty infiltrate between muscle fibers)
Myasthenia gravis
- etiology
- when does it show up
- presentation
- autoimmune, antibody to Ach receptor on muscles that impairs the neuromuscular junction
- early adulthood
- abnormal muscular fatigue and weakness
Myasthenia gravis tx
- Cholinergic meds or meds that block Ach-esterase
- if don’t treat diaphragm won’t work - die
How to test for myasthenia gravis
- blink a bunch of times, lids will tire
- give tensilon, Ach burst will let them blink again
- test for antibodies
Prion
- define
- proteinaceous and infectious
- “ion” ending as analogy to virion
- small proteinaceous infectious particles that resist inactivation by procedures that modify nucleic acids
- everyone has prion proteins, they are not dangerous until they misfold
What is crazy about prions
- defy convention
- “replicate” without DNA
- not a true replication, induces a conformational change in other prions
Common way to transfer prions
eat misfolded prion from someone/something else
Name for prion diseases, why?
- spongiform encephalopathy
- prions kill neurons, produces vacuoles/holes in cortex
Prion diseases
- how dangerous
- cure
- cause
- what is protein resistant to?
- all are fatal
- no cure for any
- misfolded prion proteins accumulate in cytosol
- resistant to heat, proteases, anti-invectives, UV irradiation, etc.
Prion disease MC 3 sx
- dementia
- ataxia
- myoclonus
Prion disease other sx other than three MC
- progressive loss of motor function
- loss of speech
- hallucinations
- seizures
- visual agnosia
List 6 common prion diseases
- Scrapie in sheep
- Bovine spongiform encephalopathy (aka BSE or mad cow disease)
- Chronic wasting syndrome (white tailed deer, elk, moose)
- Feline spongiform encephalopathy
- Kuru - New Guinea women
- Creutzfeldt-Jakob disease
Iatrogenic transmission of prion disease
- human growth hormone injections in France 2009
- dura grafts
- corneal transplants
- neurosurgical instruments up to 2 years after autoclaved (now all disposable)
Creutzfeldt-Jakob disease
- etiology
- mostly sporadic, can be iatrogenic, variant, familial
Familial defect in prion gene
Fatal familial insomnia
- 35 families
- symptomatic in 40s, can’t sleep
- die from insomnia
