Patho Quiz 2 Flashcards
Loss of distrophin protein leads to muscle tissue degeneration; genetic disease with adolescent onset
Muscular dystrophy
Autoimmune destruction of ACh receptors; muscle weakness worsens through the day
myasthnia gravis
inflammatory mononeuropathy causing loss of fine motor and pincer grip in hand
carpal tunnel syndrome
inflammatory demylination causing progressive muscle weakness, often preceded by an illness
Guillian Barre
slow degenerative disease of substantia nigra causes a decrease in dopamine activity and unopposed ACh activity; impairment of extrapyrimidal tracts inhibits ability to coordinate and control movement
Parkinson’s disease
Symptoms of Parkinson’s disease
*first can be loss of sense of smell, can precede rest by years
Resting tremors, pill-rolling
Muscle rigidity and bradykinesia, dec arm swing
Poor balance, shiffling gait, stooped posture
Loss of facial expression, soft voice
chronic, progressive, exacerbating/remitting demylination of CNS tracts leading to many symptoms including weakness, pain, and cognitive impairment
Multiple sclerosis
preganglionic fibers travel to ganglia close to organs before synapsing with shorter postganglionic neurons
Parasympathetic NS
cell bodies in craniosacral areas of SC
PNS
preganglionic axons synapse shortly after leaving SC in sympathetic ganglia; long postganglionic fibers branch so multiple organs can respond at once; exception is innervation of adrenal medulla, which bypasses ganglia for immediate effect
sympathetic NS
SNS meds cause more side effects because
their action is more systemic; PNS action is more specific to target organ
released by adrenal medulla and postganglionic sympathetic fibers
norepinephrine
NT synthesized in substantia nigra and ventral tegmental areas of brain; precursor or NE;
dopamine
all purpose NT released by SNS preganglionic fibers, PNS pre and post fibers, and motor neurons
acetylcholine
alpha 1 SNS reception effects
*Vasoconstriction*
peripheral arterial constriction
decreased GI and urinary motility
release of Renin from kidneys
pupil dilation
arrector pili
alpha 2 SNS receptor effects
*The Regulator*
slows CNS during times of stress to promote clear thinking
PNS muscarinic M2 and M3 receptor effects
M2: decreases heart rate at the SA and AV node
M3: acts on smooth muscle in organs
increased GI motility
increased urinary motility promoting bladder constriction and sphincter relaxation
SNS Beta 1 receptor effects
Acts on HEART
to increase rate, conduction velocity, contractility, and automaticity
(also works on glands to dec saliva and inc sweat)
Beta 2 SNS receptor effects
Acts on LUNGS
*Bronchodilation*
dilates arteries in skeletal muscle
decreased GI motility (relaxes muscles in bladder and GI)
Beta 3 SNS receptor effects
Acts on adipose tissue
to mobilize for gluconeogenesis
vagus nerve effects
decreased heart rate
bronchoconstriction
stimulates peristalsis and acid secretion
stimulates bile release
simple vs. complex seizure
Simple: consciousness is not impaired
Complex: consciousness is impaired
automatism (repetitive movements like smacking lips) occurs in
complex partial seizures
partial vs. generalized seizure
partial: restricted to one hemisphere
generalized: both hemispheres
incidence of stroke greatly increases after
75 year of age
excitatory CNS NT
glutamate
inhibitory CNS NT
GABA
seizures are a dysfunction of
ion channels. paroxysmal discharges from groups of neurons
in epileptics, this is low
seizure threshold; neurons are hyperexcitable
There’s 2-4 hours to save this salvagable tissue around the core of infarction in a stroke
penumbra
severe unilateral headache with nausea and vomiting
brain tumor
fever, HA, AMS, neck stiffness, n/v, photophobia
CNS infection
severe HA with or without photophobia, younger age
migraine
confusion with or without loss of consciousness, incontinence, tongue biting, tonic-clonic movements
seizure
sudden onset severe HA with photophobia
subarachnoid hemorrhage
generalized dizziness, and diaphoresis with or without hearing loss
vertigo
hyperreflexia and spasticity occur in
upper motor neuron lesions
hyporeflexia, fasciculations, and atrophy occur in
lower motor neuron lesios (peripheral NS)
motor neuron degeneration with muscle weakness and hyperreflexia, no sensory loss; loss of speech, swallow, respiration, death in 2-5 years
Amyotrophic lateral sclerosis (ALS)
spinal nerve root disease signified by radiating pain that can “shoot” down extremities
radiculopathy; can be caused by disk herniation, trauma, or degenerative changes (OA)
Gram positive characteristics
thick peptidoglycan layer in cell wall
only one membrane (inner; outer and inner in Gm-)
techoic acid in CW (induces inflamm response)
Gram negative characteristics
thin PG layer
two membranes (outer and inner)
larger periplasmic space (houses beta lactamases)
can live with or without oxygen
facultative anaerobes
bind to MHC II and T cells to overpromote immune reponse; induces AI activity (Kawasaki’s disease, toxic shock, rheumatic fever)
superantigens
Probable causative organism:
impetigo
Staph aureus
Probable causative organism:
AOM
viral
Strep, moraxella, Hib
Probable causative organism: cellulitis
Staph aureus
Probable causative organism: periorbital cellulitis
Strep pneumoniae
Staph aureus
*medical emergency, infection can travel up optic nerve to brain
Probable causative organism: pharyngitis
viral-adenovirus
strep pyogenes (group A)
EBV, coxackie, herpes
Probable causative organism: UTI/pyelo
E. coli
Klebsiella
Proteus
Probable causative organism:
bronchitis
usually viral (RSV, adenovirus, coxackie, Flu, rhinovirus)
Probable causative organism: CAP, 6 mos-5yrs
RSV, parainfluenza
Probable causative organism:
CAP, school age kids
mycoplasma, Flu A
Probable causative organism: CAP, young adult
mycoplasma
Probable causative organism:
CAP, older adult
Hib, Strep pneumo
thick consolidation on CXR means it’s probably
bacterial
patchy, diffuse consolidation on CXR means it’s probably
viral
Acetylcholine action in CNS
Neuromodulator, not exactly excitatory or inhibitory
helps encode new memories
promotes neuroplasicity
triages responses: is immediate action needed?
(low ACh –> dementia)
these drugs are GABA mimetics
benzodiazepines
high levels of this NT in CNS can lead to toxicity, cell death, seizures
glutamic acid
pain neurotransmitter of the dorsal (sensory) horn of the SC; involved in emotional response to pain
released during inflammation and nerve damage
substance p
neuropeptides that act on opioid receptors to reduce the perception of pain
endorphins
where do endorphins come from?
produced by pituitary and hypothalamus, induced by exercise, excitement, sex ,love, spicy food
Protein deposits (Lewy bodies) develop in CNS–> Lewy body dementia. What are the early symptoms?
difficulty making decisions
visual hallucinations of animals and children
