Meningitis causes 6mo-60yrs
S. Pneumoniae, N. Menigiditis, H. Influenza
Meningitis causes ages 0-6mo
Listeria, E. coli, GB Strept
Meningitis causes age 60+
S. Pneumoniae, Listeria
TB meningitis involves what part of brain
Basal aspect with cranial nerve involvement
Most common cause of lymphocytic aseptic meninigitis
Enterovirus
herpes or mumps less likely
Most common cause of non-herpetic viral encephalitis
Arbovirus (seasonal)
Causes of herpetic encephalitis
HSV1 (most common), CMV, VZV
-Bilateral, asymmetrical hemorrhagic necrosis of the temporal lobes
Key microscopic pathological feature of rabies encephalitis
Negri bodies in purkinje cells or large pyramidal cells
Poliomyelitis
- What is it?
- What causes it?
- Microscopic pathology (key)
- Enterovirus that targets spinal cord grey matter
- Neuronophagia (dying neuron surrounded by microglial cells)
Most common causes of viral meningitis/menigoencheph
Eterovirus, herpes virus, arbovirus
Two main histological features of viral enceph
- Perivascular chronic inflammatory infiltrates
2. Neuronophagia
What receptor is involved in MOA of LSD?
5HT-2 post-synaptic receptor
List 3 treatments for LSD
- Ride the wave
- Support/reassurance
- Benzos to calm them down
-no chronic damage, but can unmask psychiatric vulnerabilities like panic, paranoia or depression
Clinical manifestations of LSD
- Unpredictable
- Micropsia, macropsia, derealization, depersonailization, visual hallucinations, synethesia (hear colors eg), euphoria/lability, ego fragmentation
Clinical manifestations of PCP
- Euphoria, peaceful floating sensation, disconnection from world, oblivious to surroundings
- Flat affect (Sz like), uncommunicative, staring gaze, rigid muslces
- Slurred speech, rotary nystagmus (arch of eyes), rolling gait, hand/feet numbness, depersonalization, distortions of body image/space/time, delusions, perceptual disturbances
- Large doses can be lethal: hyperacusis, amneisa, hostility/paranoia, excessive salivation without a gag reflex, muscle rigidity, increased BP & pulse, coma and convulsions
-recovery can take days
MOA PCP
- NMDA receptor antagonist (blocks glutamate activity)
- DA/5HT, sigma and K+, Na+ receptor involvement
Treatment for PCP
- No chronic use permanent damage, but do have neuro and cog dysfxn for 2-3 weeks
- do not reassure, it doesn’t work
- Benzos target seizure risk
- Acidification of urine
- Antipsychotics for paranoia
- Gastric suction
Clinical manifestations of MDMA
- Euphoria/loving feeling, loss of boundaries between self and others, disinhibition (decreased defensiveness), increased intimacy
- Cognitive distortions-shifts in thought form and content, slowed mentation, cognitive apathy
- Perceptual distortions-intensified visual perceptions, visual hallucinations, altered sense of time/space
- Increased BP, HR, dry mouth, brxism (teeth grinding)
MOA MDMA
-Increased vesicular release of DA and Serotonin
Treatment of MDMA
- dehydration treatment
- reassurance
- support
- edu
-Chronic use causes long lasting destruction of serotonergic pathways leading to greater risk of depression
Clinical manifestations of anticholinergics
(atropine, TCAs, etc)
- Delirium (waxing/waning of consciousness, impulsivity, impaired judgement, hallucination)
- Hallucinations (misperceptions, dysphoria, estrangement, depersonalization, agitation)
- Toxicity (fever, warm, dry skin, fixed dilated pupils, tachycardia, decreased peristalsis, atonic bladder)
Treatment of anticholinergic
- Discontinue offending agents
- Protect pt against involuntary harm
- Gastric lavage, parenteral physostigmine
Clinical manifestations of inhalants
- Stimulation
- Disinhibition
- Nystagmus (regular)
- Muscular incoordination
- Perceptual distortions
MOA Inhalants
GABA-A receptor agonist (like alcohol)
