Things I struggle with Part 3 Flashcards
VPL nucelus
spinothalamic and dorsal columns/medial lemniscus- pain and termpature, pressure, touch, vibration, proprioception. first degress somatosensory
VPM nucelus
trigemenial and gustatosy- facial and taste sensation
LGN nucleus
CNII for ision
medial geniculate nucleus
superior olive and inferior colliculus of the tectum for hearing
ventral lateral nucelus
basal ganlgia and cerebellam for motor
limbic system- what are parts of it and function
hippocampus, amygdala, cingulate gyrus, and feeding, feeling, fighting, fleeing, fucking
mesocortical pathway
decreased activity leads to the negative symptoms of schizophrenia
mesolimbic pathway
increased activity leads to positive sympotms- target of anyipsychotic drugs
nigrostriatal patwhay
decreased activity leads to EPS symptoms-
tuboinfundibular pathway
decreased activity leads to increased prolactin
cerebeller lesion affects ipsi or contral
ipsilateral lesion=ipsi defect
the nuclei of the cerebellum from the lateral to mesail
dentate, emboliform, globose, fastigal
lateral cerebellar lesions do what
affect voluntary movement of extremities when injured there is propensity to fall towards the injured side
medial lesions of the cerebellum do waht
involvement of midline structures- tranquil ataxia, nystagmus, head tilting- bilateral axial defects
what does the basal ganglia do
it provides feed back to the cortex to modulate the movemetn
excitatory pathway of the basal ganglia
cortical inputs stimulate the striatum, stimulating the release of GABA which inhibits GABA release from the GPi disinhibiting the thalamus via GpI to increase motion
inhibitory pathway of the basal ganglia
cortical inputs stimulate the stiratum releasing GAB that disinhibits STN via GPe inhibition and STN stimulates GPi to inhibit the thalamus so decreased motion
dopamine in the basal ganglia
it binds D1 and this stimulates the excitatory pathway and D2 binds the inhibitory pathway to increase motion
athetosis
slow writhing movements especially with the fingers from the basal ganglia- writhing snake like movements
chorea
sudden jerky movemntts thatare purposeless from the basal ganglia
dystonia
sustains involuntar muscle contractions- like writers cramp and blepharspams eye lid twitch
essential tremor
high frequency tremor sustained with posture worsened with movement- contant tremor that tends to run in families-patients self medicate with alcohol- decreased tremor amplitude- beta blockers and primidone
hemibalsimus
sudden wild flailing of one arm and ipsilateral leg- contralaterla sub thalamic nucelus-
intention tremor
slow zigzag motion when posting extending toward a sudden target- tremor with movement from cerebellar dysfunction
myoclonus
sudden, brief uncontrolled muscle contraction- jerks, hiccupus, commong in metabolic abnormalities as enal and liver failure
resting tremor
uncontrolled moment of distal appendages- noticeble in hands and tremor is alleviated by movement
parkinson disease
degeneration of CNSs associtatd with Lewy bodies composed of alpha synuclein- intracellular eosinophilic inclusions and loss of dopaminergic neurons- depigmentation of substantial nigra- has tremor, rigidity, akinesia, postural instability, shuffling gait
Huntington disease
AD- CAG repear on the fourth chromosome- manifest between 30-50 and it is choreiform movements, aggression, depression, dementia- initially mistake for substance abust. increased dopamine, decreased GABA, neural death from NMDA-R binding and glutamate excitotoxicity. There is atrophy of the caudate and putamen with hydrocephalus ex vacuo.
what happens with the huntington gene
mediated gene causes transcriptional silencing and causes increased in histone deacetylation, which silence genees fro neuronal survival
confluent speech with intact comprehension but cannot repeat- what aphasia
brocaas area
fluent speech, impaired comprehension, impaired repetition- what aphasia
wenicke
fluent speech fluidity, intact comprehension cannot repeat- what aphasia
conduction aphasia- it is from damage to the arcuate fasiculus
nonfluent speech, impaired comprehension, impaired repetition- what aphasia
global- arcuate fasiculus, braca nad wernicke areas
nonfluent, intact comprehension, intact repetition- what aphasia
transcortical motor aphasia- affecting frontal lobe around broads are but broca is spared
fluent, impaired, intact- what aphasia
transcortical sensory- affects the temporal lobe around whence area but wenches area is spared
nonfluent, impaired comprehension, repetition intact- what aphasia
broca and wrench areas and arcuate fascicles remain intact surrounding watershed areas are affected
disinhibited behavior with hyperphagia, hyper sexuality, hyperorality associated with HSV1- where is the lesion
amygdala lesion-kluver bucy
hemispatial neglect syndrome- agnosia of the contralateral side of the world- where is the lesion
nondominant parietal cortex
agraphia, acalculia, finger agnosia, left and right orientation- where is the lesion
dominant parietal cortex
reduced levels of arousal and wakefullness- where is the lesion
reticular formation
confusion, opthalmoplegia, ataxia, memory loss (anterograde and retrograde), and confabulation and personality changes- where is the lesion
mamillary bodies
when B1 is given with glucose what is not fixed in wernicke korsakoff
the memory problems are not fixed
what enzyme is decreased with Werknicke B1 deficiency
eryhtrocyte transkelotase is decreased
tremor at rest, chorea, athetosis - where is the lesion
it is in the basal ganglia
intention tremor, limb ataia, loss of balance, damage to cerebellum fall towards lesion- where is the lesion
cerebellar hemisphere
what is degeneration of the cerebellum most commonly from
chronic alcohol
truncal ataxia and dysarthria- where is the lesion
cerebellar vermis which is central located because the middle parts are always affecting the middle
contralateral hemiballisums- where is the lesion
it is from sub thalamic nucelus
anterograde amnesia- inability to make new memories- where is the lesion
hippocampus bilaterally
eyes look away from the lesion- where is the lesion
it is paramedian pontoon reticular formation
eyes look away from the lesion- where is the lesion
frontal eye fields
what supplies the central sulcus of the brain
ACA
what supplies the outside of the brain
MCA
how do you treat increased intracranial pressure with ventialtion
if you hyperventilate the patients then there is vasoconsticrion and decreased blood flow and decreased intracranial pressure
watershed areas of the brain
between ACA and MCA and PCA
obstruction of the R brachiocephalic
impaired drainage of the right subclavlian and IJV so it drains to the right lymphatic drug and this leads right sided congestion and encouragement
contralateral paralysis and sensory loss of the face and upper limb, aphasia if dominant usually the left, and it is the left hemisphere. hemineglect if lesion is nondominat- what vessel is occluded
middle cerebral artery
contralateral paralysis and sensory loss of lower limb cam have some behavioral and urinary incontience- what vessel is occluded
anterior cerebral artery
contralateral paralysis and or sensory loss- face and body. absence of cortical signs like neglect, aphasia, visual field loss- what vessel is occluded
lenticulostriate artery
what does the lenticulostriate artery supply
the internal capsule and striatum
where do saccular aneurysms tend to be
bifurcatiosn at the circle of willis
wehere is the most common saccular aneurysm
it is at the ASA and ACA but and can cause subarachnoid hemorrhage
where is the aneurysm that squashes CNIII
from posterior communicating artery
charcot bouchard microanerusysm
associated with chronic hypertension affects small vessels in the basal ganglia and thalamic and not seen on agiogram. wit acute hypertesnive get intracerebral hemorrhage, and creates deep hemorrhage. The HTN leads to hyalinization and fibrosis of the vessel wall leads to bright sports on CT
what is the aneurysm causing- bitemporal hemianopia, and visual acuity defects- if ruptured it leads to contralateral lower extremity hemiparesis and sensory defects
ACA
what is the aneurysm causing- down and out and mydriasis, see ptosis and out
posterior communicating artery
what is the aneurysm causing- rupture leads to ischemia causing contralateral upper extremity and facial hemiparesis, sensory defits
middle cerebral artery
what causes- neuropathic pain and initial paresthesias followed by weeks to months of allodynia (painless stilmuli causes extreme pain, dyestheias
central post stroke pain syndrome of the thalamus
rupture of middle meningeal artery due to skull fracture, lucid itneraval and rapid expansion leading to transtentoral herniation and CNIII palsy- lens shaped lesion
epidural hematoma
rupture of riding brains from mild trauma, cerebral atrophy, elderly alcoholoism- crescent shaped crosses sutures
subdural hemtoma
rupture of aneurysm or AV malformation leading to rapid course and worse headache, bloody or yellow tinged spinal tap. 4-10 days after hemorrhage, vasospasm can occur leads to ischemic infarct
subarachnoid hemorahage
what do you give when there is a subarachnoid hemorrhage
nigedopine to prevent ischemic infarct
systemic HTN, and amyloid nagioathy recurrent locar hemorrahge storoke, vascultitis, neoplasm, reperfusion is from ischemic stroke, occurs in basal gnaglia, and internal capsule can be lobar or from lacuna strokes
intraparenchymal hemorrhage
what happens to the brain after 12-48 hours of ischmia
red neucons
24-48 hours of ischemia
necosis and neutrophils
3-5 days after ischemia
macrophages
1-2 weeks after ischemia
reactive gliosis, vacualr proliferation
more than 2 weeks after ischmia
glial scar and astocytes surround the cystic cavity
venous sinus thrombosis
increased intracranial pressure, and headache, seizures, focal neurologic deficits. May lead to venous hemorrhage associated with hyper coagulable states like pregnancy, OCP use ,factor V leiden
where are the arachnoid granulations located
superior saggittal sinus
what do you see if the cerebral aqueduct is blocked
the fourth ventricle is normal but the third and lateral ventricles are dilated
idiotpathic intracranial hypertension- pseudotumor cerebri
increased ICP with no apparent cause on impaging- increased with woman of child bearing age, vitamin A excess, danazol, tetracycline, obese- headache diplopia from Vi without change in mental status
why are their transient vision changes with pseudo tumor cerebri
transient vision changes from impaired axoplasmic flow in optic nerves that is worse with valsalva maneuvers
communicating hydrocephalus
decreased CSF absorption by arachnoid grannies from meningitis
normal pressure hydrocephalus
wacky, wobbley, wet- urinary incontinence, ataxia, cognitive dysfunction- elderly- increased CSF pressure but does not result in increased subarachnoid space volume. Expansion of centrical of the corona radiata
noncommunicating hydrocephalus
causes by structural blockage of CSF circulation in the ventricular system aka stenos of the aqueduct of selves like colloid cyst or forma on of monro
ex vacuo ventriculomegaly
appearance of CSF increase on imaging but actually due to decreased brain tissue and neuronal atrophy like advance HIV, AD, or Picks- ICP is normal
vertebral disc herniation
nucelus pulposis squirts out and it causes ocompression usually of s1 which causes absent ankle reflex
nerves C1-C7 it above the corresponding vertebrae. and the others exit below there.
In the c spine, the nerves sit on top and after C8 they exist below
where does the spinal cord end on adults
L1-L2
where is the lumbar puncture performed
L3-L4-5 or L4-L5
where in the dorsal columns are the arms and legs
arms are lateral legs are central
what is the lateral corticospinal tract
saracl and cervical
what is in the anterior corticospinal tract
voluntary motor
what does the anterior spinothalamic do
crude touch, pressure
what is the lateral spinothalamic doing
pain and temperature
dorsal columns: path and function
ascending pressure, vibration, fine touch, proprioception- sensory nerve ending-cell body in dorsal root ganglion- enters the ipsilateral DC- ispisalteral nucleus cuneatus or gracilis and decussated n the medulla and ascendds contra laterally in the medial lemmings then synapses at the VPL in the sensory cortex
spinothalamic: path and function
sensory ad and c fibers cell body in dorsal root ganglia, and enters the spinal cord and ipsilateral gray matter- decussate the anterior white commissure and ascends contralleraterlly VPL in the thalamus to the sensory cortexx- pain termapreue for lateral tract
anterior -crude touch and pressure
lateral coricospinal: path and function
decending is voluntary movement- UMN cell body in the motor cortex then internal capsule then pyramidal decussation and descends contralaterlly and cell body is in the anterior horn of the spinal cord
what are characteristics of LMN lesions
weak, atrphy, fasiculations, decreased reflexes, decreased tone, no babinski, flaccid paralysis
what are the characteristics of UMN lesions
hyperreflized, babinski, spastic paralysis, increased tone, no atrophy or fasiculations
clasp knife spasticity
can be caused by stroke to the internal capsule leading to pure motor weakness on contralateral side of arm, leg, face, and other UMN sides can be present
congential degeneration of anterior horns of spinal cord with LMN lesions only. Floppy baby syndrome with marked hypotonia and tongue fascinations. Influential type median death is around 7 months. It is autosomal recessive
Werdnig Hoffman syndrome
combined UMN and LMN deficits with no sensory or bowel/bladder dysfunction- due to loss of cortical and spinal cord motor neurons, can be caused by defect in superoxide dismutase 1, and commonly presents as asymetric limb weakness, fascinations, eventual atrophy
ALS
spares the dorsal columns and lesser tract in the upper throacic ASA territory is watershed area as the artery of Adamkiewisz supples the AS before T8
complete occlusion of the anterior spinal artery
degeneration and dymyleination of dorsal columns and roots progressive sensory ataxia and impaired proprioception- poor coordination. Associated with chariot joints, shooting pain, argyll robertson pupil
tertiary syphillus causing tabes dorsalis
syrinx expands and damages anterior white commissure of spinothalamic tract- bilateral loss of pain and temperature sensation in cpae like distribution seen with chair I malformation
syringomeyelia
subacute comobines degneration-demylination of spinocerebellat tracts lateral corticospinal tracts, dorsal collumns- ataxic gait an dimparied position and vibration sense
B12 deficiency
caused by poliovirus from fecal oral transmission. replicated in the oropharynx and small intestine spreading via bloodstream to CNS. Infection causes anterior horn destruction of spinal cord and LMN death- LMN lesion- weakness, hypotonia, flaccid paralysis, fascinations, hyporeflexia, muscle atrophy, increased WBC, increased slight of protein in the CSF and WBC in the CSF- virus is recovered from the stool or throat
poliomyelitis
AR recessive GAA repeat on chromosome 9 leading to gratin genre issues- degradation of multiple spinal tract and muscle weakness. Lose vibration sense, proprioception, staggering gait, frequent flailing, nystagmus, dysarthria, pets caves, hammer toes, diabetes, hyeprtrphic cardiomyopathy and kyphoscoliosis
friederich ataxia
what is the most common cause of death of friderich ataxia
it is from hypertrophic cardiomyopathy
what does the gene for friederich ataxia do
it is part of DNA replication and repair and leads to mitochondrial dysfunction
hemisection of the spinal cord so ipsilateral UMN sings below lesion level from corticospinal. Ipsilateral loss of tactile and vibration below lesion from dorsal column damage, contralateral pain and temperature loss below the level of the lesion from spinothalamic tract, ipsilateral loss of all sensation at the level of the lesion, ipsilateral LMN signs- if it is above T 1 then it could lead to hroner syndrome
Brown squared syndrome
rupture discleading to low back pain radiating to one or both of the legs ,saddle anesthesia, loss of anal wink, bowel and bladder dysfunction, loss of ankle jerk and plantar flexion
cauda equina
what is the anal wink level relfex
S4
compression at L2 leading to flaccid paralysis of the bladder and rectum leading to saddle anesthesia and impotence
conus medularis syndrome
what is the dermatome for the nipple
T4
what is the dermatome for the belly button
T10
what is the dermatome for the inguinal ligament
L1
what is the dermatome for knee caps down the leg
L4
what is the S,23,4, dermatomes
erection and sensation of penile and anal zones
what is the biceps reflex
C5,5
what is the triceps reflex
C7,8
what is the patella reflex
L3,4
what is the achilles reflex
S1,2
what is the anal wink reflex
S3,S4
moro reglex
hang on for life
rooting reflex
head moves toward one side if cheek is stroked
sucking reflex
sucking response on roof of mouth
palmar reflex
curling fingers in hang
plantar reflex
dorsiflexion of large toe and fanning of other toes with plantar stimulating. Babinski reflex is in the child but in adult it is from UMN lesion
galant reflex
smoking along one spine while newborn is in suspension
S1 radiculopathy
compression by disc herniation. posterior thigh and calf lateral foot and sensation. weakness of thigh extension, knee flexion, absent ankle jerk
L5 radiculopathy
- weakness of dorsiflexion, inversion and eversion of the foot and toe extension. No missing reflexes
what is parinaud sudnrome
paralysis of conjugate vertical gaze due to lesion of the superior colliculus- store, hydrocephalus, pinealoma
what does the interior colliculi do
it is from auditory
what does superior colliculus do
conjugate vertical gaze
what cranial nerve passes through the cribriform plate
CN I
what cranial nerve passes through the optic canal
CN II
what cranial nerve passes through the superior orbital fissure
V1, IV, III, VII
what cranial nerve passes through the foramen rotundum
v2
what cranial nerve passes through the foramen ovale
V3
what cranial nerve passes through the internal auditory meatus
VI, VIII
what cranial nerve passes through the jugular foramen
IX, X, XI,
what cranial nerve passes through the hypoglossal canaal
XII
what cranial nerve passes through the foramen magnus
XI
what does the nucleus solitarius do
visceral sesory information like taste, barorectoptions, and gut distention from VII, IX, X
what does the nucleus ambiguous do
motor innervation of pharynx, larynx, upper esophagus, swallowing palate elevation- aka swallow and speech
what odes the dorsal motor nucleus do
sends autonomic parasympathetic fibers to heart, lungs, upper GI
corneal reflex: afferent and efferent
afferent V1 and efferent is VII
lacrimation reflex: afferent and efferent
afferent V1 and efferent is VII
jaw jerk reflex: afferent and efferent
afferent V3 and efferent V3
pupillary reflex: afferent and efferent
afferent II and efferent is III
gag reflex: afferent and efferent
afferent Ix and efferent x
if the jaw is deviating is it towards or away from the lesion- and what is the nerve involved
it is jaw towards the lesion and it is from a CNV motor lesion
uvula deviates is it towards or away from the lesion- and what is the nerve involved
away from the lesion and it the vagus nerve for the lesion
the head is weak at turning and there is shoulder droop is it on the same side or way and what is the nerve
CN XI lesion and the head turns away from the lesion and shoulder droops on the side of the lesion
the tongue deviates is it towards or away from the lesion- and what is the nerve involved
the tongue deviates towards the side of the lesion and due to weakened tongue muscles on the side of the lesion
what are the muscles of mastication
masseter, temporalis, and medial pterygoid.
what innervates the muscles of mastication
V3
if the facial nerve lesion spares the forehead, where is the lesion
destruction of motor cortex or connection between motor cortex and facial nucleus in pons to contralateral paralysis of lower muscles of facial expression. Forehead is spared due to its bilateral UMN innervation
if the facial nerve lesion is full face, where is the lesion
it is a destruction of the facial nucleus or CN VI anywhere along the side of the course. Ipsiplateral paralysis of the upper and lower muscles of face. It also leads to hyperacusis
what causes hyperacusis
increased sound from paralysis of stapedius has high pitched sounds from facial nerve palsy
What can cause Bells Palsy
it can be from lyme disease, herpes simplex, herpes zoster, sarcoidosis, tumors, diabetes mellitus, treatment si acyclovir and corticosteroids
what are the signs of bells palsy
impaired eye closure, eyebrow sag, can’t smile, can’t frown, no nasolabial fold, decreased tearing, hyperacusis, decreased taste on the posterior part of the tongue
what CN are in the cavernous sinus
II, IV, V1, VI and V2
cavernous sinus syndrome
opthalmoplegia, decreased corneal sensation, orner syndrome, and occasional decreased maxillary sensation. can be secondary to pituitary tumor or mass effect carotid cavernous fistula cavernous sinus thrombosis related to primary infection.
which nerve in the cavernous sinus is most susceptible to injury
VI
what infections are most common in cavernous sinus
staph aureus, mucor, strep, rhizopus,
what are some of the symptoms of palsies with II, IV, VI
common with proptosis, conjunctival swelling, impaired ophthalmic draining
what order are they on the sides down the cavernous sinus
III, Iv, VI, V1, V2 down the sides and the trochlear is right next to the internal carotid artery
where is low frequency heard in the inner ear
low frequency heard at apex near helicotrema
where is high frequency heard in the inner ear
high frequency heard best at the base of the cochlea
conductive hearing loss
abnormal bone>air and localizes to the affected ear
sensorineural hearing loss
air>bone and localizes to the unaffected ear
the rinne test
it is to test for bone conduction
the weber test
it is the test for the midline of the fork and it localizes to one side or the other
what is a cholesteatoma and were dos it come from
it is a lesion of the tympanic membrane that can rupture the middle ear- it is an overgrowth of desquamated keratin debris within the middle ear that may erode the ossicles and the mastoid air cells- conductive hearing loss
what forms the superior of the orbit
thick orbital plate of the frontal bone
what forms the lateral side of the orbit
zygomatic bone and sphenoid wings form it
what forms the orbital floor
it is a think wall that separates from maxillary sinus- break common- the inferior rectus herniate into the maxillary sinus
what forms the medial wall of the orbit
ethmoid and lacrimal bones fracture and medial rectus gets trapped
what does the trabecular outflow do in the eye
it drains through the trabecular meshwork through the canal of scheme and episcleral vasculature and it can increase with M1 agonist
uveosceleral outflow
it drains into the uvea and sclera and increased prostaglandin agonist
aqueous hunmor production
produced by non pigmented epithelium on ciliary body- decreased by beta blockers, alpha 2 agonists, and accarbonic anhydrase inhibiotrs
hyperopia
eye too short for refractive power of cornea and lens- light focusses behind the retina
myopia
eye is too long, so it focusses in front of retina
astigmatism
abnormal curvature of the cornea and different refractive power at different axis
presbyopia
age related impaired accomindation focusing on near objects, and primarily die to decreased lens elasticity and often nessicitates reading glasses
cataract
painless often bilateral opacification of the lens. decreased vision. Acquired risk factors of increased age, smoking, excessive sunlight, prolonged corticosteroid use, diabetes, trauma, infection
what are the congenital risk factors for cataracts
galactosemia, galactokinase deficiency, trisomies, toche infections like rubella, marfan syndrome, alport syndrome, myotonic dystrophy, and NF2
open angle glaucoma
increased with age, race, family history, and painless and more common. Primary cause is unclear. secondary is blocked trabecular network from EBC or RBC can be from blocked retinal elements
closed angle glaucoma
primary is enlargement or forward movement of the lends against the central iris and obstruction of normal flow o fhumor through the pupil and flip builds up behind the virus pushing the peripheral iris against the cornea. it impedes frlow through the trabecular netwrk. Secondary is from hypoxia and retinal disease
chronic closure
asymptomatic with damage to optic nerve and peripheral vision
acute closure
true ophthalmic emergency. increased IOP pushes the iris forward and angle closes abruptly and very painful red eye, sudden vision loss, halos around lights, rock hard eye frontal headache
what do you not give with acute closure glaucoma
do not give epinephrone because of mydriatic effect
conjunctivitis
inflammation of conjunctiva and red eye .Allergic itchy eyes bilateral and could be from bacterial which treat and see pus. Viral is from adenovirus and sparse mucus discharge and swollen pre auricular node self-resolving
uveitis
inflammation of urea and it can have pus accumulated in the anterior chanmber of the ye and can be associated with system inflammatory disdeae
age related macular degeneration
degeneration of the macula and central area of the retina causes distorting and loss of central vision.
what is dry age related macular degeneration
deposition of yellowish extracellular material in and between bruch membrane and retninaly pigment epithelium with gradual vision loss and prevent progression with vitamins
what is wet age related macular degeneration
it is rapid loss of vision due to bleeding secondary to choroidal neovascularization treat with anti-vegf this is called ranibizumab
diabetic retinopathy and difference between non proliferative and proliferative
- retinal damage de to chronic hyperglycemia.
- nonproliferative- damaged capillaries leak bloos and lipids and fluid seep into retina causing hemorrhage and macular edema. Treat with blood sugar control
- proliferative- chronic hypoxia results in new blood vessel formation with resultatt traction on tretina
retinal vein occlusion
blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis and retinal hemorrhage and venous engorgement and edema in the affected area
retinal detachment
separation of the neurosensory layer of the retina from the outermost pigmented epithelium and degradation of photoreceptors and vision loss. May be secondary to retinal breaks, diabetic traction, inflammatory effusions. visualized on fundoscopy as crinkling of retinal issue and changes in vessel direction. Breaks are more common with high myopia or head trauma. Often proceed by flashes and floaters. It has eventual monocular loss of vision like a curtain draw down
central retinal artery occlusion
acute painless monocular vision loss, and retina is cloudy with attenuated vessels and cherry red spot at fovea- center of the macula- theres an embolic source from carotid artery atherosclerosis, vegetations, patent foramen ovale
what signs of reflex would you see on central retinal artery occlusion
no constriction of other eye with direct light because of destroyed retinal ganglial cells
retinitis pigmentosa
inherited retinal degneration. Painless progressive vision loss beginning with night blindness and rods are affected first- bone spicule shaped deposits around the macula
retinitis
retinal edama, necorsis, and leads to scar
what are the causes of retinitis
CMV, HSV, VZV and can be bacterial or parasitic or associated with immunosuppression
papiledema
optic disc swelling usually bilateral with increased ICP and it is engaged blind spot and elevated opt disc with blurred margins
miosis- what is the reflex
first neuron is the dinger wasteful nucleus to the chillily ganglia via CNIII and second neuron is short ciliary nerves to pupillary sphincter muscles
where is the origination of the Edinger westfall nucleus
it is in the midbrain
myadriasis
dilation it is from sympathetic.
marcus gunn pupil
afferent pupil light defect due to optic nerve damage or severe retinal injury. decreased bilateral pupillary constriction when light is shone in affected eye relative to unaffected eye.
horner syndrome
sympathetic denervation of the face- ptosis, anhidrosis, miosis- pan coast tumor, brown squared, late stage syringomyelia
what CN innervates the lateral rectus
CN VI
what CN innervates the superior oblique
CN IV
what CN innervates superior rectus, inferior rectus, , medial recturs, and inferior oblique
CN III
what motion does the superior oblique perform
it abducts, interest, and depresses while adducted
internuclear opthalmoplegia
when looking left, the left nucleus of the CNVI fires, which contacts the left lateral rectus and stimulates the contralateral right nucleus of the CNIII via the right MLF to contract the right medial rectus. Convergence stays normal
AD
most common cause of dementia in the elderly. Increased risk with ApoE2 decree and increased risk with APOE4. App, presenilin and have an increase risk. see widespread cortical atrophy, and narrowing of gyro and widening of the sulk. There is decreased ACh. Senile plaques are in the grey matter and extracellular beta amyloid core. May cause amyloid angiopathy and intracranial hemorrhage. AB synthesized by the cleavage of APP. Neurofibbrillary tangles are intracellular hyperphosphorylated tau proteins. Number of tangles determines how bad the disease is
why are people with downs at an increased risk of AD
they have an extra APP gene on chromosome 21
frontotemporal dementia
early changes in personality and behavior or aphasia. Aphasia is from primarily progressive aphasia. May have associated movement disorders. ALS like UMN/LMN degeneration. Previously called pick disease. Ave frontotemporal dementia and lobe degeneration. Inclusions of hyperphosphorylated taw protein and round eosinophilic lesions and TDP43 postiive
Lewy body dementia
initially dementia and visual hallucinations followed by parkinson like deatures- intracellular levy bodies with insoluble aggregates of alpha synuclein primarily in the cortex
vascular dementia
multiple arterial infarcts and or chronic ischemia. It is a step wise decline in cognitive function and impairment. It is theseoncd most common cause. Look at MRI which shows multiple cortical and subcortical infarcts
CJD
rapidly progressive dements with myoclonus. Spongiform cortex and protons from beta pleated sheet which is resistant to degradation
what are some other causes of dementia
HIV, hypothyroidism, vitamins B1, B3, or B12, wilson disease NPH
Central pontine myelinosis
acture paralysis, dysarthria, dysphaga, diplopia, loss of consciousness- caused locked in syndrome- massive axonal degeneration in pontine white matter. Secondary to osmotic changes. Commonly iatrogenic from rapid correction of hyponatremia.
what happens if hypernatremia is corrected too quickly
it causes edema and herniation
Charcot triad
scanning speech, intention tremor, incontinence, internuclear ophthalmoplegia, nystagmus
what is the CSF sign of MS
it is oligoclonal banding in the CSF.
what is seen on MS MRI
it is gold standard and there are periventricular plaques with destruction of cons. multiple white matter lesions.
pseudobulbar palsy
associated with MS. There is dysarthria, dysphagia, dysphonia, impaired tongue, facial movements
acute inflammatory demyelinating polyradiculopathy
GBS subtype that is an autoimmune condition attacking the schwann cells and inflation and demyelination of the peripheral nerve fibers. results in symmetric ascending muscle weakness/paralysis and beginning in lower extremtities. Can have some autonomic dysregulation. Increased CSF protein count. Associated with campylobacter jejuni and viral causes. Need respiratory support
acute disseminated post infectious encephalomyelitits
multifocal periventricular inflamtion and demyelination after infection or vaccination- rapidly progressive multifocal neurologic symptoms altered mental status
Charcot Marie Tooth
hereditay motor and sensory neuropath- progressive herditary nerve disorders related to defective production of proteins involved in the structure oand function of peripheral nerve or the myelin sheath. Typically autosomal dominant inherticane pattern associated with foot deformities, lower extremity weakness and sensory deficits
Krabbe disease
AR- lysosomal storage disorder due to degiceinct of galactocerebrosidase. buildup of glactocerebroside and pyochosine destroys myelin sheath. It is peripheral neuropathy, and developemental delay, optic atrophy and globoid cells
Metachromatic leukodystrophy
ar lysosomal strage disorder of arylsulfatase A deficiency. Buildup of sulfates impaired production and destruction of myelin sheath. Find central and peripheral demyelination with ataxia and dementia
PML
demyelination of the CNS due to destruction of oligodendrocytes and it is from reactivation of JC virus in MS or AIDs rapidly progressive and fatal from natalizumab and rituximab
adrenoleukodystrophy
X linked disorder of disrupted metabolism of long chain fatty acids and build up in nervous system, adrenal gland, testes- leads to long term coma death, and adrenal crisis
partial siezures
affect a single area of the brain and commonly originate from the temporal lobe often proceeded by an aura
simple partial
consciousness stays intact but it is only motor sensory and autonomic psychic
complex partial seizure
lose consciousness
epilepsy
a disorder of recurrent seizures fertile are not it
status epilepsy
continous or recurring siezures that may result in brain injury>5 min
causes of seizures by age: children adults, elderly
- children- genetic infection, febrile, trauma, congenital, metabolic
- adults-tumor, trauma, stroke, infection
- elderly- stroke ,tumor, trauma, metabolic infection
absence seizures
3hx frequency and no postictal confusion- treat with ethosuximide- staring spells
myoclonic seizures
repeated jerks
tonic clonic seizures
alternating stiffening and movement
tonic seizures
just tensing
atonic seizures
drop seizures where they fall to the floor
cluster headaches
unilateral in young male smokers, 15 minute 3 hour repetitive- repetitive brief headaches excruciating periorbiral pain with lacrimation and rhino rhea or Horners syndrome
treatment for cluster headahces
sumatriptan and O2
CNS tunmor that is in the cerebal hemispheres can cross the corpus collosum and its pseudopalisading pelomophic tumors cells with central areas of necrosis and hemorrhage and positive for GFAp
glioblastoma multiforme- grade IV astrocytoma
benign primary brina tumor. most often occurs near surfaces of brain and pasasagittal region arises from arachnoid cells it is extra acial- and may have a dural attachment often asmyptomati but can have focal neurological signs and seizures- see psammoma bodies which are calcifications
meningioma
cerebellla tumor associated with VHL and it is found with retinal angiomas- can produce erythropoetin like polycythmia- thin walled capillaries with minimal parenchyma
hemangioblastoma
cerebellopontine angle typically but can be from other peripheral nerves. vestibular is CNVVIII- bilateral vestibular are in NF2 are S100
these are schwannomas
rare slow growing tumors of fried egg cells, chicken wire capillaries and are in the frontal lobes
olidendroglioma
usually a prolactinoma with biemporal hemianopia with lactotrophy cells
piutiary adenoma
what brain lesion do AIDs patients tend to get
CNS lymphoma single ring enhancing lesion are high grade, poor prognosis and positive for EBV
pineal mass
germinoma with mass effect and cause obstruct hydrocephalus
well circumscribed in children found in posterior fossa like cerebellum- may be supratentorial and positive for GFAP= see rosenthal fibers- eosinophilic corkscrew fibers- cystic and solid
pilocytic astrocytoma
highly malignant cerebellar tumors a form of primitive neuroectodermal tumor can compress fourth ventricle causing noncommunicating hydrocephalus can send drop metastases to spinal cord- midline posterior fossa- increased intracranial pressure and cerebella dysfunction- homer wright rosettes and small blue cells
meduloblastoma
perivascular rosettes and rod shaped belpharoplasts- basal ciliary bodies found near the nucleus- can be in the 4th ventricle
ependymoma
childhood tumor with bitemporal heianopia- childhood supratentorial tumor- slow benign tumor of super cellar region with cyst and calcification and motor oil in the cells from ruthless pouch and have calcification and cholesterol crystals
craniopharyngioma
tumor of pineal gland causing compression of the tectum and vertical gaze palsy and obstructive hydrocephalus and compression of cerebral aqueduct and processors puberty and increased beta HCG- similar to seminoma
pinealoma
cingulate and subflacine herniation
flax cerebra can compress anterior cerebral artery
central herniation
downward transtentorial hernaition- durrette hemorrhage from basilar artery rupture- caudal displacement of the brainstem
uncal herniation
CNIII palsy with blow pupil, down and out
cerebellar tonsil herniation
coma and death and go through the foramen magnum
trigmeinal neuralgia
sudden pain in CN V stabbing and electric shock in short bursts from chewing, tooth brush ,temperature changes, carbamazepoins is first line and decrease NA channel recovery to decreased firing of neurons. CBC monitor for aplastic anemia
DRESS syndrome
2-8 weeks post drug exposure- fever, lymphadenopathy, facial edema, mobeliform skin rash and confluent erythema, actor I neurhoathy, cough, increased ALT and eosinophilia
what is the path of the ACL and what test do you use for ACL injury
it is from the lateral femoral tubercle to the anterior tibia- you should use the anterior drawer or Lachman test for it
what is the path of the PCL and what test do you use for PCL injury
PCL is from medial femoral condyle to the posterior tibia. Use the posterior drawer test
what is injured if the there is lateral force placed on the knee and it starts to bed that way from valgus force
it is an MCL tear
what is injured if there is varus force applied to the knoee and the lateral space widens
LCL
for the McMurray test, if there is external rotation applied and pain then its the
medial meniscus
for the McMurray test, if there is internal rotation applied and pain then its the
lateral meniscus
Osgood Schlatter: where is the injury, what should you feel on testing, and what is the repetitive stress from
there is an overuse injury to the secondary ossification centre of the apophysis f the tibial tubercle. Knee pain in adolescent and pain and swelling at the tibial tubercle and at the insertion of the patellar ligament which connects the tibia to the patella and quadriceps can avlse. This can lead to a callus formation at this tendon. It is from repetitive use of the quadriceps and from jumping
what is the function of the patella
it improves knee extension and provides nutrients to distal femur cartilage.
if the patella is broken, what movement cannot be performed
extension of the knee against gravity and there is a palpable gap in extension
what is injured in the unhappy triad and what causes this injury
ACL, MCL, medial meniscus- due to lateral force applied to a planted leg
what causes prepattellar bursitis and what is the inflammation
it is inflammation of the from and largest bursal sac of synovial fluid- it is from repeated trauma or pressure from excessive kneeling like gardening or housemaids
where is a Baker cyst and what is the common related condition
it is a popliteal collection in gastrocneumus-semimenbranous bursa and communciated with the synovial space and related to chronic joint disease
what are the muscles of the rotator cuff
supraspinatur, infraspinatus, subscapularis, teres minor
what motion does supraspinatus perform, when is it injured and what nerve innervates it
it does shoulder abduction and it is the most common injury should test the can test and its innervated by the supra scapular nerve
what motion does infraspinatus perform, when is it injured and what nerve innervates it
It is the lateral or external rotator of the shoulder and it is from a pitching injuryy and its innervated by the supra scapular nerve
what motion does theres minor perform, when is it injured and what nerve innervates it
it adducts and internally rotaties the arm/lateral rotation- it is from the axillary nerve
what motion does subscapularis perform, when is it injured and what nerve innervates it
it medially rates the arm so internal rotation and adduction- its from the sub scapular nerves
what is the repeated motion for medial epicondylitis
it is repeated flexion of the wrist
what is the repeated motion for lateral epicondylitis
repretitive extension so repetitive wrist extension
what is a scaphoid injury from and why
it is from the fall on the outstretched hand. It is in the anatomical snuff box, and it is retrograde blood supply. It sits on the radius and it is closest to the thumb
where is the lunate injury and why
it is from fall on the outstretched hand with acute carpal tunnel syndrome from dislocation- it is on the radius more medial than the scaphoid but next door
what is the hamate injury and why
it is the hook of the hamate which dits close to the fingerso n the pinky side and it causes lunar nerve injury
carpal tunnel involves which nerve and ligament
medain nerve entrapment by the transverse carpal ligament- it is causing paresthesia, pain and numbness in the thinner eminence atrophy but sensation here is spared
who gets guyot canal syndrome and what nerve is there
ulnar nerve issue and its in cyclists
what is a shoulder dislocation
the head of the humerus rotates out of the glenoid
what is a shoulder seperation
clavicle separates from acromion and cricoid process of the scapula
anterior should dislocation can damage what- how to test for damage
axillary nerve and posterior circumflex artery- lose feeling in the deltoid
what causes posterior shoulder dislocation
seizures
hip disloaction is from what and what does it damage
it is from a MVA and there are medial and lateral circumflex femoral arteries and femoral vein damage and sciatic nerve, and head of femur
what nerve and artery is injured with the fracture of the surgical neck of the humerus and anterior dislocation of the humerus
axillary nerve and circumflex arteries
what nerve and aftery is injured from pitching or shoulder dislocation
musculocutanous nerve
what nerve and artery is injured by mid shaft frcture of the humber, compression of the axilla, and crutches or saturday night palsy, supracondylar fracture with anterolateral displacement of the proximal fracture fragment
radial nerve- it is the deep brachial artery with the mid shaft break of the humerus
supracondylar fracture anteromedial of the humerus, carpal tunnel, and distal wrist laceration- nerve and artery
median nerve sometimes the brachial
fracture of the medial epicondyle of the humerus fractured hook of hamate- what nerve is injured
ulnar nerve
superficial laceration of the palm- nerve injury
recurrent branch of the median nerve
what nerve injury leads to flat deltoid, loss of arm abduction and loss of sensation of deltoid and lateral arm
axillary nervve
what nerve injury leads to loss of forearm flexion, and supination and loss of sensation over lateral forearm
musculocutanous nerve
what nerve injury leads to wrist drop aka loss of elbow, wrist, and finger extension, decreased grip strength, loss of sensation over postior arm and forearm and dorsal hand
radial nerv
what nerve injury leads to ape hand and pope blessing, loss of wrist flexion, and flexion of lateral fingers, and thumb opposiotn, and lumbricals, loss of sensation over lateral fingers nan tingling when pushing on carpal tunnel
median nerve
what nerve injury leads to loss of wrist flexion, flexion of medial finders and abductio and adduction of all fingers
ulnar nerve
what nerve injury leads to loss of thanr muscle group so thumb stuff
recurrent branch of median nerve
what causes the lesion and where is the lesion when the arm hangs by the side with abduction, lateral rotation, flexion and supination
lateral traction on neck during delivery, or trauma in adults- lesion-Erbs palsy is the avulsion of the C5-6 roots
what causes the lesion and where is the lesion when the hand is a total claw hand
in infants its from upward force during delivery and adults it is from trauma when grabbing a tree branch and it accuses the C8-T1
what causes the lesion and where is the lesion when there is atrophy of the intrinsic hang useless esteemi and pain and edema from vascular compression
it is from the cervical rib. Pan coast tumor, repetitive overhead exercises- lower trunk and subclavian vessels
what causes the lesion and where is the lesion when inability to anchor the scapular to the thoracic cage and cannot abduct arm above horizontal
it is a lesion of the long thoracic nerve (C5-C7) and this is the innervation of the serrates anterior which is at the 4-5 intercostals on the midaxillary line it is damaged by axillary nerve dissection after mastectomy or stab wounds
what muscles are paralyzed by an anterior shoulder dislocation or humeral neck fracture
it is the axillary nerve so the deltoid and the theres are paralyzed
what is going on when there is pain at the costosternal angel wit palpation and worse with repetitive activity- prolonged pain
costotchondriasis
what is the risk with a COPD patient with an inter scalene nerve block
can paralyze the phrenic nerve which is C3,4,5
what is the ulnar claw from
it is the extension of the 1-3 fingers at rest, but the 4-5 cannot relax because of a distal ulnar nerve injury
what is the pope hand from
it is that way when patient tries to make a fist because the 1-3 cannot bend so there is a proximal median nerve injury
what is the median claw
1-3 are bunched up and 4-5 can extend- it is a distal median nerve injury
what is the ok gesture from
it is a proximal ulnar nerve injury so the fingers can’t curl up
what do the dorsal inteossei do
dorsals abduct
what do the palmar interossei do
palmar adduct
what nerve does pelvic surgery injure
obturator nerve
what nerve does pelvic fracture injure
Femoral nerve
what nerve does trauma or compression of lateral aspect of leg and fibular neck fracutre- cast compression-injure
common perennial nerve
what nerve does intramuscular injection to upper medial gluteal region injure
superior gluteal
what nerve does posterior hip dislocation injure
inferior gluteal nerve
what presents as decreased medial sensation of the thigh and decreased adduction
obturator
what presents as decried thigh flexion and leg extension
femoral nerve
what causes foot drop that is inverted at resd and with a stopgap gate and loss of sensation to the dorsum of the foot
common perennial nerve
what causes inability to curl toes and loss of sensation on the sole of the foot and eversion of the foor
tibial
what causes trendeleberg gait and the lesion is contralateral to the side of the hip drop
superior gluteal
what causes difficulty climbing stairs, rising from seated and loss of hip extension
inferior gluteal
what does the people nerve do
everts and dorsiflextes- PED
what does the tibial do
inversts and plantarflexes TIP
where do you find the pudenal nerve and what can injuryy do
find it at the ischial spine and it is the landmark for injection if injured it can led to incontience and painful sex
what runs through the sciatic foramen
the piriformis, gluteal arteries, internal pudendal ,ecstatic nerve
piriformis syndrome
sciatica from enlarge piriformis
ankle sprain injures what ligament
it hurts the anterior talkofibular ligament
what motion does the illipsoas perform and what levels does it run from
psoas is T12 through L5 and can have an abscess back there it performs hip flexion so sit up
what performs hip flexion
illipsoas ,rectus femoris, tensor fascia lata
what performs hip extension
gluteus maximus, semitendinouss, semimembranosis, biceps femoris
what performs hip abduction
gluteus medius nad gluteus minimus
what performs hip adduction
adductor brevis, longus, and magnus
what nerve roots are compressed if there is weakness of knee extension, and decreased patellar reflex
L3-4
what nerve roots are compressed if there is weakness of dorsiflexion, difficulty heel-walking
L4-L5
what nerve roots are compressed if there is weakness of plantar flexion, difficulty in toe-walking, and decreased achilles reflex
L5-S1
what is the tibial nerve run with
popliteal artery
what can injure the popliteal artery
posteiro dislocation of the knee
what does anterior compartment syndrome mess up-what nerve and artery are compromised
it is bad foot extension, anterior tibial artery, deep perennial nerve so decreased sensation between first and second toes so decreased dorsiflexion, foot drop, and claw foot.
what parts of the sarcomere contract
H and I bands between the Z lines
what does Ca bind to in the muscle
it binds to troponin C and it moves the tropomysin off so the myosin and actin can bind
what cocks the myosin head
it is the hydrolysis of ATP to ADP
Type 1 muscle fibers
slow twitch with high mitochondria and myglobin
type 2 muscle fibers
- fast twithc fibers with increased anaerobic glyoclysis
what do high levels of PTH do
resorb bone
what do low levels of PTH do
it keeps bone building going
what does estrogen do to bone
it inhibits the apoptosis of the osteoblasts and induces the apoptosis of the osteoclasts
what is MLCK inhibited by
dihydropyridine CC< epinephrine, and prostaglandin E2
what is mutation does a kid with short limbs and normal torso and head have and what does this mutation do. What are the risk factors for the mutation
activating mutation of FGF3 and it decreases chondrocyte growth and increase paternal age and AD can be the mutations
what is OI from and what is the defective from and why are their sclera blue
it is from a defect in type 1 collage, and it is AD and it has multiple fractures and blue sclera from the exposure of choroidal veins. there is also hearing loss
what is osteopetrosis from and what is the mutation in, and what do you treat it with
it is defect of bone resportion and thick heavy bone with that cracks. It is poor last fucntion and it is from a carbonic anhydrase mutation which decreases the ability of the bone to create an acidic environemnet to resole the Ca from the bone. Can create hearing loss, compression of CN and hydrocephalus and RTA, Treat with bone marrow transplant
Ricketts and osteomalacia
it is defective mineralization of the bone due to decreased vitamin D. It can be decreased in serum and poor diet, and malabsorption, and liver and renal failure. IN children there is pigeon breast, frontal bossing, and rosary on the chest, and bowed legs. Osteomalacia and weak bone with increased fracture and decreased CA, decreased phosphate, and increased PTH. increased alkaline phosphatase.
what increases the alkaline phosphatase
blasts are active which increases the alkaline phosphatase activity
osteoporosis
increased breaks and it is dependent on peak bone mass. It is diet, d receptror and exercise determines the peak bone mass. has bone paine, features in weight berarign areas
when does bone mass peak
30 years old
what are the labs for osteoporosis
it is normal labs
Pagets disease
inbalance between clast and blast activity. Overactivity of the class usually kicked off by viral illness then the clasts eventually cause mixed then it is blast activity. only involves 1-2 bones. It is from sclerotic bone that fractures easily. Lamellar mosaic bone. Increased hat size, hearing loss, lion face, increased all phos
what are the bad outcome from pagets
it is high output cardiac failure or osteosarcoma from the screwed up blasts
how to treat Pagets
it is treated with calcitonin and bisphosphinates which decreases the activity of the clasts
where do kinds get osteomyelitits
metaphysis
where do adults get osteomyelitits
epiphysis
what patients get pseudomonal osteomyelitits
it is from diabetic or IV drug use
avascular necrosis
from decreased flow or trauma and fracture shock or sickle cell can cause osteoarthtitis and fracture
osteoma
surface of face like Gardners. It is fibroelastosis in peritoneum.
osteoid ostemoa
benign osteorid tumor with a rim of a reactive bone cortex of long bone in diaphysis- get bone pain that gets better at aspirin. radiolucent with reactive core
osteoblastoma
larger arise in the vertebrae and does not respond to aspirin
osteochrondroma
cartilage/bone tumor from lateral projection of growth plate. like like pedunculate mass off the bone. it is continuous with the marrow space. can go to chrondrosarcoma
osteosarcoma
malignancy of the bone and teens and elderly with bimodal development. It is Rb and pages, radiation of the metaphysics of long bone of distal femur or proximal tibia. Pathologic fracture or bone pain and swelling. Creates a pereosteal tending and Codmans angle is important and has hay sunburst appearance.
what is the morphological feature of osteosarcoma
Creates a pereosteal tending and Codmans angle is important and has hay sunburst appearance. and cells are pleomorphic and produce lots of osteoid pink
Giant cell bone tumor
tumor of multinucleated giant cells and stream cells. Occurs in the young adult at the epiphysis and its soap bubble lesion. It is locally aggressive tumor and can recur
Ewing sarcoma origin
neuroectoderm
ewing sarcoma
it is neuroectoderma in the medulla at the diaphysis and it is in male kids
ewing sarcoma morphology
it is onion skinning lesion with small blue cells and it looks like lymphocytes can have fevver
what is the translocation for Ewing sarcoma
11:22 translocation
chrondroma
bening in medullar of small bones of the hands and feet
chondrosarcoma
middle of pelvis or central skeleton
what kind of mets in the bone are blastic
prostate
degenerative bone disease
it is i progressive destruction of bone and articular cartilage eburnation, and can be from age and obesity, and hits the hip, lumbar spine, and knees, DIP and PIP, and it is worse during the day.
Rheumatoid arthritis
middle age women and HLADR4- synovititis causing a panes formation, and it has joint fusion, and contraction of pants can cause deviation. Worse in he morning but better wit activity. Joint narrows, loss of cartilage, and osteopenia, and increased fever, malaise, weight loss, and myalagia. rheumatoid nodules- central necroses with histiocytes. Baker cysts and pleural effusion
what is the Ra antibody
it is IGM against Fc portion of IgG.
what is ankylosing spondylitits
sarcoiliac joint fusion, males, low back pain, uveitis, and fusion of the spine. can get aortic dilation
Reiters arthrtitis
can’t see, can’t pee, can’t climb a tree- after GI or STD
what is the presentation no infective arthritis
it is neisseria and staph aureus
what is psoriatic arthritis
axial, peripheral with sausage fingers
what are the causes of gout (why does it happen)
from increased uric acid or not excreted in the kidney
what can increase uric acid
tumor breakdown
Lesch Nyhan
decreased HGPRt but increased PRPP
renal insufficiency gout
can’t excrete the uric acid
what do the crystals look like
negatie biofringent and it is parallel and yellow needles
gout what are the depositions from
it is monosodium rate crystals
chronic gout- what shoes up
tophi with debris and giant cell recactio with white chalky lesion
pseudo gout what are the crystals and what are they made of
it is rhomboid crystals and it is calcium pyrophosphate and its weakly positive under polarized light
dermatomyositits
gastric carcinoma and it is bilateral proximal weeks, can’t comb hair or climb stairs, heliotropic rash, malaria rash, and red papillose on elbows, knuckles, knees. increased CK, anti-o1,
where is the inflammation in the muscle fascicel
it is perimysial inflammation along the muscle edges
where is the muscle fasicle inflammation in polymyositits
endomysela inflammation
polymyositits
it is muscle only involvement which is not skin involved at all
what is the genetic issue with Duchenne muscular dystrophy
deletion of dystrophin gene
Ducheene muscular dystrophy
it is calf pseudo hypertrophy and proximal weakness starting at one years old
what is the function of dystrophin
it is the anchor between muscle cells and extracellular matrix
what is the genetic issue in Becker
it is a mutation in dystrophin, so it still produces some dystrophin
Myasthenia gravis
it is a postsynaptic issue. It is against the postsynaptic, so ACh cannot bind. It is no ache, and ptosis and double vision, muscle weakness is wore with use- thymoma and thyme hyperplasia
Lambert Eaton syndrom
presynaptic Ca channel is affected. Paraneoplastic from small cell lung cancer. decreased ACh release. weakness improves with use and it does not happen with the eyes
what is the dominant cell of liposarcoma
lipoblast
what muscle tumor is associated with TS
cardiac rhabdomyoma
where can a rhabdomyosarcoma be and what marker is here
it is in the heart of vagina and desmin positive
what are the layers of the epidermis deep to superficial
it is basalis, spinosum, granulosum, corneus.
atopic dermatitis
it is eczema and red itchy wet wit small vesicles. HSN1
contact dermatitis
HSN4 and it is from an irritant
acne vulgaris- what is the bug
it is from chronic inflammation no the hair follicles and sebaceous glands. It is in the hair share and paces breakdown the stuff with lipases
benzyl peroxide
it kills the pacnes
what does vitamin A do for acne
it decreases the keratin production
psotiasis
extensor surfaces, it is scale due to excess keratin and from trauma, and is HLA-C. hyperplasia of Keratinocytes. and parakeratosis, and longer dermal papilla. peel off skin and it bleeds.
how to treat psoriasis
it is treated with PUVA- psoralen and UVA light
lichen planus
purple polygonal papules, planar with white lines in the oral music and on the wrists and elbows. Inflammation at the DE junction and sawtooth pattern
what is lichen planus associated with
HCV
pemphigus vulgaris
IGG against desmoglein and it creates intraepidermal blisters and acantholyis from the basal layer staying attached. It is IGG fishnet. oral blisters when Q-tip is drug across it
bullous pemphigoid
detroy the hemidesmosomes and it blisters and has ED junctions and so large tense bullae. Oral is spared
erythema multiforme
HSR with target rash and bull assocaited with white central necroses. Can be fro SLE, or drug reaction or malignant
if the erythema multiform is associated with oral mucosa what is the lesion
it is from SJS
what is TEN
sloughing of skin from SJS and from adverse drug reaction
subbereic keratosis
it is stuck on coin lesions and this is a revised lesion of pseudocysts with pink swirls
what is the cause and name for sudden onset sobererc keratosis
it is the lesser treat sign and it is from gastric or GI cancer
acnathosis nigricans
velvet skin with epidermal hyerplasia- DM or gastric cancer
BCC risks, and what is seen
all is uvb exposure,and it is elevated nodule with central ulcer and telangtactase, and upper lip and nodule of basal cell with peripheral palisading. excise
SCC risk and what does it look like
it is UVB and from immunosuppressant, arsenic, chronic inflame of skin, ulcerated noudle hits the lower lip, treat wit hexcision
actinic keratosis
precursor to SCC, scaly plaque on the back, neck , face
keratoacanthoma
well defined SCC that rapidly develops then regresses. it is cup shaped with central ulcer full of keratin debris
vitiligo
autoimmune destruction of the metlanocutes. can be see in a white person that can’t tan
albinism
congential lack of pigment lack of tyrosine so normal metlanocytes
what is increased in freckles
iti can be increased number of melanosomes
junctional nevus
it is grown at the DE junction- child
compound nevus
it is down to D but in the E
intradermal nevus
it is down into the dermal only so it is adult
melanoma
assymtery, broad irrusialt, color, big diameter
phase of melanoma growth
radial growth and vertical
what determines how bad the melanoma is
depth
lentigo malgina
melanoma is only at junction good prog
superficial melanoma
early radial phase- good prog
nodular melanoma
early vertical phase- bad
acral lentiginous
it is on the nails and toes, which is not associated with sun light and it is in darker skinned people
impetigo
honey colored crusts with strep pyogenes and staph aureaus
cellulitis
dermal infection and it is trauma or insult
necrotiszing fascitis
it is necrosis of subcutaneous tissue and due to infection of flesh eating bacteriaa causes creptitis, and surgical emergency
staph scalded skin syndrome
it is from exfoliative tons a and B and removes the stratum granulosum- staph
where does TEN hit
the DE junction
veruca
warts with hPV
what is mollucusm contangiousum
large umbilicate pustule and it has inclusions called inclusion bodies
what is the typical arm fractures of osteoporosis
it is dinner fork fracture of the radius
what group has higher bone density
african american femaes
progressive groin and hip pain with exacerbation of wait bearing and decreased range of motion
avascular necrosis of bone
polyostatic fibrosis
bone mineral replaced by collagen Part of Macune albright syndrome
Macune Albright Syndrome
precocious puberty, and cafe au last spots and polyostatic fibrosis
what are the levels in primary hyperparathyoidism
it is increased serum calcium, decreased phase, increased ALP,ad increased PTH
what are the levels in secondary hyperparathyoidism
decreased CA, increased phos, increased ALP, and increased PTH from CKD
what are the levels in hypervitamin D
it is increased CA, and increased phos, and decreased PTH
what are the genetic predispositions to osteosarcoma
it is PAgets, ratiation, RB and Li-Fraumani which is a p53 mutaiton
what medication can exacerbate gout
thiazide diuretics
Sjogren syndrome
autoimmune disorder characterized by destruction of exocrine glands and it is expecially of the lacrimal and salivary glands by lymphocytic infiltrate
what are the complications of Sjogren
it is dental caries, MALTomas, and lymphoma
how do you diagnose it and what are the antibody markers
it is diagnosed by lip biopsy and it has anti SSA (ro) and SSB la
what are the findings associated with Sjogrens
inflammatory joint pain, keratoconjunctiitis, xerostomia and bilateral parotid enlargement
gonoccocal arthritis triad
polyarthralgias, tenosynovitits, and dermatitis, pustules
what should you look for with AS to diagnose progress in
it is with a chest XR to look at if it gets worse in thoracic to prevent chest wall movemetn
SLE presentation
rash, joint pain, fever- female of reproductive age and african american descent
libman sachs endocarditis
nonbacterial verrucous thrombi usually on the mitral or aortic valve
lipus nephritis
it is homerular deposition of complexes hematural and proteinuria
what are the symptoms of SLE
rash, arthritis, serositits, hematologic disroders, oral nasal ulvers, renal disease, photosensitivity, antinuclear antibodies, immunologic disorder, nuerologic disorder
what is the sensitive test and specific test of SLE
sensitive- ana
specific- anti dSDNA or Anti smith
what does SLE do to complement
decreased complete form increased consumption of the immune complexes
antiphopholipid syndrome
an be with SLE- thrombosis, spontaneous abortion, anticardiolipin and anti b2 glycoprotein antibodies- can be false positive on VDRL
mixed CT disorder
SLE, systemic scleoriss, and polymyositis- associatd wit hanti-U1 RNP antibodies
sarcoidosis
widespread noncaseating granulomas- elected ACE, and elevated CD4/CD8- bilateral adenopathy and coarse reticular opacities. Extensive hailer and mediastinal adenopathy. It is associated with restrictive long disease, and erythema podium, lupus perinea on skin, and bell palsy, epithelium granulomas, uveitis, hypercalcemia. increased 1 alpha hydroxylate mediated vitamin D activation.
what cytokines are active in sarcoid
it is Th1 and iL2 and IFN gamma increased so macrophages to granulam
what are the lab levels of calcium and vitamin D for sarcoidoisis
increased 1,5 vitamin D, decreased PTH and increased Ca
polymyalgia rheumatica
pain and stiffness in shoulders and hips with fever, males weight loss no weakness associated with temporal arteritis
what is the vacillates associated with polymyalgia rheumatica
temporal arteritis
fibromyalgia
females 20-50 and chronic musculoskeletal pain at stiffness, paresthesia, poor sleep, fatigue, and cognitive disturbance, and some fatigue and neurospych symptoms
what specific part of the NMJ does MA hit
the postsynaptic Nicotinic at receptors
myositis ossificans
hetertrpic ossification of skeletal muscle following muscle trauma- presents as suspicious mass at site of known trauma or as incidental finding on radiology
scleroderma diffuse
widespread skin involvement rapid progression and early visceral involvement, anti scl70 and anti DN toposionmerase I
limited scleroderma
limited skin involvement confined to fingers and gave. Also sclerodactyl, calcinocis, wryness, esophageal dysmotily, and telangatase- pulmonary HTN from deposition of collage
what is the antibody for limited scleroderma
anti-centromere
Ryanauds phenomenon
decreased blood flow to hands due to arteriolar vessel vasospasm i response to cold or stress, white and blue to red- raunaud is secondary to SLE, Crest or mixed CT disorder. it is the limited form of crest
what do you treat raynauds with
CCB
hyperkeratosis
thickness increased of strum corneum
parakeratosis
hyperkeratosis with mention of nuclei in statum coneum
hypergranulosis
increased thickness of stratum grnaulosum
spongiosis
epiderma accumulation of edematous fluid in intercellular spces
acantholysis
operation of epidermal cells
acanthosis
epderma hyperplasi and increased spinosum
rosacea
inflammatory facial skin disorder characterized by erythematous papillose and pustules but no comedones- may assocaited with facial flushing in response to extremal stimuli- alcohol and heat- phymatous rosacea and cause rhinopehyma deformation of the nose
urticaria
hives prurutic wheals that form after mast cell degranulation. supeficial dermal edema and lymphatic channel draining
angiosarcoma
rare blood vessel malignancy occurring in the head, neck and breast usually in elderly on unexposed areas- chronic psomastectomy lymphadeam
what is the associated with hepatic angiosarcoma
it is vinyl chloride and arsenic exposure
what is the marker for angiosarcoma
CD31
bacillary angiomatosis
benign capillary skin papillose in AIDS from bartonella henselae infection looks like kaposi but has neutrophilic infiltration
cherry hemangioma
benign capillary hemangioma of elderly does not regress increase wit hage
cystic hygroma
cavernous lymphagioma of the neck- translucent and it is in turners
glomus tumor
bening red blue tumor under finger nails arises from bodied smooth muscle cells of the thermoregualtor gloms body
kaposi sarcoma
endothelial malignancy most commonly associated wit skin , but mouth GI tract, and respirator tract, HHV8 and HIV. mistaken for bacillary angiomatousin but has lymphocytic infiltrate
pyogenic granuloma
polypoid capillary gemanioma that can ulcerate and bleed associated with trauma and pregnancy
strawberry hemangioma
bening capillary hemangioma of infancy and appear in first few weeks of life, and grows and rapidly regress spontaneously by 5-8 years
erysipelas
it is infection involving the upper dermis and superficial lymphatics usually from strep progenies and present with well defined demarcation between infection and normal skin
what organisms most often cause abscesses
it is staph aureus usually
why does erythema multiform happen
it is from the immune deposition in the skin which causes the reaction.
what viruses are often a cause of erythema multiform it is usually
hsv
scaly erythematous plaques in the shape of a christmas tree on the trunk
pityriasis rosea
what drug can you use for specific mutations of melanom
veruafenib- BRAF kinase inhibitor
what is the origin of melanocytes
neural crest cells
when does lung development start
4 weeks
what can errors in the embryonic period of lung development lead to
TE fistula
when is the pseduoglandular phase of lung development and what happens
it is 5-16 weeks. It is incompatible with life. it is endodermal tubes to terminal bronchioles
when is the cannilicular phase and what does it do
terminal bronchioles and respiratory bronchioles and alervelor dructs. airways increase in diameter
at what phase and week can respiration be capable
it is at 25 weeks and its in the cannilicular phase
what is the saccular phase and what does it do
it is development of pneumocytes. it is 26 weeks to brith
how is breathing in utero accomplished
it is breathing by aspiration.
what can causes pulmonary hypoplasia
diaphragmatic hernia or bilateral renal agencies which leads to poorly developed bronchial tree with abnormal histology
what is a bronchogenic cyst, where are they located
mediastinal mass in a child and it is from abnormal bugging can be infected or cause respiratory distress from compression of other structures
what are the cells that line the alveoli and are thin for gas exchange
type 1 pneumocytes
what cells secrete pulmonary surfactant and decrease alveolar surface tension and decrease lung recoil and increase the lung compliance. Proliferate in the face of damage
type II pneumocytes
what are club cells
nonaffiliated low columnar/cuboidal cells with secretory granules. Secrete a component of surfactant and degrade toxins and act as reserve cells
when do alevoli have a tendency to collapse
when they have a decreased radius according to lap laces law, they have an increased collapsibility.
what is the main component of surfactant
dipalmitoylphosphotidylcholine
what can you give to mother and when to increase surfactant production
48 hours before delivery give steroids
what does neonatal distress syndrome look like
alveloar collapse from increased surface tension and ground glass appearance on imaging
what is the screening for fetal lung development
it is L/S ratio of greater than 2 and foam stability test. Amniotic fluid is placed in ethanol and shaken
what does persistently low O2 cause
PDA
risk factors for neonatal RDS
prematurity, maternal diabetes from increased insulin, c section form decreased glucocorticoids produced form the baby
what can therapeutuc supplemental O2 cause in an infect
it can cause retinopathy of prematurity, intraventiruclar hemorrhage, bronchopulmonary dysplasia. The retinopathy is from increased O2 and the intraventricular hemorrhage is from the immature germinal matrix rupturing
what composes the conducting zone of the lung, what is the function and what are the epithelium made of
it is large airways of nose, pharynx, larynx, trachea, and bronchi- small airways are bronhioles to terminal bronchioles- it is warming humidifying, and filtering the air, but it does not permit in gas exchange so it is anatomic dead space. It is pseudo stratified because it has cilia to remove particles and then traditions to cuboidal cells at the terminal bronchioles. Smooth muscle gets to the terminal bronchioles
what composes the respiratory zone, and what are the epithelium and what clears the area of debris
it is respiratory bronchioles, alveolar ducts, and alveoli, and it participates in gas exchange. It has alveolar macropahges to clear the debris.
what happens to the resistance as you move down the airways
it decreases the resistance since the tubes are in parallel
a person aspirates while reclining in bed, where does it go
the superior segment of the inferior Right lobe
a person aspirates while sitting up in bed, where does it go
the inferior segment of the inferior right lobe
how many lobes do the right and left lung have
the right lung has 3 and the left lung has 2 and a lingula
what structure is at T8
IVC
what structure is at T10
esophagus, vagus
what is at T12
aorta, thoracic duct, and azygous vein
where does pain from diaphragm irritation go to
shoulder which is C5 and trapezius which is C3 and 4
what bifurcates at C4
common carotid
what bifurcates at T4
trachea
what bifurcates at L4
abdominal aorta
formula for minute ventialtion
Ve=Vt x RR
formula for alveolar ventilation
VA= (Vt-Vd) x RR
elastic recoil
tendency for the chest wall to want to go out and the lung to pull in
when are the elastic forces equal
at the FRC
At FRC what is the airway and alveolar pressures
it is 0 and the intrapleural pressure is negative to prevent the pneumothorax and PVR is the lowest
compliance of the lungs
change in lung volume for a pressure change. It is inversely proportional to the stiffness.
what are high lung compliance states
lung is easier to fill and its with normal aging and emphysema
what are low lung compliance states
lung is harder fill so edema, pneumonia, fibrosis
what does surfactant do to compliance
it increases compliance
hysteresis
it is lung inflation following a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation
what is the taut form of hemoglobin
iti s the deoxygenated form that promotes the release of oxygen
what is the relaxed form of hemoglobin
it is a form that has high affinity to grab O2
what favors the taut form over relaxed
increased Cl, H, Co2, 2-3 BPG, and temperature increased
why does fetal hemoglobin have higher affinity
it is does not respond to 2-3BPG
what type of iron is in hemoglobin
the F2 iron is in normal O2
what is the ferric iron and what does it do if its in hemoglobin
it is Fe3 and it has an increased affinity for cyanide and its called methemoglobin
chocolate colored blood and cyanosis
methemoglobinemia
what can induce metheglobinemia
it can be induced by nitrites plus thiosulfate or benzocaine and can be used to treat cyanide poisoning
treatment for metheglobinemia
methylene blue and vitamin C
what level does not change with metheglobinemia
PaO2
carboxyhemoglobin
form of Hb bound to CO in place of O2. It decreases the oxygen binding capacity and so decreased unloading to tissue. treat with O2
what is positive coopertivity
after one O2 binds to hemoglobin it increases affinity of binding for the others
does myoglobin have cooperatvity
no
what things cause Hb right shift
acid, Co2, exercise, 2-3 BPG, altitude, temperature
Left shift
can be from increased EPO and erthyrocytosis or fetal hemoglobin
what lab values do not change with changes in the hb content of the blood
PaO2 and O2 saturation
what is the hb concentration, o2 sat, PaO2, total O2 content: Co poisoning
Hb concentration: normal
%O2- decreased
PaO2- normal
total O2 content- decreased
what is the hb concentration, o2 sat, PaO2, total O2 content: anemia
Hb concentration: decreased
%O2- normal
PaO2- normal
total O2 content- decreased
what is the hb concentration, o2 sat, PaO2, total O2 content: polycythemia
Hb concentration: increased
%O2- normal
PaO2- normal
total O2 content- increased
perfusion limited lung:
gas equilibrates early on the capillary so it is can only increase if flow is increased
diffusion limited lung:
emphysema, fibrosis, CO- gas does not equilibrate by the time blood reaches the end of the capillary
DCLO
extend to which oxygen passes from air sacs into the blood
diffusion area is decreased in
emphysema
alveolar wall thickness is increased in
pulmonary fibrosis
equation for pulmonary vascular resistance
PVR= P(pul artery)-P(left atrium)/CO
alveolar gas equation
PAo2=PIO2-PaCO2/R
when can increased A-a gradient occur
hypoxemia causes shunting, V/Q mismatch, fibrosis
what decreases O2 delivery to the tissue
decreased CO, Co poisoning, hypoxemia, anemia
what decreases PaO2 with normal A-a gradient
high altitude, hyperventilation aka opioid use
what decreases PaO2 with an increased A-a gradient
V/Q mismathc, diffusion limitation like fibrosis, right to left shunt
ischmia or loss of blood flow is from
impeded blood flow or decreased venous drainage
what can obesity do to breathing
hyperventilation from increased CO2 and no A-a gradient
what is the difference in zone one of the lung
it is wasted ventilation because there is less perfusion
what makes the V/Q mismatch less
exercise from vasodilatin
why does TB like the apex of the lung
extra O2 hangs out up there
when does the V/Q equal 0
when there is an obstruction, so extra O2 does not help because it can’t get to the alveoli.
when is the V/q equal to infinity
it is equal to infinity when there is not enough perfusion. It can be improved by increasing O2 content
what are the ways that CO2 is carried in the eblood
HCo3, carboaminohemoglobin when the CO2 binds the N terminus of global. which is in the taut state, and dissolved in the blood
Haldane effect
oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equillibrium toward CO2 formation therefore Co2 is released from RBCs
Bohr effect
increased H+ from the tissue metabolism shifts the curve right to unload O2
what does the body do in response to high altitude
it decreased PaO2, increased ventilation, decreased Pa CO@, respiraotry alkalosis, altitude sickness
what are the signs of acute altitude sickness
it is headache, fatigue, acute cerebtal edema, and pulmonary edema from vasofialtion in the brain and vasoconstriction of the lungs from shunting which increases the pressure leading to edema
chronicly what does high altitude do
it increases ventilation, increased 2,3BOG, increased EPO, and increased cellular mitochondria, increased renal excretion of HCO3 which is also augmented by acetazolamide which is compensation for the respiratory alkalosis
what does chronic hypoxic pulmonary vasoconstriction lead to
pulmonary hypertension and RVh
what happens to the levels of PaO2, PaCO2, venous Co2 and venous O2
there is no change in PaO2, and PCo2, but the venous content of Co2 increases and the venous content of O2 decreases
what is the most common viral cause of rhinitis
adenovirus
what type of HSN is allergic rhinitits and what is seen histologically
it is HSN1 . see eosinophilic inclusions and associated with asthma and eczema.
child with nasal polyps what might you be worried about
CF
if there is asthma and nasal polyps, what should you not give him
aspirin
adolescent male with profuse nose bleeding
it is angiofibroma- benign tumor of nasal mucosa
nasopharygeal carcinoma
it is a EBV associated tumor with cervical lymphadenopathy and pleomorphic and keratin positive cells of epithelial cells in the lymphocytes
acute epiglotitis
HIb is the cause and there is airway inflammation, drooling, dysphagia, and insipraory stridor and protect airway
larygneotraceheal bronchitis
parainfluenza with seal back cough
vocal cord nodules
it is excessive use, mixed tissue, and hoarsness and it is bilateral
laryngeal papilloma and cause and histology
it is HPV 6,11- koilocytes and multiple in kids and single in adults
laryngeal carcinoma
squamous cell cancer from epithelial lining and cause alcohol, smoking, hoarseness, stridor, and some increased risk of HPV
risk factors for pneumonia
impaired cough, decreased mucocilliary elevator, and circus can known down the cilia which causes risk of superinfection. mucus plug
symptoms of pneumonia
fever, chills, sputum, pleuritic chest pain from increased bradykinin and PGE2, decreased breath sounds, dull to percussion, and increased WBC
what are the common causes of lobar pneumonia
klebsiella from aspiration in alcoholics, elderly, and diabetics and have thick mucoid capsule and currant jelly sputum and abscess.
strep pneumo is common in old people
are the stages of lobar pneumonia and what do they look like
- congestion-dilated vessels and edema
- red hepatization- neutrophils and blood increased RBC leads to the consolidation
- grey hepatization- RBC get broken down still consolidated
- resolution- scar leads to increased activity of pneumocytes II
Bronchopneumonia causes and what does it look like and which are associated with
- staph aureus- number 1 cause of virus knock out the elevator. Can cause empyema(infection in pleura in the infection), and abscess
- hib- COPD
- pseudomonas- it is CF
- moraxella- community or COPD
- legionella- water source- silver stain and intracellular organism
interstitial pneumonia causes are presentation
diffuse inflammation of air sac is atypical. It has a mild URI and decrease sputum and cough, and low fever. Empty air sacs, and neutrophils in the interstitium,
- mycoplasma- can cause IgM hemolytic anemia and no cell wall
- chlamydia- teenagers
- RSV- neonates
- CMV- post transplant
- influenza- old people increased risk of pneumonia
- coxiella- atypical farmer or vets- high fever- cattle placenta lots of spore- rickettsia without rash
aspiration pneumonia- where does it occur and what causes it
anaerobe- bacteriodes, fusiform, and peptococcus- right lower lobe abscess
TB primary infection
Ghon ocmplex, fibrosis, calcification of hillier LN, and lower lobe. positive PPD and sub pleural and hillier.
secondary TB
AIDs, age increase the likelihood of reactivation. Apex for increased O2 and foci of caseating necrosis, and military TB which seeds other organs. Fever, night sweats, caveating necrosis granulomas, look for acid fast positive
what part of the brain does TB seed
base of brainstem
what does TB cause in the kidney
sterile pyuria
what does TB in the bone cause
Potts disease
what does airway obstruction lead to in terms of values
decreased FVC, decreased FEV1, decreased ration, and increased TLC
Chronic bronchitis presentation
it is 3 months over 2 years from smoking large areas. It is glandualr hyperplasia leading to increased mucus which forms plus and then leads to cough and increased PaCO2 and decreased PaO2, and
chronic bronchitis complications
increased risk of infections and for pulmonate, clamp down to shunt from O2 low region and move it to other areas, but if its all over from disease all over can create increased RH work which led to right heart hypertrophy and failure.
emphysema presentation
destroy alveolar sacs from exchange so increased collapse because cant have enough elastic roil to stay open. It is dyspnea, airway collapse of small ones, purse lips for increased back pressure to prevent trapping, and pink offer ,weight loss from increased breathing work ,and wide chest from increased chest pull out
what is emphysema pathophysiology of smoking caused
centracinar emphysema- it is increased proteases because of the extra inflammation which is more than the alpha 1 can handle
what is the pathophysiology of alpha 1 antitrypsin
it is no protection from protease damage because too much proteases. It is panacean emphysema and lower lobe pneumonia get cirrhosis from misfolded protein build up in the hepatocytes and this causes pink PAS positive globules. these are in the endoplasmic reticulum
what is the gene for alpha 1 anti-trypsin and what is the difference with a heterozygote and homozygote
-PiM is normal allele and the common mutation is PiZ. If you are homozygous, you will get it. There is PiZ and PiM together then it is you are heterozygous so should not smoke, but need to keep lungs protected because some increased risk from decreased production,
what are the cytokines that induce asthma
TH2, IL4-IgE, IL5-eosinophils, IL10- inhibit Th1, and so increased Th2
pathophysiology of asthma
it is re-exposure causes cross linking of IgE and this activates mast cells and dump histamine and causes vasodilation,in venues and it causes fluid from posterior capillary venues. Leukotriene C4, D4,E4- constriction and inflammation leads to bronchoconstriciton and perpetuats the constriction.
what is it called if asthma doesn’t want to stop
status asthmaticus
bronchiectaasis
abnormal dilated airways - lose tone and air trapping whorls because the air can’t get out. Large airspaces and necrotizing inflammation and damage to the wall
who gets bronchiectasis
CF (thick sputum), Kartageners (dynein arm less movement), tumor or foreign body, necrotizing infection like Kleb, and allergic bronchopulmonary aspergillum (asthmatics or CF gets HSN reactions to aspergillum.
what are the complications of bronchiectasis
hypoxia and cor pulmonale, and secondary amyloidosis
foul smelling sputum, dyspnea, cough
bronchiectasis
what are the lab values for restrictive lung diease
decreased TLC, decreased FVC, decreased FEV, and increased ration
idiopathic lung fibrosis what causes it and cytokine and symptoms
TGF-beta from injured pneumocytes induce fibrosis and can be from bleomycin, amnioderone, dyspnea, progressive cough, and sub pleural fibrosis, honey comb lungs
coal workers lung
carbon to the macrophages, shrunken lung
what is associated with coal workers lung
rheumatoid arthritis
what is seen with mild carbon
build up in macrophages, and anthracosis, and hilar LN, and common with just polution
silicosis patient, what does it inhibit, and what are they at increased risk of
sand blaster and miners, impaired phagolysossome in macrophages, and increased risk of TB in the upper lobes
beryllium lung
aerospace injury, non caseating granulomas like sarcoid. increased risk of lung cancer
asbestosis
constuction, plummer, ship year, fibrosis of the lung and pleura increased risk of lung cancer and mesothelioma
what are the cells seen in a sample of asbestos exposure
ferruginous bdies which are iron barbells
sarcoid what causes it and histology and symptoms
systemic non-caseating granulomas, black female and CD4 + T cell response, and Cutaenous nodules, uveitis, and asteroid bodies, Sjogrens syndrome, and lung can become less compliant. dyspnea, cough, increased ACE in suerm, hypercalcemia, treat with steroids and can resolve without it
why does sarcoid cause hypercalcemia and what other conditions can cause it
it increases activation of vitamin D because it has 1 alpha hydroxylase activity and it is increased in anywhere that has noncaseating granulomas
what can cause HSN pneumonitis and what are the features
it is fever, cough, dyspnea, and remove exposure and it gets better. granulomas form- eosinophilic granulomas and it is pigeon breeders comtimes
what is seen with pulmonary HTN
it is increased MAP and the women with exertion dyspnea
primary pulmonary HTN
young adult females, increased BMPR2 inactivation leads to increased vascular smooth muscle
causes of secondary pulmonary HTN
it is hypoxemia, increased surface tension, and so increase volume current like congenital heart disease
ARDs
damage to alveolar cap interface and protein fluid forms hyaline membrane like dense pink. Increased diffusion barrier so hypoxemia, and increased surface tension so collapse air sacs. Diffuse white out o lung
what are the causes of ARDS
sepsis, infection, shock, trauma, aspiration, pancreatitis, DIC, HSN, drugs
pathogenesis of ARDs
activation of neutrophils inducing protease mediated damage and free radical damage to type I and II penumocytes
what do you treat ARDS wit hand what are the complications
PEEP to prevent collapse and complication increased fibrosis
neonatal RDs
inadequate surfactant so increased surface tension.
what are the populations at risk for neonatal RDs
premature before 34 weeks, C section from decreased stress, and maternal diabetes because insulin prevents surfactant activation
what is seen on the XR for NRDS
hazy granularity
what is the main component of surfactant
lecithin has phosphatidylcholine mainly
what is the complications of NRDS
it is necrotizing enterocolitis, and PDA
what can supplemental O2 do in a neonate
retina with free radical injury and bronchopulmonary dysplasia
what is the bad part of cigarette smoke causing cancer
polycyclic aromatic hydrocarbons
what do you look for if there is a mass on lesion on the lung
look at old XR to see if anything has changed
what are the benign lung lesions and what can cause them
benign hamartomas and grnulomas (histoplasma and TB)
what are hamartomas composed of
calcified on imaging and has cartilage and lung tissue
small cell lung cancer what does it look like
poor differentiated small cells, central tumor on smokers and increased mitosis
small cell lung cancer: what are the paraneoplastic syndromes
ADH, ACTH, and Lambert Eaton (presynaptic calcium channels)
squamous cell carcinoma histology
keratin pearls and intracellular bridges which are desmosomal connections
where is the squamous cell tumor and what are the paraneoplastic syndromes
PTHrP and increased Ca, and central tumor of male smokers
large cell tumor histology
poor differentiation with poor prognosis
bronchioloalveloar tumor
tumor on small airway and malignant Clara cells and peripheral looks like pneumonia and walls of alveoli are replaced by tall columnar cells
carcinoid tumors
neuroendocrine tumors and polyp mass on the bronchi positive chromogranin
what cancer is involved or moves to the pleura
adenocarcinoma
what are some of the complications of lung cancer
pleural involvement (adenocarcinoma), obstruction of the SVC, phrenic or laryngeal nerve, pan coast tumor (pinpoint pupil, and anhidrosis of the forehead , and ptosis
where does a lung tumor met to
adrenal glands
which way does the trachea go on a spontaneous pneumothorax
it is an emphysematous bleb and young male and trace goes towards it
which way does the trachea go in a tension pneumothorax
penetration causses a one way valve the trachea goes away from it.
mesothelioma
pleural tumor that encases the lung. it is dyspnea, and chest pain, rind around the lung- asbestos exposure
where do the maxillary sinuses drain to
middle meatus
epistaxis where is the life threatening bleed from
posteior segment in the sphenopalatine artery branch of maxillary artery
what are the typical HEENT tumors and what causes them
squamous cell cancer and HPV16 usually multiple tumors
Virchow triad
stasis, hypercoagulability, endothelial damage
D dimer is used to rule out DVT why
high Sn and low Sp
who to treat DVT
heparin and LMWH for the first bit then use warfarin and rivaroxaban
aviation what happens to the lung and body
G forces that are positive then increased blood to lower body and blackout at 4-6 Gs and scpaship is 8-9 so use G suit or change the angle. G- is all the blood to the head
space what happens to the body
prolonged light leads to decreased BV and RBC and muscle street, decreased CO, and Ca and phos decrease
nitrogen narcosis does what
N dissolves into neural membrane leading to decreased neuronal excitability act drunk
decompression sickness
nitrogen is liquid in blood and comes out if start to come up to fast occluding vessels leading to dizziness, paralysis, sycope, and and SOB and pulmonary edema
pulmonary emobolism
hypoxemia, resp alk, and sudden onset chest pain, dyspnea, and tachypena and tachycardia.
what are typical histology of PE
it is lines of zahn which are interdigitating areas of pink platelets and red RBC and the thrombus is formed before death
what are the types of emobil
fat, air, thrombus ,bacteria, amniotic fluid, tumor
what causes fat emoboli
it is from bone fractures or liposuction. hypoxemia, neurologic abnormalitiy, and petechial rash
amnitic fluid emboils is from
DIC and postpartum
air embolus
from bends and it is treated with hyperbaric O2
what can cause sudden death in a PE
it is a saddle embolus
what stain is used for asbestosis
it is prussian blue
why does TB have increased risk with silicosis
the silicosis impairs the phagolysosome of the macrophages which increases the infectious potential of TB
why does pancreatitis cause ARDS
it is from increased cytokines and pancreatic enzymes so neutrophils get into the intersitium chasing pulmonary edema and exudate and free radical damage
what happens to the lung and PCWP during ARDS
normal PCWP decreased lung complicate and V/Q mismatch
sleep apnea
repeated cessation of breathing>10 seconds during sleeping disrupted sleep and daytime somnolence. Normal PaO2 during the day. Nocturnal hypoxia leading to systemic/pumonary hypertension and arrhythmia atrial fib and flutter. sudden death and hypoxia nadi increased EPO and increased eryhtropoesis
obstructive sleep apnea
repiraoty effort against airway obstruction, associated with obesity, loud snoring, caused by excess paraphayrngeal tissue in adults, adenotonsillar hypertrophy in children, Weight loss and Cpap
what can kinda of nerve stimulator do you use for sleep apnea
hypoglosal stimulator
central sleep apnea
norespiratory effort due to CNS injury/toxicity, HF, and opioids
obesity hypoventilation sydnrome
obestity, hypoventilation, decreased RR, decreased PaO2, and increased PaCO2 during sleep, increased PaCo2 during waking hours from retention
what are increased and decreased values in pulmonary HTN
increased endothelia, decreased NO, and decreased prostacyclin
what heart sounds are heard with pulmonary HTN
accentuation of S2 from increased VR and increased JVP, and peripheral edema and hepatic congestion
what is transudate pleural effusion
decreased protein content due to increased hydrostatic pressure or decreased oncotic pressure like nephrotic syndrome and cirrhosis
what is exudate pleural effusion
increased protein content, cloudy, due to malignancy, pneumonia, collagen vascular disease,e trauma occurs with increased vascular permeabiltiy and must be drained due to infection risk
lymphatic pleural effusion is from what
thoraci duct injury from trauma or malignancy, milky appearing fluid increased triglycerides
lung abcess
aspiration of oropharyngeal contes like loss of consciousness like alcoholics or epileptics or bronchial obstruction. Air fluid levels on CXR
lung abscess with upright lesion where
basal segments of right lower lung
lung abscess with supine lesin
posterior segments of right lobe or superior segment of right lower lobe
is smoking a risk factor for mesothelioma
no
why does pulmonary destruction happen with abscess
partially because of the release of lysosomal enzymes by neutrophils and macrophages it helps kills the pathogen and clean debris but can cause parenchymal damage as well
treatment for lung abscess
clindamycin
what structures does Pancoast tumor compress
recurrent laryngeal nerve, superior cervical ganglia, superior vena cava, and sensorimotor deficit
SVC syndrome
an obstruction of the SVC that impairs blood drainage from the head with jugular distention, and upper extremity edema, and caused by malignancy, and thrombosis of indwelling catheter, and can raise intracranial pressure if obstruction is severe and headaches, and dizziness and increased risk of aneurism and rupture of intracranial arteries
