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160 Cards in this Set

  • Front
  • Back
what is a motor unit?
the functional unit of the neuromuscular system
what are the 3 components of the motor unit?
low motor neuron in the anterior horn of the spinal cord
the axon of the lower motor neuron
the multiple muscular fibers that the neuron innervates
how does the ratio depend on the muscles involved?
finer control muscles have higher ratios, while larger and more broad ovements have lower ratios.
what is the difference between a nerve and a nerve fiber?
one fiber is an axon with its schwann cells.
a nerve is a bundle of nerve fibers.
what king of nerve fibers are found in the peripheral nerves?
both myelinated and non-myelinated
what is the difference between the myelinated nerves in the CNS and the PNS?
PNS- have a higher amount sphingomyelins and glycoproteins. MPZ and MPB are both proucts common to the myelinted PNS.
are schwann cells found on non-myelinated axons as well as myelinated?
yes, but they cover more axons with non-myelinated, one for every 5-20, while the myelinated are a 1:1 ratio.
what regulates the nerve environment, and how does it work?
perineural barrier- tight junctions between nerves, between cells that form the outer layer of the arachoid membrane, and by endothelial cells in the capillaries derived from the vasa nervorum
what normal cell function does not occur in peripheral nerves?
no protein synthesis, only by axoplasmic flow are they delivered and feedback is done by retrograde transport.
what is the difference between type 1 and type 2 muscle fibers?
1- weight bearing, sustained force, slow twitch. High in myoglobin, lots of mitochondria, red, fatigue resistant, lots of lipids, scant glycogen. Postural muscles, they rely on oxidative phosphorylation. no lactic acid.
2- sudden movement, fast twitch, few mitochondria, abundant glycogen. Increase with androgenic steroids, decrease with no activity. Make lactic acid.
are more than one type of muscle fiber found within the same motor neuron?
no, the motor neuron determines the myofibril type.
what are the 2 general reactions of the motor unit?
1- schwann cells affected = demyleination
2- neuronal or axonal degeneration, or group atrophy.( sometimes can recover- type grouping)
describe segmental demyelination?
dysfx of schwann cells or damage to the myelin sheath.
not a primary abnormality of the axon.
Affects some schwann cells while sparing others.
denuded axon provides stimulus for remyelination.
new ones are smaller and thinner.
what is sequential episodes of remyelination to a peripheral nerve called?
onion bulb formation
describe axonal degeneration and muscle fiber atrophy.
primary destruction of the axon with secondary disintigration of the myelin sheath. Wallerian degeneration in the distal end of the axon that has been transected.
describe the muscle atrophy associated with axonal degeneration
myofibers become angular.
loss of myofilaments and myofibrils
if not reinnervated, proceeds to complete loss
condensation and aggregation of the nuclei.
what is guillian barre syndrome?
acute inflammatory demyelinating polyradiculoneuropathy.
preceeded by a viral illness, and patient has recovered by the time the neuropathy develops. No infectious agent is found in the peripheral nerve. Felt to be immunologically mediated with circulating antibodies damaging the nerve. Causes inflammation, segmental demyelination, and occasionally damage to the axons.
Ascending paralysis (affects the longer neurons fisrt)
loss of dependant reflexes
increase in the CSF protein.
decreased velocity
COD is usually respiratory paralysis.
can cause autonomic instability, causing severe orthostatic hypotension, diarrhea or constipation.
what is leprosy?
caused by mycobacterium leprae
involves schwann cells
loss of myelinated and non-myelinated axons.
symetric polyneuropathy involving pain fibers and leads to loss of sensation.
what causes diptheria?
diptheria exotoxin causes parathesis and weakness in the peripheral nerves. Loss of proprioception and vibratory sensation.
selective demyelination that extends into the anterior and poterior roots, as well as into the sensorimotor nerves.
what virus can cause lesions in the peripheral nerve?
varicella zoster virus
describe shingles?
latent infection of neurons in the sensory ganglia of the spinal cord and brain stem following chicken pox. After reactivation it causes painful vescicular skin eruptions in a dermatomal distribution. It can cause neuronal destruction and axonal regeneration
what are the commonalities associated with hereditary neuropathies?
all are heterogenous
progressive
affect both strength and sensation
what is HMSM1?
charcot marie tooth disease
usually appears in childhood
ADprogressive atrophy of the calf. presents as muscle weakness in calf or cavus foot
palpable nerve enlargment with onion bulbs.
still has normal life span.
what is HMSM2
similar to HMSM 1, but no nerve enlargment
presents at later age
no segmental demyelination
AD
HMSM3?
Dejerine-Sottas Disease
AR
begins in childhood.
delayed motor skills
areflexia
large often palpable peripheral nerves.
distal weakness is accompanied by truncal weakness.
what is the morphology of type 3?
onion bulbs
segmental demyelination
axonal loss
peripheral neuropathy with type 2 diabetes?
distal symmetric sensory or sensory motor loss (most common)
autonomic
can cause ulcers
what percentage of diabetics have neuropathy after 25 years of disease?
50%
100% have conduction abnormalities
20-40% have autonomic neuropathy.
what is autonomic neuropathy in diabetics usually associated with?
distal sensorimotor abnormalities
what is mononeuropathy associated with diabetics?
disorder of a single individual peripheral or cranial (occulomotor) nerve or several individual nerves.
how are the kidneys affected by peripheral neuropathy?
axonal degeneration with degeneriating fibers and fiber loss.
what nutritional deficiencies can cause peripheral neuropathy?
Thiamine (dry beriberi)
B6, B12, E
what drugs can affects B12 levels and can cause peripheral neuropathies?
PPIs
what can cause neuropathies associated with malignancies?
infiltration or compression by the tumor
paraneoplastic syndromes- diffuse neuropathy in patients with distant cancer (small cell lung cancer). An example would be plasma cell dyscrasias (MM) that cause amyloid to be depoisitied in peripheral nerves.
what can cause toxic neuropathies?
exposure to environmental chemicals, biologic toins, or therapeutic drugs
what is a traumatic neuropathy that is not due to direct damage?
carpal tunnel syndrome
what predisposing factors can cause carpal tunnel syndrome?
pregnancy
DJD
hypothyroidism
amyloidosis
excessive use of the wrist.
what is a morton's neurona?
impingement of the common digital nerve between metatarsal heads. Commonly in the 2nd and 3rd interspaces. Usually diagnosed by parasthesia between 3rd and 4th digits.
what is type 1 neurofibromatosis?
also known as von recklenhausen's disease
AD - chromosome 17
multiple neural tumors that can be located anywhere on the body (arise within or attached to nerve trunks).
skin lesions called cafe au lait spots
pigmented iris hemartomas (lisch nodules)
these
what are the 3 types of neurofibromas that are associated with type 1?
1- cutaneous- sessile or peduncualted
2- subcutaneous- just below the skin, often painful
3- plexiform, huge multilobar pendelous masses, as big as 20cm diameter.
describe the cafe au lait spots
round to ovoid with long axis parallel to underlying nerve.
6 or more spots with a diameter of more than 1.5 cms is necassary
what are lisch nodules?
pigmented hemartomos of the iris, asymtomatic, but aid in diagnosis.
what gene has been linked to NF-1?
NF-1 gene, AD, chromosome 17
what types of lesions are assocoated with NF-1?
skeletal- erosive defects, scoliosis, cystic lesions.
increased risk of developing other tumors
increased risk of decreased intelligence.
what is type 2?
much less common than type 1
AD
patients develop bilateral acoustic schwanoma, multiple meningiomas, gliomas on the spinal cord, and non-neoplastic lesions.
have cafe au lait spots, but no lisch nodules.
what is amyotrophic bilateral sclerosis?
neuronal muscle atrophy
upper and lower motor neurons are affected
loss of nerves in the anterior horn and corticospinal tracts
most common in older maes
AD
reactive gliosis
precentral gyrus can be atrophic in severe cases.
early- asymetric weakness in hands, cramps in arms and legs
late- decreased muscle stength and bulk, and fasiculations and respiratory muscles can become involved.
what are muscular dystrophies?
heterogenious group of inherited disorders characterized by progressive severe muscle weakness and wasting often beginning in childhood.
what is duchenne's muscular dystrophy
most common form
x-linked
normal at birth, delayed walking
use gauer's manuver to get in walking position.
usually death by 20's due to repiraotry distress or infection or cardiac degeneration.
usually begins at pelvic girdle
pseudohypertrophy of calves. (1st fiber hypertrophy, but leads to fat and CT hypertrophy).
X-linked Recessive- Xp21- causes dystrophin to be produced which dauses deletions, frame-shifts, and point mutations.female carriers are asymptomatic.
what is dystrophin?
normally located adjacent to the sarcolemmal membrane in myocytes. It maintains the myocyte membrane integrity during shape change associated with muscle flexing.No dystrophin is found in Duchenne's syndrome.
morphology of DMD?
variation in muslce fibers
increased # of internalized nuclei
degeneration, necrosis, and fibrosis of myocytes
regenertion of muscle fibers
both type 1 and 2 are involved.
what is becker muscular dystrophy?
X-linked recessive
has diminished amounts of dystrophin.
similar to DMD, but lower progression and may have a normal life span and is less common.
what are limb girdle autosomal muscular dystrophies?
affects the proximal musculature of the trunk and limbs. they are similar to duchennes?
what is the most common form of adult muscular dystrophy?
myotonic dystrophy- sustained involuntary contacture of muscle groups.
in respect to myotonic muscular dystrophy, what does anticipation mean?
the disease tends to get more severe and has an earlier onset with succeeding generations (autosomal dominant).
what do we need to know about the gene involved with myotonic dystrophy?
it codes for mytonin protein kinase and it is a trinucelotide repeat.
what is the main difference between myotonic dystrophy and DMD?
the ring fibers- myofober with a subsarcolemmel bandof cytoplasm distinctfrom the center of the fiber.
what are the S & S of myotonic dystrophy?
gait abnormalities, especially with foot dorsiflexors.
weak hands and wrists
cataracts
atrophy of facial muscles
myotonic response by percussion of thenar area.
what causes the glycogen storage diseases?
mcCardle syndrome: type V. glycogen being stored in the skeletal muscles. painful cramps with strenuous activity.
describe mitochodrial myopathies and their different classes
aggregation of abnormal mitochondira. They have Red Ragged fibers.
I- AD or AR, on nuclear DNA
II- point mutations onmtDNA
III- deletions or duplications on mtDNA.
drug-induced myopathies?
cushing's syndrome (endogenous or idiopathic) - causes proximal muscle weakness., and type 2 muscle fiber atrophy.
Chloroquine- vacuoles in myocytes
what is thyrotoxic myopathy?
acute or chronic proximal muscle weakness with hyperthyroidism, it can preceed the other signs of thyroid dysfunction.
hypothyroidism can also cause fiber atrophy and cramps and achings and loss of the DTRs
ethanol myopathy is significant because of what two molecules that are toxic to the kidneys?
rhabdomyolysis
myoglobin
myasthenia gravis?
auto immune disease
immune mediated loss of ACh receptors because of ACh receptor antibodies.
65% have thymic hyperplasia
15% have thymoma
what do we need to know about the AChr antibodies associated with myasthenia gravis?
increases degredation of AChr
blocks receptors
fixes comlpement to damage the postsynaptic membrane
antibody levels does not correlate with severity of the disease.
what happens in severe cases of myasthenia gravis
type 2 fiber atrophy
simplification of the post synaptic membrane
deposition of immune complexes and complement to the post synaptic membrane.
what are the clinical S&S of myasthenia gravis?
extraoccular muscles
ptosis
double vision
the weakness can flucuate
improved with anticholinesterase agents
treat with prednisone, and reesction of the thymomoa if present
what is Lambert-Eaton Myasthenia syndrome?
another disease of the neuromuscular junction.
typically a paraneoplastic syndrome, but can occur without cancer. Get proximal muscle weakness and autonomic dysfunction.
fewer vescicles are released with presynaptic action potential.
how do the ostecytes communicate with eachother?
they use the caniculi and the haversian systems.
Is bone a static organ once it is matured?
no it is continually being broken down and built back, so much that 10% of the skeleton is replaced each year.
what mediates bone resorption?
osteoblasts - by stimulating osteoclasts via paracrine chemical signalling
what triggers osteoblasts to lay down new bone?
cytokines and growth factors released during resorption.
what is craniorachischisis
failure to close the cranium or the spinal column (meningomyelocele and meningoencephalocele)
what genetic mutation is responsible for causeing achondropasia, or dwarfism?
fibroblast growth factor receptor 3 (FGFR3), which causes unorganized growth plates.
osteogenesis imperfecta is commonly made manifest by what?
blue sclerae, and multiple fractures seen in children, so often that eventually doctors start wondering if the kids are being abused. Abnormal teeth, and hearing loss.
what are the important factors in causing secondary osteoporosis that we were told to remember?
bed rest (physical inactivity)
paralysis
dietary- Vit D, calcium, protein deficeincies
steroids
what does a decrease in estrogen cause in bones?
increase in cytokines that stimulate osteoclasts, most commonly in the femoral neck.
what is osteopetrosis?
abnormally thickened bones due to insuffificinet osteoclast activity. Marbe bone disease. Very brittle. No room for hematopoeisis. Nerve root are compressed that can cause cranial paulsey.
what is paget's disease?
overactive osteoclasts, followeed by osteoblasts. Thin, then abnormaly large and brittle bones. End stage the bones are very dense and sclerotic. Patients usually present with pain.
what are brown tumors and cutting cones associated with?
hyperparathyroidism- increased coritcol resorption. Controling it may cause recession.
with osteonecrosis of the femoral head, what are the usual signs of it occuring histiologically?
dead bone surrounded by necrotic adipocytes and necrotic marrow.
what is the difference betweeen sequestrum and involucrum?
sequestrum is an island of dead bone, and involucrum is the repairative bone that is growing around the edges.
what kind of infection is common in children when they have chronic osteomyelitis with an abcess involved?
septiv arthritis- the abcess will track into the joint.
what type of infections are seen with staph aureus?
folliculitus- inflammation of a hair follicle
furuncles- infected hair follicle that causes accumulation of pus and dead tissue.
carbuncles- a collection of furuncles draining pus onto the skin.
cellulitis
fasciitis
peronychia
wound infection
respiratory tract infections.
VRSA
MRSA
Bronchopneumonia- causes abcesses, fistulas, empyema, and is very destructive.
what non-suppurative (non-pus forming)diseases can Staph Aureus cause?
scalded skin syndrome- staph pharyngitiscommon in newborns. Fever, erythema, and exfoliation
toxic shock syndrome- staph vaginalis.
food poisoning- from ingested enterotoxin in unrefridgerated dairy and meats. N/V/D.
what kind of infections can staph epidermitis cause?
endocarditis
catheder and shunt infections
prosthetic joint infections.
what non-suppurative diseases can strept cause?
pharyngitis
impetigo- honey crusts
erysipilis- rash
scarlet fever- strawberry tongue and rash on thigh and trunk.self limitied but at risk for post complications
rheumatic fever
Post strept glomerulonephritis
what are the two pathogenic species of neiseria?
meningiditis- suppurative sporadic or epidemic. fever, headache, purulent spinal tap with low glucose and high WBCs and proteins. Can cause septicemia.
meningococcemia- can occur with or withour meningitis. Cause small petechial lesions on the skin. Endotoxin can cause waterhouse syndrome (in adrenal glands) and DIC.
gonococcemia- arthirits, rash, fever.
decribe the arthritis seen with gonococcus infections.
acute polyarticular type.
freee of cultural gonnococci

chronic type has purulent exudate and has positive cutures.
what is more common, metastatic cancers or primary bone neoplasms?
metastatic cancers
why is radiography important in diagnosis of a bone tumor?
to determine if it is in the epiphysis, metaphysis, or diaphysis. Also to determine if it involves the cortex or the medulla. And also to determine if the borders are well defined or if they are infiltrative.
what does periosteal growth indicate on a radiograph?
rapid growth
describe an osteoma.
benign, sub periosteal, solitary, may be in association with gardner's syndrome. Located in the head and neck (it can inpinge on outside tissues). It has woven and lamellar (mature) bone. The hematopoeitic element may be present.
osteoid osteoma?
less mature lamellar bone and woven bone. Loose connective tissue surrounding it. Less than 2cm. Common in femur and tibia. Painful, but can be releived by aspirin.
what is the difference betweeen an osteoid osteoma and an osteoblastoma?
osteoblastoma- larger than 2cm, usually occurs in the vertebral column and usually is not relieved by aspirin.
describe the radiographic findings for osteoid osteomas and osteoblastomas
well circumscribed
only involves cortex
rim of sclerotic bone at the edge
nidus- radioluscent center of the tumor. (osteoma is more sclerotic than osteoblastoma)
describe an osteosarcoma
malignant from mesenchyme
second most common malignant (MM is first)
4th most common in general.
very aggressive.
most common metastatis in the lungs.
can be due to paget's disaese or a history of exposure to radiation. It has bimodal occurrance due to the two different ways of appearing.
Knee is most common location.
large, ill defined.
what is codman's triangle and what does it indicate?
new subperiosteal bone formation that raises the periosteum. It indicates osteosarcoma.
what is an osteochondroma?
also known as an exostosis.
benign
mature bone covered by hyaline cartilage.
usually asymptomatic
what is a chondroma?
also called an enchondroma (when inside the medulla)
benign
mature hyaline cartilage
most common in the hands and feet.
usually located within the medullary cavity
what syndromes are associated with chondromas?
ollier disease (skeletal deformities)
maffucci disease (associated with benign vascular soft tissue tumors and brain gliomas).
what is the prognosis for chondromas?
if solitary, it is good.
if multiple, it has an increased risk of developing chondrosarcomas.
what is a chondroblastoma?
rare
benign
usually in young patients
most common in shoulders and knees.
can be confused with giant cell tumors of bone.
describe a chondrosarcoma
no osteoid
older patients
shoulder, ribs, proximal femur, pelvis.
associated with multiple chondromas.
arises in medullary cavity and erodes through the cortex.
glistening cut surface
lacunae are filled with 2 chondrocytes.
what is fibrous dysplasia?
normal bone is replaced by fibrous tissue and disorderly islands of malformed bone.It gives rise to metaplastic bone.
what is it called when a patient has multiple bones with fibrous dysplasia and endocrine abnormalities?
McCune-Albright
describe a giant cell bone tumor.
benign but locally aggressive
usually found in the epihpysis of bones in the knee.
may erode through the cortex.
composed of multinucleated cells.
what is a ewing sarcoma?
malignant
small round blue cell tumor
common in kids
arises in medullary cavity in the diaphysis.
causes pain
causes onion skin periosteal reaction.
what causes syphyllis?
treponema pallidum
what are the 4 type of aquired syphilis?
primary- chancre (firm nodular, at site of inoculation, goes away)
secondary- diffuse macular rash (2-10 weeks later, widespread, on palms and foot, white oral lesions, headaches, will resolve, is infectious)
latent- asymptomatic
tertiary- gummas, neurosyphilis, cardiovascular disease (years later, aortic aneursm, aortic valve incompetence)
what is tabes dorsalis?
associated with syphilis
posterior root in lumbosacral degeneration, causes wide gait, loss of proprioception and vibratory sensation.
Causes charcot joint.
argyle robinson pupils- don't react to light very good.
what diseases are associated with congenital syphilis?
multiorgan malformation
hutchinson teeth
8th nerve deafness
osteochondritis
hepatosplenomegaly
interstitial keratitis
what are mycobacteria?
acid fast non-spore forming bacilli. Sinlge most infectious cause of death.
multi-drug resistent strains.
what are the 2 species that cause tuberculosis?
m. tuberculoisis
m. bovis
how is it transmitted?
m. tuberculosis- aerosol
m. bovis- unpasteurized milk.
where is primary tuberculosis usually found?
lower portion of the lung in a single lesion. It is called a ghon focus.
where is secondary TB usually found?
reinfected or reactivated dormant lesions. Lesions are located in the apical portion of the lungs. It is casseous necrotic.
what is milliary TB?
disseminated- caused by hematogenous or billiary spread. Fatal. Resembles millet seeds.
when is atypical TB seen?
immunocompromised
usually in GI tract.
what organisms can cause fungal skin infections?
Tichophyton
Microsporum
Epidermophyton
what usually causes subcutaneous fungal infections? what causes it?
trauma- usually in the hands and feet.
Sporotrichosis- in the soil. Causes a nodular lesion, it ulcerates, diagnosis requires PAS positive yeast coming from lesion.
what do the deep fungal infections all have in common?
involve the viscera
gain entry thruogh the lungs
identified by yeast and spores
usually in the soil from bird and bat droppings
what is histoplasmosis?
inhalation of microconidia
parasite of macrophages
self-limiting
widely dissiminated
what is blastomycosis?
inhaled conidia of B. dermatiditis. infection usually limited to lungs but can spread outside lungs
what is coccidioidomycosis?
inhaled spores cause delayed hypersensitivity reaction
what do opportunistic fungal infections have in common?
in compromised hosts
come from soil, decaying plants, and endogenous.
what is candidiaisis?
superficial skin and systemic infections
part of normal flora.
most common fungal infection
thrush
vaginitis
can be invasive and when it is it usually involves the kidneys.
what is aspergillosis?
allergic response to spores (type 3 and 4)
can cause asthmas or COPD
can grow in lung cavities without invasion of tissue (cavities from previous disease)
can invade lungs with immunosuppressed and cause serious problems.
what is cryptococcosis?
encapsulated
can cause meningoencephalitis
inhaled
what is HSV 1 and 2
spread by physical contact
latency in nerve ganglia
skin or mucosal infection causing vescicles
keratoconjunctivitis
esophogitis
encephalitis
can be dissiminated in immunocompromised.
what about HZV?
inhaled
chicken pox and shinlges
nerve latency
what about epstien barr virus?
mono and burkitt's lymphoma
can cause splenomegaly
atypical lymphocytes in the blood, sore throat.
what about CMV?
vertical transmission
in milk
resp droplets
body fluids
congenital infection resembles erythroblastosis fetalis.- hemolytic anemia, jaundice,, hepatosplenomegaly, extensive brain damage.
Can also infect the immunosuppressed and can cause pneumonia and other sucky things.
HHV- 6?
associated with rosiola infantism
most commonly associated with getting it with infancy
HHv-8?
associated with diffuse large B-cell lymphoma and kaposi's lymphoma
what do all prion diseas have in common?
all are associated with abnormal forms of a specific protein that is infectious and transmissable
what is the prion protein?
an alpha sheet that is changed to a beta-pleated sheet.isoform that is no longer able to be digested and accumulates. an infected species can transmit it to other species. Spongifrm trasformation of cerebral cortex, and deep grey matter. Cuases Kuru plaques.
what is CJD?
rapidly progressing dementia
involuntary muscle jerking contractions on muslce stimulus. Cerebellar dysfunction.
what is the difference between primary and secondary hyperfunction?
primary- increased secretion due to idsease of endocrine gland itself
secondary- increased secretion due to stimulation by trophic hormone
with pituuitary disease, what are the mass effects?
enlarged sella tursica
visualt field abnormalities
Increased intracranial pressure
headache, N/V
what can cause hyperpituitarism in the anterior lobe?
adenoma- most common
hyperplasia
carcinoma
hypothalamic problems
how are pituitary adenomas classified?
on the hormones they produce.
most secrete one, some secrete two, some are silent.
what is the second most common type of pituitary adenoma and causes subtle manifestations in adults?
Growth Hormone Adenomas - large, granulated and stain positive for growth hormone.
what difference does it make if the adenoma occurs prior to eh ephisyeal plate is fused?
prior- causes giantism (really tall and long bones)
after- acromegaly, causes bone and soft tissue enlargement. can cause Diabetes, HTN, sterile, nerve entrapment
what lab abnormalities are seen with acromegaly and giantism?
GH levels abnormal (not a good diagnostic tool because it can be high in other circumstances too)
elevated serum IGf-1
Insulin resistance
increased GH even after oral glucose is administered.
what is the most common type of hyperfunctioning pituitariomas?
prolactinomas, usually large. Prolactin levels are in proportion to the size of the tumor.
how do you know if someone has it?
causes amennorrhea
galactorrhea
loss of libido
infertility
what affect would a prolactinoma have on a male?
hypogonsdism
decreased libido
impotent
DDx for prolactinoma?
pregnancy
high dose estrogen therapy
renal failure
hypothalmic lesions
mass in the supra sellar department.
what are corticotroph cell adenomas?
excessive production of ACTH
small
produce secondary adrenocortical hyperfunction
what are gonadotroph adenomas?
hypersecretion of LH and FSH
usually in midde aged men and women
large
what are thyrotroph adenomas?
produce TSH
rare cause of hyperthyroidism
20% of adenomas in the pituitary are what?
null cell adenomas, but still suffer from mass effects.
how much of the pituitary must be lost before it is seen as being in hypofunction?
75%
what can cause hypopituitirism?
adenomas
surgery or radiation
rathke cleft cyst
ischemic necrosis of the pituitary gland.
what are the S&S of hypopituitarism?
pallor
hypogonadism
impotence
loss of libido
loss of secondary sex characteristics
amenorrhea.
what can cause ischemia and necrosis of the pituitary?
sheehen syndrome- post partum necrosis of the pituitary gland. Left with inadequate function. It happens during pregnancy, it gets bigger during pregnancy. Increased risk for ischemic changes.
DIC
trauma
sickle cell anemia
HTN
shock
what are the two types of empty sendrome?
primary- herniation of the subarachnoid space compressing the pituitary asymptomatic
secondary- mass enlarges the sella, then is removed by radiation or surgery, symptomatic.
what is ADH deficiency?
usually caused by tumor, radiation, or trauma.
Can't concentrate their urine.
what is inappropriate ADH secretion?
ectopic hormone production
non-neoplastic diseases on the lung
trauma
very concentrated urine.
what are the signs and symptoms associated with syndrome of inapproriate ADH?
hyponatremia
cerebral adema
neurologic dysfunction