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Goljan Transcripts - Nts - Day5Edited
Goljan Transcripts - Nts - Day5Edited
Amenorrhoea
Primary amenorrhea and secondary amenorrhea
When you think amenorrhea, it can be a prob with
the hypothalamus/pituitary. In other words, is the
hypothalamus putting out GnRH or not? Is the pit
putting out FSH/LH or not? So, is it a hypothalamicpit abnormality? Is it an ovarian prob? Maybe the
ovary is not making enough estrogen. Is its an end
organ prob?
This is anatomically related maybe she doesnt
have a vagina - Rokitansky-Kuster-Hauser
syndrome, or maybe she has an imperforate
hymen shes been having periods all along, and
has blood built up behind it, or cervical stenosis
(DES exposure) these are all anatomical reasons
for the amenorrhea.
Ashermans syndrome secondary amenorrhea,
woman has repeated dilatation and curotoshes(?),
where the stratum basalis is scraped away; have to
leave something behind from which you can
proliferate endometrial mucosa if you scrape all
the way down the the muscle, will not be able to
menstruate again, and will scar everything off,
leading to an infertile woman.
So, amenorrhea is primary or secondary :
hypothalamic-pit problem, ovarian prob, or end
organ prob. FSH and LH levels help in
distinguishing those 3.
If pt has hypothalamic-pit prob, what would FSH
and LH be? Low.
If had a primary ovarian problem, what would they
be? High.
If you have an end organ defect, what would FSH
and LH levels be? Normal.
What is the first step in the workup of any case of
amenorrhea? Pregnancy test.
Turners syndrome:
Primary cause of amenorrhea, webbed neck,
females
Majority are XO, therefore do not have a barr body.
Defects in lymphatics. Can make dx at birth via PE
Ovarian masses
Surface derived derived from the surface of the
ovary
Germ cell types - dysgerminomas (men have
these, too)
Sex chord stromal tumors make estrogens (ie
granulosa cell tumors - therefore can have
hyperestrinism which leads to bleeding and endo
carcinomas), some make androgens (sertoli leydig
cell tumors of the ovary assoc with virulization
and hirstuism).
(males just have germ cell tumors)
Follicular cyst
MCC of ovarian mass in a young woman =
follicular cyst
Follicle that ruptured, not neoplastic, accumulates
fluid and leads to peritonitis. It is bad if its on the
right side bc it can be either ruptured follicular cyst,
appedicitus, ectopic pregnancy (ruptured), PID;
look at with ultrasound
Under 35 yo, most ovarian masses are b9
Over 35 yo, most ovarian masses have a greater
potential of being malignant.
Surfaced derived (overall MC)
MC surfaced derived = serous cystadenoma (B9);
serous cystadenocarcinoma (malignant)
(these are the MC overall b9 and malignant
ovarian tumors)
These are also the MC that are bilateral, and the
cystadenocarcinoma has psommoma bodies
(bluish colored due to apoptosis, destruction of
the tumor cell and replacement with dystrophic
calcification). Also seen in papillary carcinoma of
the thyroid and in meningiomas
Example:: 65 yo, bilateral ovarian enlargement
(remem they tend to arise at this age)
Any woman that is over 55 and has palpable
ovaries is cancer until proven otherwise bc a
postmenopausal woman should be have ovaries
that are atrophying.
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Causes of choriocarcinoma:
15% of choriocaricnomas are from preexisting
hyadiform mole
25% from spontaneous abortion
25% from normal pregnancy
Hyatidiform moles are b9 tumors of the chorionic
villus; choriocarcinomas are a malignancy of the
trophoblastic tissue (do not see chorionic villi).
Loves to go to the lungs and responds well to
chemotherapy (can even go away in the presence
of mets)
Breast
Picture a schematic with nipple, lactiferous duct,
major ducts, terminal lobules (where milk is made),
and the stroma
Nipple = Pagets dz of the breast
Lactiferous duct = Intraductal papilloma (MCC of
bloody nipple discharge of woman under 50) b9
papillary tumor, if you press on it, blood will come
out of the areola
Major ducts = where most of the cancers arise from
invasive ductal cancers, medullary carcinomas,
mucinous carcinomas
Terminal lobules (where milk is made) MC tumor
= lobular carnicoma, is famous be BILATERAL (so,
lobular tumors are to the breast as serous tumors
are to the ovary in terms of their bilatterallity);
mammography doesnt pic up lobular cancers.
MCC of mass in breast of woman under 50 =
fibrocystic change
MCC of mass in breast of woman over 50 =
cancer: infiltrating ductal carcinoma (not
intraductal this means that we are not picking up
the cancer early enough by mammography and
picking up in the intraductal phase, and our
techniques are insensitive so we are missing the
ductal stage and we are picking up the cancer
when it has invaded to pick up early, need to get
at 5mm or less).
So, if they are intraductal, has a good prognosis
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Thyroid
Thyroid studies do NOT have to know resin T3
uptake and T4 indexes; 3 things need to know: T4,
TSH, I 131 uptake
If TSH is normal, the thyroid is normal. If TSH is
decreased, pt has hyperthyroidism or
hypopituitarism. If TSH is increased, have high
primary hypothyroidism.
Thyroid binding globulin is the binding protein for
thyroid hormone
What is the binding protein for
cortisol? Transcortin;
calcium? Albumin;
Fe? Transferrin;
Cu? Ceruloplasmin; what % of binding sites
occupied? 30%).
3 of 9 binding sites on TBG are occupied by thyroid
hormone.
Free T4 level. When we measure total T4 level,
there is free T4 and bound T4. The free T4 is the
part that is metabolically active and is converted to
T3. This part is doing all the work (that part that is
bound is not).
What happens if you are on an OCP with an
increase of estrogen? TBG and transcortin
increase. So, increased syn TBG, and is
immediately 1/3 occupied (9 sites on TBG, and 1/3
occupied by T4, so that is 3 T4s). Bc everything is
in equilibrium, the thyroid senses that it lost 3 T4s
and replaces them immediatetly. So, has the
FREE T4 altered? No. So what is the TSH?
Normal. What is the T4? Increased (but the free
hormone level and TSH not altered). So, an
increase T4 with a normal TSH means the pt is on
estrogens. This is true for any woman on estrogen
or any pregnant women. So, the total T4 is
elevated bc increased TBG (not be increased free
hormone level) and it automatically has 3 sites
occupied by T4). Same is true for cortisol if pt is
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Gestational Diabetes
Def: Woman who did not have diabetes, but after
becoming pregnant develops diabetes.
Risk factors for baby:
RDS, premature delivery
Women with GD, are at a higher risk for developing
diabetes later on.
Amyloid in Beta islets: Type 2
Antibodies against islets; inflammation: Type1
(Coxackie virus implicated)
HLA correlation: HLA DR3 and DR4=Type 1;
propensity for developing Type 1, if certain
environmental factor comes in such as infection:
Coxsackie, mumps, EBV
HLAB27: Ankylosing Spondylitis
Env factors:
Chlamydeal Infection
Ulcerative Colitis,
Shigellosis
Psoriasis
Musculoskeletal System
Need to identify crystals in synovial fluid
Gout
Pseudogout
Rhomboid crystals in synovial fluid==pseudogout
But Pseudogout could also have needle-shaped
crystals (like those of mono-sodium urate in Gout)
which makes DD difficult. So you use a special
filter to make the whole slide red and then the
crystals are made to look yellow or blue.
When the color of the crystals is yellow when the
plane of filter is parallel to the analyzer=
Negatively birefringent =GOUT
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Rx: Ceftriaxone
Bone Disorders
Osteogenesis imperfecta
Slide: Kid with an eyeball, blue sclera: AD disorder
with defect in synthesis of type I collagen, note the
blue sclera- loss of collagen in sclera allows bluish
color of choroidal vessels to shine through:
Osteogenesis imperfecta (NOT foreign body!)
brittle bone disease cant break bone down
Question: whats the defect? Defective synthesis of
type 1 collagen
Question: whats the mechanism of development of
blue sclera?
Collagen in sclera, type 1 is defective, so it is so
thin, so you can see the underlying choroidal veins
that gives the blue color.
Osteopetrosis = marble bone disease
Defect in too much bone: defect in osteoclasts
Osteoporosis
Slide: Decreased width of inter vertebral cartilage.
Note the collapse of the vertebra due to loss of
bone mass: patients lose more bone than is
replaced
Slide: Dowagers Hump
Mech: Postmenopausal osteoporosis is due to the
loss of the inhibitory effect of estrogen on the
release of interleukin 1 from osteoblasts; not
enough estrogen to stop the activity of Interleukin-1
(osteoclast activating factor) from breaking your
bone down.
Osteoporosis: Overall reduction in bone mass.
Both mineral AND organic component. WHOLE
mass of bone is reduced.
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Skin
Basal cell carcinoma (upper lip)
Squamous cell carcinoma (lower lip)
Psoriasis silvery lesion that is red and raised.
Can involve the hands, scalp pts think they have
dandruff (aka seborreic dermatitis from malasezia
furfura), but they really have psoriasis. On black
person wont see red lesion, will see silver one.
Rash at pressure points esp the elbow.
Atopic dermatitis child with allergic diathesis
starts dz; have eczema (aka atopic dermatitis);
type I HPY.
Contact dermatitis ie to metal (nickel); type IV
HPY
Example: pathophys is equalant to what? + PPD,
bc both are type IV HPY
Seborrheic Dermatitis
Due to Malassezia furfur (a fungus)
IC pt (ie AIDs)
This is a preAIDs lesion
Tinea capitis
Example: pt with bald spot on head, fluouresces
and seen with black light blacklight (UV-A light)
Can cause Tinea capitis (now Trichophyton
tonsurans is MCC)
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CNS
Spinal fluid derives from choroid plexus in the
ventricles. In the lateral, 3rd and 4th ventricles. Its
an ultrafiltrate of plasma. What is the difference in
serum and spinal fluid? Way more protein in spinal
fluid bc its an ultrafiltrate. Cell? Hardly any cells in
spinal fluid (none). Glucose? Lower in spinal fluid
about 60% of what it is in serum (if the spinal fluid
glucose level were low, then something is in there
utilizing it for energy such as bacteria or fungus or
cancer cells). Is there anything MORE in spinal
fluid than serum? Chloride (way higher in spinal
fluid than serum) - around 120. These are imp bc
there are injuries to the head.
Example: baseball that hits the eye in an orbital
blowout fracture can potentially break cribriform
plate, leading to dripping fluid out, which could be
snot, serum, or spinal fluid. So, its imp to know
diffs btwn the two.
Example: wacked in the head fluid out of ear
(otorrhea), hemorrhage leads to battle sign. This is
a fracture of the basilar plate and there is spinal
fluid there.
Most of the fluid comes out the aqueduct of sylvius
which is the MCC of hydrocephalus in children bc
it gets blocked off until you get a build up of spinal
fluid in the 3rd vent and lateral vent, which is a
narrow area and leads to hydrocephalus. Then, it
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AD
Hamartomas (noneoplastic proliferation of things)
Ventricles have bumps called tubercles which are
hamartomas which have proliferation of astrocytes.
They produce hamartomas that bulge into the
ventricle, called candle stick dripping. Hemartomas
of the kidney called angiomyolipomas, MR, cardiac
tumors (rhabdomyomas), shagreen patches, areas
of hypopigmentation, woods light shine out
Anencephaly
Worst of neural tube defects
Absent brain
Vertebral arch defects
Spina bifida occulta tufts of hair come out, vert
arches do not touch, no meninges come
Meningoceole meninges come out
Meningomylocele both meninges and spinal
cord come out
High alpha feto protein levels in blood of mother;
decreased in downs syndrome
Have to be on folate to prevent neural tube defects
(neural tube finished forming by 30 days, so make
sure she is on folate if she is trying to get
pregnant).
Neurofibromatosis
Albright syndrome (precocious puberty, caf au lait,
bone zits)
Sturge weber
Caf au lait (coffee colored non raised lesions)
spot, plexiform neurofibromas, hyperpigmentation
in the axilla (axillary freckling), neurofibromas
AD , therefore late manifestations (esp for
neurofibromatosis), penetrance, variable
expressivity (you are expressing the dz, but diff
levels of how severe the dz is)
Example: pt with HTN and pic, what test would you
get? Relationship of neurofibroma with
pheochromocytoma, therefore get a 24 hr urine for
VMA and metanephrine.
Acoustic schwannoma
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Rabies
Example:: meningitis, cerebral abcess, Rabies
(MCC in States = skunks, dogs in 3rd world)
Negri bodies (perkinje cell inclusion)
CMV
Periventricular calicifications
Example: section of kid (brain) - see white stuff
going around ventricles
MC congental infection = CMV
What body fluid is best to culture from? Urine
Meningitis
What is MC meningitis/sepis in first month of life?
Group B strep strep agalactae bc many women
have this organism in their vagina, so they are
carriers. Premature ruptured membranes lets the
organism get up, get an chorioamnionitis and into
the bloodstream.
2nd MCC is E coli
3rd MCC is listeria monocytogenes (gram + rod with
tumbling motility as does Trichomonas vaginalis)
What food should pregnant women avoid? Soft
cheeses (ie feta cheese, but listeria is present).
MC in 1 month 18 yo = N meningitides
(not H influenza bc vaccination)
MC in 18+ = Strep pn
Example: 52 yo man, nuchal rigidity, tap shows
increased protein, increased neutrophils and
decreased glucose dx? Strep pn. what is the
gram stain? Gram + diploccus
Cryptococcus
India ink see narrow based bud for Cryptococcus
Who do you think this is in? ICd pts
What is MC immunodef in USA? AIDs
MCC meningitis in AIDs pts? Cryptococcus
Mucormycosis
In frontal lobe, therefore from a diabetic in
ketoacidosis
Example: special stain on AIDs pt with CD 4 ct of
50, CT showed space occupying lesion
Dx? Toxoplasmosis
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Hydrocephalus Ex Vacuo
Severe atrophy of brain and ventricles look bigger
than they should be
Dementia
Alzheimers Dz
Classic lesion: senile plaque, neurits, amyloid
(Beta!!) so beta amyloid is toxic and the more you
have the more toxic pathognomonic of
alzheimers, on csome 21, therefore seen in
downs, neurofib tangles (in any dementia and HD)
Alz probs in higer levels dementia
Only way to dx is autopsy (confirmation) see
senile plaques
Parkinsons Dz
Resting tremor
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