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204 Cards in this Set
- Front
- Back
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mc testic tumor men over age 60
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testicular lymphoma
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testic tumor with alveolar or tubular appearance; sometimes has papillary convolutions
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embryonal carcinoma
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rod-shaped crystals of Reinke
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Leydig cell tumor
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Androgen producing testic tumor a/w precocious puberty
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leydig, poss sertoli
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tx of BPH that causes gynecomastia and edema
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finasteride, dutasteride
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ovarian tumor that produces afp? testicular tumor that produces afp?
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both are yolk sac tumors (endodermal sinus tumor)
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estrogen secreting ovarian tumor that produces precocious puberty
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granulosa cel tumor
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testosterone secreteing ovarian tumor that leads to virilization
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leydig cell tumor
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lined w fallowpian tube-like epithelium
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serous cystadenoma
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ovarian cancer w psamomma bodies
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serous cystadenocarcinoma
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ovarian tumor w call-exner bodies
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granulosa cell tumor
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ovarian tumor +ascites +hydrothorax
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meig's syndrome in fibromas
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elevated hCG
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choriocarcinoma, dysgerminoma
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RFs for endometrial carcinoma
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PCOS
obesity granulosa-theca tumor HRT w/o progesterone age |
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RFs for ovarian cancer
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ovulation
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hormone changes in menopause
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increased LH, FSH, GnRH
decreased estrogen |
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mc breast tumor in women < 35
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fibroadenoma
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mc breast mass in premenopausal women
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fibrocystic change
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mc breast mass in postmenopausal woman
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invasive ductal carcinoma
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breast mass with histological leaflike projections
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phylloides tumor
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commonly presents w mipple discharge
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intraductal papilloma
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diffuse breast pain and multiple bilateral fluid filled lesions
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fibrocystic breast changes
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l/o e cadherin cell adhesion gene on chromosome 16
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invasive lobular carcinoma
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ER and PR + always
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LCIS
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Padget's dz of breast means there is
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underlying adenocarcinoma
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placenta previa
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goes over os--> painless bleeding
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placenta bruptio
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hematoma b/n placenta and uterus -> 3rd trimester bleeding
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placenta accretia
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no separation bc attached to myometrium
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low beta hcg but a mole
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partial mole
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46xx karyotype mole
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complete (partial is 69XXX or 69XXY)
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causes meig's syndrome
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fibroma
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causes mucinous materal accum in peritoneal cavity
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mucinous cystadenocarcinoma
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hormones in PCOS
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incr LH, testosterone
decr FSH tx is gonatotropin analogs, clomiphene, srx, ketoconazole, spironolactone |
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Schiller-Duval bodies are
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histologic endodermal sinus structures in yolk sac tumors
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red velvety plaques on penis that involve the glans
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erythroplasia or queyrat
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multiple reddish-brown papular lesions
epidem? cancer risk? |
bowenoid papulosis
younger age group than other types, usually doesn't become invasive, no predisposition to SqCC |
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gray solitary crusty plaque on shaft of penis or on scrotum
epidem? cancer risk? |
Bowen's disease
5th decade of life progresses to invasive SCC in <10% cases |
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acquired fibrous tissue formation w/in corpus cavernosa
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peyronie's disease
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infxn of foreskin w candida
tx? |
Ballanitits
fluconazole, 1 dose |
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PLAP + and painless testicular mass
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seminoma
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Penis: Solitary, thickened, whitish plaque with slightly ulcerated, crusted surface. Markedly dysplastic epithelial cells with many mitoses. Disordered epithelial maturation, intact BM.
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A Gray, solitary, crusty plaque is Bowen's disease, a typ of penile CIS.
(red velvety is erythroplasia of querat, reddishbrown papules is bowenoid papulosis) |
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PGE2 analog causing cervical dilation and uterine contraction; inducing labor
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dinoprostone
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B2 agonists that relax the uterus
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ritrodrine, terbutaline, IV Mg
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Aromatase inhibitor used in postmenopausal women with breast cancer
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anastrozole
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partial agonist at estrogen receptors in pituitary gland
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clomiphene--incrases release of LH and FSH
stimulates ovulation...may cause hot flashes (as do the other SERMs, Tamoxifen and Raloxifene) |
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Uses of progestins
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tx endometrial cancer and abnl uterine bleeding
OCPs |
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GnRH analog with agonist properties when used pulsatile, antagonist properties when used continuously
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Leuprolide
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Uses of leuprolide
Sfx |
Infertility (pulsatile dosing)
Prostate cancer (continous dosing, w flutamide) Uterine fibroids sfx: antiandrogen, N/V |
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5-alpha reductase inhibitor
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Finasteride
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Nonsteroidal competitive inhibitor of androgens at testosterone receptor
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Flutamide
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Used for prostate carcinoma, inhibits testosterone receptor
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Flutamide
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Used for BPH and baldness
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Finasteride
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Impaired blue-green color vision
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Sildenafil, vardenafil, tadanifil
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Mech of sildenafil
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Inh cGMP phosphodiesterase, causing incrased cGMP, smooth m. relaxation in corpus cavernosum, incr bld flow, penile erection
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What do you give with Mifepristone (RU-486) for termination of pregnancy?
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PGE1 (misoprostol)
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Signs of cavernous sinus thrombosis
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down and out eye
miosis and mydriasis |
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lesion cn 3 (cavernous sinus)
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down and out, ptosis (lose levator plapebrae superioris) and mydriasis (lose parasymp to ciliary ganglion)
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lesion cn 6 (cavernous sinus)
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lateral gaze palsy
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lesion cn V1 and V2 (cavernous sinus)
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incrased or decreased sensation
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bugs that get into cavernous sinus
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mucor and rhizopus
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frontal sinuses are above
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ethmoidal air cells
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most posterior sinuses
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sphenoidal
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ethmoidal air cells are located
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btwn eyes, in front of sphenoid sinuses
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if a pituitary tumor expands laterally,the first nerve it hits is
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Cn 6
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looking for gene expression
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northern blot (DNA probe for RNA)
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Where you add a labeled antigen to see if immune system recognizes it
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Elisa test antigen
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Where you add a labeled antibody to see if an antigen is present
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Elisa test antibody
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Cathode of gel electrophoresis
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negative, on top
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Anode of gel electrophoresis
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positive, on bottom, attracts the DNA
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Looking for a gene
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use southern blot (DNA probe for DNA)
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Blood flow through caverous sinus
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Blood from eye and superficial cortex-> cavernous sinus-> internal jugular vein
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Ophthalmoplegia
Ophthalmis and maxillary sensory loss (V1 and V2) |
Cavernous sinus syndrome
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What goes thru cavernous sinus?
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CN 3, 4, 6 (eye mvmt)
CN V1 and V2 Postganglionic sympathetic fibers to orbit Internal carotid |
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Free floating in cavernous sinus
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CN 6
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incomplete penetrance
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not all ppl w dominant genotype show phenotype
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mutations at different loci can produce the same phenotype (e.g., albinism)
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locus heterogeneity
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HW: heterozygous
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2pq
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HW: homozygous dominant
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p^2
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HW: homozygous recessive
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q^2
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Formulae in Hardy Weinberg
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p^2 + 2pq + q^2 = 1
p + q = 1 |
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HW: frequency of the dominant allele
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p
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HW: frequency of the recessive allele
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q
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fraction of the population that is homozygous for B
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p^2
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Fraction of the population that is homozygous for b
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q^2
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Fraction of the population that is heterozygous
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2pq
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Hardy weinberg assumptions
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no mutation occurring at the locus
no selection for any of the genotypes at the locus mating completely random no migration into or out of population being considered |
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MC defect in autosomal dominant diseases
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defects in structural genes
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When do AD diseases ususally present?
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usually after puberty, family hx critical to dx
they are pleiomorphic often |
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If mother is not affected and father is not affected for an X-linked disease, then what about the son?
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Son cannot be affected bc mother gives him the X, and she is not affected.
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When do AR diseases usually present
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childhood, often more severe than AD
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MC deficiencies/defects caused by AR diseases
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enzyme deficiencies (which is why heterozygotes can get along with only one good allele)
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Chance that a daughter of a carrier mother will be a carrier of an X recessive linked disease
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50%
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chance that a son of a carrier mother for an X linked recessive dz will be diseased
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50%
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chance that a daughter of an affected father will be a carrier of an X-linked recessive disease
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100%
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Father + for an X-linked dominant disease, Mother - for the disease.
Chance of son getting the disease? |
Zero. Fathers only pass Y to their sons. BUt all the daughters will be affected.
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Example of X-linked dominant disease
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Hypophosphatemic rickets
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Examples of mitochondrial inheritance
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Leber's hereidatry optic neuropathy
Mitochondrial myopathies |
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Expression in population (of mitochondrial diseases)
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variable due to heteroplasmy
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What percent of offspring of mothers with mitochondrial disease get the disease
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100%
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Renal cell carcinoma
Hemangioblastomas of retinal/cerebellum/medulla Pheochromocytoma increased EPO-> polycytemia |
vHL
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FAP plus brain tumors
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Turcot's syndrome
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FAP plus mandibular osteomas or other bumps
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Gardener's syndrome
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Blood findings in hereditary spherocytosis
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MCHC
Osmotic fragility test |
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Floppy mitral valve, dissecting aortic aneurysm, berry aneurysm
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Marfans
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Mitral valve prolapse, liver disease, berry aneurysms
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APCKD
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Pigmented iris hamartomas
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Lisch nodules in NF1, also see neural tumors, cafe au lait sposts, scoliosis, optic pathway gliomas, pheochromocytomas
chromosome 17 long arm |
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Autosomal recessive diseases
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CF
Albinism alpha 1 antitrypsin deficiency phenyketonuria thalassemias sickle cell anemia glycogen storage diseases mucopolysaccharidoses (except hunter's) Sphingolipidoses (except Fabry's) Infant PCKD Hemochromatosis |
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X linked recessive diseases
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Fabry's tale: Fabry's disease
Duke the muscular: Duchenne's Muscular dystrophy Hunter: Hunter's Brutally: Bruton's agammaglobulinemia Lysed: Lesch-Nyhan the Albino- Albinism (Ocular) Gopher: G6PD deficiency without aWAreness: Wiskott-Aldrich that it was a Fragile: Fragile X Hemophiliac: Hemophilia |
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albinism is
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autosomal recessive
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HIV infected ___ fuse to form multinucleated gianat cells in CNS
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microglia
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myelinate multiple axons
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Oligodendroglia
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myelinate one axon
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Schwann cells
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myelinate CNS axons
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Oligodendroglia (multiple axons in CNS)
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myelinate PNS axons
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Schwann cells (one axon in PNS)
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Permeability layer of the nerve
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Perineurium is permeability barrier
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Locus ceruleus makes
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NE
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Ventral tegmentum and SNc make
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DA
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Raphe nucleus makes
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5-HT
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Basal nucleus of Meynert makes
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ACh
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Reticular activiating system
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locus ceruleus
raphe nuclei reticular formation |
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Ht nuc regulates prasymp ns
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anterior and preoptic
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Ht nucleus regulates symp ns
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post and lateral
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destruction of ht nuc that results in hyperthermia
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AC Anterior Cooling and preoptic as usual
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makes adh
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supraoptic
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makes oxytocin
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paraventricular nuc of ht
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stimulation -> eating
destruction -> starve |
lateral nuc of ht
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stim-> savagery and obesity
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dorsomedial
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stim-> dont eat, act civilized
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ventrolateral
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lose-> savage behavior and obesity
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ventrolateral
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destroy-> can t stay warm
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post and lateral
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releases dopamine
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arcuate
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regulates release of ant pit hormones
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preoptic? or arcuate?
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somatosensory from body via ML and STT
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VPL
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somatosensory from face
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VPM
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cerebellar dentate nucleus and basal ganglia -> motor ctx
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VL
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basal ganglia->prefrontal ctx
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VA
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mammilothalamic tract to cingulate gyrus (part of Papez circuit)
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Anterior
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thalamic nuclei that stimulate the cerebral cortex to produce movement
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VA and VL
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What inhibits VA and VL
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globus pallidus internal segment
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what inhibits the globus pallidus interna to activate VA and VL
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substantia nigra pars compacta inhibits GPi directly and indirectly ny inhibiting Gpe to inhibit Subthalamic nucleus (which usually turns up the GPi)
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contain alpha synuclein
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lewy bodies
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inhibits monoamine oxidase used in parkinsons
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selegiline (kind of prevents mptp exposure)
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treatments of parkinsons
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balsac
bromocriptine amantadine levodopa + carbidopa selegiline antimuscarinics COMT ihibitors (entocapone< tolcapone) or SR LAP BEAT |
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selective mao b inhibitor
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selgiline
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ergot alkaloid and partial dopamine agonist used in parkinsons
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bromocriptine
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other agonists at da receptors
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pramiprexole, ropinirole
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toxicity of amantidine
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ataxia
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increased ne
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mania
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decreased ne
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depression
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never give l-dopa with an maoi bc
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inh mao increases da which increases ne and can lead to mania or cocaine like symptoms
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5HT1D agonist that causes vasoconstriction
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sumatriptan
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complications of selegiline
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hypercalcemia and hyperkalemia
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why would you want to inhibit comt?
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comt activates 3-0 methyldopa which inhibits levodopa conversion to dopa in CNS
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ant communicating artery aneurysm can cause
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bitemporal homonymous hemianopia
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can cause bells palsy
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alaxander bell with an std
aids lyme bells palsy sarcoid tumors diabetes |
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bilateral bells palst
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guillian barre syndrome
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dmg r vagus nerve
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uvula deviates to the left (riht site palate does not rise)
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what lesions could cause uvula to deviate to left?
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r vagal nerve
r nucleus ambiguus l corticobulbar tract soft palate portion of left motor cortex |
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damg r hypoglossal nerve or nuclei
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tongue will deviate right
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dmg r motor cortex that innervates tongue
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tongue deviates to the left
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damage to which areas can cause tongue to deviate to the left?
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left hypoglossal nerve
vertebral artery or anterior spinal artery (innnervate the medial medulla where the hypoglossal nucleus lives) right corticobulbar tract ? right tongue portion of motor cortex |
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Pt has spastic paralysis on R side of body. He has left sided ptosis and mydriasis (pupil dilation).
His eyes show lateral strabismus (I think this is where you can't look laterally) |
This sounds like a lesion to a cerebral peduncle ( spastic paralysis is corticospinal, and the eye stuff means a lesion of the 3rd CN as it exits midbrain medially)
so this is Weber's syndrome |
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where is the anterior spinal artery
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it is the little artery between the two vertebral arteries
it supplies the medial medulla |
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Pt has spastic paralysis on the left and tactile and kinesthetic defects on the left.
HIs tongue deviates to the right. Where is the lesion? |
a tongue thing makes you think maybe the medulla is involved (likely but not always the case). where in teh medulla does the corticospinal tract run? the pyramids. and where does CN 12 exit? medially. so this is probably a medial medullary syndrome.
the medulla is innervated by a paamedian branch of the anterior spinal artery |
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innervates medial medulla
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paramedian branch of anterior spinal artery
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pt has lost pain and temp sensation over his right face and his left body. He also c/o hoarseness, difficulty swallowing. You try to gag him but it doesn't work. He has right sided Horner's syndrome.
He also has vertigo, nystagmus, and n/v. You test his cerebellum and find that he has right sided past-pointing |
We see damage to the STT/TTT from the right face and left body. The sTT from the left body is on the right, so we assume we are on the right side of the brainstem.
Hoarseness is caused by a CN 9/10 lesion--the nucleus ambiguus/motor area This is in the medulla. A right sided Horner's syndrome results from sympathetic damage. The clincher is the cerebellar damage on the right--it indicates ICP damage, which puts us in the right lateral medulla. The vestibular nucleus damage also helps decide this (vertigo, n/v) This is lateral medullary syndrome, in which the PICA is damaged |
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PICA supplies
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lateral medulla
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Pt comes in with left-sided spastic paralysis and loss of light touch/vibration/kinsthetic sensation on the left.
He can't look to the right. He can't abduct his right eye. He has no deficits in pain and temp sensation |
left sided spastic paralysis plus decreased vibration sense on the left indicates a lesion where these guys run together. Moving on, we see that he can't look to the right. So this puts us in the brainstem, with a CN 6 palsy. CN6 and the PPRF are located in the pons. If the pt can't look to the right and can't abduct his right eye, we are thinking right pons.
So a right pontine lesion that incorporates all these things would have to be medial, since CN6 exits the brain medially This is right medial inferior pontine syndrome. The artery damaged is the right paramedian branch of the basilar artery |
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Medial nuclei
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3, 6, 12
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supplies the pons
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medially: paramedian branches of basilar (Willis' fat belly)
laterally: AICA |
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Pt comes in complaining of hearing loss and tinnitus on the left as well as nystagmus, vertigo, NV. He also has a left sided bell's palsy. You find that his tongue has loss of taste on the left. He can't feel any pain or temperature on the left side of his face or on the right side of his body. He also has a left sided Horner's syndrome. Finally, he has left sided limb and gait ataxia.
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The left sided facial nerve paralysis/loss of taste means CN 7. The unilateral deafness/tinnitus means CN 8. The nystagmus, vertigo, n/v means vestibular nucleus. The limb and gait ataxia on the left points you toward a cerebral peduncle, which makes you think of the pons. The left face sensory loss and the right body sensory loss put you somewhere where the pyramids and the TTT are near each other. This is lateral and on the left. The Horner syndrome means there is damage to the descending sympathetics. It looks like you are in the lateral inferior pons, supplied by the left AICA
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Pt comes in complaining of hearing loss and tinnitus on the left as well as nystagmus, vertigo, NV. He also has a left sided bell's palsy. You find that his tongue has loss of taste on the left. He can't feel any pain or temperature on the left side of his face or on the right side of his body. He also has a left sided Horner's syndrome. He has left sided limb and gait ataxia.
He also has a loss of vibration and light touch on the left. His jaw deviates to the left. |
Wow, this is a problem with CN7 on the left, STT and TTT on the left, and CN V3 on the left, also well as descending sympathetics. If you are including CN 5, then this is a lateral superior pontine problem
Damage to AICA. |
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alternate routes for the mediateion of voluntary movement
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reticulospinal and rubrospinal tracts (reticular formation and red nucleus)
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claw hand
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ulnar
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wrist drop
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radial
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scapular winging
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long throacic
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unable to wipe bottom
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thoracodorsal
adduction, medial rotation, pronation |
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weak lateral rotation of arm
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suprascapular and/or axillary
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l/o arm and forearm flexion
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musculocutanous
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l/o arm abduction
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AXILLARY
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l/o forearm extension
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radial
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cant abduct arm beyond 10 degrees
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axillary
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can't raise arm above horizontal
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long thoracic and spinal accessory
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can't initate arm abduction
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suprascapular
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weak extension of thigh
loss of knee flexion loss of foot dorsiflexion |
sciatic
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weak flexion of hip, loss of knee extension
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femoral
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weak thigh adduction
weak thigh medial rotation |
obturator
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weak hip extension and lateral rotation of thigh
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inferior gluteal
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loss of abduction of the leg
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superior gluteal
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loss of hip extension and lateral rotation of thigh
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inferior gluteal nerve
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loss of hip abduction and medial rotation of the thigh
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trendelenberg gait seen in superior gluteal injury
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results from trauma to lateral aspect of leg or from fibula neck fracture
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common perioneal (PED: peroneal everts and dorsiflexes; if injured, foot dropPED)
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foot drop
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common Peroneal (droP)
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cant stand on toes
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TIP: Tibial Inverts and Plantarflexes
Injury: can't stand on TIP toes |
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cant jump, climb stairs or rise from seated position
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inferior gluteal nerve
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damaged in posterior hip dislocation
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superior and inferior gluteal nerves, leading to + trendelenburg (superior gluteal) and inability to jump, climb staris, or rise from seated
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Injured by polio
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superior gluteal nerve
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cannot abduct the thigh
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trendelenberg sign, superior gluteal nerve injury
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caused by knee trauma
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damage to tibial nerve; can't invert or plantarflex foot and can't flex toes (can't stand on tip toes)
l/o sensation on sole of foot |
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caused by anterior hip dislocation
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inability to adduct thigh due to obturator nerve injury
l/o sensation in medial thigh |
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sensory deficit in medial thigh
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obturator nerve
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sensory deficit in anterior thigh and medial leg
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femoral nerve
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caused by pelvic fracture
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femoral nerve injury: can't flex thigh or extend leg
l/o sensation in anterior thigh and medial leg |
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lumbrical muscles
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flex at MP joint
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