sessh Flashcards
(156 cards)
1
Q
enzymes for iodide uptake
other important enzymes
A
NIS(na I, brings into thymocyte)
pendrin(chloride iodide exchanger, transports across the cell) to arrive in the follicular lumen
this is the first step of making iodide hormone
once in the lumen TPO-thyroidal peroxidase turns iodide to iodine via oxidization…. once in this form iodide can ionize tyrosine molecule (organifying them) making MIT and DIT. MIT and Dit couple up which is catalyzed by TPO
2
Q
megalin
A
member of the LDL family that helps endocytize the iodine rich colloid. proteolysis is the final enzyme to make T4
3
Q
5′ deiodinase
A
turns t4 to t3
then t3 can enter the nucleus to bind to thyroid receptor
4
Q
Radioiodine uptake is usually markedly elevated
A
hyperthyroidism
5
Q
inhibiting the peroxidase, thus blocking iodine organification, and coupling of the iodotyrosines.also blocks peripheral deiodination
A
thiamines
-does not block the uptake of iodide into the gland just stops the production. causes delayed effect because the thyroid will use up all its stores first.
6
Q
DOC for Graves’ disease.
A
methimazole
7
Q
_______preferred in severe hyperthyroid states or thyroid storm because_______
A
Propylthiouracil PTU
because blocks t4 to t3
8
Q
pregnancy considerations with hyperthyroidism
A
1st trimester give PTU after give Methimazole
never give radioactive iodide
9
Q
thiamin AE
A
pruritic rash, agranulocytosis, severe hepatitis*
PTU spa associated with liver failure
10
Q
used prior to surgery to decrease vascularity of the thyroid gland and used in….
A
iodide
also used in a cytokine storm of cytotoxicosis
11
Q
iodide AE
A
swelling of the neck and mouth, metallic taste in mouth, mouth ulcers
12
Q
therapeutic effect is due to emission of β rays
A
radioactive iodine
contraindicated in pregnancy
13
Q
amiodarone therapy can induce
A
either hyper or hypothyroidism
hypo esp in pts with AI thyroiditis(can add levothyroxine if meds cant be stopped)
hyper1. iodine in the amiodarone causes inc production of hormone esp if preexisting goiter(thioamine)
hyper2. destructive thyroid in previously normal pt causes inc in hormone release(glucocorticoids)
14
Q
the obvious and not obvious side effects of glucocorticoids
A
metabolic effect(fat deposition), immunosupressive, anti-inflammatory
behavioural(insomnia, depression), pseudotumor cerebri(inc intracranial pressure), development of peptic ulcers(provokes H pylori and inc, stimulated fetal surfactant production, inc platelets and RBC
15
Q
Weakness, fatigue, weight loss, hypotension, hyperpigmentation and
inability to maintain the blood glucose level during fasting.
tx
A
chronic adrenal insufficiency, Addisons
Daily hydrocortisone (with higher doses during periods of stress)
* Must be supplemented with fludrocortisone
16
Q
antagonist at glucocorticoid & progesterone receptors
use?
A
MIFEPRISTONE
-Inoperable patients with Cushing’s syndrome due to ectopic ACTH production or adrenal carcinoma who failed to respond to other therapeutic manipulations
17
Q
competes with aldosterone for its receptor
use?
A
spironolactone
Aldosteronism (diagnosis & treatment), hirsutism in women (acts as androgen antagonist), K+ sparing diuretic
18
Q
spironolactone AE
A
Hyperkalemia, cardiac arrhythmia, impotence, menstrual abnormalities, gynecomastia,
19
Q
potent & non-selective inhibitor of adrenal & gonadal steroid synthesis
use?
A
KETOCONAZOLE
-cushings syndrom
-prostate cancer
20
Q
KETOCONAZOLE AE
A
hepatotoxicity
irregular menses, decreased libido, impotence, gynecomastia
21
Q
blocks conversion of cholesterol to pregnenolone which leads to reduced synthesis of all hormonally active steroids
use?
AE?
A
AMINOGLUTETHIMIDE
Cushing syndrome due to adrenal cancer
lethargy, skin rash
22
Q
relatively selective inhibitor of steroid 11-hydroxylation (interferes with cortisol & corticosterone synthesis)
use?
A
METYRAPONE
to test adrenal function
Tx for pregnant women with Cushing syndrome
23
Q
METYRAPONE AE
A
hirsutism, salt and water retention
24
Q
DKA management
A
replace fluid loss with saline, Insulin IV, possassium support, bicarb supp
25
advanced glycosylation end products
causes sone of the diabetic complications
-this and non enzymatic glycosylation, and inc TGFb will be caused from hyperglycemia and lead to diabetic glomerulosclerosis
26
diabetic glomerulosclerosis becuase of
non enzymatic glycosylation, inc TGFb, and advanced glycosalation end products appear from hyperglycemia and will cause:
-inc mesangial matrix formation
-inc type 4 collagen fibronectin
-glomerular hypertroph
27
parathyroid adenoma mutation
MEN1 mutation(MEN 1 and 2) and Cyclin D1 gene rearrangement
28
Preventing addition of iodine to tyrosine residues on thyroglobulin
organification
thioamines
29
prostatic carcinoma metastisis
hematogenous to axial selection
-osteoBLASTIC lesions which can present as low back ache
if spread to lymph will spread obturator and para-aortic lymph nodes
30
mϋllerian-inhibiting hormone`
stimulates the descent of the testes from the abdomen, the rest of the descent is due to androgen
31
cryptorchidism risks
infertility and germ cell neoplasm in the normal testicle
32
mutations for testicular germ cell tumors
Mutations involving genes encoding for the ligand for tyrosine kinase KIT and BAK.
* Reduplication of short arm of chromosome 12 (isochromosome 12p) is strongly associated
other associations are cryptorchidism, hydrospias, adrenal insufficiency
33
On a cut section they appear as homogenous, gray-white and lobulated masses, with minimal hemorrhage or necrosis.
* Histologically they are composed of uniform cells divided into lobules by fibrous septa, interspersed with lymphocytic infiltrate.
* The tumor cells are large round cells with a glycogen-rich (clear or watery appearing) cytoplasm, a round nuclei and prominent nucleoli.
seminoma
34
may secrete β-hCG and its levels may be elevated and used as a tumor marker.
seminoma, choriocarcinoma
35
On a cut section they have a variegated appearance due to presence of hemorrhage and necrosis.
* Histologically they are composed of sheets of large tumor cells with a basophilic cytoplasm, large nuclei and prominent nucleoli.
* The cells may be poorly differentiated (anaplastic) or forming tubular or papillary patterns.
embryonal carcinoma
36
endodermal sinus tumors
yolk sac
37
Histologically they are composed of lace-like or reticular network of cuboidal epithelial cells.
* The cells may be arranged in papillary structures or solid cords.
* Some tumor cells are arranged to have a mesodermal core with a
blood vessel along with surrounding parietal and visceral layers of
cells, like primitive glomeruli, known as
yolk sac tumor
known as Schiller-Duval bodies
38
tumor cells also have eosinophilic globules that have α1- antitrypsin and α feto protein (AFP)
yolk sac tumor
39
The tumors where the pluripotent germ cells differentiate into cells resembling placental trophoblastic tissue.
* It is a highly malignant and aggressive tumor with a poor prognosis.
choriocarcinoma
-this is in men and women
40
Histologically they are composed of neoplastic syncytiotrophoblasts and cytotrophoblasts.
what are features of each cell
choriocarcinoma
-Syncytiotrophoblasts are large multinucleated cells with eosinophilic cytoplasm containing hCG,
-Cytotrophoblasts are mononuclear polygonal cells with clear cytoplasm.
41
These tumors arise when the totipotent germ cells differentiate into various cellular components representing more than one germ cell layer.
teratoma
good prognosis, esp the mature ones with all three germ types there (immature has worse prognosis)
42
testicular germ cell tumor metastisis and non germ cell tumors
lymphatics for germ cell -retroperitoneal para-aortic lymph nodes → mediastinal →supraclavicular nodes.
non germ cell: hematogenously to the lungs
43
LDH is elevated in what tumor
large testicular germ cell tumors
44
Abnormal urethral opening on the ventral surface, anywhere along the shaft of the penis vs dorsal
ventral: hypospadias
dorsal: epispadias
both lead to many complications.
45
Is a condition where the orifice of the prepuce is too small to permit normal retraction. This could be due to developmental anomalies or infection with scarring of the preputial ring.
Phimosis
-clinically present as painful, urethral constrictions and recurrent urinary tract infections. Circumcision is curative.
46
Occurs when a phimotic prepuce is forcibly retracted over the glans penis, causing marked constriction & swelling.
Paraphimosis
-clinically present as painful, urethral constrictions and recurrent urinary tract infections. Circumcision is curative.
47
warty benign condition of penis shaft
caused by
progression?
CONDYLOMA ACUMINATUM
caused by HPV 6 and 11
-DOES NOT cause cancer
(other HPV infections the penis will cause caner)
48
Histologically they are composed of papillary infoldings of squamous epithelium which show
koilocytic changes (vacuolization of keratinocytes and nuclear abnormalities) that are characteristic
of
viral benign lesion
CONDYLOMA ACUMINATUM
49
risk factors for developing invasive squamous cell carcinoma of penis
cig smoking and Bowen disease
circumcision is protective
50
The lesions are papillary or flat and progress to large infiltrating masses involving the entire shaft of penis.
* Histologically they show squamous differentiation of tumor cells, keratin pearls and inter-cellular bridges may be seen. They may also have areas of necrosis and hemorrhage.
➢ Clinically they are painless growths until there is ulceration and secondary infection. They usually
spread to the inguinal lymph nodes early in the disease, however, widespread metastasis is rare and
until the lesion is very advanced.
invasive squamous cell carcinoma of penis
51
persistence of epidermal thickenings along the milk line, which extends from the axilla to the perineum
Polythelia, extra nipples
51
Dilated ducts
* Filled with inspissated secretions
* Numerous lipid-laden macrophages
Granulomas may form around cholesterol deposits and secretions
* Subsequent fibrosis produces an irregular mass with skin and nipple retraction
duct ectasia
52
Acute lesions: hemorrhagic and necrotic with neutrophils and few macrophages.
Later over the next few days→ proliferating fibroblasts and chronic inflammatory
cells
* Subsequently→ giant cells, calcifications, and hemosiderin
* Eventually→ focus replaced by scar tissue or is encircled and walled off by fibrous
tissue
* Grossly: ill-defined, firm, gray white nodules containing small chalky-white foci of
calcification
fat necrosis
53
Frequently multiple and bilateral, mobile masses
* Epithelial component is hormonally responsive
fibroadenoma of the breast
54
rubbery, grayish whiteish nodule (1) that
bulges above the surrounding tissue (2) and often contain slit like spaces
fibroadenoma of the breast
55
leaf like
phyllodes
56
phyllodes metastisis
hematogenously
57
“lumpy bumpy” breas
fibrocystic change,
benign
blue dome cyst
58
apocrine metaplasia
benign in fibrocystic change
can also be seen in intraductal papilloma
59
increase in the number of acini per
lobule seen in
adenosis
seen in pregnancy and fibrocystic change
60
what breast lesion mimics carcinoma
sclerosing adenosis(slinically and histologically)
intraductal papilloma(bloody discharge)
61
Components of sclerosing adenosis, papillomas, and epithelial hyperplasia- also called complex sclerosing lesions
radial scar
62
breast cancer metastisis
bone(see hypercalcemia) , brain, lungs, liver
63
Clonal proliferation of epithelial cells limited to ducts and lobules by the basement membrane
* Myoepithelial cells preserved in involved ducts/lobules
ductal carcinoma in situ
64
toothpaste out the nipple
comeo ductal carcinoma in situ
65
Mucin-positive signet ring cells are commonly present
* Loss of________________
lobular carcinoma in situ
loss of E cadherin
66
Usually ER-negative and overexpress HER2
pagets disease, DCIS with bad prognosis
67
lobular carcinoma mutation
double loss of CDH1 (E cadherin)
will also be at risk for signet cell carcinoma of the GI
68
lobular carcinoma metastisis
peritoneum and retroperitoneum, the
leptomeninges (carcinomatous meningitis), the gastrointestinal tract, and the
ovaries and uterus
specific
69
medullary carcinoma of breast mutation
BRCA1
70
Presents as breast erythema, swelling, and skin thickening (resembling acute
mastitis/abcess)
* Characteristic gross appearance caused by extensive plugging of the
lymphovascular spaces of the dermis with carcinoma cells
* Edematous skin tethered to the breast by Cooper ligaments and mimics the
surface of an orange peel : peau d’orange appearance`
inflammatory carcinoma of the breast
-clinically appears inflamed but is not! the underlying carcinoma is diffusely infiltrative with no palpable mass
71
Consist of normal looking endometrial
glands + stroma + RBC + hemosiderin
Induce fibrosis, adhesions, pain
usually associated with infertility
Endometriotic cyst in ovary
= chocolate cyst
72
LH are increased, FSH decreased, and androgens increased.
effects?
PCOS
-inc in FSH: LH ratio
inc estrogen= endometrial hyperplasia(then to carcinoma), stimulate adipose tissues
inc androgen= hirtuism, virilization(male features)
73
PCOS diagnostic criteris
2 out of 3
1. hyperandogenism
2. menstral irregularities
3. ultrasound string of pearls appearence
74
thick, smooth capsule and absence of corpora lutea and corpora albicans
Cysts lined by granulosa cells and hypertrophied theca interna cells
PCOS
75
investigations of ovarian tumors
CA 125
Ascitic fluid tap
FNAC
76
type 1 ovarian tumor mutations
this one progresses from benign to Bassline to type 1
KRAS, BRAF = low grade
all kinds of epithelial tumors
77
type 2 ovarian tumor
starts with cyst from fallopian tube, high grade, most commonly serous
78
areas of marked epithelial atypia in fallopian tube epithelium: observed in fallopian tubes of women
STIC: Serous tubal intraepithelial carcinoma/ type 2
79
Serous tubal intraepithelial carcinoma mutation
p53, Rb, BRCA1/2
80
Psammoma bodies
calcified papillae in serous ovarian tumor
81
mutation for mutinous carcinoma of ovart
KRAS
82
ENDOMETRIOID TUMORS
mutations
PTEN, microsatellite instability (MSI due to mismatch repair
genes), KRAS
83
clear cell tumor mutations
KRAS, PTEN, p53
84
sheets of large epithelial cells with abundant clear cytoplasm
-polygonal shape
* Very aggressive and poor outcom
clear cell carcinoma of ovary
-associated with clear cell adenocarcinoma and endometriosis
-glycogen containing cytoplasm
85
Contain neoplastic epithelial cells resembling urothelium
transitional cell tumors-brenner tumors
-most benign
86
Dysgerminoma genes and serum tumro markers
c-kit
LDH and hCG
87
large uniform vesicular cells in sheets with clear cytoplasm, well defined cellboundaries, and centrally placed regular nuclei; fibrous stroma diving into lobules and rich in
infiltrating lymphocytes and can see a granulomatous reaction
* Very responsive to chemotherapy
dysgerminoma
88
cervical ripening agents(induce labor
prostaglandins misoprostol (PGE1), and dinoprostone (PGE2).
and stimulate contractions
89
prostaglandin AE
tachysystole, fever, N, V, D
90
the preferred pharmacologic agent for inducing labor when the cervix is favorable or ripe
oxytocin
91
oxytocin receptor type and effect
Gq-PLC
inc Ca with IP3 and inc PKC with DAG
Ca activate MLCK resulting in myometrial contraction
also activated MAPK cascade to activate PLA2, to stimulate more prostaglandins and more contractions (positive feedback loop)
92
oxytocin AE
excessive uterine contraction(fetal distress, uterine rupture, placental rupture)
*activation of the vasopressin receptor(fluid retention, hyponateremia, HF, Seizure, death)
93
management of post partum hemorage
uterine message,
oxytocins(oxytocin-IV, DOC, ergot alkaloids-methylergonovine, prostaglandins)
94
partial agonist at α-adrenergic receptors and some serotonin receptors
methylergonovine -ergot alkaloid
acts on the smooth muscle of the uterus and increases the tone, rate, and amplitude of rhythmic contractions(used for hemorage and can induce labor)
95
contraindications for postpartum hemorage agents
most heart or vascular problems- HTN, MI, angina, stroke
-long term use of methylergonovine is contraindicated because it can lead to ergot posioning/gangrene in the feeding infant through the milk
96
synthetic analogue of PGF2α
Carboprost tromethamine
97
management of preterm birth
uterine relaxants- tocolytics, Glucocorticoids, and rest
-used in labor that begins before 34 weeks. 37 is considered preterm
98
tocolytic agents
magnesium sulfate (MgSO4), indomethacin, and nifedipine.
99
uncouples excitation–contraction in myometrial cells through inhibition of cellular action potentials.
AE
magnesium sulfate
-flushing , N, V, blurred vision. high levels rep depress, cardiac arrest and can cross the placenta= resp and motor depress
100
NSAID used to slow preterm labor
AE
indomethican
-crosses the placenta and can cause oligohydramnios from dec renal blood flow
-not recommended after 32 weeks bc it will close the ductus arterioles in the kid
101
The calcium channel blocking agent _____________acts by impairing the entry of Ca2+ into myometrial cells via voltage-dependent Ca2+ channels, and thereby inhibiting contractility.
nifedipine
-most safe
102
Peptide analog of oxytocin. Competitive antagonist at oxytocin receptors.
Atosiban
-not available in US
103
Activation of ____________ on myometrial cell membranes activates adenylyl cyclase. This causes a rise in cAMP which in turn activates protein kinase A. Protein kinase A phosphorylates smooth-muscle myosin light chain kinase (SmMLCK). Phosphorylation of SmMLCK results in a lower affinity of SmMLCK for the Ca2+-calmodulin complex. As a result, SmMLCK does not phosphorylate myosin, and the myometrial smooth muscle relaxes, delays birth for several hours
B2 adrenoreceptor agents- Terbutaline
104
abortion drugs
for less than 8 weeks gestation
mifepristone (antiprogestin), misoprostol (prostaglandin analog) and methotrexate (folic acid antagonist).
105
steroidal estrogens most commonly used clinically
Ethinyl estradiol and mestranol
106
estrogen side effects
-dec bone resorbtion
-inc HDL and dec LD
-inc production of platelet factors and inc risk for thromboembolism
-inc hepaticc production of proteins
-inc production NO
-water retention
107
* Oral Contraceptives
* Endometrial Cancer
* Abnormal Uterine Bleeding
* Hormone Replacement Therapy
* Infertility
* Diagnostic Test of Estrogen Secretion
use of progestins
108
vaginal malodor
thin off white/grey discharge
no vaginal inflammation
causes?
bacterial vaginosis
bacterial overgrowth
from antibiotics, contraception, sex
109
Candida virulence factors
-dimorphic
-adhesion on the surface of pseudohyphae = Als3
-hydrolyase: lipase, hydrolipase, protease
-candidalysin (invade and evade)
110
Ciliate
Free-floating trophozoite
aquired through sexs
Trichomonas vaginalis -parasite
111
Trichomonas vaginalis MOA
sex, convert to ameba to adhesive to epithelium. digest lactobacilli, erythrocytes . produces cell detaching factor to slough off the epithelial discharge. **degrades iGg and igA
112
thin green/yellow odorous vaginal discharge, vaginitis
Trichomoniasis
113
clahmydia virulence factors
ER can bind to receptors on the mucosa anywhere inside the vaginal area.
then turns into RB to multiply(can damage cells during replication and a pro inflammatory cytokine release)
114
New or increased discharge
* Purulent, cloudy or bloody
* Intermenstrual bleeding * Pain during intercourse
clahmydia
115
New or increased discharge
* Purulent, cloudy or bloody
* Intermenstrual bleeding * Pain during intercourse
-fever
-N
-low ab pain
Pelvic Inflammatory disease induced by clahmydia
116
Urethritis
* Urethral discharge: clear or cloudy with mucus strands
clahmydia
117
lacks a cell wall
Triple layer external membrane contains sterol
* Serum or cholesterol must be added to growth media
mycobacterium genitalium
consider if have been treated many times for a STI
118
mycobacterium genitalium virulence factor
MgTa tip adhesions which can cause evasion, H2O2 cell damage, inflammation
119
* Gram negative, facultatively
intracellular flattened diplococci
* obligate aerobes
* catalase +, oxidase+
* Lipooligosaccharide (LOS) instead of LPS
* dissemin
neisseria gonnerhea
120
* disseminated infection (DGI) * “septic arthritis”
neisseria gonnerhea
121
* Highly antigenically variable pili (>1 million different types!)
* No protective immunity post- infection
neisseria gonnerhea
122
neisseria gonnerhea virulence factors
On the surface: LOS(endotoxin), Type 4 pilli(very variable), porins
-porins helps with iron aquisistions
-DNA detoxer
-regulatory networks
-antibiotic resistance bc of efflux pump, mutations in antibiotic target, DNA gyros
123
twitching motility
neisseria gonnerhea
124
* Humans are only host
* Enters via microtrauma
* Does not Gram stain; visualize with?
motility?
-painless lesions
Treponema pallidum (syphilis)
dark field microscopy
corkscrew motility
endoflagellum seen as actin filaments
125
Treponema pallidum MOA
-inflammation at sight on innoculation
-rapidly in the lymph and blood
-produces metalloprotinase1 in dermal cells to go deeper causing inflammation from the epithelial cells
126
surface is antigenic ally inert
Treponema pallidum
-they are very sneaky with the immune system, keep low numbers, go to immune underserved areas, slow growth, doesnt need iron sequestration
127
nonspecific cardiolipin-
cholesterol-lecithin antigen
(“beef heart cardiolipin”)
non-treponemal
-used in nonspecific syphillis test
the specific test will use the actual antibody
128
Gram –ve, encapsulated
* oxidase +, catalase -, facultative anaerobe.
* Pleomorphic, “railroad tracks” or “school of fish” arrangement
Haemophilus ducreyi
129
Haemophilus ducreyi virulence factors
LOS & Fimbria-Like-Protein (Adherence to epithelial cells and fibroblasts)
required factor X for growth
tissue, cell damage with Cytolethal distending toxin (CDT) and Cytotoxin hemolysin
130
* Gram-negative pleomorphic * “safety-pin appearance”
* Characterized by intracellular inclusions in macrophages, called?
* Encapsulated.
* Highly fastidious
Klebsiella granulomatis
inclusions are called Donavan bodies
lesions are painless
131
icosahedral, non-enveloped, circular dsDNA viruses
HPV
-human epithelial cells are effected
-group1
132
HPV moa
gains entry through micro wound and goes to the basal cell of the epithelium. E6and E7 promote host cell proliferation and prevents apoptosis, viral genome incoperates itself into host genome which will upregulat E6,7 causing more instability and risk for aneuploidy, dysplasia, carcinoma`
133
HPV vaccine based on
capsid
134
The placenta implants in the lower uterine segment or cervix, often leading to serious third trimester bleeding
placental previa
Patients with placenta previa can present with painless vaginal bleeding or postcoital spotting at or more than 30 weeks’ gestation. Ultrasound is diagnostic and should be performed prior to vaginal examination in any third trimester bleed to avoid tearing the placenta and causing hemorrhage.
135
abnormally implanted, invasive, or adhered placenta.
PLACENTA ACCRETA
villi grow into the myometrium
The condition can cause severe post-partum hemorrhage because of failure of placental separation. A hysterectomy might be required to stop the bleeding.
136
Premature and abrupt separation of placenta from the uterus due to hemorrhage between the placenta and the uterine wall
risk factors:
ABRUPTIO PLACENTA
risk: Increasing maternal age, multiparty, hypertension, preeclampsia, trauma, smoking and cocaine use.
-will present with painful bleeding, DIC, fetal distress
137
characterized by widespread maternal endothelial dysfunction that presents after 20 weeks’ gestation with hypertension, edema, and proteinuria.
pre-eclampsia
sx dissapead after taking out the placent. due to placental ischemia which will cause the endothelial dysfunction potentially bc of failure to revacularize the placenta
risk: hydatidiform mole
-htn presents as headache
138
preeclampsia conplication
HELLP Syndrome (Hemolysis(micrangiopathic with schistocytes), Elevated Liver enzymes, and Low Platelets).
hyper coagulability, acute renal failure, DIC, pulmonary edema
139
gun powder
describes endometriosis
140
what drug can cause endometrial polyps
tamoxifen
-proestrogen in the uterus
141
what stimulates a endometrial polyp and what is a complication
stimulated by estrogen and not by progesterone.
can lead to adenocarcinoma
the excess estrogen will also stimulate the endometrium cells to hyperplasia(PTEN gene has both these pathologies in common)
142
what condition is closely associated with type 1 endometrial carcinoma
Lynch syndrome
143
red degeneration,what induces this
necrosis of fibroids when they grow quickly in pregnancy(or with proliferative phase of cycle)
coagulative necrosis seen in leiyomyosarcoma
144
Retention (Nabothian) cysts may be seen in what condidiotn
chronic cervicitis
145
Wolffian (mesonephric) duct rests
seen in Gartner duct cyst on the lateral wall of the vaignal
-fluid filled
146
Diethyl stilbesterol (DES) causes what
which has what complication
vaginal adensosis
-red patches in the vaginal made of mutinous columnar epithelium that has failed to turn into squamous epic
clear cell carcinoma complication
147
cambium layer
fibromyxomatous stroma where will see immature rhabdomyoblasts seen in SARCOMA BOTYROIDES
seen as bunch of grapes
147
Bartholinitis caused by what orgs
strep, staph, gonococci, e coli
147
lichen simplex chronicus
squamous cell hyperplasia
clinically looks like leukoplakia
147
Auotimmune condition of white plaques or macules that in time may enlarge and coalesce, producing a surface that resembles porcelain or parchment.
lichen sclerosis
may lead to SCC
148
cells positive for Periodic acid Schiff stain, cytokeratin 7 (negative in its differential diagnosis- melanoma).
Paget
148
resulting from rubbing or scratching the skin to relieve pruritus.
squamous cell hyperplasia
not premalignent
149
small, distinctive, glandlike structures filled with an acidophilic
material recall immature follicles
Call-Exner bodies in granulosa cell tumors
150
granulosa cell tumors serum marker
inhibin
151
two types of monodermal teratoma and what do they secrete
1. Struma Ovarii = thyroxine
2. carcinoid = 5HT
