26/03 Flashcards
(36 cards)
layers of the scrotum
Some Damn Englishman Called It The Testes
S: skin
D: dartos fascia and muscle
E: external spermatic fascia
C: cremasteric fascia
I: internal spermatic fascia
T: tunica vaginalis
T: tunica albuginea
Blood supply to fallopian tube
uterine (medial 2/3rd) (from internal iliac) + uterine plexus
ovarian arteries (lateral 1/3rd) (from aorta) + pampiniform plexus
USS torsion
edema
peripheralization of follicles
pain when scanning over the adnexa
Doppler flow within a torsed ovary may be present (normal), decreased, or absent.
Cardinal ligament
The female ureter, uterine artery, and inferior hypogastric (nervous) plexus course within the cardinal ligament.
Broad ligament subdivisions
Mesometrium
Runs laterally
covers external iliac vessels and proximal part of the round ligament
Mesovarium
post surface of broad lig –> posterior surface of ovaries (but does not cover the surface of the ovary itself).
Mesosalpinx
superiorly to the mesovarium, enclosing the fallopian tubes.
Contents of the broad ligament
uterus, fallopian tubes and ovaries
ovarian (in suspensory/infundo lig) and uterine (in cardinal lig) arteries
3 ligs within the broad ligament
Ovarian ligament.
inf ovary –> side of uterus
Round ligament of uterus.
gubernaculum
uterine horns- lab maj
Suspensory ligament of ovary (also known as the infundibulopelvic ligament).
–> contains ovarian vessels
Cardinal Ligaments
arise from the side of the cervix and the lateral fornix of the vagina —> lateral pelvic wall at the level of the ischial spines
Note: When a hysterectomy is being performed due to a malignancy, the cardinal ligaments are often removed as they are common reservoir of cancerous cells.
Which ligaments play a part in pelvic organ prolapse?
cardinal and uterosacral ligaments
Neisseria
- nonmotile
- non-sporeforming
- Gram NEG diplococci with adjacent sides flattened. The KIDNEY-shaped concave sides face each other.
OXIDASE (+)
- possess cytochrome C
- will oxidize dimethyl- or tetramethyl-paraphenylenediamine → purple (oxidase test)
CATALASE (+)
- catalyzes decomposition of H₂O₂ → H₂O + O₂
- bubbles are rapidly formed.
Present as normal flora: N. lactamica, N. sicca, N. flavescens, N. mucosa, and N. subflava.
Two pathogenic species:
1. N. gonorrhoeae (gonococcus)
→ gonorrhea
2. N. meningitidis (meningococcus)
→meningitis and septicemia
N. meningitidis:
- capsule= virulence factor
Some N. gonorrhoeae possess a loosely associated capsule or slime layer
**NATURAL COMPETENCY—take up free DNA by TRANSFORMATION. This helps to repair DNA damaged by ROS in neutrophils
Human beings are the only known reservoir of these two species.B
Neisseria growth and cultivation
- obligate aerobes
- somewhat delicate bacteria
- require special culture techniques
- sensitive to drying and to certain toxic trace metals and fatty acids present in blood agar and other ordinary media
Thayer-Martin medium (Chocolate agar containing vancomycin, colistin, nystatin, and sometimes trimethoprim) has been used for this purpose.
chocolate agar = brown color»_space; contains blood which has been heated to 80°C (chocolatized)
somewhat capnophilic (need high concentration of CO₂), especially N. gonorrhoeae → chocolate agar plates are incubated at 37°C in a 5% CO₂ atmosphere
lipopolysaccharide (LPS) vs lipooligosaccharide (LOS)
Gram-negative bacteria possess LPS or LOS in their outer membrane
Both are endotoxins → fever, shock, and other pathophysiologic changes
LOS DOES NOT have the long O-antigen polysaccharide chain present in typical Gram negative lipopolysaccharide (LPS).
LOS has core oligosaccharide + lipid A
- can incorporate sialic acid and thus mimic the host cell for immune evasion
- appears to play a role in ADHESION to host cells.
Pili
mediate the initial stage of attachment to mucosal surfaces. Piliated strains are usually capable of infecting mucosal surfaces, while non-piliated strains are not. Pili are long and thin.
GC pathogenesis
- colonize mucosal surfaces
- attach to cells using pili, outer membrane proteins including Opa, and LOS
- can become intracellular in mucosal cells where they multiply
- can also enter and multiply within neutrophils
- can be transferred to the submucosa by exiting the epithelial cells (transcytosis), entering in areas with damage to the cellular monolayer, or through phagocytes.
GC pen resistance
Developed trough chromosomal mutations and plasmid acquisition.
Low-level resistance is due to mutations in the bacterial chromosome,
High-level resistance is due to plasmid-mediated production of penicillinase.
other Gram-negative coccobacilli of the normal flora of the oropharynx, nasopharynx, and vaginal tract
Moraxella, Kingella, Acinetobacter
Bactericidal abx
Very Finely Proficient At Cell Murder
V ancomycin
F luoroquinolones
P enicillin
A minoglycosides
C ephalosporins
M etronidazole
+ Rifampicin
Bacteria gram positive make up
1, THICK peptidiglycan layer
2, Tightly bound acid polysac –> teichoic and lipoteichoic acid
3, retain CV
Gram neg bacteria
1, Thin later of peptidoglycan sandwiched between surface and plasma memb
2, outer membrane containing LPS - lipid A plus O plus other thing
Sildenafil
sildenafil (Viagra) = selective for PDE5.
inhibit cGMP-specific PDE5 enzyme on endothelial cells –> sm muscle relaxation –> increased BF
Within endothelial cells there is an enzyme NO synthase (converts L-arginine –> o2 into NO).
NO goes from endothelial cells –> sm muscle cells where it activates guanylyl cyclase (GTP -> cGMP). cGMP induced sm m relaxation.
PDE5 breaks down cGMP - causing its inactivation.
PDE5 inhibitors - inhibit
cGMP-specific PDE5 in CC (and retina) –> less breakdown of cGMP - more increased sm m relaxation in response to NO –> increase BF/ enhanced response.
Half life approx 1 hour therefore take one hour before SI
SE
Hypotension
Flushing
Headach
Dyspepsia
Impair vision
** CANNOT GIVE WITH NITRATES**
Capasases in apoptosis
2, 3, 6-10
Capasases in Pyroptosis
1, 4, 5, 11, 12
Apoptosis vs Pyroptosis
both forms of programmed cell death,
Apoptosis= “silent” process that doesn’t cause inflammation
Pyroptosis=lytic cell death that triggers inflammation and immune responses, characterized by cell swelling, pore formation, and release of intracellular contents