26/03 Flashcards
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
Hypersensitivity rxns can be classified in into four types:
* Type I: fast and it occurs within min to hrs. EX= allergic rxn
* Type II: complement activation rxn induced due to antibodies binding to cell surface antigens. It occurs within hrs to days
* Type III: complement activation induced by soluble antigen-antibody complex that occurs in serum. It occurs within hrs to days
* Type IV: delayed type hypersensitivity rxn. The cells that participate in the type IV rxn include macrophages and T cells. It takes 2 to 4 days.
Actinomyces israeli
Gram positive (purple branching filaments)
Rod shaped
Faculative anaerobe
Non motile
Dont form spores
Non- acid fast bacteria
Z-N stain - BLUE
Catalase NEG
Molar tooth appearance on blood agar culture
Clotting cascase
Extrinsic
PT(playing tenis)
3 (TF) and 7
Intrinsic
APTT (table tenis)
12, 11, 9, 8
Common
10
2 (a = thrombin)
1 (a = fibrin)
heparin - antithrombin III (ATIII)
vit k - 2, 7, 9, 10
HSV Antibody Tests
Type Specific Tests
IgG Tests (commonly used) → Detect past infection but cannot determine when it occurred.
IgM Tests (not recommended) → Not type-specific, cannot distinguish recent vs. recurrent infections, short-lived (7–14 days).
IgG Avidity Tests → Measure binding strength over time but cannot confirm recent primary infection (primary from past but not recent primary)
detecting seroconversion only by paired serum samples looking at IgG
Up to 12% of patients lose IgG antibodies over time, complicating serology interpretation.
When to do hsv ab testing
Recurrent genital lesions with negative HSV PCR → Helps rule out HSV infection.
Pregnant women with first-time genital herpes in the third trimester → Helps determine need for C-section.
Asymptomatic partners of preg patients → Helps detect serodiscordant couples (important for pregnancy planning).
pyknosis karyorrhexis karyolysis apoptosis or necrosis
pyknosis
both
shirnking
karyorrhexis
fragmenting
both but diff mechanisms
karyolysis
nuclear fading/ disolution
necrosis only
PCOS dx
- Irregular cycles + clinical hyperandrogenism (HA) (exclude other causes) = diagnosis
- If no clinical hyperandrogenism, test for biochemical HA (exclude other causes) = diagnosis
- If only irregular cycles or hyperandrogenism:
> > Adolescents: consider at risk of PCOS and reassess
> > Adults: USS for PCOM or AMH (exclude other causes) = diagnosis
Turners synd
45XO
No barr body, can be mosiac
Non disjunction meiosis - paternal gamete
LOW OESTROGEN
HIGH FSH/LH
Congen malformations
horseshoe kidney
bicuspid a / coarctation
lymphatic disease
streak ovaries - ammen and infertility
Clinical fts
short stature
webbed neck
extensively spaced nipples
shorted 4th metacarpals
Kleinfelters
47 XXY
Barr body present
LOW testosterone (leydig) and inhibin B (sertoli)
HIGH LH/FSH/oestrogen
Clinical fts
Eunuchoid body shape
Less facial and body hair
Gynaecomastia
Hypogonadism -> dysgenesis of SN tubules and testicular atrophy -> infertility
Voiding and filling urine nerves
Peeing = PNS
Pelvic N (S2-4)
Muscarinic (Ach)
M3 in bladder
PP MAM
PNS
Pelvic N (S2-4)
Muscarinic
Ach
M3
Stop (filling) = SNS
Hypogastric N (T12-L2)
Adrenergic (NE/NA)
Α1, β3 in bladder
SHAT (can’t pee while you shit)
SNS
Hypogastric
A1, β3 , Adrenergic (Adrenaline)
T12-L2 (hypogastric)
Onuf’s nucleus
S2-4 = the micturition centre/ Onuf’s nucleus
Receives afferent from stretch receptors in bladder wall
Sends efferent signals – both somatic (pudendal nerve) and autonomic (e.g. parasympathic pelvic nerve)
