26/03 Flashcards

(36 cards)

1
Q

layers of the scrotum

A

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

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2
Q

Blood supply to fallopian tube

A

uterine (medial 2/3rd) (from internal iliac) + uterine plexus

ovarian arteries (lateral 1/3rd) (from aorta) + pampiniform plexus

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3
Q

USS torsion

A

edema
peripheralization of follicles
pain when scanning over the adnexa

Doppler flow within a torsed ovary may be present (normal), decreased, or absent.

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4
Q

Cardinal ligament

A

The female ureter, uterine artery, and inferior hypogastric (nervous) plexus course within the cardinal ligament.

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5
Q

Broad ligament subdivisions

A

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.

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6
Q

Contents of the broad ligament

A

uterus, fallopian tubes and ovaries

ovarian (in suspensory/infundo lig) and uterine (in cardinal lig) arteries

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7
Q

3 ligs within the broad ligament

A

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

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8
Q

Cardinal Ligaments

A

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.

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8
Q

Which ligaments play a part in pelvic organ prolapse?

A

cardinal and uterosacral ligaments

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9
Q

Neisseria

A
  • 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

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10
Q

Neisseria growth and cultivation

A
  • 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&raquo_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

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11
Q

lipopolysaccharide (LPS) vs lipooligosaccharide (LOS)

A

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.

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12
Q

Pili

A

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.

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13
Q

GC pathogenesis

A
  • 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.
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13
Q

GC pen resistance

A

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.

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14
Q

other Gram-negative coccobacilli of the normal flora of the oropharynx, nasopharynx, and vaginal tract

A

Moraxella, Kingella, Acinetobacter

15
Q

Bactericidal abx

A

Very Finely Proficient At Cell Murder

V ancomycin

F luoroquinolones

P enicillin

A minoglycosides

C ephalosporins

M etronidazole

+ Rifampicin

17
Q

Bacteria gram positive make up

A

1, THICK peptidiglycan layer

2, Tightly bound acid polysac –> teichoic and lipoteichoic acid

3, retain CV

18
Q

Gram neg bacteria

A

1, Thin later of peptidoglycan sandwiched between surface and plasma memb

2, outer membrane containing LPS - lipid A plus O plus other thing

19
Q

Sildenafil

A

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**

20
Q

Capasases in apoptosis

21
Q

Capasases in Pyroptosis

A

1, 4, 5, 11, 12

22
Q

Apoptosis vs Pyroptosis

A

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

23
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.
24
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
25
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
26
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.
27
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).
28
pyknosis karyorrhexis karyolysis apoptosis or necrosis
pyknosis both shirnking karyorrhexis fragmenting both but diff mechanisms karyolysis nuclear fading/ disolution necrosis only
29
PCOS dx
1. Irregular cycles + clinical hyperandrogenism (HA) (exclude other causes) = diagnosis 2. If no clinical hyperandrogenism, test for biochemical HA (exclude other causes) = diagnosis 3. If only irregular cycles or hyperandrogenism: >>Adolescents: consider at risk of PCOS and reassess >> Adults: USS for PCOM or AMH (exclude other causes) = diagnosis
30
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
31
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
32
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)
33
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)
34