Genitourinary Disorders Flashcards

1
Q

How and where does the enlargement occur in BPH?

A

Periurethral enlargement from proximal to distal

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2
Q

Etiologic risk factors for BPH?

A

gaining (age related changes in androgen levels)
genetics
race
diet

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3
Q

What coverts DHT to T?

A

5a-reductase

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4
Q

What is the function of DHT?

A

Supports prostate str and fx

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5
Q

What imbalance occurs in BPH?

A

T:E imbalance. Quantitative decrease in T and relative increase in E

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6
Q

What is the role of E in BPH? How does it work within its pathology?

A

E sensitizes prostatic cells to DHT.
More E = more sensitive
= increased growth

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7
Q

What 2 cellular adaptations occur in BPH?

A

Hyperplasia of periurethral tissue

Hypertrophy of smooth muscle

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8
Q

2 compensations during BPH?

A

bladder wall thickens

trabeculations & diverticula form

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9
Q

2 complications from BPH and why do they occur?

A

calculi formation and infection due to urine stasis

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10
Q

Consequential structural changes during BPH?

A

hydroureter (ureters distend w urine)
fishhook ureters (ureters loop downward)
hydronephrosis (distention of renal pelvis and calices with urine)

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11
Q

5 Diagnostics for BPH?

A
DRE
PSA 
BUN
Creatinine
Urinalysis
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12
Q

What is PSA and what is it used for?

A

Prostate specific antigen
Normal component of prostatic fluid
Proportional to prostatic mass

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13
Q

What additional diagnostic test is needed to calculate PSAD and PSAV?

A

US

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14
Q

What kind of neoplasia occurs in prostate CA? (4)

A

Adenocarcinoma of peripheral origin, multi centric, beneath the capsule

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15
Q

Where does extension occur in Prostate CA

Where does mets?

A

Bladder & seminal vesicle

Bone, liver, lungs

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16
Q

Manifestations of Prostate CA and why?

A

Prostatitis r/t mets and invasion

Hip & back pain r/t bone mets

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17
Q

1st line tx for prostate CA?

A

anti androgens (eg. estrogen)

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18
Q

What does a radical prostatectomy include?

A

prostate and seminal vesicle

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19
Q

What is inflamed in PID

A

reproductive tract beyond cervix (excluding vagina)

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20
Q

What is affected in PID

A

uterus (endometritis)
tubes (salpingitis)
ovary (oophoritis)

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21
Q

Etiologic factors (specific bacteria) for PID

A

POLYMICROBAL/PYOGENIC

chlamydia, gonococci, staphylococci, strepcocci, E-coli

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22
Q

What untreated STIs can cause PID?

A

gonorrhoea or chlamydia

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23
Q

When do the microbes enter the cervix in PID? Why is this time beneficial for their survival?

A

Menstruation

Menstrual slough is rich in nutrients

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24
Q

Complications of PID (4)

A

Pelvic abscess
Peritonitis
Systemic Spread
Parametritis

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25
Q

Manifestations of PID (7)

A
abd pain 
heavy purulent vaginal discharge
dyspareunia (pain during intercourse)
adnexal tenderness 
fever
vaginal bleeding 
leukocytosis
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26
Q

What will be elevated in PID

A

ESR and CRP

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27
Q

Tx PID

A

multiple broad spectrum Abx

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28
Q

What hormonal factors are risks for developing breast CA?

A

E admin for menopause, early menarche, late menopause, nulliparity

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29
Q

What hereditary genes contribute to breast CA?

A

BRCA1 gene on Chr 17

BRCA2 gene on Chr 13

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30
Q

8 types breast CA?

A
ductal carcinoma in situ
infiltrating ductal carcinoma
infiltrating lobular carcinoma
inflammatory carcinoma
medullary carcinoma
mucinous carcinoma 
tubular ductal carcinoma
Paget's disease
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31
Q

What stage in ductal carcinoma in situ? What does this mean? Is it invasive?

A
  1. If not treated, will become invasive
    No
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32
Q

Most common breast CA?

A

infiltrating ductal carcinoma

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33
Q

Where do most malignancies occur in breast CA?

A

Tail of spence

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34
Q

Where does infiltrating ductal carcinoma mets to?

A

Axillary lymph nodes, liver, bone, brain

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35
Q

What is the mass like in infiltrating ductal carcinoma?

A

fixed
irregular
painless

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36
Q

Later manifestations of infiltrating ductal carcinoma?

A

nipple discharge, retraction and edema

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37
Q

What is the biopsy looking for in breast CA?

A

surface receptors for E and Progesterone.

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38
Q

If there are lots of surface receptors for E or P in breast CA biopsy, what does this mean?

A

The tumor is dependent on hormones for support

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39
Q

Serum marker for breast CA?

A

CEA (carcinoembryonic antigen)
protein needed for cell adhesion
also for Colorectal CA

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40
Q

Why would we treat a hormone dependent tumor with more of the hormone?

A

High doses of hormones will decrease number of receptors on tumor

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41
Q

If E/P receptors high in breast CA, what is a tx?

A

tamoxifen (antiestrogen, non steroidal)

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42
Q

Lumpectomy

A

removal of tumor and surrounding tissue

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43
Q

Quadrantectomy

A

removal of quadrant

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44
Q

Mastectomy

A

entire breast

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45
Q

What determines the prognosis of breast CA?

A

not the breast tissue involved, but lymph node involvement

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46
Q

Why is ovarian CA the most lethal CA? (4)

A

no screen
difficult to dx
silent advancement
mets at dx

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47
Q

Et/risks for ovarian CA?

A

age, increased ovulatory age (age of oocytes, first menses - menopause), autosomal dominant, familial history, nullipatiry, infertility, dysmenorrhea

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48
Q

What familial history is pertinent in ovarian CA?

A

breast/ovarian CA of 1st/2nd degree relatives

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49
Q

What kind of malignancy is ovarian CA usually?what other kinds of tumors are possible?

A

epithelial

germ cell, stromal

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50
Q

Where does extension in ovarian CA happen?

A

tubes, uterus, ligaments, other ovary

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51
Q

Where does seeding occur in ovarian CA?

A

mesentery, bowel, liver

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52
Q

How does mets occur in ovarian CA?

A

via lymph/blood

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53
Q

Early manifestations of ovarian CA?

A

nonspecific GI disturbances

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54
Q

Uterine CA is also known as

A

Endometrial CA

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55
Q

Why is obesity a risk for uterine CA?

A

adipose tissue stores and synthesizes E & hyperestrogenism is a risk factor for this CA

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56
Q

Risk factors for uterine CA?

A

obesity, hyperestrogenism, age, pelvic radiation, DM, HTN

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57
Q

Every month, what normal cellular adaptation happens in the uterus? How does this become abnormal in uterine CA?

A

hyperplasia of endometrium

++ E = hyperplasia -> dysplasia -> anaplasia

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58
Q

What kind of neoplasia is uterine CA?

A

adenocarcinoma

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59
Q

Type 1 uterine CA

A

E dependent, from hyperestrogenism

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60
Q

Type 2 uterine CA

A

non E dependent
associated c atrophy of endometrium (those with atrophied endometriums who get uterine CA will get type 2)
poor prognosis

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61
Q

Et/risks for cervical CA

A

HPV infection, early age sex, multiple partners, unprotected sex, smoking, hx of STDs

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62
Q

What strains of HPV cause genital warts? Which ones cause cervical CA?

A

6 & 11

16 & 18

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63
Q

What kind of cell origin is cervical CA?

A

squamous cell origin

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64
Q

3 stages cervical CA (not CIN)

A

dysplasia
carcinoma in situ
invasive CA

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65
Q

CIN levels

A

CIN1: preCA, mild dysplasia
CIN2: PreCA, moderate dysplasia
CIN3: severe dysplasia, carcinoma in situ

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66
Q

What scope is done to dx cervical CA?

A

colposcopy

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67
Q

What 2 factors can contribute to menstrual pattern changes?

A

lack of ovulation

disturbances of hormone patterns

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68
Q

What is amenorrhea?

A

No menstruation

69
Q

What is primary amenorrhea?

A

no menstruation if over 15 years or 13 years if the woman has no secondary sex characteristic

70
Q

What is secondary amenorrhea?

A

cessation of menses for at least 6 months when normal cycles were present

71
Q

What causes primary amenorrhea? (4)

A

gonadal dysgenesis, congenital mullerian genesis, testicular feminization, hypothalamic-pituitary ovarian axis

72
Q

What causes secondary amenorrhea? (8)

A
ovarian, pituitary or hypothalamic dysfunction
intrauterine adhesions
infections (syphilis or TB)
pituitary tumor
anorexia
\++ physical activity
73
Q

How can menstruation be induced in the treatment of amenorrhea?

A

cyclic P and E

74
Q

What is dysmenorrhea?

A

Pain and discomfort with menstruation

75
Q

Primary dysmenorrhea is

A

menstrual pain not associated pathologically, after menarche, systemic symptoms

76
Q

secondary dysmenorrhea

A

caused by organic conditions such as endometriosis, uterine fibrosis, adenomyosis, IUDs, PID

77
Q

Tx of dysmenorrhea

A

symptom control, prostaglandin synthetase inhibitors, ovulation suppression (oral contraceptives)

78
Q

What is the significance of prostaglandins in dysmenorrhea?

A

++ PG = painful uterine contractions and arteriolar vasospasm

79
Q

What is Menorrhagia?

A

Prolonged/excessive bleeding at time of regular flow

80
Q

What causes menorrhagia?

A

EARLY IN LIFE
endocrine imbalance

LATER IN LIFE
inflammatory disturbances, tumors in uterus, hormonal imbalance

81
Q

What is metorrhagia?

A

Vaginal bleeding between regular menstrual periods

82
Q

What kind of renal CA occurs in children?

A

Wilms Tumor

83
Q

Why is Wilms tumor called an embryonic kidney tumor?

A

Composed of elements that resemble normal fetal tissue

84
Q

What congenital abnormalities are associated with Wilms tumor?

A

Anirida, hemihypertrophy

85
Q

What gene mutation is associated with Wilms tumor?

A

WT1 gene on Chr 11 encoding for factor needed for kidney development

86
Q

What does Wilms tumor look like?

A

solitary mass, encapsulated, distends kidney

87
Q

Manifestations of Wilms tumor?

A

asymptomatic abdominal mass, HTN, abd pain, vomiting

88
Q

What Renal CA affects adults?

A

Renal Cell Carcinoma

89
Q

Risk factors for Renal Cell Carcinoma

A

smoking, kidney CA, obesity, exposure, chronic renal insufficiency, acquired cystic kidney disease

90
Q

5 Kinds of Renal Cell Carcinoma and the most common?

A
Clear cell carcinoma (most common)
Papillary tumors
Chromophoric tumors 
oncocytomas
collecting duct tumors
91
Q

What features of clear cell carcinoma?

A

clear cytoplasm
Chr 3 deletion
proximal epithelial cell origin

92
Q

Symptoms of Renal Cell Carcinoma indicate…

What are they…

A

Advanced disease

Hematuria and flank pain, presence of palpable flank mass

93
Q

What MO is associated with bladder CA

A

S. Maematobium parasite

94
Q

What 2 kinds tumors bladder CA

A

High grade invasive and low grade invasive

95
Q

Risks for bladder CA

A

carcinogens excreted in urine (dyes), smoking, UTIs, stones

96
Q

What is a the neoplasm derived from in bladder CA?

A

Transitional epithelial cells lining bladder

97
Q

3 hematuria associated with bladder CA?

A

painless, gross, microscopic

98
Q

What diagnostics are done for high risk patients bladder CA

A

periodic urine cytology, cystoscopy, biopsy, US, CT

99
Q

What tx bladder CA

A

endoscopic resection, diathermy

100
Q

What 4 defences does the UT have?

A

mucin layer (secreted by bladder cells prevents contact with urine), washout, prostatic fluid (antimicrobial), women = periurethral flora (microbial antagonism)

101
Q

What bacteria usually causes lower UTI and pyelonephritis?

A

E coli

102
Q

Pyelonephritis is the inflammation of…

A

The upper UTI including the renal pelvis and parenchyma

103
Q

What risks associated with pyelonephritis?

A

suppressed immunity, catheterization, urinary reflux, DM

104
Q

Chronic for pyelonephritis, 3 points

A

recurrent inflammation = obstr/reflux
renal damage = renal failure
fibrosis and scar tissue

105
Q

Pyuria in pyelonephritis is

A

pus in urine

106
Q

what is a serious manifestation in chronic pyelonephritis?

A

Severe HTN

107
Q

5 Categories of glomerular disease

A
Nephrotic syndromes
Nephritic syndromes
Sediment disorders
Chronic glomerulonephritis 
Rapidly progressive glomerulonephritis
108
Q

Characteristics of nephrotic syndromes

A

increase perm of G = increased filtrate and abnormal urine composition

fluid and protein loss

109
Q

Characteristic of nephritic syndromes

A

decreased permeability of G, fluid and NW retention = azotemia

110
Q

Patients with glomerular disease can often present with both…

A

nephritic and nephrotic syndromes

111
Q

Sediment disorder characteristics

A

hematuria and or proteinuria

112
Q

Acute post infectious glomerulonephritis is an example of what glomerular disease?

A

Rapidly progressive glomerulonephritis

113
Q

What precedes Acute post infectious glomerulonephritis?

A

An A beta hemolytic strep infection

dermal or pharyngeal

114
Q

Who does Acute post infectious glomerulonephritis affect mostly?

A

children

adults - 30% will develop RF

115
Q

Patho Acute post infectious glomerulonephritis

A

T3HS
IC traps in G = GF impeded
Hypercellularity (leukoytes, endothelial cells, mesangeal cells)
glomerular enlargement d/t inflm

116
Q

What are some initial and late mnfts of Acute post infectious glomerulonephritis

A

initially = oliguria d/t impaired filtration d/t IC imbedding

then = proteinuria and hematuria d/t later inflammatory damage

Increased BUN and Creatinine

HTN & edema

117
Q

Where do renal calculi occur?

A

Anywhere in the UT

118
Q

What 3 factors can contribute to the formation of renal calculi?

A

Structural changes
Increased [blood/urine]
dietary & metabolic factors

119
Q

What usually inhibits crystallization for renal calculi formation?

A

3 kidney proteins

120
Q

4 types of kidney stones

A

Calcium (oxalate+phosphate)
Magnesium ammonium phosphate (struvite)
Uric Acid (urate)
Cystine

121
Q

What quality of pain occurs with renal calculi?

A

Renal colic

122
Q

When does non colicky pain occur with renal calculi?

A

staghorn calculi

123
Q

IVP is what and for which condition?

A

intravenous pyelogram

renal calculi

124
Q

renal calculi

A

Passed spontaneously

125
Q

What 3 drugs are given for renal calculi?

A

Morphine
Dimenhydrinate
Buscopam (antispasmodics)

126
Q

Sx for renal calculi?

A

Lithotripsy

127
Q

Stress incontinence (3)

A

change in urethro-vesicular angle (d/t pelvic distention/childbirth)
weak sphincter
Increased intrabdominal pressure (coughing/laughing)

128
Q

Overflow incontinence (2)

A

intravesicular pressure > urethral pressure

retention and bladder distension

129
Q

Overactive bladder (2)

A

Hyperactive detrusor muscle

Neurogenic/myogenic problem

130
Q

Why are alpha adrenergic agonists used for urinary incontinence?

A

They cause contraction of the urethral sphincter (fortify and strengthen)

131
Q

2 major problems in ARF

A

fluid/electrolyte imbalance

azotemia

132
Q

How much urine must be produced each day to avoid azotemia?

A

400 mL/day

133
Q

What is oliguria?

A

100-400 mL/day

134
Q

What is anuria?

A
135
Q

Main etiologic factors for ARF?

A

hypotension/hypovolemia

136
Q

Pre Renal ARF presents with

A

oliguria and ischemia

137
Q

Infrarenal ARF 3 stages

A

Initiating phase = precipitating event -> manifestations
Maintenance phase = Decreased GFR, oliguria
Recovery phase = tissue repair and gradual increased in GFR

138
Q

Why are you monitoring closely when administering fluids to those in ARF

A

Kidneys cannot make adjustment

139
Q

3 stages CRF

A

Diminished renal reserve
Renal insufficiency
Renal failure

140
Q

Diminished renal reserve

A

GFR

141
Q

Renal Insufficiency

A

GFR 20-50% of normal

142
Q

Renal Failure

A

GFR

143
Q

End stage CRF

A

GFR

144
Q

How can STDs be transmitted?

A

Via genitalia, mouth, rectum, skin, placenta

145
Q

Why are females at a higher risk for contracting STDs?

A

Higher SA = higher probability of transmission

146
Q

What are the viral STDs

A

Herpes, warts, AIDS

147
Q

What are the bacterial STDs

A

syphilis, chlamydia, gonorrhoea, chancroid

148
Q

What predisposes someone at a higher risk of contracting a STD

A

multiple partners, unsafe practices, drug abuse, underserved medically, prior STDs, noncompliant STD tx

149
Q

What virus causes genital herpes

A

HSVT2

150
Q

What kind of virus is herpes simplex two

A

A neurotrophic microbe = replicates in neurons

151
Q

Does genital herpes always present with symptoms?

A

No. Can be subclinical

152
Q

What causes genital warts?

A

HPV 6 & 11

153
Q

What topical drugs are available for genital warts?

A

Antimitotic and cytotoxic

154
Q

What causes syphilis? What kind of organism is it?

A

Treponema pallidum
Spirochetes
Long gen time

155
Q

How is syphilis spread?

A

Contact with lesions and through placenta

156
Q

How does the syphilis microbe replicate?

A

Replicates and distributes systemically

157
Q

Complications of syphilis?

A

Blindness, paralysis, heart disease, death

158
Q

At which stages can syphilis be eradicated?

A

primary and secondary

159
Q

What happens in the primary stage of syphilis?

A

Painless chancre at exposure site
Healing 3-12 weeks
Regional lymphadenopathy

160
Q

What happens in the secondary stage of syphilis?

A

Maculopapular rash to palms/soles
Patches on mucous meds/flat papule
Generalized lymphadenopathy
Fever, malaise

161
Q

Why is long acting penicillin used for syphilis?

A

long generation time

162
Q

What causes chlamydia?

A

Chlamydia trachomatis

163
Q

Male symptoms chlamydia

A

white clear DC, mild dysuria, testicular pain

164
Q

Female symptoms chlamydia

A

mucopurulent vaginal DC, dysuria, bleeding, pelvic pain d/t PID

165
Q

Tx for chlamydia

A

Doxycycline or azithromycin

166
Q

What bacteria causes gonorrhoea?

A

Neisseria gonorrhoeae (Gm -, diplococcus)

167
Q

Local symptoms of gonorrhoea M/F

A
Female= purulent vaginal DC, dysuria, late = pelvic pain
Male= urethral DC, dysuria
168
Q

Systemic manifestations of gonorrhoea

A

bacteremia/septicemia, pharyngeal infection, conjunctivitis, arthritis-dermatitis syndrome

169
Q

Tx gonorrhoea

A
1st line: cepholasporins 
2nd: increase dose + another class of Abx