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GI/Endo/Repro > Assessment 6 > Flashcards

Assessment 6 Flashcards

1
Q

Location and time of fertilization

A

Usually in ampulla of uterine tubes

Within 24hrs of ovulation

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2
Q

Time of implantation

A

Day 20-24 of menstrual cycle

3 weeks gestation

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3
Q

hCG

A

Human chorionic gonadotropin

Secreted by syncytiotrophoblasts

Bind LH receptors and promote progesterone secretion from corpus luteum

Detectable 9-11 days after LH surge

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4
Q

hCG other effects

A

Stimulates testes to secrete testosterone from Leydig cells (just like LH)

Promotes differentiation of cytotrophoblasts to syncytiotrophoblasts

Increase thyroid activity

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5
Q

Corpus Luteum secretion

A

Progesterone

17 hydroxyprogesterone - marker of corpus luteum b/c placenta cannot produce

Relaxin

Estradiol

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6
Q

hCG secretion change

A

hCG doubles every 2 days until peak @ 10 weeks

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7
Q

Pregnancy symptoms

A 
Amenorrhea
Vaginal bleeding/spotting
Nausea w or w/out vomiting
Elevation of temperature
Fatigue
Breast enlargement
Increased urination with no dysuria
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8
Q

Pregnancy symptoms that are concering

A

Heavy bleeding

Nausea/vomiting after 10weeks gestation

Lightheadedness w/abnormal HR and rhythm

Dyspnea and other pulmonary symptoms

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9
Q

hPL and hPGH

A

hPlacental Lactogen: Secreted throughout, higher levels than hPGH

hPlacental Growth Hormone: Secreted later in gestation, shuts down maternal GH

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10
Q

Hormone involved with maternal insulin

A

hPL - decrease maternal insulin sensitivity

Increases lipolysis, decrease glucose uptake, increase gluconeogenesis

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11
Q

Glucose homeostasis in mother and fetus

A

Maternal: Insulin insensitivity, mobilize more free glucose for fetal use. fasting hypoglycemia, post prandial hyperglycemia, hyperinsulinemia

Fetus: Take glucose from mother

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12
Q

HPAdrenal Axis changes in pregnancy

A

Placenta produces CRH

Maternal hypercortisolism - Cushings levels, but progesterone can prevent other cushings symptoms

Fetus protected from high cortisol levels because of 11BHSD2: Cortisol –> Cortisone

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13
Q

Placental CRH difference from maternal

A

Cortisol has positive feedback on pCRH

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14
Q

Near term HPA axis change

A

Positive feedback from Cortisol increases - started by drop in CRH-BP

Less 11BHSD2 = increased fetal exposure to cortisol: Necessary for lung development and surfactant synthesis

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15
Q

Preterm labor steroids

A

Dexamethasone or betamethasone for babies born 23-34 weeks - hydrocortisone metabolized by 11BHSD2

Greater than 34 weeks not necessary

Less than 23 weeks lungs not developed enough for drug to work

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16
Q

Estriol

A

Major estrogen in pregnancy

Comes from 16a hydroxyDHEA-S in fetus liver

Travel to placenta and converted to estriol

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17
Q

Maternal-Placental-Fetal Unit

A

Placenta cannot make cholesterol - taken from mother

Placenta cannot make androgens (DHEA)

Fetus cannot make estrogens from androgens

Fetus and mom supply placenta with DHEA which gets converted to Estrogens

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18
Q

Progesterone functions during pregnancy

A

Increased secretions to nourish pregnancy

Decrease uterine contractility

Breast development

Alters cardiac and pulmonary parameters

Suppress immune function so fetus not rejected

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19
Q

Estrogen pregnancy functions

A

Increased uterine blood flow

Breast enlargement and ductal growth

Sink for weak androgens produced by fetus

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20
Q

Estrogen during labor

A

Increase uterine contraction and release of placental prostaglandins

Stimulates proteolytic enzymes in cervix for cervical dilation

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21
Q

Pregnancy and pituitary gland

A

Enlarges but no increase in blood flow

Hyperprolactinemia

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22
Q

Prolactin and pregnancy

A

Increase

Promotes alveolargenesis in breast

Milk synthesis post partum

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23
Q

Thyroid and pregnancy

A

Increase in TBG

Stimulation of TSHr by hCG
-Decrease TSH with increase FT4

Euthyroid hyperthyroxinemia

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24
Q

Pregnancy and renin angiotensin system

A

Increase in total body water

Estrogen drives activation of R-A-A system

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25
Q

Normal weight gain in pregnancy

A

25-35lbs

~22lbs gets lost after pregnancy

2/3 weight gain occurs in last 1/2 of pregnancy

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26
Q

Obesity and pregnancy

A

Increased risk of miscarriage, GD, preeclampsia, congenital defects, Csection

15lbs weight gain if BMI>30

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27
Q

Cardiovascular changes in pregnancy

A

Improve oxygenation and nutrient flow to fetus

Increase SV and HR

Decrease PVR = decrease in BP

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28
Q

Decreased vascular resistance mechanism

A

Progesterone and NO mediated smooth muscle relaxation

BP lowered

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29
Q

Maternal position and CVSystem

A

Sleeping on back can compress IVC and decrease SV and BP

Decrease uterine perfusion as well

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30
Q

GI and pregnancy

A

Increase appetite

Increase reflux - decrease LES tone

Nausea and vomiting - week 4-8 until 14-16. Increase hCG = stomach muscle relaxation

Decrease GI motility - decrease in motilin

Hemorrhoids

Cholestasis - empties slower (progesteron)

LDL increase, hemodilution, increase ALP

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31
Q

REnal changes in pregnancy

A

Ureter compression

Bladder loses tone (Progesterone), also compressed by uterus

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32
Q

Breast changes

A

Size increase

Ductal growth

Everything gets bigger/more pronounced

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33
Q

Delivery and breastfeeding

A

Decrease in hormones (prog, estrogen etc) removes feedback inhibition on PRL so milk synthesis can occur

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34
Q

Suckling

A

Oxytocin release

Contraction of myoepithelial cells in breast

PRL release

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35
Q

Ectopic pregnancy

A

Implantation not in uterus, usually in fallopian tubes

1/150 pregnancies

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36
Q

Ectopic pregnancy risk factors

A 
PID
Endometriosis
Surgery
Smoking
IUD
Age
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37
Q

Ectopic pregnancy symptoms

A

Late menses
Pelvic pain
Vaginal bleeding

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38
Q

Placental abruption

A

Placenta breaking off from uterus

Concealed bleeding or visible bleeding

Irritation from blood = uterine contraction = further breaking of placenta = more blood

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39
Q

Placental abruption risk factors

A 
Smoking
Trauma
HTN
pre-eclampsia
Cocaine
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40
Q

Placental abruption grading

A

Based on amount of bleeding, severity of contractions, fetal distress/HR, BP, ab pain

Grade I, II, III (most severe)

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41
Q

Intrauterine growth restriction

A

IUGR = EFW less than 10%

Maternal HTN, smoking, cocaine, diabetes, renal disease, autoimmune, malabsorption

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42
Q

Macrosomia

A

EFW greater than 4000-4500g in diabetic pregnancy

EFW greater than 5000 in non diabetic

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43
Q

Diabetes in pregnancy

A

Due to insulin insensitivity caused by hPL

Decrease glucose uptake, increase lipolysis, increase gluconeogenesis

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44
Q

White classification

A

Takes into account duration/cause and if any end organs are involved

F - nephropathy
R - Retinopathy
H - CAD
T - transplant

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45
Q

Diabetic screening in pregnancy

A
  1. history at first visit
  2. Physical exam
  3. Glucola (1hr) test @ 240=-28 weeks
  4. Glucose tolerance test (if glucola is positive), 3hr test
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46
Q

Diabetic management with pregnancy

A

Patient education on diet

Glucose monitoring

Test for end organ damage

Fetal growth monitoring

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47
Q

Total amniotic fluid

A

500-1000mL

Replaced every 3hrs

Primarily from renal excretion

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48
Q

Oligohydraminos: Definition, cause, management

A

Not enough amniotic fluid - AFI less than 5

Causes: Rupture, placental insufficiency, fetal renal anomalies

Management: Inpatient care, rehydration, delivery at term

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49
Q

Polyhydraminos

A

AFI > 24

Causes: Maternal diabets, idiopathic, abnormal fetal swallowing, GI malformation (duodenal atresia)

Management: Fetal testing, delivery at term

7x increase of IUFD over Oligo

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50
Q

Hypertension and pregnancy incidence

A

Affect up to 10% of all pregnancies

Gestational HTN: 6-18% nulliparous, 6-8% multiparous

Pre-eclampsia: 3-5% nulliparous, .8-5% multiparous

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51
Q

Distinguishable features of pre-eclampsia compared to Gestational HTN

A

Occurs >20 weeks

Variable HTN

Proteinuria
Increased Uric acid
Hemoconcentration
Thrombocytopenia (severe case)
Hepatic dysfunction (severe case)
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52
Q

Pre-eclampsia classification: Mild

A

BP > 140 sys, >90 diastolic

Proteinuria

Protein/creatinine >.3

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53
Q

Pre-eclampsia classification: severe

A

BP > 160 sys, >110 diastol

Oliguria
Visual disturbances
Epigastric pain
Edema
HELLP
IUGR
Eclampsia (seizures)
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54
Q

Gestational hypertension

A

Most cases occur late, after 37 weeks

Increased progression to pre-eclampsia if diagnosis is remote from term

Delivery at term

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55
Q

Potential etiologies of Pre-eclampsia

A

Abnormal trophoblastic invasion

Coagulation abnormalities

Vascular endothelial damage

Immune issue

Genetics

Dietary deficiency

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56
Q

Normal vs pre-eclampsia pregnancy prostacyclin and thromboxane

A

Normal pregnancy: Prostacylin and thromboxane in balance

Pre-eclampsia: Shift towards thromboxane - Vasoconstriction, platelet aggregation, uterine activity increase, decrease uteroplacental blood flow

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57
Q

Pre-eclampsia risk factors

A 
Nulliparous
Fam Hx or previous Hx
Obesity
Multifetal gestation
Molar pregnancy

Preexisting medical conditions
Preexisting thrombophilias

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58
Q

Complications of severe pre eclampsia by organ system

A

Cardiovascular: Severe HTN, pulmonary edema

Renal: Oliguria, renal failure

Neurologic: Cerebral edema, eclampsia (seizures), hemorrhage, amaurosis

Hepatic: Hepatic dysfunction and subscapular hematoma

Hematology: Hemolysis, DIC, thrombocytopenia

Uteroplacental: Abruption, IUFD, fetal distress, IUGR

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59
Q

HELLP Syndrome

A

Hemolysis

Elevated Liver enzymes

Low Platelets

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60
Q

Pre eclampsia Diagnosis

A

Identify risk first

Assess symptoms

BP monitoring

Proteinuria

Weight gain/edema assessment

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61
Q

Pre eclampsia management

A

Continuous fetal and uterine monitoring

Anesthesia

Antihypertensives

Delivery - base on severity

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62
Q

Recommendation for exclusive breast feeding?

A

First 6 months

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63
Q

Recommendation for breastfeeding + complimentary foods

A

At least 1 year old

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64
Q

No breast feeding increases risk of…

A

Acute otitis media (2 fold)

Gastroenteritis (3 fold)

Lower respiratory tract infection (3 fold)

SIDS (50%)

Necrotizing enterocolitis (1.5 fold)

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65
Q

Only formula increases risk for…

A

Atopic dermatitis

Asthma

Obesity

Diabetes

Leukemias

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66
Q

Breast milk contents

A 
Immunoglobulins
Cytokines
Growth factors
Anti microbial
Metabolic hormones
Oligosaccharides (anti infection)
Mucins (infection block)
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67
Q

Breast milk supply and demand

A

Increase supply by adherence to breast feeding

No skipping/milk substitutes

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68
Q

Milk production stages

A

Lactogenesis I, II, III

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69
Q

Lactogenesis I

A

Secretory differentiation

Preparation of mammary gland to make milk

Mid pregnancy, increased prolactin

Lactocytes differentiate

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70
Q

Colostrum

A

First milk

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71
Q

Lactogenesis II

A

Secretory activation

Onset of copious milk production

Triggered by expulsion of placenta, decrease in hormones removes PRL inhibition

Lactose activates, water drawn into lactocyte

Increase from 20-30mL to 500+mL week 1 post partum

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72
Q

Lactogenesis III

A

Maintenance of milk output

Production dependent on continual removal, less on hormones

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73
Q

Oxytocin and lactation

A

Secretion stimulated by suckling, baby smell/sound

Milk ejection via myoepithelial cell contraction

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74
Q

Common breast feeding problems

A

Milk supply issue

Difficulty feeding

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75
Q

Solutions for breast feeding issues?

A

Baby friendly hospitals
Steps for successful feeding
Peer and professional support post partum

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76
Q

Benefits of scrotum

A

Thermoregulation

Sperm fitness

Social signal

Clitoral stimulation?

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77
Q

Spermatic cord contents

A

Pampiniform plexus

Cremaster muscle

Testicular artery

Vas deferens

Genitofemoral nerve

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78
Q

Thermoregulation of testis - pampiniform plexus

A

Counter current between plexus and testicular artery

Heat from body blood transferred to venous plexus blood traveling back to body leaving testes blood cooler

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79
Q

Varicoceles

A

10% men affected

Abnormal dilation of veins in spermatic cord

Palpable/enlarged vein, atrophy, lower testosterone levels

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80
Q

Varicocele cause

A

Idiopathic - incompetent valves

Secondary - compression of venous drainage: nutcracker, pelvic/abdominal malignancy

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81
Q

Left sided varicoceles?

A

Left testicular vein drains into left renal vein instead of larger IVC

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82
Q

Dartos fascia

A

First layer under skin

Smooth muscle components contract and relax testes to bring closer or move further from body

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83
Q

Cremaster muscle

A

Arise from internal abdominal oblique

Lowers and raises testes to regulate temperature

Brings testes closer to body during running/fighting/stress

84
Q

Cremasteric reflex

A

Cremaster muscle innervated by genital branch of genitofemoral nerve (L1/L2)

Inner thigh stimulation induces cremaster contraction

85
Q

Spermiogenesis

A

Process where spermatids become mature spermatozoa

Development of middle piece/tail

Formation of acrosome

86
Q

Sertoli cell

A

Epithelial cell of seminiferous

AMH secretion
Inhibin and activin secretion
Androgen binding protein to increase testosterone accumulation
Establish blood testes barrier

87
Q

Glial cell line derived neutrophic factor

A

Produced by sertoli cell

Spermatogonia self renewal during perinatal period

88
Q

ERM transcription factor

A

Produced by sertoli cell

Maintenance of spermatogonial stem cells in adults

89
Q

Spermatogenesis and 2 cell theory

A

LH binds to Leydig cell and induces androgen synthesis which travel to Sertoli cell and bind to receptors in nuclei

FSH binds to Sertoli cell and weakly stimulates spermatogenesis

Presence of BOTH FSH and Androgens = strong stimulus for spermatogenesis

90
Q

Sertoli cell only syndrome

A

Germ cell aplasia

Only sertoli cells present

Infertility, azoospermic

Deletions in AZF region of Y chromosome

91
Q

Exogenous androgen

A

Exogenous androgen exerts inhibitory effect on pituitary gland –> Decrease LH –> Decrease in spermatogenesis

92
Q

Path of sperm

A

Seminiferous tubules –> Straight Tubules –> Rete Testis –> Epididymis –> Vas deferens –> Ejaculatory Duct –> Urethra –> Penis

93
Q

Testicular cancer risk factor

A

Cryptorchidism

Previous testicular cancer

Previous male infertility

Family history

Downs

94
Q

Orchitis

A

Inflammation of testes

Blood in sperm/urine, sever pain, swelling

Causes: STD, mumps, ischemia

Treatment: Oral antibiotics, NSAIDS

95
Q

BPH

A

Benign prostatic Hyperplasia

Plastic growth of prostate gland

Polyuria, urgency, nocturia, hesitancy

Enlarged prostate on digital rectal exam

96
Q

BPH surgery

A

Transurethral Resection of Prostate Gland

97
Q

Pharma options for BPH

A

Alpha 1 adrenergic antagonists

5a reductase inhibitors

98
Q

Alpha 1 adrenergic antagonists

A

Prazosin, Doxazosin, Tamsulosin

Antagonize alpha 1 receptors, inhibit bladder smooth muscle contraction

Can also affect vascular smooth muscle - risk of orthostatic hypotension, nasal congestion, reflex tachycardia

99
Q

Tamsulosin benefit

A

Tamsulosin is specific for bladder alpha 1 receptors

Less likely to cause hypotension and dizziness

100
Q

5 alpha reductase inhibitor

A

Prevent production of DHT which can limit plastic growth of prostate gland

Finasteride, dutasteride

Sexual dysfunction, ED

Can lower PSA so may hide other issues such as malignancy

101
Q

Bulbourethral gland

A

Cowpers gland

Secrete salty mucous secretion

Lubricates urethra, neutralize acidity

102
Q

Parts of urethra

A

Spongy, membranous, prostatic

103
Q

Bladder blood supply

A

Internal iliac artery supplies bladder - Superior and inferior vesicle arteries

Venous return to vesical and prostatic venous plexus

104
Q

Bladder innervation

A

Internal sphincter - parasympathetic from pelvic splanchnic nerves

External sphincter - somatic from pudendal nerve (perineal nerve deep branch)

105
Q

Balantis

A

Inflammation of glans peins

Bacteria, irritation, HPV, diabetes

Antibiotics/antifungal, hygeine

106
Q

Phimosis

A

Foreskin too tight and cant be pulled back

Congenital, injury, inflammation

Treat with steroid creams or circumcision

107
Q

Rupture of penile urethra but not Buck’s fascia

A

Swelling contained to penis only

108
Q

Rupture of penile urethra and Buck’s fascia

A

Collection of liquid deep to Colle’s fascia

Lower abdominal wall, testes

Superficial pouch

109
Q

Prostomembranous junction rupture of urethra

A

Retroperitoneal hematoma and urine extravasation

Limited to deep perineal pouch

110
Q

Peyronie’s diseas

A

Connective tissue disorder

Scar tissue in tunica albuginea

Pain, abnormal curvature

Trauma/injury

111
Q

Penis blood supply

A

Internal pudendal artery from internal iliac

112
Q

Penis innervation

A

Somatic nerve supply from pudendal nerve

Dorsal nerve of penis

113
Q

Detailed penis vasculature

A

Pudendal artery –> Dorsal and deep artery of penis –> Helicine arteries –> Sinusoids –> Emissary veins –> Circumflex veins –> Deep dorsal vein –>

114
Q

Flaccid vs erectile state of penis

A

Flaccid: Lacunar space compressed and sufficient venous outflow

Erectile: Dilation of lacunar space (trabeculae SM), blood inflow increase and venous compression (decreased outflow)

115
Q

Erection and nervous system

A

Sensory or touch stimulus to penis –> Dorsal nerve of penis –> S2-4

Pelvic splanchnic parasympathetic nerves dilate erectile tissue arteries

116
Q

Secretion

A

Release of fluids from seminal vesicle, prostate, bulbourethral glands

Cholinergic axons from inferior hypogastric plexus

117
Q

Emission

A

Movement of ejaculate into prostatic urethra

Postganglionic sympathetic neurons of inferior hypogastric plexus

Peristaltic contractions of epididymis and vas deferens

SM contraction of prostate and seminal vesicle

Internal urethral sphincter contraction prevents retrograde ejaculation

118
Q

Ejaculation

A

Release of ejaculate from penile urethra

Pudendal nerve fibers cause contractions of bulbospongiosus muscle

Synonymous with orgasm

119
Q

Detumescence

A

Cessation of sexual stimulus

Vasoconstriction of arteries, trabecular contraction, loss of blood filling erectile tissue

120
Q

Normal signaling pathway for erection vs ED

A

Normal: Stimulus –> NO increase –> Guanylyl cyclase increase –> cGMP formation –> smooth muscle relaxation –> increase blood flow

ED: cGMP converted to inactive GMP –> no SM relaxation and erection

121
Q

Phosphodiesterase 5 inhibitors

A

PDE-5 inhibitors

Sildenafil (Viagra)

Vardenafil (Levitra)

Tadalafil (Cialis) - long lasting

Avanafil (Stendra) - absorbed quickly

122
Q

PDE 5 inhibitor interactions

A

Metabolized by CYP3A4

Transiently lowers BP

Don’t use organic nitrates for angina

123
Q

PDE 5 inhibitor selectivity

A

Sildenafil and Vardenafil inhibit retinal PDE5 - blue eyes

PDE1 in vascular smooth muscle inhibited by sildenafil and varendafil - vasodilation, tachycardia, flushing

124
Q

Steps of viral infection

A 
Attachment
Penetration
Uncoating
Biosynthesis
Assembly
Release
125
Q

HPV: Structure, pathogenesis, diagnosis, prevention/treatment

A

Structure: Circular DNA genome, no capsid

Pathogenesis: Direct contact. Replication basal cell nuclei of epithelium, no systemic spread. Transform wart–>carcinomas

Diagnosis: Cytology, immunohistochemistry, nucleic acid

P/T: Vaccine, Pap smear, surgery

126
Q

Herpes simplex virus

A

Can be latent or active

Virus present in axons

Virion protein 16 acts with HCF

VP16 transcription factor not transported to neuronal nuclei = latency

VP16 promoter promotes prduction of VP16 which initiates replication and end of latency

127
Q

Complete hydatidiform mole

A

Total lack of fetus but placenta present and growing

Enlarges because continually absorbing fluid

Uterine enlargement, first trimester bleeding, second trimester pre-eclampsia

Elevated hCG

Large avascular chorionic villi, trophoblastic atypical proliferation

128
Q

Complete hydatidiform mole genetics

A

Two sets of paternal chromosomes, empty egg

p57 gene (paternally imprinted): Tumor suppressor and cell cycle inhibitor

No maternal gene to express

p57 negative

129
Q

Partial hydatidiform mole

A

Variable uterus size
Variable hCG
Fetus MAY be present, usually abnormal

Two populations of chorionic villi: Large avascular villi with convoluted outlines and small vascularized villi

130
Q

Partial hydatidiform mole genetics

A

Triploid and diandric: Two paternal, one maternal

p57 expressed (maternal chromosomes)

131
Q

Invasive mole

A

Hydatidiform mole that penetrates uterine wall

Persistent elevation of hCG after curettage

Responds to chemo

Can cause uterine rupture

132
Q

Choriocarcinoma

A

Malignant neoplasm with atypical trophoblasts, no chorionic villi

Biphasic tumor (cyto and syncytiotrophoblasts

LARGE amounts of hCG

133
Q

Acute chorioamnionitis

A

Cloudy membrane, smelly amniotic fluid

Premature rupture of membrane and premature labor

Most common cause of death in 2nd trimester

Placental membrane inflammation - neutrophils

134
Q

Acute subchorionitis

A

Maternal response to amniotic sac infection

Leukotactic signal

Neutrophilic infiltration of subchorionic fibrin

135
Q

Chorionic plate vasculitis

A

Fetal inflammatory response

Severe ascending infection

Polymorphonuclear leukocytes migrating from fetal blood

136
Q

Umbilical cord vasculitis and funisitis

A

Fetal inflammatory response

Umbilical cord compression

Polys of fetal origin

137
Q

Intrauterine pneumonia

A

Poly leukocytes in terminal air spaces

Usually lethal

138
Q

TORCH infection

A 
Toxoplasmosis
Other (Syphilis)
Rubella
CMV
Herpes
139
Q

TORCH clinical features

A 
Fetal growth restriction
BRain lesions
Eye lesions
Hepatosplenomegaly
Skin lesions
140
Q

Listeriosis

A

Placental inflammation, stillbirth, neonatal sepsis

Abscess formation in lungs, liver, lymph nodes

141
Q

Most common fetal virus

A

CMV

142
Q

Oligohydraminos causes

A

Renal agenesis/malformation

Urethral obstruction

Chronic leakage of amniotic fluid

Decreased production or increased absorption of amniotic fluid

143
Q

Oligohydraminos clinical presentation

A

Amnion nodosum

Fetal compression - Potter’s face, abnormal limbs, Breech

Pulmonary hypoplasia - Respiratory insufficiency and death

144
Q

Amniotic band syndrome

A

Disruptions and deformations caused by amniotic bands

Craniofacial, abdominal wall defects

145
Q

Monosomy X

A

99% die in utero

Generalized edema, cystic hygroma, aortic coarctation, bicuspid aortic valve

146
Q

Trisomy 21 prenatal screening

A

Quintuple test: 2nd trimester maternal screen -

hCG - High

Urinary Estriol - Low

AFP - Low

Inhibin A - High

Pregnancy associated plasma protein A - Low

147
Q

Trisomy 13

A

Pateau syndrome

1:5000

No separation of cerebral hemispheres
Cleft lip/palate
Omphalocele
Renal anomalies
Cardiac malformations
148
Q

Trisomy 18

A

1: 8000

Less than 5% survive to term

Quintuple test: All 5 components low

Polyhydraminos, globular head, low set ears, cardiac malformations, overlapping fingers

149
Q

Thanatophoric dysplasia

A

Most common lethal dwarfism

Gain of function mutation in FGFR3 - different than achondroplasia

Micromelic limb shortening, telephone receiver femora, large head, narrow thorax

Disorganization and retardation of bone growth plates

150
Q

Osteogenesis imperfecta

A

Autosomal mutation in genes for alpha 1 and alpha 2 collagen chains

Deficiency in type 1 collagen synthesis

Most common connective tissue inherited disorder

Four subtypes

Most severe: Type II - intrauterine fractures, blue sclerae, thin calvarium

151
Q

Environmental causes of congential anomalies

A

TORCH infection

Maternal diabetes

Drugs/chemicals: FAS, Retionic acid, Thalidomide

152
Q

Diabetes embryopathy/fetopathy

A

Cardiac anomalies, neural tube defects, caudal regression syndrome - Embryopathy

Fetal macrosomia due to maternal hyperglycemia induced fetal - fetopathy

153
Q

Neural tube defects

A

Environment and genetic

Folate deficiency and hyperthermia during early gestation

Diagnosis: Very elevated AFP
Confirm with ultrasound

154
Q

Signs and symptoms of fetal hypoxia

A

Abnormal fetal movements
Passage of meconium
Abnormal fetal HR
Abnormal fetal blood sampling

155
Q

Fetal hypoxia pathogenesis

A

Reduced placental perfusion –> Increase stress and decrease fetal oxygenation –> CO2 accumulation and metabolic acidosis

Acidosis = impaired cardiac function

Severe birth asphyxia = brain damage, can lead to death

156
Q

Fetal hydrops causes

A 
Intrauterine heart failure
Chromosomal anomalies (Turners, Tri 18/21)
Structural abnormalities that interfere with circulation
Chronic anemia = cardiac failure
157
Q

Chronic anemia and hydrops

A

Parvovirus B19 transplacental infection

Infect erthyroid precursor, inhibit red cell maturation

Immune hydrops: Rh

158
Q

Chlamydia life cycle

A

Elementary body: Hard, small, extracellular, infectious

Reticulate: Large, intracellular, replicative

159
Q

Chlamydia serovar D-K

A

Urethritis, PID

Co infection with gonorrhea

Less acute manifestations, more chronic sequelae

160
Q

Chlamydia Serovar L 1-3

A

Lymphogranuloma venereum

Sex organs–> inguinal lymph nodes and abscess formation

Rectal infection –> proctocolitis

161
Q

Chlamydia diagnosis

A

Nucleic acid amplification tests

Sensitivity >90%

162
Q

Chlamydia Treatment

A

Azithromycin PO once

Doxycycline 100mg BID 7x a day

Only test for cure in pregnant women

163
Q

Gonorrhea

A

G(-) diplococcus

Multi drug resistant

Hard to grow - oxidase positive, CO2

164
Q

Gonorrhea transmission

A

Guys more likely give to girl

Short incubation

No lasting immunity

165
Q

Gonorrhea virulence factor

A

Pili - adherence to host tissue, multiple genes to avoid antibody binding, antigenic variation as well

Opa proteins - Surface proteins, bind to neutrophils and T/B cells

166
Q

Gonorrhea antigenic variation

A

Change pili AA sequence to adhere to host tissue

High frequency changes

Can avoid immune response

167
Q

Gonorrhea lipooligosaccharide

A

Outer membrane of G(-) - LPS

Hide from Ab

Membrane rupture of organism = Lipid A activation = immune activation and tissue damage

Also TNF-alpha release

168
Q

Gonorrhea testing

A

Nucleic acid amplification test

Culture - resistance

Gram stain of urethral specimen

169
Q

Gonorrhea treatment

A

Ceftriaxone shot x1
Azithromycin x1

Test cure if alternate regimen is used

170
Q

Syphilis

A

Cant be cultured or seen on gram stain

Dark field microscopy or fluorescence

Human reservoir only

Painless chancre at site of disease - primary

Secondary - Systemic disease after untreated primary - rash/fever/lymphadenopathy

Tertiary - CNS involvement

171
Q

Latent syphilis

A

Early - within year acquisition

Late - Over a year ago/unknown acquisition

NO SYMPTOMS

172
Q

Syphilis diagnosis

A

Serologic test:

Non treponemal (RPR, VDRL) - antibodies directed against indirect signs of active synthesis

Treponemal (FTA-ABS, TP-PAA) - Antibodies against specific antigens on bacterial surface

Positive for life

173
Q

Syphilis treatment

A

Penicillin always

174
Q

Haemophilus ducreyi

A

Causative agent of chancroid

Gram (-)

School of fish appearance

Painful ulcer and lymphadenopathy

175
Q

Leuprolide: MoA, Use

A

GnRH agonist

Prostate cancer, central precocious puberty, endometriosis

176
Q

Gosrelin

A

GnRH agonist

Prostate cancer

177
Q

Flutamide

A

Inhibits androgen uptake/binding to target tissues

Hepatic toxicity

178
Q

Clomiphene and Te

A

Partial agonist to Estrogen receptor (acts as antagonist)

Increase Te production and spermatogenesis by blocking negative E feedback on Leydig cell

179
Q

Hypogonadism diagnosis

A

Low 8am Te concentration on 3 separate occasions

180
Q

7 Cardinal movements of Labor

A
  1. Engagement - Head moves to level of ischial spine
  2. Descent - Fetus moves towards pelvic inlet
  3. Flexion - Head reaches pelvic floor, bends forward onto chest (smallest anteroposterior diameter)
  4. Internal rotation - Head rotates, enters pelvic inlet
  5. Extension - Internal rotation complete, head exits
  6. External rotation - Body rotates so shoulders can fit
  7. Restitution/expulsion - Anterior then posterior shoulder exits
181
Q

Definition of true labor

A

Contractions at regular intervals

Interval shortens

Intensity increases

Duration of contraction increases

Progressive cervical dilation and effacement

Not stopped by sedation

182
Q

3 P’s of labor

A

Power

Passage

Passenger

183
Q

Fetal lie types

A

Longitudinal

Transverse (Can’t be delivered)

Oblique

184
Q

Stages of Labor

A

First stage: Initial onset of true labor pains to complete cervical dilation

Second stage: Complete cervical dilation to birth of baby - Pelvic and perineal phases

Third stage: Delivery of placenta

Fourth stage: Contraction and retraction of uterus

185
Q

Prostatitis

A

Infection of prostate

Perineal or back pain

Acute bacterial - fever/chills/dysuria

Chronic bacterial - Hard to treat

186
Q

Prostatic Intraepithelial neoplasia

A

Precursor lesion to prostatic carcinoma

Basal cells present. Superficial cells show nuclear enlargement and prominent nucleoli

Base grade on atypia

187
Q

Prostate adenocarcinoma

A

Most common male cancer, 2nd leading cause of cancer death

Grading and staging important

TNM - T = How far tumor has moved
N = lymph node
M = distant metastases

Travel to bone

188
Q

Testicular Lipoma

A

Proximal spermatic cord

189
Q

Testicular adeomatoid tumor

A

Upper pole of epididymis

190
Q

Rhabdomyosarcoma

A

Distal end of spermatic cord

191
Q

Types of Testicular tumors

A

Germ Cell
Mixed Germ Cell
Sex Cord Stromal

192
Q

Germ Cell Tumors

A

Seminomatous

Non seminoma

193
Q

Seminoma tumors

A

Seminoma

Spermatocytic seminoma

194
Q

Pathogenesis of germ cell tumors

A

Most originate from intratubular germ cell neoplasias

Cryptochordism, genetics, tetses dysgenesis are all predisposing factors

195
Q

Seminoma

A

Large polyhedral clear cytoplasm

20-40yo

196
Q

Spermatocytic seminoma

A

Males over 65

3 types: Small, medium, giant

Rarely metastasize

197
Q

Non seminoma tumors

A

Embryonal carcinoma
Yolk Sac
Mature/immature teratoma
Choriocarcinoma

198
Q

Embryonal carcinoma

A

20-30yrs

Only 3% aggressive

Many mitotic figures

199
Q

Yolk Sac tumor

A

Elevated AFp
Schiller Duval bodies
Most common testicular tumor before age 3

200
Q

Testicular Choriocarcinoma

A

1% of testicular tumors

Aggressive

Beta hCG

201
Q

Mixed germ cell tumors

A

Have components from multiple individual germ cell tumors

202
Q

Leydig cell tumor

A

Rare, 2%

Crystalloids of Reinke

Majority benign

203
Q

Sertoli cell tumor

A

Rare

Cord like structures form

Majority benign

204
Q

Staging of germ cell testicular tumor

A

Stage I - Confined to testis

Stage II - Spread to lymph nodes below diaphragm

Stage 3 - Metastasized above diaphragm or to other lymph nodes

205
Q

Condyloma Acuminatum

A

HPV 6/11

Papillary excrescences

206
Q

Bowen’s disease

A

Solitary plaque on shaft or scrotum

Atypical cells

Bowenoid papulosis

207
Q

Verrucous carcinoma

A

Invasive carcinoma

Rare nodal involvement or metastasis

GI/Endo/Repro (8 decks)

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