HYPOGONADISM + MISC DISORDERS (PAGET'S) Flashcards

1
Q

hypogonadism

A

occurs when gonads produce low levels ofhormones due to HPA gonadal disruption

  • sex hormone release reg by hypothalamus, AP gland, and hormones they secrete
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2
Q

hypogonadism normal pathway

A

hypothalamus—GnRH—pituitary gland—FSH + LH —-gonads—sex specific hormones (reg via neg feedback)

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3
Q

estrogen
- primary v secondary traits

A

control development primary sex characteristics in females
- vagina, uterus, fallopian tubes, clitoris, cervix, bear children ability
- secondary: breasts + fat distribution
- other secondary controlled by androgens: pubic + axillary hair, libido

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4
Q

progesterone

A

prepares endometrium for potential of pregnancy aftr ovulation
- trigger lining to thicken to accept fertilized egg, dec muscle contractions in uterus that would reject egg

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5
Q

testosterone controls what

A

controls male physical features and promotes physical changes in puberty
- growth of penis + testes
- facial, pubic, body hair growth
- deeper voice
- muscle + bone development, taller
- sperm production

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6
Q

how do testosterone levels fluctuate
- when is highest/lowest
- what age highest

A
  • change from hr to hr
  • highest in morning, lowest at night
  • highest age 20-30, start to decline slowly after 30-35
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7
Q

primary v. secondary hypogonadism causes

A

primary
- dysfunc of gonads–> low/no sex hormones

secondary
- dysfunc hypothalamus or pituitary—> low FSH + LH –> low/no sex hormones

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8
Q

primary hypogonadism
- what levels are high/low
- acquired v. congenital causes

A

no neg feedback to pit+hypothal = FSH+LH OVERPRODUCTION

acquired
- radiation, chemo, trauma, autoimmune ds, infx (mumps)

congenital
- genetic d/o (klinefelter or turner syndrome)

hypergonadotropic hypogonadism

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9
Q

secondary hypogonadism
- what levels are low/high
- acquired v. congenital causes

A

dysfunc hypothal or pit = LOW FSH + LH

acquired
- tumors of hypothal or pit, pit hemorrhage or necrosis (sheehan), head trauma

congenital
- panhypopituitarism (all pit hormones), kallman syndrome (GnRH def), chronic illness (CF, celiac)

hypogonadotropic hypogonadism

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10
Q

hypogonadism dx
- general testing
- primary v. secondary dx

A

check serum levels of sex hormones (testosterone, estradiol, LH, FSH)

primary
- high LH+FSH, low estradiol or testosterone
- karyotyping to r/o genetic conditions

secondary
- low LH+FSH, low estradiol or testosterone
- pit/brain MRI to assess underlying cause

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11
Q

hypogonadism tx
- male and female
- risks

A
  • underlying cause tx

long term hormone replacement therapy (HRT)
- testosterone IM injx, patch, gel (inc risk edema, thomboemboli)
- estrogen + progesterone pills, skin patch (inc RBC and risk thromboemboli)
—-> estrogen w out prog = risk endometrial hyperplasia and ca

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12
Q

hypogonadism tx secondary only

A

chorionic gonadotropin and/or GnRH therapy (can help w fertility)

  • HRT will induce puberty but not help w fertility
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13
Q

pagets ds (osteitis deformans)
- define
- osteoclast v osteoblast nl function

A
  • osteoclasts nl absorb/break down bone
  • osteoblasts make new bone

chronic bone d/o marked by disorganized remodeling of the bones
- osteoclasts more active than blasts (inc bone breakdown, lead to deformities + potential fractures)

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14
Q

pagets ds patho
- 3 phases

A

3 stages
- lytic phase: osteoclast hyperactive (inc bone breakdown rate)
- mixed (lytic-blastic): compensatory osteoblastic hyperactive, inc bone formation (disorganized)
- sclerotic phase: thick, sclerotic, disorg bone (woven), prone to fracture, HYPERVASC

burned out phase: inactive

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15
Q

pagets RFs + onset

A
  • unclear cause
  • can be triggered by infx (measles)
  • linked to genetic mutations (SQSTM1, RANK genes)
  • onset after age 55
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16
Q

pagets ds presentation
- intially v. overtime

A

initial- no sx
over time
- impinged nerves–> sensory losses (auditory and optic)
- skulll involvement–>lion like face (leontiasis)–> INC HAT size
- bone/joint pain w microfractures
- low linb weakness
- BOW LEGGINGS

can lead to osteosarcoma

17
Q

pagets ds complications

A
  • osteoarthritis
  • HF
  • neuro tissue compression
  • malig transformation to sarcoma
18
Q

pagets ds labs+ imaging dx

A

labs
- alk phos high

xray
- lytic lesions
- thickened bone (tunneling)

if these both pos—> baseline radionuclide bone scan to see extent/location of skeletal involvemtn
- bone bx (exclude osteosarcoma)
- dexa scan (osteoporosis)

19
Q

pagets ds management/tx

A
  • analgesia–>pain control, NSAID, APAP
  • bisphosphonates (alendronate)–> monitr for GERD, ulcers, alph phos monitor to see success tx
  • surgery to correct bone deform/decompress impinged nerves
  • PT
  • assistive devices based on Sx (walker, hearing aids)