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endocrine > Conditions > Flashcards

Conditions Flashcards

1
Q

How does obesity cause hypertension in metabolic syndrome?

A

Increased adipose production of angiotensinogen leads to production of Ang II–> which leads to vasconstriction

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2
Q

what is the primary cause of low HDL (good cholesterol)

A

liver insulin resistance

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3
Q

What is the framingham risk calculator?

A

includes the risk factors of age, total cholesterol, HDL cholesterol, systolic BP, treatment for HTN and cigarette smoking- Gives 10 year risk estimate for myocardial infarction and/or coronary death

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4
Q

fasting plasma glucose of 110-125 range

A

impaired tolerance

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5
Q

fasting plasma glucose equal or greater than 126

A

Diabetes Mellitus

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6
Q

2 hour glucose test levels of 140-199

A

Impaired tolerance

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7
Q

2 hours glucose test greater 200

A

diabetes mellitus

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8
Q

random plasma glucose over 200

A

diabetes mellitus

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9
Q

water content independent of temperature and pressure

A

osmolality

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10
Q

water content dependent on temperature and pressure

A

osmolarity

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11
Q

what is the action of ADH at the V1 receptor?

A

it mediates vasoconstriction, enhancement of corticotropin release, and renal prostaglandin synthesis

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12
Q

what is the action of ADH at the V2 receptor?

A

It mediates the antidiuretic response

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13
Q

what values would you expect to see in Central DI?

A

decreased ADH release form posterior pituitary–> polyuria and polydipsia
an elevated serum Na+ (increase in osmo) stimulates thirst to replace urinary water loss
- increase serum osmolality and decrease urine osmolality

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14
Q

what are symptoms of hypernatremia?

A

lethargy, edema, weakness, irritability and NM excitability

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15
Q

what happens to the urine in chronic renal disease?

A

Increased solute excretion due to nephron (V2) damage

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16
Q

what can be used to distinguish central from nephrogenic DI?

A

central= reduction in urine output+ increase in urine osmolality

nephrogenic= continued production of large amounts of dilute urine

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17
Q

what medications can be used to treat central diabetes insipidus?

A

Chloropropamide- most commonly used antidiuretic after desmopressin
carbamazepine: good for partial central DI
Clofibrate: increases posterior pituitary ADH release- also for “partial” Central DI

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18
Q

what is an example of positive feedback? How does that mechanism work?

A

Oxytocin
this mechanism allows the release of the oxytocin horomone when a trigger occures. The hormone then causes an action in the body, such as milk release or the start of labor contractions, which signals more production of oxytocin

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19
Q

what is an example of negative feedback? How does that mechanism work?

A

insulin
High blood glucose is detected by insuling secreting cells of the pancreas. The pancreas secretes the hormone insulin in response, insulin causes the liver cells to take up glucose. As the body takes up glucose, blood glucose declines -release of insulin stops

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20
Q

what type of complication is diabetic neuropathy? what usually causes it?

A

Microvascular complication
occulsion of vasa nervosum

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21
Q

what is the most common type of diabetic neuropathy?

A

distal symmetric sensory neuropathy

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22
Q

loss of touch and temperature
minor trauma goes unnoticed

A

Sensory neuropathy

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23
Q

abnormal weight bearing, callus formation, ulceration

A

disorders of proprioception

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24
Q

abnormal foot biomechanics
structural changes

A

motor neuropathy

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25
Q

what are diabetic patients more prone to getting with peripheral arterial disease?

A

Arteriosclerosis obliterans

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26
Q

peripheral arterial disease can cause?

A

calcification of the tunica media
increased blood flow with lack of elastic properties of the arterioles
complicates ulcer healing

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27
Q

what are some risk factors for diabetic foot?

A

DM> 10 years duration
peripheral neuropathy
abnormal foot structure
peripheral arterial disease
smoking
previous ulceration/amputation
poor glycemic control

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28
Q

what are non-invasive vascular evaulations that can be done for diabetic foot?

A
  • Doppler segmental pressure and waveform analysis (PVR)
  • ankle brachial pressure index
  • transcutaneous CO2
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29
Q

What is the classification system for diabetic foot ulcerations?

A

Wagner’s classification

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29
Q

What is the classification system for diabetic foot ulcerations?

A

Wagner’s classification

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30
Q

what is the wagner classification for diabetic ulcer (from 0-5)

A
  • 0- intact skin (impending ulcer)
  • 1 -superficial
  • 2- deep to tendon or ligament
  • 3- deep abscess, osteomyelitis
  • 4- gangreen of toes or forefoot
  • 5- gangreen of entire foot
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31
Q

where is the most common site of ulcers for diabetic foot?

A

plantar surface of the foot

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32
Q

what are treatment options for diabetic foot?

A

offloading
debridement
wound dressing
antibiotics
surgery

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33
Q

benefits of debridement?

A

removes biofilm
stimulates capillary growth- bleeding
good for chronic to acute wound

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34
Q

what are the phases of wound healing?

A

inflammatory phase- first 2 days
cellular proliferaton phase- peak 10-12 days
maturation phase- neodermis

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35
Q

what would you use for wound care of a large exudate?

A

foam
alignates= debridement

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36
Q

what would you use for wound care for light to moderate exudate?

A

hydrocolloid= not with infection
collagen

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37
Q

what would you use for wound care when there is no exudate?

A

hydrogel = necrotic wound

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38
Q

what would you use for an infected wound?

A

antimicrobial

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39
Q

what type of antibiotic would you use for diabetic wounds? why?

A

broad spectrum
most diabetic wounds are multimicrobial

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40
Q

what are indications for amputation?

A
  • uncontrollable infection or sepsis
  • inability to obtain a plantar grade foot that can tolerate weight bearing
  • non-ambulatory patient
41
Q

severe non-infective bony collapse with secondary ulceration?

A

charcot foot

42
Q

decreased sensation + repetitive trauma= joint and bone collapse

A

neurotramatic charcot foot

43
Q

increased blood flow–> increased osteoclast activity—> osteopenia—> bony collapse

glycolization of ligaments—>brittle and frail–> joint collapse

A

neurovasclar charcot foot

44
Q

what is the classification of charcot foot called? what are the classifications?

A

Eichenholtz
1- acut inflammatory process (often mistaken for infection)
2- coalescing phase
3- reconstructive

45
Q

most common location for charcot foot?

A

midfoot

46
Q

what is prolactin’s function in reproduction?

A

it negatively modulates gonadal function by inhibiting GnRH release

47
Q

what is the clinical presentation of hyperprolactinemia?

A

hypogonadism- both sexes
galactorrhea/amenorrhea- women
Mass Effect- greater in men

48
Q

what two hormones is growth hormone under the influence of? what causes the negative feedback?

A

under the influence of GHRH and somatostatin
negative feedback from IGF-1

49
Q

what are some pharmacologic causes of GH excess

A

insulin induced hypoglycemia
norepinephrine
clonidine
estrogen

50
Q

diagnosis of Acromegaly-Gigantism?

A

serum growth hormone- post glucose administration
IGF-1(insulin- like growth factor)
Head MRI

51
Q

what medications can be used to treat acromegaly-gigantism?

A

octreotide
dopaminergic drug
GH receptor blocker (pegvisomant)

52
Q

best way to diagnose varicoceles?

A

Duplex Ultrasonography

53
Q

release inhibin- keeping FSH low

A

sertolli cells

54
Q

responsible for the release of testosterone?

A

LH

55
Q

which class of medications can cause ejaculatory disfunction?

A

alpha blockers
5- alpha reductase inhibitors

56
Q

the consisten or recurrent inability of a man to attain and/or maintain a penile erection sufficient for sexual activity

A

erectile dysfunction

57
Q

what would organic erectile dyfunction look like

A
  • Gradual onset
  • risk factors present
  • consistent dysfunction
  • masturbation a problem
  • orgasm may be preserved, even if flaccid
  • sleep erections absent
58
Q

what would psychogenic ED look like?

A
  • sudden onset
  • risk factors absent
  • situational and varying dysfunction
  • non-coital erections may be present
  • orgasm absent
  • sleep erections present
59
Q

what is an important thing to consider for younger patients presenting with Erectile dysfunction?

A

ED may be the first sign of underlying CVD

60
Q

What are some shared risk factors for ED and cardiovascular disease?

A

Hypertension
diabetes
dyslipidemia
Depression
smoking
obesity
sedentary lifestyle

61
Q

The pathogenesis of ED is related to ?

A

Endothelial dyfunction
* decrease endothelium dependent vasorelaxation
* increased adhesion of leukocytes to endothelium

62
Q

symptoms of low testosterone?

A
  • diminished libido/erectile dysfunction
  • diminished energy/ vitatlity
  • depressed mood
  • cognitive changes
  • decreased muscle mass/ strength
63
Q

signs of low testosterone?

A

Decreased bone density
anemia
truncal obesity

64
Q

Fluid imbalance marked by polyuria, nocturia and polydipsia

A

diabetes insipidus

65
Q

increased levels of ADH causes water retention

A

SIADH

66
Q

what is the urinary output (osmolarity) in diabetes insipidus?

A

High- polyuria

67
Q

what is the urianry output for SIADH?

A

low- oliguria

68
Q

treatment for diabetes insipidus?

A

central- desmopressin
Nephrogenic- hydrochlorthiazide

69
Q

treatment for SIADH?

A

fluid restriction

70
Q

water retention/decrease urine production

A

increase in ADH

71
Q

increase urine production

A

decrease in ADH

72
Q

major stimuli for relase of ADH hormone?

A

plasma hyperosmolality
circulating volume depletion

73
Q

excessive thirst and excretion of a large amount of dilute urine. Decreasing the intake of fluid does not change urine concentration

A

Diabetes insipidus

74
Q

site of defect for central diabetes insipidus?

A

hypothalamus or possibly posterior pituitary

75
Q

central diabetes insipidus left untreated would result in ______ serum Na+

A

high to normal range

76
Q

Increase serum osmolality and decreased urine osmolality

A

Central DI

77
Q

which receptor mediates vasoconstriction, enhancement of corticotrophin release and renal prostaglandin synthesis?

A

V1

78
Q

Mediates the antidiuretic response

A

V2

79
Q

What is needed for diagnosis of SIADH?

A
  • Hyponatremia
  • serum osmolality <275
  • urine osmolality >100

must have nml cardiac, renal, hepatic and thyroid fxn

80
Q

type of SIADH where patient may have decreased reaction times, cognitive slowing, ataxia resulting in frequent falls

A

chronic SIADH

81
Q

SIADH that may be relatively asymptomatic, but may also have anorexia, nausea, malaise, headache, muscle cramps, weakness, seizures or coma

A

Acute SIADH

82
Q

what pharmacologic agents are responsible for hyperprolactinemia?

A

anti-depressants
H2 blockers
opioids

83
Q

excess growth hormone after growth plates closed

A

Acromegaly

84
Q

excess growth hormone before the epiphysis closes

A

Gigantism

85
Q

what do you have to give in order to get a correct serum GH

A

glucose

86
Q

what is first line treatment of acromegaly/gigantism? what second line?

A

1st line: transsphenodial surgery
pharmacologic: dopaminergic like ocretinide/pegvisomant

87
Q

what genetic testing should be offered for patients entering IVF/ICSI with nonobstructive azoospermia or counts <5mil/ml

A

Karyotyping
Y chromosome analysis

88
Q

what genetic test should be offered for patients with vasal agenesis or unexplained epididymal/ED obstruction (absence of vas defrens, blockage in prostate)

A

CFTR testing to rule of cystic fibrosis mutations

89
Q

retrograde or anejaculation can be caused by?

A

alpha blockers (tamulosin)

90
Q

ejaculatory dysfunction is can be caused by?

A

5 alpha reductase inhibitors

91
Q

Total testosterone =

A

Free T + albumin bound T + sex hormone binding globulin (SHBG) bound T

92
Q

bioavailabe testosterone =

A

Free T + albumin bound T

93
Q

intramuscular dosing of testosterone?

A

every 2-3 weeks

94
Q

absorbable gel dosing of testosterone?

A

once daily

95
Q

oral dosing of testosterone?

A

3-4 times daily

96
Q

nonscrotal patch dosing of testosterone?

A

once daily

97
Q

mucoadhesive dosing of testosterone?

A

twice daily

98
Q

nasal dosing of testosterone?

A

three times daily

99
Q

SQ pellets dosing of testosterone

A

every 3 months

100
Q

one step glucose test for gestional diabetes

A

fasting >92mg
1 hr >180mg
2 hr >153mg

101
Q

two step criteria for gestational diabetes

A

after 50g oral glucose
if 1hr > 130mg/dl
step 2: diagnosis is confirmed if
fasting >95mg
1hr >180mg
2 hr > 155mg
3 hr> 140mg

endocrine (2 decks)

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