Conditions Flashcards

(102 cards)

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
what are diabetic patients more prone to getting with peripheral arterial disease?
Arteriosclerosis obliterans
26
peripheral arterial disease can cause?
calcification of the tunica media increased blood flow with lack of elastic properties of the arterioles complicates ulcer healing
27
what are some risk factors for diabetic foot?
DM> 10 years duration peripheral neuropathy abnormal foot structure peripheral arterial disease smoking previous ulceration/amputation poor glycemic control
28
what are non-invasive vascular evaulations that can be done for diabetic foot?
* Doppler segmental pressure and waveform analysis (PVR) * ankle brachial pressure index * transcutaneous CO2
29
What is the classification system for diabetic foot ulcerations?
Wagner's classification
29
What is the classification system for diabetic foot ulcerations?
Wagner's classification
30
what is the wagner classification for diabetic ulcer (from 0-5)
* 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
31
where is the most common site of ulcers for diabetic foot?
plantar surface of the foot
32
what are treatment options for diabetic foot?
offloading debridement wound dressing antibiotics surgery
33
benefits of debridement?
removes biofilm stimulates capillary growth- bleeding good for chronic to acute wound
34
what are the phases of wound healing?
inflammatory phase- first 2 days cellular proliferaton phase- peak 10-12 days maturation phase- neodermis
35
what would you use for wound care of a large exudate?
foam alignates= debridement
36
what would you use for wound care for light to moderate exudate?
hydrocolloid= not with infection collagen
37
what would you use for wound care when there is no exudate?
hydrogel = necrotic wound
38
what would you use for an infected wound?
antimicrobial
39
what type of antibiotic would you use for diabetic wounds? why?
broad spectrum most diabetic wounds are multimicrobial
40
what are indications for amputation?
* uncontrollable infection or sepsis * inability to obtain a plantar grade foot that can tolerate weight bearing * non-ambulatory patient
41
severe non-infective bony collapse with secondary ulceration?
charcot foot
42
decreased sensation + repetitive trauma= joint and bone collapse
neurotramatic charcot foot
43
increased blood flow--> increased osteoclast activity---> osteopenia---> bony collapse glycolization of ligaments--->brittle and frail--> joint collapse
neurovasclar charcot foot
44
what is the classification of charcot foot called? what are the classifications?
Eichenholtz 1- acut inflammatory process (often mistaken for infection) 2- coalescing phase 3- reconstructive
45
most common location for charcot foot?
midfoot
46
what is prolactin's function in reproduction?
it negatively modulates gonadal function by inhibiting GnRH release
47
what is the clinical presentation of hyperprolactinemia?
hypogonadism- both sexes galactorrhea/amenorrhea- women Mass Effect- greater in men
48
what two hormones is growth hormone under the influence of? what causes the negative feedback?
under the influence of GHRH and somatostatin negative feedback from IGF-1
49
what are some pharmacologic causes of GH excess
insulin induced hypoglycemia norepinephrine clonidine estrogen
50
diagnosis of Acromegaly-Gigantism?
serum growth hormone- post glucose administration IGF-1(insulin- like growth factor) Head MRI
51
what medications can be used to treat acromegaly-gigantism?
octreotide dopaminergic drug GH receptor blocker (pegvisomant)
52
best way to diagnose varicoceles?
Duplex Ultrasonography
53
release inhibin- keeping FSH low
sertolli cells
54
responsible for the release of testosterone?
LH
55
which class of medications can cause ejaculatory disfunction?
alpha blockers 5- alpha reductase inhibitors
56
the consisten or recurrent inability of a man to attain and/or maintain a penile erection sufficient for sexual activity
erectile dysfunction
57
what would organic erectile dyfunction look like
* Gradual onset * risk factors present * consistent dysfunction * masturbation a problem * orgasm may be preserved, even if flaccid * sleep erections absent
58
what would psychogenic ED look like?
* sudden onset * risk factors absent * situational and varying dysfunction * non-coital erections may be present * orgasm absent * sleep erections present
59
what is an important thing to consider for younger patients presenting with Erectile dysfunction?
ED may be the first sign of underlying CVD
60
What are some shared risk factors for ED and cardiovascular disease?
Hypertension diabetes dyslipidemia Depression smoking obesity sedentary lifestyle
61
The pathogenesis of ED is related to ?
Endothelial dyfunction * decrease endothelium dependent vasorelaxation * increased adhesion of leukocytes to endothelium
62
symptoms of low testosterone?
* diminished libido/erectile dysfunction * diminished energy/ vitatlity * depressed mood * cognitive changes * decreased muscle mass/ strength
63
signs of low testosterone?
Decreased bone density anemia truncal obesity
64
Fluid imbalance marked by polyuria, nocturia and polydipsia
diabetes insipidus
65
increased levels of ADH causes water retention
SIADH
66
what is the urinary output (osmolarity) in diabetes insipidus?
High- polyuria
67
what is the urianry output for SIADH?
low- oliguria
68
treatment for diabetes insipidus?
central- desmopressin Nephrogenic- hydrochlorthiazide
69
treatment for SIADH?
fluid restriction
70
water retention/decrease urine production
increase in ADH
71
increase urine production
decrease in ADH
72
major stimuli for relase of ADH hormone?
plasma hyperosmolality circulating volume depletion
73
excessive thirst and excretion of a large amount of dilute urine. Decreasing the intake of fluid does not change urine concentration
Diabetes insipidus
74
site of defect for central diabetes insipidus?
hypothalamus or possibly posterior pituitary
75
central diabetes insipidus left untreated would result in ______ serum Na+
high to normal range
76
Increase serum osmolality and decreased urine osmolality
Central DI
77
which receptor mediates vasoconstriction, enhancement of corticotrophin release and renal prostaglandin synthesis?
V1
78
Mediates the antidiuretic response
V2
79
What is needed for diagnosis of SIADH?
* Hyponatremia * serum osmolality <275 * urine osmolality >100 | must have nml cardiac, renal, hepatic and thyroid fxn
80
type of SIADH where patient may have decreased reaction times, cognitive slowing, ataxia resulting in frequent falls
chronic SIADH
81
SIADH that may be relatively asymptomatic, but may also have anorexia, nausea, malaise, headache, muscle cramps, weakness, seizures or coma
Acute SIADH
82
what pharmacologic agents are responsible for hyperprolactinemia?
anti-depressants H2 blockers opioids
83
excess growth hormone after growth plates closed
Acromegaly
84
excess growth hormone before the epiphysis closes
Gigantism
85
what do you have to give in order to get a correct serum GH
glucose
86
what is first line treatment of acromegaly/gigantism? what second line?
1st line: transsphenodial surgery pharmacologic: dopaminergic like ocretinide/pegvisomant
87
what genetic testing should be offered for patients entering IVF/ICSI with nonobstructive azoospermia or counts <5mil/ml
Karyotyping Y chromosome analysis
88
what genetic test should be offered for patients with vasal agenesis or unexplained epididymal/ED obstruction (absence of vas defrens, blockage in prostate)
CFTR testing to rule of cystic fibrosis mutations
89
retrograde or anejaculation can be caused by?
alpha blockers (tamulosin)
90
ejaculatory dysfunction is can be caused by?
5 alpha reductase inhibitors
91
Total testosterone =
Free T + albumin bound T + sex hormone binding globulin (SHBG) bound T
92
bioavailabe testosterone =
Free T + albumin bound T
93
intramuscular dosing of testosterone?
every 2-3 weeks
94
absorbable gel dosing of testosterone?
once daily
95
oral dosing of testosterone?
3-4 times daily
96
nonscrotal patch dosing of testosterone?
once daily
97
mucoadhesive dosing of testosterone?
twice daily
98
nasal dosing of testosterone?
three times daily
99
SQ pellets dosing of testosterone
every 3 months
100
one step glucose test for gestional diabetes
fasting >92mg 1 hr >180mg 2 hr >153mg
101
two step criteria for gestational diabetes
after 50g oral glucose if 1hr > 130mg/dl step 2: diagnosis is confirmed if fasting >95mg 1hr >180mg 2 hr > 155mg 3 hr> 140mg