Endocrine Flashcards

(32 cards)

1
Q

patho of SIADH

A

There is a hypersecretion of ADH from posterior pituitary gland. This goes to kidneys and promotes excessive water reabsorbtion.
This leads to dilutional hyponatremia.
Think H2O intoxication

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2
Q

causes of SIADH

A

oat cell carcinoma AKA bronchogenic tumor
viral pneumonia
neurologic disorder
analgesics, anesthetics, & stress

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3
Q

serum osmolality normal level

A

275-295

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4
Q

how to quickly calculate serum osmolality

A

2x sodium level

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5
Q

fluid status in low serum osmolality?

A

fluid volume overolad

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6
Q

fluid status in high serum osmolality

A

concentrated/dehydration

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7
Q

urine specific gravity normal levels

A

1.005-1.030

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8
Q

assessment of SIADH patient

A
decreased LOC/lethargy
confusion/personality changes
Headache
NVD
anorexia
hyponatremia (cerebral edema)
seizures/coma
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9
Q

medical management of SIADH

A

treat underlying cause - surgery/radiation/chemo
fluid restriction
Na replacement w/ 3%NS
Lasix if overloaded after 3%

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10
Q

medications for SIADH

A
ADH inhibitor (vaprisol)
demeclocycline (abx) - abx that interferes with ADH effects in tubules
phenytoin/fludrocortisone - blocks effects of ADH in tubules
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11
Q

nursing management for SIADH

A

fluid volume status
neuro
seizure precautions
oral care

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12
Q

patho/causes of DI

A

improper posterior pitutitary development
neuro trauma
pituitary tumor
kidney disease - nephrogenic DI from failure to respond to ADH
dilantin - blocks effect of ADH on tubules

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13
Q

what is the one thing you think of when you hear DI?

A

water wasting

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14
Q

assessment of patient with DI

A
polyuria
polydipsia
dehydration
hypotension
tachycardia
decreased LOC
seizures
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15
Q

what labs would you see with DI?

A

low urine osmolality/specific gravity/sodium

high serum osmolality/specific gravity/sodium

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16
Q

what labs would you see with SIADH

A

high urine osmolality/specific gravity/sodium

low serum osmolality/specific gravity/sodium

17
Q

medical management of DI

A

fluid replacement w/ hypotonic crystalloids

exogenous ADH - DDAVP/pitressin/vasopressin

18
Q

nursing management of DI

A

fluid/electrolyte monitoring
seizure precautions
neuro

19
Q

what form of DM is DKA most prominent in?

20
Q

normal hyperglycemia range for DKA?

21
Q

risk factors for DKA?

A

decrease insulin intake, increase dietary intake, growth spurts, surgery, infection, trauma, emotional stress

22
Q

3 components of DKA?

A

hyperglycemia
ketosis
acidemia

23
Q

patho for DKA

A

not enough insulin leads to increased glucagon release because cells are not receiving glucose d/t lack on insulin.
Leads to hyperglycemia and increased serum osmolality which causes cellular dehydration and fluid excretion
Ketoacidosis occurs when fatty acid metabolizes in cells

24
Q

assessment for DKA

A
polyuria
polyphagia
glucosuria
polydipsia
NV
weight loss/dehydration
fruity breath
decreased LOC
dry skin/mucous membranes
tachycard/hypotensio
kussmaul respirs
25
DKA is common in which type of DM1 patients?
newly diagnosed patients
26
What is important with DKA patients when it comes to curing them?
Treat DKA, but also treat the underlying cause of DKA (infection)
27
DKA/HHNK protocol?
NS 0.5-1L/hr x 2 hr bolus then 1/2NS @ 250-500mL/hr until BS <250 When BS reaches <250 then D5,1/2NS until DKA resolves ``` stat EKG to r/o hyperK if K >5.5, treat if symptomatic 4-5.5 give 20meq to each L of fluid 3-4 give 40meq to each L of fluid <3 give PO/IV 10meq K q1h or PRN ``` insulin 0.1units/kg initial bolus IV then continuous 0.1units/kg/hr with BSBG q1h until resolution
28
Nursing management of DKA/HHNK
``` fluid management BSBG q1h neuro q4h UOP q1h Lab analysis cardiac monitor pt education ```
29
HHNK Hallmark sign
grossly elevated BG w/o ketosis
30
patho of HHNK
same as DKA, but insulin is produced but not effective in pushing glucose fast enough into cells
31
Which DM is HHNK most associated with?
DM2
32
How high can BG get in HHNK?
2000