Endocrine Flashcards

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?

A

DM1

20
Q

normal hyperglycemia range for DKA?

A

300-600

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
Q

DKA is common in which type of DM1 patients?

A

newly diagnosed patients

26
Q

What is important with DKA patients when it comes to curing them?

A

Treat DKA, but also treat the underlying cause of DKA (infection)

27
Q

DKA/HHNK protocol?

A

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
Q

Nursing management of DKA/HHNK

A
fluid management
BSBG q1h
neuro q4h
UOP q1h
Lab analysis
cardiac monitor
pt education
29
Q

HHNK Hallmark sign

A

grossly elevated BG w/o ketosis

30
Q

patho of HHNK

A

same as DKA, but insulin is produced but not effective in pushing glucose fast enough into cells

31
Q

Which DM is HHNK most associated with?

A

DM2

32
Q

How high can BG get in HHNK?

A

2000