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NCLEX > Endocrine Part 2 > Flashcards

Endocrine Part 2 Flashcards

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1
Q

3 main issues with Addison’s disease

Aldosterone is a what?

A

(Too little aldosterone; lose Na and water, ^K)

  1. Not enough steroids
  2. SHOCK
  3. ^K

mineralocorticoid

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2
Q

S/S Addisons

A

Hyperkalemia (twitching –> weakness –> paralysis)

Hypotension - low Na, ^K, low glucose
Anorexia/nausea
GI upset
Decreased bowel sounds
Vitiligo
Hyper pigmentation (bronzing of the skin and mucous membrane)
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3
Q

How to treat Addison’s
Diet?
Main ND
Medication to give

A

Fix shock/hypotension, I/O/wt
^ Na - fruit juice/broth

Fluid volume deficit
Fludrocorticoid / Aldosterone

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4
Q

Rule of thumb to daily weights

A

Keep wt within 2-3 lbs or their normal weight

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5
Q

What happens when steroids are stopped abruptly? Why? What do we think of when we think of this?

A

Addisonian Crisis (Adison’s disease x 100)

Because when we take steroids, our own adrenal glands go to sleep and we we stop taking them all of the sudden, there are NO steroids in our body!

Sever hypotension and vascular collapse

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6
Q

What to we think of first when we think of fluid problems?

A

HEART PROBLEMS

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7
Q

No aldosterone = _____ retention of Na and Water

So what if we gain or lose too much weight?

A

NO - losing it all

Gain weight - hold dose
Lose weight - increase dose

*Doses will not be the same throughout life

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8
Q

How do you need to DC steroids?

A

TAPER THEM

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9
Q

What happens to our blood sugar in Addison’s Disease?

A

Normally when we are taking steroids, our blood sugar is going to increase. BUT in this disease, we don’t have any of these steroids so our blood sugar is going to DECREASE

LOW GLUCOSE

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10
Q

Cushings = ________ steroids

A

TOO MANY (glucocorticoids, mineralocorticoids, sex hormones)

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11
Q

S/S in Cushing’s Disease due to too many GLUCOCORTICOIDS

A

Remember 4 functions of glucocorticoids* (alter mood, inhibit insulin, break down fats & proteins, alter defense mechanisms)

Growth arrest
Lipolysis (this extremities)
Hyperglycemia
Psychosis or depression
Increased risk of infection

Moon face, truncal obesity, buffalo hump - D/t fat redistribution

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12
Q

S/S in Cushing’s Disease due to too many SEX HORMONES

A

Oily skin / acne
Women with male traits
Poor sex drive

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13
Q

S/S in Cushing’s Disease due to too many MINERALOCORTICOIDS (aka ______)

A

Aldosterone

Fluid volume EXCESS
Hypertension
Weight gain
CHF

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14
Q

Because the patient has too much mineralocorticoid, what happens to our potassium?

A

DECREASES Potassium

*Remember
Aldosterone = retain Na and water, lose K

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15
Q

How do we treat Cushing’s?

A

Adrenalectomy

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16
Q

What does the patient need to do if they have both adrenal glands removed?

A

Take replacements for life

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17
Q

what kind of environment should the post-adrenalectomy patient have? Why?

A

Quiet because when our steroids are messed up, our body does not have the ability to handle stress

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18
Q

What should the patient’s diet be before Cushing’s Treatment?

*What 4 things are affected?

A 
Increased K (They are losing it)
Increased Protein (They are breaking it down)
Increased Calcium (Losing it)
Decreased Na (They are retaining it)
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19
Q

How do steroids affect calcium again??

What kind of precautions are we going to take?

A

They decrease serum calcium by excreting it through the GI tract

They are going to have more brittle bones so we want to be careful with things like turning, and protecting fragile bones like the ribs (CPR)

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20
Q

Can a Cushing’s patient’s body handle infection well?

A

NO! Avoid it! This is stress and when our steroids are all messed up, their bodies aren’t going to be able to handle it and increased steroids = suppressed immune system

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21
Q

What 2 things are going to appear in the urine of Cushing’s patient? Why?

What are we not going to have in our urine of a Cushing’s patient and why?

A

Ketones - Result of breaking down protein
Glucose - steroids increase blood sugar and when we have excess blood sugar, it will spill over into our urine

NO PROTEIN in their urine!! Proteinuria to deal with glomerular / kidney damage

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22
Q

Causes of T1 diabetes

A 
Autoimmune response (Type 1A)
Idiopathic response (Unknown Type 1B)
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23
Q

What is often the first sign of T1 DM

A

DKA

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24
Q

You need ______ to carry ______ out of the _______

A

You need insulin to carry glucose out of the vascular space

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25
What happens to our blood when there is no insulin? How does insulin work?
It becomes hypertonic (like s sponge) and pulls fluid into the vascular space Decreases glucose and K by driving them out of the vascular space and into the cell
26
Why to the 3 P's occur?
The kidneys filter excess glucose and fluids causing polydipsia and polyuria This causes the cells to starve because of low glucose so they start breaking down fat and proteins for energy causing polyphagia
27
What happens when our body breaks down fat and protein? How do we compensate?
We produce ketones and become acidotic (metabolic acidosis) Body tries to compensate by increasing respirations to blow of CO2 (Kussmauls)
28
With polyuria, think _____ first
SHOCK! Because we are losing fluid
29
Glucose normal
70-110
30
How is T2 DM usually found?
By accident - Coming to the doctor frequently for things like wounds that won't heal, repeated vaginal infections Sugar loves bacteria!
31
What do T2 DM need to be evaluated for?
Metabolic Syndrome
32
What are the 6 components of Metabolic syndrome?
1. Insulin Resistance 2. Abdominal obesity (waist >40 M, >35 F) 3. Increased Triglycerides 4. Decreased HDL 5. Increased BP 6. CAD
33
Steps to treat T2 DMaaa
Start with diet and exercise, then add oral agents, then they may need insulin
34
What is the major difference between T1 and T2 DM
Metabolic acidosis will only occur with T1 because they aren't making any insulin so it is only their bodies that will breakdown fats and proteins
35
Gestational DM resembles what? Does mom need more insulin? When should we screen? What if they have risk factors? What are the complications to baby?
T2 Yes - 2-3x more insulin Screen all moms at 24-28 weeks and at the 1st prenatal visit if they are at risk Increased birth weight and hypoglycemia
36
When we think of extreme blood sugar, we should think what? | What does this put the patient at risk for?
Vascular damage Risk for CAD because the sugar destroys the vessels *Same kind of deal when there is high fat in the vessels causing narrowing
37
DM DIET Where should we get most of our calories? What should we limit? Why? High or low fiber -Why?
Complex carbs, then fats, and LASTLY protein Limit protein by 10-20% because diabetics tend to have renal disease and messed up kidneys can't handle increased protein to break down High fiber - keeps their sugar steady by slowing glucose absorption in the intestines and eliminated sharp rise/falls in good sugar -- May be able to decrease insulin with this diet!
38
``` DM EXERCISE When should patient exercise? How does exercise affect blood sugar? How should they prevent hypoglycemia? Parameter to follow for daily exercise? Is it better to exercise when blood sugar is at it's highest or lowest point? ```
``` When their glucose is normal Exercise decreases blood sugar EAT before exercising Do it at the same time and amount daily HIGHEST ```
39
How do oral hypoglycemic agents work?
Most will stimulate the pancreas to make insulin for T2 DM (Nclex - they all do) All in all: They work to decrease circulating glucose
40
Insulin dose is based on what? | How is it adjusted?
Body weight | Adjusted until BS is normal and there aren't any ketones or glucose in the urine
41
What is the Basal/Bolus method of giving insulin? When given?
Giving a long-acting and a rapid-acting insulin Long - Morning once Rapid - before meals (never give without food)
42
RAPID insulin Types Onset Peak Duration
Aspart, Lispro (Humalog, Novolog) Onset : 15 min Peak: 1-3 hours Duration: 3-5 hours GIVE W FOOD
43
REGULAR Insulin Types Onset Peak Duration
Short Acting- Humulin R, Novolin R Onset: 30 min Peak: 2-4 hours Duration: 6-8 hours
44
NPH Insulin - clear or cloudy? Types Onset Peak Duration
Intermediate- Acting: Humilin N, Novolin N Cloudy Onset: 1.5 hours Peak: 4-12 hours Duration: 16-24 hours
45
LONG ACTING Insulin Types Onset Peak Duration
Glargine, Detemir (Lantus, Levemir) Onset: 2-4 hours Peak: None Duration: 24 hours
46
Do you need snacks with Basal/bolus insulin?
No BUT patients still must eat when dosing rapid acting insulin - so have food available
47
When should clients eat during the day in regards to their insulin?
At the insulin's peak because that's when their blood sugar is the lowest
48
Always monitor for what when a patient is taking insulin regardless?
Hypoglycemia
49
Clear and cloudy insulin, which do we draw up first?
Clear
50
Hub A1c tracks aver blood sugar over what time period?
Last 3 months - Want less than 6
51
NCLEX: Illness = ______
DKA
52
How do we rotate injection sites? Aspirate?
Within the area first for a week then don't use again for 3-6 weeks NO
53
What kind of insulin is given in an infusion pump?
Rapid acting - will give a continuous and boluses
54
Only insulin that can be given in fluids as an IV infusion?
Regular
55
Hyperglycemic Mnemonic
Polyuria Polydipsia Polyuria Hot & Dry, Sugar high - fruity odor
56
Hypoglycemic Mnemonic
TIRED ``` Tired, tachycardia Irritable, Headache Restless/anxiety/shakiness Excessive hunger Diaphoresis, Cold & Clammy, need some candy ```
57
What should patient do if hypoglycemic
Eat/drink simple sugar 4 oz Coke, juice, milk - Increase sugar FAST Unconscious: put honey under tongue
58
How is glue absorbed when eating fat?
Glucose has delayed absorption
59
Once blood sugar is up after consuming a simple sugar, what should the patient do?
Eat a complex carb Ex: PB and crackers, protein
60
If someone is unconscious, will we treat hypo or hyperglycemia? What to do when they wake up?
HYPOGLYCEMIC - more sugar will hurt the brain is that's what they are unresponsive Have them eat something
61
What to give if patient does not have IV access for hypoglycemia? What if they do?
Injectable glucagon D50W IVP
62
How to prevent hypoglycemia
Eat Know S/S Take insulin regularly Check sugar regularly
63
S/S DKA
Hyperglycemia Kussmauls Decreased LOC
64
How to treat DKA
1. IVF - NS until BS is around 300m then switch to D5W to prevent hypoglycemia MD may want to add K at some point 2. IV insulin
65
Things to monitor with DKA
Hourly glucose, K, I/O ECG ABG
66
DKA think _____ | HHS think _____
DKA - T1 | HHS - T2
67
How is HHS different than DKA?
No acidosis present because they aren't breaking down fat No kussmauls
68
Vascular damages d/t DM What do these lead to?
Poor circulation d/t vessel damage Diabetic retinopathy -> blindness Nephropathy -> renal failure
69
4 Complications with DM neuropathy
1. Sex probs - impotence/decreased sensation 2. Pain/paresthesia/numbness in feet and legs - Need to inspect daily! no Betadine/harsh chemicals 3. Neurogenic bladder - incontinence or retention / UTI 4. Gastropharesis - delayed gastric emptying - risk for aspiration

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