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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
Q

What happens to our blood when there is no insulin?

How does insulin work?

A

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

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26
Q

Why to the 3 P’s occur?

A

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

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27
Q

What happens when our body breaks down fat and protein?

How do we compensate?

A

We produce ketones and become acidotic (metabolic acidosis)

Body tries to compensate by increasing respirations to blow of CO2 (Kussmauls)

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28
Q

With polyuria, think _____ first

A

SHOCK! Because we are losing fluid

29
Q

Glucose normal

A

70-110

30
Q

How is T2 DM usually found?

A

By accident - Coming to the doctor frequently for things like wounds that won’t heal, repeated vaginal infections

Sugar loves bacteria!

31
Q

What do T2 DM need to be evaluated for?

A

Metabolic Syndrome

32
Q

What are the 6 components of Metabolic syndrome?

A
  1. Insulin Resistance
  2. Abdominal obesity (waist >40 M, >35 F)
  3. Increased Triglycerides
  4. Decreased HDL
  5. Increased BP
  6. CAD
33
Q

Steps to treat T2 DMaaa

A

Start with diet and exercise, then add oral agents, then they may need insulin

34
Q

What is the major difference between T1 and T2 DM

A

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
Q

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?

A

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
Q

When we think of extreme blood sugar, we should think what?

What does this put the patient at risk for?

A

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
Q

DM DIET
Where should we get most of our calories?
What should we limit? Why?
High or low fiber -Why?

A

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
Q 
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?
A 
When their glucose is normal
Exercise decreases blood sugar
EAT before exercising
Do it at the same time and amount daily
HIGHEST
39
Q

How do oral hypoglycemic agents work?

A

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
Q

Insulin dose is based on what?

How is it adjusted?

A

Body weight

Adjusted until BS is normal and there aren’t any ketones or glucose in the urine

41
Q

What is the Basal/Bolus method of giving insulin? When given?

A

Giving a long-acting and a rapid-acting insulin

Long - Morning once
Rapid - before meals (never give without food)

42
Q

RAPID insulin

Types
Onset
Peak
Duration

A

Aspart, Lispro (Humalog, Novolog)

Onset : 15 min
Peak: 1-3 hours
Duration: 3-5 hours

GIVE W FOOD

43
Q

REGULAR Insulin

Types
Onset
Peak
Duration

A

Short Acting- Humulin R, Novolin R

Onset: 30 min
Peak: 2-4 hours
Duration: 6-8 hours

44
Q

NPH Insulin - clear or cloudy?

Types
Onset
Peak
Duration

A

Intermediate- Acting: Humilin N, Novolin N
Cloudy

Onset: 1.5 hours
Peak: 4-12 hours
Duration: 16-24 hours

45
Q

LONG ACTING Insulin

Types
Onset
Peak
Duration

A

Glargine, Detemir (Lantus, Levemir)

Onset: 2-4 hours
Peak: None
Duration: 24 hours

46
Q

Do you need snacks with Basal/bolus insulin?

A

No BUT patients still must eat when dosing rapid acting insulin - so have food available

47
Q

When should clients eat during the day in regards to their insulin?

A

At the insulin’s peak because that’s when their blood sugar is the lowest

48
Q

Always monitor for what when a patient is taking insulin regardless?

A

Hypoglycemia

49
Q

Clear and cloudy insulin, which do we draw up first?

A

Clear

50
Q

Hub A1c tracks aver blood sugar over what time period?

A

Last 3 months - Want less than 6

51
Q

NCLEX: Illness = ______

A

DKA

52
Q

How do we rotate injection sites? Aspirate?

A

Within the area first for a week then don’t use again for 3-6 weeks
NO

53
Q

What kind of insulin is given in an infusion pump?

A

Rapid acting - will give a continuous and boluses

54
Q

Only insulin that can be given in fluids as an IV infusion?

A

Regular

55
Q

Hyperglycemic Mnemonic

A

Polyuria
Polydipsia
Polyuria
Hot & Dry, Sugar high - fruity odor

56
Q

Hypoglycemic Mnemonic

A

TIRED

Tired, tachycardia
Irritable, Headache
Restless/anxiety/shakiness
Excessive hunger
Diaphoresis, Cold & Clammy, need some candy
57
Q

What should patient do if hypoglycemic

A

Eat/drink simple sugar

4 oz Coke, juice, milk - Increase sugar FAST

Unconscious: put honey under tongue

58
Q

How is glue absorbed when eating fat?

A

Glucose has delayed absorption

59
Q

Once blood sugar is up after consuming a simple sugar, what should the patient do?

A

Eat a complex carb

Ex: PB and crackers, protein

60
Q

If someone is unconscious, will we treat hypo or hyperglycemia? What to do when they wake up?

A

HYPOGLYCEMIC - more sugar will hurt the brain is that’s what they are unresponsive

Have them eat something

61
Q

What to give if patient does not have IV access for hypoglycemia? What if they do?

A

Injectable glucagon

D50W IVP

62
Q

How to prevent hypoglycemia

A

Eat
Know S/S
Take insulin regularly
Check sugar regularly

63
Q

S/S DKA

A

Hyperglycemia
Kussmauls
Decreased LOC

64
Q

How to treat DKA

A
  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
Q

Things to monitor with DKA

A

Hourly glucose, K, I/O
ECG
ABG

66
Q

DKA think _____

HHS think _____

A

DKA - T1

HHS - T2

67
Q

How is HHS different than DKA?

A

No acidosis present because they aren’t breaking down fat

No kussmauls

68
Q

Vascular damages d/t DM

What do these lead to?

A

Poor circulation d/t vessel damage

Diabetic retinopathy -> blindness
Nephropathy -> renal failure

69
Q

4 Complications with DM neuropathy

A
  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

NCLEX (23 decks)

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