Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NUR 141 > 2.3 Nutrition and Fluid Balance, Endocrine > Flashcards

2.3 Nutrition and Fluid Balance, Endocrine Flashcards

1
Q

Type I Diabetes

A

Type I Diabetes (10-15%)
Auto-immune= body attacks beta cells in pancreas that produce insulin.
Occurs before age of 30 (usually)
No insulin is produced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type II Diabetes

A

Type II Diabetes (85-90%)results from
Risk Factors: obesity, family hx, inactivity, middle age or older (can develop younger ages)
Insulin resistance (overweight people)
Inadequate insulin production (lean people)
A combination of both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyperglycemia signs and symptoms

A 
POLYDIPSIA
POLYURIA
POLYPHAGIA
WEIGHT LOSS
FATIGUE
Frequency of infections
Rapid onset
Insulin dependent
Early onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Polyuria
Cause:
Effect:

A

Polyuria
Cause: High blood sugar causes water to enter intravascular space

Effect: Increased intravascular fluid causes increased urine output= electrolyte imbalances.
Blood Glucose >180 glucose is excreted in urine “glucosuria”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Polydipsia
Cause:
Effect:

A

Polydipsia
Cause: Increase urine output causes dehydration

Effect: Mouth becomes dry and thirst sensors activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Polyphagia
Cause:
Effect:

A

Polyphagia (excessive hunger)
Cause: Glucose can’t enter cells to provide energy when insulin not present or ineffective.

Effect: Energy production decreases = stimulates hunger= in hopes of providing body with energy = glucose still can’t enter cell to provide energy = body breaks down fats and proteins to restore energy = person loses weight.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DM Monitoring

A

Capillary Glucose Monitoring:

  • Frequency of monitoring individualized
  • Isopropyl alcohol, food residue & some lotions will alter the results.

HGB A1C or HBA1C or Glycosylated hemoglobin (A1C)

  • Represents average glucose level during 2-3 month period. (Kees p. 225)
  • A1C ≥ 6.5% diagnostic for diabetes (new 2014 guidelines)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypoglycemia signs and symptoms

A

Sudden onset: Blood glucose < 60 mg/dL

Symptoms: anxiety, shaky, irritability, tachycardia, difficulty thinking, poor concentration, slurred speech, blurred vision, decrease LOC, seizures, coma, pale cool skin, sweaty.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypoglycemia treat

A

Treat: Needs sugar!
Alert? Oral juice, glucose gel/tabs, reg soda
Unresponsive? IV D50
Brain requires glucose!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hypoglycemia in Elderly

A

What does an insulin reaction look like in an older patient?

Speech Disorder
Slurring
Confusion
Disorientation

Not the typical diaphoresis and clammy skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hypoglycemia vs. stroke

A

Hypoglycemia can produce symptoms similar to a stroke

Blurred vision
Weakness, dizziness
Slurred speech

All suspected strokes should receive hypoglycemia treatment, just in case

Many strokes have been “cured” this way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diabetic Ketoacidosis

what is it

A

A state of insulin deficiency resulting in hyperglycemia and an accumulation of ketones in the blood. Fat stores used for energy results in metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diabetic Ketoacidosis

Causes/ risk factors

A

Causes/ risk factors:
Sick or infection (most frequent)
Decrease or omission of insulin.

Occurs in Type 1 DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diabetic Ketoacidosis Labs

A 
Labs:
Ketones elevated in blood or urine.
Blood glucose >250
PH <7.30
Bicarb<15
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diabetic Ketoacidosis Symptoms

A 
Symptoms
Lethargy, coma
Kussmaul’s respirations
Warm, dry, poor turgor
Fruity breath from ketones 
Hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Somogyi Phenomenon what is it

A

Is a combo of hypoglycemia in the night with rebound hyperglycemia in the morning.

Caused by too much insulin

Hyperglycemia = more insulin =hypoglycemia =secretion of counter-regulatory hormones (epinephrine, cortisol, glucagon, growth hormone = hyperglycemia =more insulin = cycle repeats
Treat by slowly reducing insulin

More common in Type I DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Dawn Phenomenon what is it

A

Rise in blood glucose between 4-8 AM that is not a response to hypoglycemia.

Cause unknown: thought to be r/t nocturnal release of counter-regulatory hormones that increase blood sugar

Can occur both DM I and II

Correct with timing of insulin or increase of dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Complications of DM- hyperglycemia

A

Hyperglycemia from impaired glucose & insulin resistance invokes an inflammatory process in vascular endothelial lining causing complications:

19
Q

Complications of DM

Macrovascular

A

Macrovascular:

Manifested thru atherosclerosis results in HTN, CAD, PVD, Cerebral & Carotid artery damage

20
Q

Complications of DM

Microvascular

A

Microvascular:

Basement membrane of smaller blood vessels & capillaries thickens eventually leading to decreased tissue perfusion.

21
Q

Complications of DM

Retinopathy

A

Retinopathy- micro-vascular damage & hemorrhage lead to scarring of retina. Leading cause of blindness in DM.

22
Q

Complications of DM

Nephropathy

A

Nephropathy: thickening of basement membrane of glomeruli impairing renal function.

23
Q

Complications of DM

Neuropathy

A

Neuropathy- thickening of blood vessels that supply nerve endings. Causes change in sensation (numbness/tingling), pain (ache, burn, shooting, cold) Teach importance of visually inspecting feet/legs daily to look for injury

24
Q

Diabetic Foot Care teaching

A 
Teach Daily foot inspection
avoid crossing legs
Non-restrictive shoes & good quality socks
Do not self-treat foot problems
Avoid dry skin, cracks, infections
Podiatrist evaluation
Buy shoes late afternoon- feet @ largest
25
Q

Management of Diabetes

A

DIET

EXERCISE

MEDS

26
Q

Insulin Administration

A

Preferred site is Abdomen- allows most rapid absorption.
Do not give in legs prior to exercise- increases absorption rate and chance of hypoglycemic event.
If mixing insulin must draw up “clear before cloudy” (regular then NPH). Avoids contamination of NPH into regular insulin vial.
Do not massage site after injection- interferes with absorption.
Teach pt that exercise lowers insulin requirements; seek consultation prior to exercise program.

27
Q

Insulin Administration tips

A 
Tips to decrease pain with injection:
Allow alcohol to dry on skin 1st 
Room temp insulin
Don’t reuse needles
Quick penetration and removal of needle at same angle.
28
Q

Noninsulin Hypoglycemic Agents

Metformin

A

Metformin (Biguanides):
Reduces FBG (fasting blood glucose) & postprandial (after eating) hyperglycemia.
Often suspended during hospitalization r/t increased risk of lactic acidosis
Stopped prior to and 48 h after use of contrast media & surgery r/t risk of renal failure.
Low risk of hypoglycemic events

29
Q

Noninsulin Hypoglycemic Agents

Sulfonylureas

A

Sulfonylureas glipizide (Glucotrol), glyburide (Micronase), glimepirde (amaryl)

Treat type 2 DM in non-obese people not controlled by diet alone.

Stimulate pancreatic cells to secrete more insulin making peripheral tissues more sensitive to insulin.

Usually suspended during hospitalizations r/t dose adjustments must be made slowly.
Not useful in acute illness.

Common side effect hypoglycemia compounded by NPO status.

30
Q

Teaching: Sick Day rules

A

M- Monitor blood sugar levels more frequently
D- Do not stop taking insulin
C- Check urine for ketones if glucose >240
B- Be careful with over-the-counter medications
H- Have a game plan & ask for help if needed
F- Force fluids (8 oz. each hour)
C- Call provider if unable to eat >24h, vomiting /diarrhea >6 h, urine ketones mod/lg for >4h

31
Q

ADRENAL GLAND FUNCTION Medulla

A

Medulla (inner portion of adrenal gland)

Epinephrine and Norepinephrine

32
Q

ADRENAL GLAND FUNCTION Cortex

A

Cortex (outer portion) Produces hormones essential to life.
Mineralcorticoids (release controlled by renin when b/p or Na is low)
Glucocorticoids (cortisol & cortisone) released in time of stress affect CHO metabolism & regulates glucose use in body tissues.
Androgens- sex hormones
Loss of cortex hormones=death

33
Q

Cushing’s Syndrome
what is it
treated

A

Excessive cortisol produced
Chronic disorder
Taking corticosteroids long time= increased risk.
Treated: meds to suppress cortisol or adrenalectomy

34
Q

Cushing’s Syndrome

Excess cortisol effects

A

Excess cortisol effects:
Fat deposits abdomen, under clavicle, upper back “buffalo hump”
Moon face
Muscle weakness/wasting r/t change in protein metabolism.
Loss of collagen & connective tissue
Thinning of skin, abdominal striae (stretch marks)
Poor wound healing, frequent infections
Altered glucose metabolism sometimes causing DM
Emotional changes (depression/ psychosis)

35
Q

Cushing’s Disease Diagnostics labs

A 
Increased levels:
Serum cortisol
Sodium 
Glucose
Urine free cortisol

Decreased levels:
Potassium

36
Q

Cushing’s Disease Diagnostics

Treatment

A

Treatment:
Meds to suppress activity of adrenal cortex (Mitotane, aminoglutethimide)
Adrenalectomy

37
Q

Addison’s Disease what is it

A

Adrenal insufficiency - Cortisol deficiency
Autoimmune most common cause
Slow onset s/s occur after 90% adrenal function lost.

Deficient cortisol effects:
Sodium is lost & potassium retained
Extracellular fluid depleted and blood volume decreased

38
Q

Addison’s Disease S/S

A

S/S:
Postural hypotension & syncope, dysrhythmias
Dizziness, confusion, lethargy, emotional lability
Weakness, muscle wasting
Hyperpigmentation of skin
Hyperkalemia, hyponatremia, hypoglycemia

39
Q

Addison’s Disease Diagnostics labs

A

Decreased levels of:
Serum cortisol levels
Blood glucose levels
Serum sodium levels

Increased:
Serum potassium levels

40
Q

Addison’s Disease

Teaching and treatment

A

Treatment:
Meds to replace corticosteroids and mineralocorticoids
Hydrocortisone (Cortef & others)
Fludrocortisone (Florinef)
Prednisone, dexamethasone, methylprednisolone
Steroids suppress immune system
Teach: meds needed for rest of life, diet low K+ high Na+ and protein.

41
Q

Addisonian Crisis

A

Life threatening acute adrenal insufficiency caused by major stressors (surgery, acute illness, trauma)
Abruptly withdrawn from corticosteroid meds or hemorrhage into adrenal glands

42
Q

Addisonian Crisis s/s

A

S/S (develop rapidly): high fever, weakness, severe penetrating pain in abdomen/lower back/legs, severe vomiting, diarrhea, hypotension, circulatory collapse, shock and coma.

43
Q

Addisonian Crisis treatment

A

Treatment: rapid IV replacement of fluids and glucocorticoids. Fluid balance generally restored in 4-6 hours.

44
Q

Adrenal Gland Hormones

3 “S’s”

A

Sugar: glucocorticoids (cortisol and cortisone), effect carbohydrates by regulating the glucose

Salt: mineralocorticoids (aldosterone), Na and water, regulate BP, part of renin angiotensin aldosterone systems

Sex: androgens (male hormones, DHEA, testosterone)

NUR 141 (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions