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NEW NUR 141 > 2.3 NFB, endocrine > Flashcards

2.3 NFB, endocrine Flashcards

1
Q

DIABETES MELLITUS TYPE I

A 
TYPE I
auto-immune process
abrupt onset often triggered by illness/stress
insulin dependence
childhood onset
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2
Q

DIABETES MELLITUS TYPE II

A

TYPE II
decreased insulin release
insulin resistance in liver, peripheral tissues

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3
Q

Classic signs and symptoms are related to hyperglycemia

A 
Polyuria
Polydipsia
Polyphagia (hunger)
Weight loss
Fatigue
Increased frequency of infections
Rapid onset
Insulin dependent
Early onset
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4
Q

Polyuria

A

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

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5
Q

Polydipsia

A

Mouth becomes dry and thirst sensors activated

Increase urine output causes dehydration

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6
Q

Polyphagia

A

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.

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7
Q

Type II deabetes

A 
Sedentary lifestyle
Familial tendency
Average age, 50
History of high BP
Fatigue
Reduced energy
Recurrent infections
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8
Q

Hypoglycemia s/s

A 
Rapid onset: 1-3 hr
Anxious
Sweaty
Hungry
Ha
Blurred vision
Shaky
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9
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

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10
Q

Diabetic Ketoacidosis

A

A state of absolute or relative insulin deficiency resulting in hyperglycemia and an accumulation of ketones in the blood with subsequent metabolic acidosis

Ketosis
Acidosis
pH<7.30
Bicarb<15 mmol/L
Hyperglycemia
Ketones in urine/blood
BS: >250
Lethargy
Coma
Kussmaul's resp
Hypotension

Occurs in Type 1 DM

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11
Q

Diabetic ketoacidosis s/s

A

Lack of insulin
Hx:
GI upset, febrile illness
Slow onset: 4-10 hr

Fruity breath
Tachycardia
Hypotension
Acidosis
High blood sugar
Hyperkalemia

NEED:
hydration
insulin
electrolyte replacement

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12
Q

Somogyi phenomenon

A

Rebound hyperglycemia due to hypoglycemia during the night

Caused by too much insulin
Hyperglycemia- more insulinhypoglycemia- secretion of contra insulin hormones- hyperglycemia- more insulin- cycle repeats

Treat by slowly reducing insulin

Tx:
decrease evening insulin or adjust timing to prevent hypoglycemia

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13
Q

Dawn phenomenon

A

Normal morning effect increases growth hormones and decrease insulin levels

Tx:
increase basal insulin or adjust timing for better control

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14
Q

Complications of DM

Macrovascular

A

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

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

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15
Q

Complications of DM

Microvascular

A

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

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

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16
Q

Complications of DM

Retinopathy

A

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

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17
Q

Complications of DM

Nephropathy

A

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

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18
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

19
Q

DIABETIC FOOT CARE

A 
DIABETIC FOOT CARE 
Daily inspection
avoid crossing legs
Always wear shoes, Bathe feet--test water temp
do not self-treat foot problems
avoid dry skin, cracks, infections
Podiatrist evaluation
20
Q

Sick day rules

A 
Monitor blood sugar more often
Do not stop taking insulin
Check urine for ketones
Careful with OTC
Have game plan
Force liquids
Call provider if unable to eat >24 hr, vomiting/diarrhea >6 hr, urine ketones
21
Q

Insulin

A

know types

22
Q

oral

A

know meds

23
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
Teach pt that exercise lowers insulin requirements; seek consultation prior to exercise program.

24
Q

Metformin (Biguanides):

A

Reduces FBG & postprandial hyperglycemia.
Often suspended during hospitalization r/t 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

25
Q

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

A

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.

26
Q

ADRENAL GLAND FUNCTION Medulla

A

Medulla (inner portion of adrenal gland)

Epinephrine and Norepinephrine

27
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

28
Q

ADRENAL GLAND Function

A

Function-
Adrenal medulla produces 2 hormones-epinephrine (adrenalin) and norepinephrine.
Adrenal cortex secretes several hormones, all corticosteroids. (Mineralocorticoids and glucocorticoids-these are essential to life)

29
Q

ADRENAL GLAND What is ACTH?

A

What is ACTH?

Adrenocorticotropic hormone. Stimulates release of hormones especially glucocorticoids from the adrenal cortex

30
Q

HOW DOES ACTH AFFECT ADRENALS

A

ACTH: adrenocorticotropic hormone

From anterior pituitary

Stimulates secretion of corticosteroids

Diagnostics: ACTH stimulation

  • Addison’s disease-Adrenocortical Insufficiency
  • Cushing’s syndrome-Hypercortisolism
31
Q

Adrenal Gland hormones three “s”

A

Sugar: glucocorticoids
Salt: mineralocorticoids
Sex: androgens

32
Q

Diagnostic Tests related to Adrenal Function

A

ACTH suppression Test

Cortisol Levels

CT or MRI of Abdomen

33
Q

Addison’s Disease

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.

34
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

35
Q

Addison’s Disease Diagnostics

A 
Decreased levels of:
Serum cortisol levels
Blood glucose levels
Serum sodium levels
Increased:
Serum potassium levels
36
Q

Addison’s Disease tx

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.

37
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

S/S (develop rapidly): high fever, weakness, severe penetrating pain in abdomen/lower back/legs, severe vomiting, diarrhea, hypotension, circulatory collapse, shock and coma.
Treatment: rapid IV replacement of fluids and glucocorticoids. Fluid balance generally restored in 4-6 hours.

38
Q

Cushing’s Syndrome

A

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

39
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)

40
Q

Cushing’s Disease Diagnostics

A 
Increased levels:
Serum cortisol
Sodium 
Glucose
Urine free cortisol
Decreased levels:
Potassium
41
Q

Cushing’s Disease Treatment:

A

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

42
Q

ADRENAL GLAND steroid admin

A

Adrenocorticosteroids (Solu-Medrol, Decadron, Cortisol, Florinef, Prednisone) are used for replacement therapy in acute/chronic adrenal insufficiency.

43
Q

ADRENAL GLAND Side Effects

A

Side Effects: BP, edema, wt gain, bleeding/bruising-ULCERS/GI BLD, CUSHINGs Syndrome, may mask infection, Mood Swings/Changes

44
Q

ADRENAL GLAND Nursing Interventions

A

Nursing Interventions: Medication Education for pt & Family.
Monitor VS, Mental Status, Neurological Function, Wt. Edema, Glucose
Identify medication interactions with corticosteroids (Antidiabetic agents, NSAIDS)
Administer with Food to decrease ulcerongenic effect
Monitor electrolytes: K+ & Na++, Blood Glucose

NEW NUR 141 (5 decks)

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