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NUR720 FNP Review > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

1
Q

What kind of antigens and antibodies are most associated with type 1 diabetes?

A

human leukocyte antigens

Islet cell antibodies

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2
Q

What is a unique development for Type 1 DM?

A

ketone development

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3
Q

What is the pathology of type 2 DM?

A

Tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/ or impaired insulin production

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4
Q

What is syndrome X

A

DM II and associated with obesity, HTN, and abnormal lipid profiles (low HDLs and high triglycerides)

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5
Q

What does metabolic syndrome entail and how is the diagnosis made

A

3 or more of the following:

1) wait circumference >40inches (102cm) in men and >35inches (89cm) in women
2) BP>130/85
3) triglycerides >150
4) FBG>100
5) HDL

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6
Q

Diagnostics for DM type 1 and type II

A
  • Random plasma glucose >200 with polyuria, polydipsia and weight loss
  • Serum fasting (8hrs) blood sugar >126 on 2 separate occasions
  • Kenonemia, ketouria, or both for type 1
  • Oral glucose tolerance test>200 2 hours post-prandial
  • Hbg A1C- ROUTINE Diagnosis- normal 5.5-7%
  • Impaired glucose tolerance test FBG >100and
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7
Q

Dietary teaching for diabetics

A

carb intake 55-60%
fats 20-30%
protein 10-20%
Fiber 25g/1000 calories

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8
Q

When is insulin therapy warranted and how do you start insulin?

A

if a patient presents with ketones

0.5units/kg/day giving 2/3 dose in the morning and 1/3 dose in the evening

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9
Q

What is the conventional split dose mixtures of insulin

A

morning dose of insulin is 2/3 NPH and 1/3 regular

evening dose of insulin is 1/2 NPH and 1/2 regular

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10
Q

What are the insulin analogs

A

Aspart (novolog)
Glargine (Lantus)- prolonged duration
Lispro (Humalog)- rapid onset

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11
Q

What are the 5 classes of oral antidiabetics?

A 
Sulfonylureas
Biguanides 
Alph-glucosidase inhibitors 
Thiazolidinediones
Non-sulfonylurea insulin release stimulators
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12
Q

Sulfonylureas- how it works and names

A

stimulate the pancreas to release more insulin

2nd generations: glipizide(glucotrol), glyburide, glimepride

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13
Q

Biguanides- how it works and names

A

decreases hepatic glucose production and intestinal glucose absorption
Metphormin (glucophage)
Good adjunct to the sulfonylureas but can be used alone especially in obese patients

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14
Q

How do alpha-glucosidase inhibitors work and give some names

A

bind to disaccharides more readily than sucrose, so less glucose is absorbed by the gut
acarbose (precose)
miglitol (glyset)

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15
Q

What is a common thiazolidinediones and whats the popular brand?

A 
glitazones decrease gluconeogenesis
Pioglitazone hydrochloride (actos)
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16
Q

How do the non-sulfonylurea insulin release stimulators work and what are 2 brands

A

Rapidely absorbed from the intestine and mimics the effects of rapidly acting insulin
Repaglinide (Prandin)
Nateglinide (starlix)

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17
Q

How does Exenatide ( Byetta) work?

A

Injectable that mimics the effects incretins (signals pancreas to increase insulin secretion and the liver to stop producing glucagon). Causes n/v/d

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18
Q

How does Sitagliptin (Januvia) work?

A

DD-4 inhibitor, breaks down incretins

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19
Q

How does Pramlintide (Symlin) work?

A

Injectable for type 1&2DM, resembles human amylin, slows the absorption of glucose and inhibits the actions of glucagons: promotes weight loss while decreased glucose levels

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20
Q

What happens during the somogyi effect

A

nocturnal hypoglycemia and morning hyperglycemia

21
Q

treatment of the somogyi effect

A

reduce or omit the HS insulin

22
Q

what happens during the dawn phenomenon

A

tissue becomes desensitized to insulin nocturnally, becomes progressively elevated throughout the night and morning hyperglycemia

23
Q

How do you tx the dawn phenomenon

A

add or increase the HS dose of insulin

24
Q

Diabetic Ketoacidosis (DKA) is a complication of

A

DM1

25
Q

what state is DKA

A

intracellular dehydration

26
Q

What is hyperosmolar hyperglycemic non-ketosis a complication of?

A

DMII

27
Q

What happens in HHNK?

A

PAtients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis and extracellular depletion

28
Q

When is kussmauls breathing seen?

A

in DKA

29
Q

When is fruity breath seen?

A

DKA

30
Q

What are the labs/ diagnostics for DKA

A

hyperglycemia (>250)
ketonemia, ketonuria
Marked glucosuria
metabolic Acidosis (Ph

31
Q

What are the labs/ diagnostics for HHNK?

A 
serum blood glucose >600
Hyperosmolality
elevated BUN and cr
elevated hbg a1c
normal Ph
Normal anion gap
32
Q

What is the most common form of hyperthyroid

A

graves disease

33
Q

What are some other causes of hyperthyroid

A

toxic adenoma, subacute thyroiditis, TSH, secreting tumor of the pituitary, high doses of amiodorone

34
Q

Patho causes of hypothyroidism

A 
pituitary deficiency of TSH
hypothalamic deficiency of TRH
iodine deficiency
hashimotos throiditis 
damage to the gland 
idiopathic
35
Q

What is the most sensitive test for hyperthyroidism

A

TSH assay

36
Q

What is the most important test for hyperthyroidism

A

t3

37
Q

What else can elevate the ANA

A

lupus or collagen disease

38
Q

What test should be performed to establish etiology of hyperthyroidism

A

thyroid radioactive iodine uptake

39
Q

What 2 drug classes are used for hyperthyroidism

A

propranolol for symptomatic relief (especially for subacute)

Thiourea drugs for patients with mils cases, small goiters or fear of isotopes (Methimazole, propylthiouracil/ PTU)

40
Q

Treatment dosing with levothyroxine

A

50-100mcg every day, increasing the dosage by 25mcg every 1-2 weeks until symptoms stabilize
decrease dosing for >60yo

41
Q

Causes of Cushings syndrome

A

ACTH hyper secretion by the pituitary, adrenal tumor, chronic administration of glucocorticoids

42
Q

S/SX of Cushing’s syndrome

A

central obesity, moon face with buffalo hump, acne, poor wound healing, purple strake, hirsutism, HTN, weakness, amenorrhea, impotence, HA, polyuria and thirst, labile mood, frequent infections

43
Q

Labs for Cushing’s syndrome

A 
HYPERGLYCEMIA 
HYPERNATREMIA 
HYPOKALEMIA 
leukocytosis 
elevated plasma cortisol in the morning 
dexamethasone suppression test
serum ACTH
glycosuria
44
Q

Causes of addisons disease

A

deficient cortisol, androgens, and aldosterone
Autoimmune destruction of the adrenal gland
CA with mets
Bilateral adrenal hemorrhage (from anticoagulation tx)
pituitary failure resulting in ACTH

45
Q

s/sx addisons disease

A 
hyperpigmentation in buccal mucosa and skin creases 
diffuse tanning and freckles 
orthostasis and hypotension
scant axillary and pubic hair 
rapid worseing 
acute fever 
change in LOC
46
Q

labs for addisons disease

A 
HYPOGLYCEMIA
HYPONATREMIA 
HYPERKALEMIA 
elevated ESR
Lymphocytosis
47
Q

management of addisons disease

A

glucocorticoid and mineralcortiocoid replacement (aldosterone and androgen)

48
Q

what is the pathophysiology of graves disease

A

hyperthyroidism: when the thyroid gland overproduces the hormone thyroxine as a result of an immune system attack

NUR720 FNP Review (24 decks)

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