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CNUR 203 midterm > Unit 5 Endocrine > Flashcards

Unit 5 Endocrine Flashcards

1
Q

URGlucagon

A

hormone from the pancreas in response to low serum glucose, eating protein, or increased in glucose demands

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2
Q

Glycogen

A

stored form of glucose

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3
Q

Glycogenesis

A

Formation from glycogen from glucose (carbohydrates)

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4
Q

Glycemic index

A

rise in serum glucose levels after eating carbs

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5
Q

Glycemic index

A

rise in serum glucose levels after eating carbohyrates

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6
Q

Glycogenolysis

A

chemical breakdown of glycogen to glucose

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7
Q

Glucogenolysis

A

Synthesis of glucose from non-carbohydrate sources

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8
Q

Pancrease

A

secretes insulin into the bloodstream in response to circulating carbohydrates or glucose related from the liver

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9
Q

Insulin

A

Circulates enabling glucose to enter the cells to act as energy this lowers the amount of glucose in the blood stream

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10
Q

As serum blood sugar levels drop what happens to the secretion of insulin

A

The secretion becomes less

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11
Q

excess glucose is stored in

A

muscle, liver, fat cells

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12
Q

When serum glucose levels are low what does the liver do

A

the liver breaks down stored glycogen into glucose and releases it into the blood stream

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13
Q

What is the feedback loop of insulin and Glucose

A

Blood glucose rises, insulin released from the pancreas, blood glucose is reduced back to normal, normal blood glucose levels

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14
Q

Glucagon acts as an opposite to

A

insulin

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15
Q

insulin is released in response to

A

low serum levels

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16
Q

what does insulin do to the liver

A

Stimulates the liver to release stored glucose

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17
Q

Glucagon does what to the blood

A

moves glucose into the blood

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18
Q

Insulin moves what out of the blood and into the cell

A

glucose

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19
Q

Pancreas function

A

Insulin allows glucose to enter cells, Signa

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20
Q

Glycogen

A

Stores ingested glucose

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21
Q

Pancreas job

A

regulates glucose, allows glucose to enter cells, Signals liver to release stored glucose

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22
Q

Liver job

A

Provides glucose, stores ingested glucose, releases stored glucose, gluconeogenesis (makes glucose from other sources)

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23
Q

Normal Glucose

A

4-6

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24
Q

Average amount of insulin secreted daily

A

0.6 units/kg/day

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25
Q

Basal rate

A

insulin continuously released to meet base metabolic need

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26
Q

Bolus rate

A

Insulin released in response to rise in serum glucose

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27
Q

Prandial insulin (bolus/mealtime)

A

Given in anticipation of the spike in blood glucose from the ingestion of the carbohydrate bolus (by eating or tube feeds)
Either:
1. Rapid acting insulin given with meals
2. Short acting insulin given 30 mins prior to meals

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28
Q

Examples of Prandial and Correction insulin

A

Nova rapid, apidra, humalof, humbling R, Novocain Toronto

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29
Q

Correction insulin

A

Rapid or short-acting insulin is used when blood glucose levels are above the target range the correction insulin is the same product as the prandial that pateint receives. The dose will be given at the same time so only one injection is needed

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30
Q

Somogyi- Night nurse effect

A

-Hypoglycemia in response to HS insulin, liver releases sugar, serum hyperglycemia (SO Much insulin)

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31
Q

Dawn effect

A

-fasting AM hyperglycaemia
-In response to decreasing HS insulin in response to somogyi (Down insulin)

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32
Q

teach about Dawn effect

A

check 02-04 serum glucose

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33
Q

What does it mean when “Diabetes is a multi system disease” is said

A

Abnormal insulin production, impaired utilization, both

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34
Q

65-80% of people with diabetes die of

A

heart disease and stroke

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35
Q

Risk factors for type 1 Diabetes

A

Auto immune response, genetic response

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36
Q

Type 2 diabetes risk factors

A

Lifestyle, some genetics

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37
Q

Prediabetes/metabolic syndrome

A

The cells are resistant to the insulin

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38
Q
A
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39
Q

Type 2 diabetes

A

pancrease does not make enough insulin

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40
Q

High risk for diabetes

A

-people 40 years and older
-first degree relative with type 2
-pregnant

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41
Q

Type 1

A

pancreas does not make any insulin

42
Q

Types of diagnostic tests

A

fasting plasma glucose, 2h plasma glucose oral glucose tolerance test, A1C

43
Q

Impaired glucose tolerance

A

-usually asymptomatic, vessel damage may already be occurring, pre diabetes offers a warning and gives us a chance to change the future. If left untreated 50% of people will develop diabetes in their lifetime

44
Q

Hgb A1C

A

hemoglobin A1C (HbA1C) test is a blood test that shows what your average blood sugar (glucose) level was over the past two to three months

45
Q

watch for the 3 P’s

A

Polyuria, polyphasic, polydipsia

46
Q

Risk factors for type 2 Diabetes

A

Obesity, abdominal fat, lifestyle, Visceral adiposity (fat around organs)

47
Q

Endogenous

A

Insulin is still present but is either not enough, not used, both

48
Q

4 Metabolic Abnormalities

A
  1. Insulin resistance (body does not respond to the action of insulin)
  2. decreased pancreatic production of insulin (cell fatigue from compensatory overproduction of insulin)
  3. Liver inappropriately produces glucose
  4. Adipose tissue (Adipoctrokines) change in hormone production affects insulin sensitivity
49
Q

Gluconeogensis

A

“creation of new glucose”
-Process of making glucose sugar from its own breakdown products or from the breakdown products of lipids fats or protein

50
Q

Gluconeogensis occurs where

A

Liver or kidney

51
Q

which system does diabetes effect

A

ALL

52
Q

Neuropathy

A

Neuropathy is when nerve damage leads to pain, weakness, numbness or tingling in one or more parts of your body.

53
Q

Lab tests for diabetes

A

Fasting plasma glucose, Hgb A1C, non-fasting plasma glucose, oral glucose tolerance test, BGM, Urine, hematology, lytes

54
Q

What does high alert medication mean

A

that it is extra dangerous and can cause death if administered falsely

55
Q

how much insulin is needed

A

1 unit/10g carbs - grams of fibre
ex eat 30 grams of carbs, 10 grams of fibre get 2 units of insulin

56
Q

How insulin is administered

A

-Insulin pens, syringes, insulin pumps

57
Q

Rapid acting insulin (onset, peak, duration)

A

10-15 minutes onset, 60-90 minutes peak, 4-5 hours duration
-should be clear in colour, can be mixed

58
Q

Short-acting insulin (onset, peak, duration)

A

30-60 minutes onset, 2-4 hours action, 5-8 hours duration, Is able to to be mixed with other insulins should be clear in colour

59
Q

How early should short acting insulin be administered

A

30 minutes prior to meal

60
Q

Intermediate acting(onset, peak, duration)

A

1-2 hour onset, 5-8 hour duration, 14-18 hour lasting can be mixed and appears cloudy

61
Q

Long acting insulin (onset, peak, duration)

A

1.5 hour onset, no peak, 24 hour duration should be clear

62
Q

Should long acting insulin be mixed with others

A

NO

63
Q

rapid acting insulins

A

NovaRapid, Apidra, Humalog

64
Q

Short acting insulin

A

Humulin R, Novolin

65
Q

Intermediate acting insulin

A

Isophane insulin suspension

66
Q

Long acting insulin

A

Lantus, Levemir

67
Q

Part 1 of SHA subcutaneous insulin order set

A

Baseline and BGM orders

68
Q

part 2 of of SHA subcutaneous insulin order set

A

Scheduled insulin, Basal and Prandial

69
Q

Part 3 of SHA subcutaneous insulin order set

A

Correction insulin, Additional insulin that is needed according to BGM and TDI, usually same as Prandial

70
Q

Microfilament test

A

to test for nerve damage (peripheral neuropathy), which may be caused by conditions such as diabetes.

71
Q

Diet for Diabetes

A

monitor carbs (low), low fat, high fibre, fluids

72
Q

Why is fibre important

A

because number of carbs - number of fibre = the amount of carbs to be managed with insulin

73
Q

Carb foods

A

Starches/grains, fruits/sweet veggies, milk, sweets

74
Q

Non carb foods

A

protein, fat, other veggies

75
Q

hospital Consults for diabetes

A

Dietician, diabetes educator, pharmacist, endocrinologist, nephrologist, vascular surgeon

76
Q

In the community consults for diabetes

A

live well chronic disease management, Canadian diabetes association, homeware, podiatrist

77
Q

Hyperglycemia causes

A

too much glucose in blood, too little meds, insulin resistance, illness, physical or emotional stress, steroids

78
Q

Hypoglycemia causes

A

not enough glucose in the blood, too much diabetes meds, too much exercise, weight loss without weight adjustment to meds

79
Q

Diabetes Ketocidosis

A

-fat is metabolized, lack of circulating insulin means sugar cannot enter the cell happens mostly in type 1. Leads to ketones in the blood

80
Q

hot and dry

A

sugar high

81
Q

Symptoms of hyperglycemia

A

headache, polyphasic, polyuria, sweet urine, weakness/fatigue, hot/dry skin, blurry vision, abdominal cramps

82
Q

Symptoms of hypoglycaemia

A

vision changes, cool, clammy, shaky dizzy, emotional outburst, headache, hunger/nausea, tachycardia, slurred speech, unsteady gate, numbness, seizure, unresponsive

83
Q

Subjectives questions to ask diabetic patients

A

-last insulin, last glucose, symptoms of three P’s, symptoms of hyperglycaemia?

84
Q

Kussmauls

A

Kussmaul breathing is an abnormal breathing pattern characterized by rapid, deep breathing at a consistent pace.

85
Q

Assessment for Diabetic patient

A

CVS (tachycardia, hypertension, hypokalemia), Resp (Kuddmauls), CNS (confusion, may see change in LOC)

86
Q

Things to do as nursing interventions for a diabetic patient

A

Oxygen, IV fluid (Salin 500 mL/h x 4), monitor ins and outs, Serum and Urine labs, ECG/cardiac monitor, Electrolyte replacement, Insulin 0.1 unit/kg/hour, monitor BGM, treat symptoms such as nausea

87
Q

Insulin is not to be given to treat

A

Hyperglycaemia

88
Q

Insulin is given to reverse

A

ketosis

89
Q

Serum lights in a hyperglycemic pateint will appear

A

high

90
Q

ABG metablic acid results for a Hyperglycemic patient

A

-pH lower because of increased acid
-CO2 lower because the body is trying to compensate by blowing off acid in the form of CO2
-H+ lower because the base has been lost from the GI tract with the vomitting

91
Q

Sick day plan

A

-Which diabetes meds to continue which to stop, insulin adjustment, advice to contact the healthcare provider or go to the ER

92
Q

Hypersmolar hyperglycaemic state

A

Lifethreatening with sever CNS symptom, severe dehydration

93
Q

Can type 2 pateint produce enough insulin to prevent severe hyperglycaemia

A

NOPE

94
Q

What is serum glucose in severe hyperglycaemia

A

24 mmol/L

95
Q

Hyperosmolar

A

Elevated serum glucose, Fluid loss, Electrolyte loss

96
Q

DKA and HHS are

A

Medical emergencies

97
Q

Macrovascular complications

A

Vicoud blood, hypercoagulabilty, vessel damage, increased stroke, MI, Amputation, delayed healing

98
Q

Microvacular complications

A

Thickening of vessel membrane, thickening of capillaries/arterioles. Retinopathy, nephropathy, neuropathy, dermopahty (glucose, bp, lipids)

99
Q

Client foot teaching

A

wash feet daily, with mild soap and warm water, pat feet dry gently especially toes, visually inspect

100
Q

Why do diabetic patients have to get amputations

A

Nerve damage or diabetic peripheral neuropathy is one of the long-term complication of diabetes. If left untreated, the damage caused by neuropathy can potentially lead to infection and limb amputation.

101
Q
A

CNUR 203 midterm (10 decks)

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