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NURS361 - Pathophysiology II > Module 1 - Diabetes Mellitus > Flashcards

Module 1 - Diabetes Mellitus Flashcards

1
Q

Incidence

A

rate of new cases

on the rise

conveys risk of contracting disease

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2
Q

Prevalence

A

proportion of actual cases

conveys how widespread disease is

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3
Q

Diabetes Insipidus versus Mellitus

A

Insipid is a disorder of ADH

Mellitus is a disorder of blood glucose regulation

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4
Q

Exocrine

A

releases through a duct

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5
Q

Endocrine

A

Secretion right into the blood stream

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6
Q

Is the pancrease endo or exocrine

A

Both

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7
Q

Pancreas

A

Large diffuse abdominal organ functioning as both an endocrine and exocrine gland

made up of acini and islets of langerhans (the two major tissue types)

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8
Q

Acini

A

Exocrine tissue of the pancreas that secretes into ducts

Releases digestive enzymes like amylase, protease, and lipase as well as sodium bicarbonate

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9
Q

Islets of Langerhans

A

Endocrine tissue of the pancreas that secretes right into blood - key role in blood glucose levels

takes up 1-2% volume of the pancreas

Has alpha delta and beta cells releasing hormones that regulate glucose levels

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10
Q

Exocrine Pancreatic Function

A

Acini release digestive enzymes and sodium bicarbonate

Contents are released into the pancreatic duct

Exocrine function here plays an essential role in digestion and absorption of food in the smal;l intestine

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11
Q

Endocrine Pancreatic Function

A

Involves synthesis and release of hormones produced by specialized cells in the Islets of Langerhans

Key role in blood glucose levels

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12
Q

Different Cells in the Islets of Langerhans

A

Alpha
Beta
Delta

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13
Q

What do Beta cells and Amylin release?

A

Insulin

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14
Q

What do alpha cells release

A

glucagon

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15
Q

What do delta cells release

A

Somatostatin

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16
Q

Diabetes is not strictly involved with …

A

Insulin

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17
Q

Other hormones that keep glucose levels high

A

Catecholamines (EP qand NEP)

Growth Hormones

Glucocorticoids (Cortisol

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18
Q

Insulin, Glucagon, and Somatostatin are what to one another? What do they work to do?

A

They are counter regulatory hormones and work to keep glucose levels lower/regulate glucose

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19
Q

What counteracts glucagon?

A

Insulin

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20
Q

Where are the Islets of Langerhans located?

A

Around the blood vessels surrounding the pancreas

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21
Q

The only hormone known to lower blood glucose ?

A

Insulin

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22
Q

What cell releases Insulin and what is Insulins action

A

Beta

Decrease blood glucose by allowing it to enter cells (changes cell membrane makeup to allow cell opening for glucose thus lowering blood glc levels)

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23
Q

What cell releases Glucagon and what is Glucagons action?

A

Alpha

Increased release of glucose from the liver into the blood to increase blood glc levels. Causes the release of stored glycogen specifically to turn into glucose for use

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24
Q

What cell releases Somatostatin and what is Somatostatins action?

A

Delta

Extends the use of absorbed nutrients for tissues by blocking increases in glc levels after we eat to allow a slower rise and better control over the glucose levels

Decreases GI activity after ingestion –> extends time over which food is absorbed –> inhibits insulin and glucagon –> extends use of absorbed nutrients by tissues

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25
Q

How much of ingested glucose is used for metabolism?

A

1/3

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26
Q

How much glucose undergoes Glycogenesis after eating?

A

2/3

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27
Q

What happens to blood glucose after a meal?

A

Glucose levels rise –> insulin secreted in response from beta cells

2/3 of glucose stored as glycogen in the liver (Glycogenesis) while 1/3 is used for metabolism

Saturation of tissues with glycogen –> glucose converted to fatty acids –> stored as triglycerides in gat (Lipogenesis)

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28
Q

What happens to blood glucose between meals?

A

Liver releases glucose to maintain blood glucose within normal limits via Glycogenolysis and potentially gluconeogenesis

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29
Q

Glycogenesis

A

Glucose converted to glycogen and stored in the liver

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30
Q

Lipogenesis

A

Excess glycogen in the tissues leads to glucose being converted to 3 fatty acids and adipose cells and then being stored as triglyceride in fat cells

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31
Q

Glycogenolysis

A

glycogen is broken down to release glucose into the blood

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32
Q

Gluconeogenesis

A

synthesis of glucose from amino acids, glycerol, and lactic acid

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33
Q

What can be used interchangeably with glucose for energy everywhere but cardiac and skeletal muscles, kidneys, brain, and the liver?

A

Fatty Acids

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34
Q

Fatty acids cannot normally be used for energy in the brain as it requires steady glucose amount, the only exception is ..

A

During starvation situations ketone bodies can be used

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35
Q

What occurs if blood sugar is low?

A

glucagon released by pancreas –> glycogen breakdown is promoted to glucose in the blood

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36
Q

What occurs when blood sugar is high?

A
  1. Insulin is released by the pancreas to promote glycogen synthesis in the liver
  2. stimulates glucose uptake in tissue cells
  3. Over Saturation with glycogen leads to storage as triglycerides in fat cells
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37
Q

What is the action of Insulin on Glucose

A

Increase glucose transport into skeletal and adipose tissue

Increase glycogen synthesis

Decrease gluconeogenesis

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38
Q

What is the action of Insulin on Fats

A

Increase glucose transport into fat cells

Increase Fatty acid transport into adipose cells

Increase triglyceride synthesis within fat cells

Inhibit adipose cell lipase (breaking down triglycerides)

Activates lipoprotein lipase in capillary walls

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39
Q

What is the action of Insulin on Proteins

A

Increase active transport of amino acids into cells

Increases protein synthesis (anabolism) by increasing transcription mRNA and accelerating protein synthesis by rRNA

Decreases protein breakdown by enhancing use of glucose and fatty acids as fuel (prevents muscle wasting - catabolic)

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40
Q

Normal insulin release only occurs in normal conditions when..

A

Blood glucose levels are high

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41
Q

Atheroscleorosis

A

Body fats deposited on lining of blood vessels

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42
Q

HDL

A

High Density Lipoproteins

The good cholesterol

takes fats on blood cells back to the liver for use

Insulin has a beneficial effect on this process

Want levels greater than 45 and 55 in women and men respectively

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43
Q

LDL

A

Low density lipoproteins

Lousy bad cholesterol

Levels between 60-80

smaller than HDL so we want more HDL and less LDL as HDL is more effective at moving fats away and preventing atherosclerosis buildup

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44
Q

How does Diabetes mellitus impact cholesterol?

A

It increases cholesterol levels while increasing LDL and greatly decreasing HDL leading to increased triglycerides and fat/plaque buildup

DM –> Not enough insulin –> no activation –> atherosclerotic buildup as a result –> risk for stroke, heart attack, etc –> elevated LDL, cholesterol and triglycerides with lower HDL

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45
Q

Anabolic Activity

A

Promotes synthesis

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46
Q

Catabolic Activity

A

Promotes break down

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47
Q

Why do children with diabetes often lose weight rapidly despite eating a lot and being hungry?

A

Not enough insulin means protein begins to catabolize and muscle wasting occurs

Proteins are needed for AA production and use in metabolic function

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48
Q

Major activity of Insulin on tissues?

A

Decrease blood glucose by allowing it to enter cells

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49
Q

Major action of insulin in regards to anabolic action?

A

Promote synthesis of proteins, carbs, lipids, nucleic acids in liver, muscle and adipose tissue

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50
Q

major action of insulin on the liver

A

Stimulates the synthesis of glycogen and increases uptake as well as fatty acid synthesis

Inhibits glycogenolysis, gluconeogenesis, and ketogenesis

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51
Q

major action of insulin on muscle

A

increase uptake of glucose and amino acids

increase glycogen and protein synthesis

inhibit protein catabolism

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52
Q

Major action of insulin on adipose

A

increase glucose uptake and fat synthesis (Lipogenesis)

decreased fat breakdown (by inhibiting adipose cell lipase)

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53
Q

Major action of insulin on Potassium (K+)

A

increase potassium uptake by cells (GIK)

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54
Q

Major action of insulin on lipids

A

metabolism of plasma lipids and lipoproteins WNL ranges

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55
Q

___% of insulin is used or degraded and why

A

50% - so insulin is released in phases since its half life is 15 minutes

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56
Q

What follows glucose when insulin allow transport into cells?

A

K+ (potassium) which makes K levels decrease too in the blood

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57
Q

A cell does not need insulin if…

A

they have special glucose carriers: the brain cells, RBC, endothelial lining cells, glomerular lining cells

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58
Q

GIK Mechanism

A

Glucose-Insulin-Potassium Mechanism allowing potassium uptake in cells at the same time as insulin allow glucose in

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59
Q

Why may we give glucose and insulin to someone with lower serum potassium levels?

A

It can instigate intake of potassium to raise levels

it is not a long term effect but it can save lives

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60
Q

Why are too high or too low K levels bad?

A

Can cause arrhythmia of the heart

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61
Q

Normal function of insulin

A

increased uptake of blood glucose into cells

decrease blood glucose levels

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62
Q

Excess insulin leads to …

A

Hypoglycemia

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63
Q

Deficit Insulin leads to..

A

Hyperglycemia

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64
Q

What can hypoglycemia cause?

A

Decreased blood glucose:

hunger
tremors
sweating
weakness
malaise
irritability
mental changes
coma --> death
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65
Q

What can hyperglycemia cause?

A

Increased blood glucose:

Polydipsia 
Polyphagia
Polyuria
Dehydration
Fatigue
Mental Changes
coma --> death
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66
Q

What are the 3 P’s of Hyperglycemia that define it?

A

Polydipsia
Polyphagia
Polyuria

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67
Q

Polydipsia

A

Intense Thirst (to dilute sugars)

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68
Q

Polyphagia

A

Intense Hunger

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69
Q

Polyuria

A

increased urinary output (leads to dehydration)

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70
Q

Why is it better to give insulin rather than more food?

A

because the cells are starving because lack of insulin means they cannot get the glucose in so they need a way in rather than more glucose

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71
Q

How does a blood sugar of 30 differ from one of 400?

A

normal range is 60-100

30 can be deadly while 400 is less dangerous and more just uncomfortable

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72
Q

What is more dangerous, hypoglycemia or hyperglycemia?

A

Hypoglycemia

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73
Q

Always assume what if you do not know blood sugar levels?

A

Assume they have hypoglycemia since it is more dangerous and BE SAFE AND GIVE SUGAR

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74
Q

Glucagon

A

Secreted by pancreas alpha cells

action opposite of insulin

diabetics may need a glucagon pen in case of emergency

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75
Q

Insulin acts on all body cells, but glucagon…

A

primarily acts in the liver

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76
Q

How does glucagon travel?

A

via portal vein to the liver where it exerts its main effects

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77
Q

Function of Glucagon

A

Stimulate glycogenolysis and gluconeogenesis

Increase lipolysis and output of ketones by the liver

Enhance uptake of amino acids by the liver (can be used for anabolic process or gluconeogenesis)

*It will help form new glucose when glucose is depleted

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78
Q

What occurs to glucagon when blood glucose is high

A

secretion is inhibited (when low it increases)

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79
Q

How is glucagon related to diabetic ketoacidosis

A

Increases lipolysis which makes ketone waste products

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80
Q

Action of Glucagon on Glucose

A

promotes breakdown of glycogen into glucose phosphate

increases gluconeogenesis

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81
Q

Action of Glucagon on Fats

A

enhances lipolysis in adipose tissue –> liberates glycerol for use in gluconeogenesis

activates adipose cell lipase

enhances lipolysis in adipose tissue –> liberates fatty acids (so they can be used for energy - ketones produced as a waste product!)

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82
Q

Action of Glucagon on Proteins

A

increases breakdown of proteins into amino acids for use in gluconeogenesis

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83
Q

New glucose, through the help of glucagon, comes from what

A

Glucagon action on amino acids, fatty acids, and glycerols together

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84
Q

Catecholamines

A

produced by adrenal medulla

EP and NEP

an important homeostatic mechanism during periods of hypoglycemia as its purpose is to conserve glucose

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85
Q

Function of Catecholamines

A

maintain blood glucose levels during stress:

mobilize glycogen stores

decreases movement of glucose into body cells (keeps it high in the blood)

inhibits insulin release from beta cells

mobilizes fatty acids from adipose tissues (prevent storage of glucose and keep levels high)

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86
Q

The main purpose of catecholamines is to..

A

conserve glucose!

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87
Q

Main catecholamines

A

NEP and EP

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88
Q

where are catecholamines produced?

A

adrenal medulla

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89
Q

How does hypoglycemia relate to catecholamines?

A

It activates the bodies stress response - leading to autonomic symptoms like palpitations, shakiness, nervousness, sweating, pallor, irritability, etc

The catecholamines then allow glucose levels to be conserved and maintain glucose levels/raise them

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90
Q

Why is it hard to potentially manage diabetes during a hypoglycemic attack

A

Symptoms of neuroglycopenia can lead to hypoglycemia of the brain impairing ability to think making it hard to manage (alongside other symptoms like weakness and lethargy)

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91
Q

Growth Hormone’s Function relating to glucose levels

A

increase protein synthesis in ALL cells of the body (anabolic)

mobilize fatty acids from adipose tissue (to use for fuel)

antagonize the effects of insulin

decrease cellular uptake and use of glucose –> increase blood glucose by 50-100% –> stimulate further insulin secretion

Normally it helps with growth but has an antagonistic effect on insulin

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92
Q

How do the GH levels compare between adults and children

A

They are the same levels!

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93
Q

What inhibits GH

A

Insulin and increased levels of blood glucose (so there is not a prolonged effect of elevated GH)

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94
Q

When do GH levels increase

A

When fasting (and hypoglycemia)

Exercise: running, cycling, etc

Stress: anesthesia, fever, trauma

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95
Q

What does prolonged GH excess cause?

A

increased glc levels despite increased insulin release –> leads to insulin resistance in peripheral tissue –> this inhibits glc uptake by muscle and adipose tissue and contributes to diabetes

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96
Q

Acromegaly

A

chronic hypersecretion of GH in adulthood

causes symptoms of glucose intolerance, insulin resistance, and diabetes

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97
Q

Gigantism

A

GH hypersecretion / excess in childhood

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98
Q

What releases GH

A

anterior pituitary

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99
Q

Pathway for increased GH?

A

Hypothalamus –> GHRH –> Anterior Pituitary –> Increased GH

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100
Q

Pathway for decreased GH?

A

Hypothalamus –> Somatostatin –> Anterior Pituitary –> Decreased GH

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101
Q

Somatostatin is released by …

A

many places like the hypothalamus, pancreas, and GI tract

it is counterregulatory to GH

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102
Q

Glucocorticoid Hormones

A

Main: Cortisol (Hydrocortisone)

Synthesized in Adrenal Cortex

Regulates metabolism of glucose

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103
Q

95% of glucocorticoid activity comes from …

A

cortisol

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104
Q

Functions of Glucocorticoids in relation to diabetes/blood glucose

A

Regulate metabolism of glucose (critical to survival during periods of fasting and starvation)

Stimulate gluconeogenesis by the liver (increased production (6-10x)

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105
Q

When do glucocorticoid levels increase

A

During stress: infection, pain, trauma, surgery, prolonged strenuous exercise, acute anxiety

During hypoglycemia: a potent stimulus for secretion of glucocorticoids

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106
Q

Why does chronic stress relate to diabetes

A

lots of cortisol is released which increases and conserves glucose levels

stress in the hospital can lead to a need for insulin

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107
Q

Ghrelin

A

Made by GI cells / in the stomach

helps control hunger (no release = no feelings of hunger)

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108
Q

Gastrin

A

made by stomach/GI cells

important to acid secretion and satiation

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109
Q

Cholecystokinin

A

released by duodenum

gall bladder contraction

GI motility

pancreatic exocrine secretion functions

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110
Q

Secretin

A

released by duodenum

related to pancreatic exocrine secretion

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111
Q

GIP

A

released by duodenum

related to Incretin activity

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112
Q

Motilin

A

released by duodenum

related to GI motility

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113
Q

Pancreatic Polypeptide

A

released by pancreas

related to gastric motility and satiation

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114
Q

Oxyntomodulin

A

released by large intestine

relates to satiation and acid secretion

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115
Q

PYY 3-36

A

released by large intestine

relates to satiation

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116
Q

GLP-1

A

glucagon like peptide 1

released in the distal small bowel

works with GIP

incretin hormone released from your gut that signals beta cells to increase insulin secretion and decrease the alpha cells release of glucagon

this one also slows down the rate at which food empties from the stomach and acts on the brain to increase satiety (and suppress glucagon)

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117
Q

GIP

A

Glucose dependent insulinotropic polypeptide

released in jejunum

incretin hormone released from the gut that signals beta cells to increase insulin secretion and decrease the alpha cells release of glucagon

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118
Q

GLP-1 and GIP mimic the action of ____-

A

somatostatin

increase the amount of insulin made and act as messengers between the digestive tract and the pancreas

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119
Q

Amylin

A

similar to somatostatin

released along with insulin from beta cells

has a similar effect as GLP-1 (decrease glucagon levels to decrease liver glucose production; slow rate at which food empties from the stomach; increase satiety by acting on the brain)

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120
Q

Pramlintide

A

medication that encourages amylin release

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121
Q

Diabetes

A

disorder of carb, protein, and fat metabolism

mult. etiologic factors

involves absolute or relative insulin insufficiency and/or insulin resistance

glucose cannot be carried into fat and muscle cells –> cell starvation –> fat and protein breakdown

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122
Q

Examples of Etiologic Reasons for Diabetes

A

genetics

viruses

cancer

obesity

sometimes it cannot be ID’ed

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123
Q

Why is Diabetes referred to as the “Running through of sugar”?

A

Because the amount of glucose overwhelms the glomerulus and spills into the urine

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124
Q

Absolute Insulin Deficiency

A

Type 1 Diabetes

Cannot make any endogenous insulin with your beta cells

You end up needing exogenous insulin

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125
Q

Relative Insulin deficiency

A

not making enough insulin

it is either destroyed early, broken, etc

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126
Q

Insulin Resistance

A

cells do not use insulin correctly and beta cells may need to make more and more until failing

lack of ability to keep up with production can occur with endogenous insulin, but resistance can occur with exogenous OR endogenous

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127
Q

What problems can insulin resistance lead to?

A

Diabetes

Heart Problems

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128
Q

What are some insulin issue types that can lead to diabetes

A

Absolute deficiency (type 1)

no insulin being made (type 1)

relative deficiency

impaired release by pancreatic beta cells

inadequate or defective insulin receptors

production of inactive insulin

insulin being destroyed begore it carries out its action

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129
Q

Types of Cells that do not need insulin for glucose to get into them?

A

Nerve cells

RBCs

Cells lining the glomerulus

endothelial cells

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130
Q

What can the brain use as emergency energy in severe starvation situations

A

Ketones from fat breakdown

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131
Q

Cause of death rank for Diabetes in the USA`

A

7th

risk for death is twice of that for non-diabetics of the same age

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132
Q

The leading cause of end stage renal disease (ERSD) in the US is..

A

Diabetes

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133
Q

Risk for heart disease and stroke is 2-4 times more for ___ than non

A

Diabetics

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134
Q

Diabetic Comorbidities for children and adolescents with Type 1 DM

A

Nephropathy

Hypertension

Dyslipidemia

Celiac Disease

Hypothyroidism

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135
Q

Important HP2020 Diabetes Take aways

A

Prevalence has increased in the last decade but leveled off

targets have been met

2/3 of diabetics are diagnosed

A1C greater than 9% in 20% of adults

half of diabetic objectives seen little or no change in the last decade

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136
Q

Type 1 Diabetes

A

Absolute insulin deficiency (cannot make insulin)

Etiology: autoimmune or idiopathic - but strongly autoimmune since attacks on beta cells and langerhans islets occur (occurs in children often)

Treatment: Insulin (only treatment)

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137
Q

Type 1.5 Diabetes

A

Latent autoimmune disease occurring in adults

Treatment: Oral medicines at first but will need insulin within 5 years

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138
Q

Type 2 Diabetes

A

Due to: Insulin insensitivity, insulin secreting deficiency, inappropriate gluconeogenesis (either insulin is formed wrong, receptors do not work, or glucose cannot be made right)

Etiology: obesity or genetics

Treatment: Diet, exercise, hypoglycemics, transporter stimulators (first two especially for pre diabetics)

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139
Q

In what form of diabetes is genetics more important?

A

Type 2

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140
Q

What maybe the etiology and treatment for other specific types of diabetes

A

Etiology: Malnutrition, Corticosteroid use, secondary to pancreatic cancer, pancreatitis, steroid use, etc

Treatment is based on case

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141
Q

GDM

A

Gestational Diabetes

etiology: increased metabolic demands of the fetus

Treatment: Diet, metformin, insulin; usually resolves post delivery

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142
Q

If GDM occurs in 2-3 pregnancies in a row what is likely to happen?

A

It may convert to type 2 diabetes (or potentially type 1)

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143
Q

If someone is diabetic then gets pregnant…

A

it is NOT GDM, its either 1 or 2

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144
Q

Former names for Type 1 Diabetes

A

Juvenile Onset (adults could get it, its just less common)

Insulin Dependent (not good name since type II could use insulin too)

IDDM

Type I (people dont know roman numerals)

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145
Q

Former names for type 1.5 Diabetes

A

Latent Autoimmune Diabetes in Adults (LADA) - Still used

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146
Q

Former names for type II Diabetes

A

Adult onset (obese children can have occur)

Non insulin dependent (NIDDM) (not good since it could require insulin dependence as well)

Type II (no roman numerals)

147
Q

Age of onset for Type 1 DM

A

any age less than 30 usually

148
Q

Age of onset for type 1.5 DM

A

ages after 30

149
Q

Age of onset for type 2 DM

A

usually after age 40 with 8/10 diagnosed being obese

BUT, as time goes on more and more younger people get this too

150
Q

Pathophysiology of Type 1 DM

A

NO insulin production

151
Q

Pathophysiology of Type 1.5 DM

A

Damage to beta cells

genetic factors

possible insulin resistance

152
Q

Pathophysiology of Type 2 DM

A

produce insulin, BUT not enough or tissues are resistant

153
Q

Major Complications of Type 1 and 1.5 DM

A

DKA (Diabetic Ketoacidosis) (Cell Starvation)

Ketones end up being produced from fat breakdown

154
Q

Major Complications of Type 2 DM

A

HHNK - Hyperosmolar Hyperglycemic Non Ketotic Syndrome (Less ketosis)

155
Q

How is HHNK and DKA different

A

HHNK occurs in type 2 as compared to DKA in 1 and 1.5

In HHNK some insulin is made (just not enough) so there is some glucose getting in leading to no FA breakdown, thus no Ketosis occurs

So HHNK has and increase in blood glc like DKA, but no production of Ketones

But, HHNK is NOT less deadly than DKA

156
Q

Manifestations of Type 1 Diabetes

A

Hyperglycemia and Glucosuria

Symptoms in type 1 develop more acutely

3 P’s - Polyuria, Polydipsia, Polyphagia

Weight loss despite normal or increased appetite

(long term) Other: Blurred vision (recurrent), fatigue, paresthesia, recurrent skin infections

157
Q

Why does Polyuria occur in Type 1 Diabetes?

A

excessive urination d/t osmotic diuresis when reabsorption capacity of renal tubules exceeded

158
Q

Why does polydipsia occur in Type 1 Diabetes?

A

excessive thirst d/t intracellular dehydration including cells of the thirst center and mouth

159
Q

Why does polyphagia occur in Type 1 Diabetes?

A

excessive hunger d/t cellular starvation and depletion of cellular stores of CHOs, fats, and proteins

160
Q

Why does weight loss occur despite normal or increased appetite in type 1 diabetes?

A

osmotic diuresis; vomiting d/t ketoacidosis occurs

cells end up= using stored CHOs, fats, and proteins for energy since insulin isnt there to move glc into the cells

161
Q

How does DM interact with the nephron

A

Glucose is a small molecule that usually gets through the glomerulus and then is brought back through reabsorption in the proximal tubule

However, high glc levels means it cannot be filtered and reabsorbed - ability exceeded - so glc stays in the urine (abnormal)

High osmotic pressure occurs which leads to the kidneys pulling fluid into the filtrate to dilute the high glc levels until its in the collecting duct (where it then is urine) –> this leads to very dilute urine from high tonicity but this relates back to cellular dehydration, polyuria, and polydipsia

162
Q

Pathogenesis of type 2 Diabetes

A

Genetic Predisposition and/or Central Obesity

–> FFAs (free fatty acids) (increase initially and decrease later)

–> Increased hepatic glucose output (high glc levels since uptake cannot occur), decreased insulin secretion, decreased glucose uptake

–> TYPE 2 DM

163
Q

What is instrumental in Type 2 DM and Heart Disease

A

Central Obesity (Visceral Fat)

It creates free fatty acids since this is active fat

it burns out the beta cells causing Type 2 Diabetes

164
Q

Manifestations of Type 2 Diabetes

A

Hyperglycemia and Glucosuria

Only 2 P’s - Polyuria, Polydipsia

Other - Long term:
Recurrent blurred vision from exposure of lens and retina to hyperosmolarity

weakness and fatigue from lowered plasma volume

paresthesia d/t dysfunction of peripheral sensory nerves

Chronic skin infections d/t hyperglycemia and glucosuria favor growth of yeast –> pruritis and vulvovaginitis

often THESE are the symptoms that prompt individuals to seek Tx

165
Q

What is the difference in manifestation development between Type 1 and Type 2 diabetes?

A

Type 1 is more acute and quick

Type 2 usually develops more insidiously

166
Q

Why is there only 2 P’s in type 2 diabetes?

A

Polyuria occurs in the same mechanism as type 1

Polydipsia may become overlooked, but does occur, since glucose increase is more gradual with no ketoacidosis

there is NO POLYPHAGIA - there is still some insulin bringing some glc in - not starving so they do not have the type 1 intense hunger

167
Q

Examples of other types/causes of Diabetes

A

Genetic Defects of Beta Cell Function

Genetic defects in insulin action

diseases of the exocrine pancreas

Endocrinopathies

Drug or chemical induced diabetes

infections

168
Q

Casual or Random Plasma Glucose (PG)

A

Diagnostic

Done ANY time of day without regard to time since last meal

Not very useful, especially for treatment

Does not tell much and diagnoses are not based on this

It only tells something if levels are extreme

169
Q

Fasting Plasma Glucose (FPG) / 2 Hour PG

A

8 to 12 hours fast for FPG / 2 hour for PG

once preferred d/t ease of administration, convenience, acceptability to patients, and lower cost

170
Q

Fasting is defined as…

A

no caloric intake for at least 8 hours

171
Q

What type of diagnostic diagnoses more people with DM than FPG or HgA1C

A

2 Hour Plasma Glucose (2 Hour PG)

172
Q

FPG <126 mg per dL is

A

Normal (she said in lecture under 100 was normal and 100-126 is pre diabetic)

173
Q

Oral Glucose Tolerance Test (OGTT)

A

Used to check for gestational diabetes: done at 24-28 weeks gestation and then 6-12 weeks postpartum if positive

75 g glucose (sugar load) is given after fasting and the blood glucose is checked before, after 1 hour, and after 2 hours

NOT recommended for routine clinical use

174
Q

How should the blood glucose levels change in OGTT diagnostics?

A

During fasting it should be low (greater than or equal to 92)

1 hour should raise to above or equal to 180

after 2 hours it should lower some to greater than or equal to 153

175
Q

What are some diagnostic criteria for diabetes?

A

A1C greater than or equal to 6.5%

FPG greater than or equal to 126 mg/dL with no caloric intake for at least 8 hours before

2 hour PG greater than or equal to 200 mg/dL during an OGTT

Random plasma glucose great than or equal to 200 mg/dL in a person with classic symptoms of hyperglycemia (3 P’s) ( if there is no hyperglycemia, 1-3 should be checked with repeated testing)

*all should be repeated mult times

176
Q

Glycated or Glycosylated hemoglobin (HgA1c)

A

RBC does not need insulin so glucose combines with Hgb but it never unbinds until cell death - so this leads to less oxygen carrying capability

If over saturated, less and less oxygen can be carried

High levels of glycosylation indicate diabetes due to oversaturation of glucose in the blood

177
Q

HgA1c reflects what?

A

average blood glucose levels for the last 2-3 months prior to this test

178
Q

Glycosylation of blood with glucose is…

A

irreversible until RBC breakdown

179
Q

Amount of glucose bound to RBC is directly proportional to what?

A

the amount of glucose exposure over the 120 day lifespan of the RBC

180
Q

Glycohemoglobin

A

blood glucose bound to hemoglobin

181
Q

Normal A1c is? Poor/Diabetic A1c?

A

< 5.7 (about 5% glycosylation in a normal person) but it is greater than or equal to 6.5 %

Poor is between those two values

182
Q

How often should A1c be checked?

A

every 3 months to determine if medicine is working

if there is good control then they may be able to go longer without testing

183
Q

What may give abnormal A1c results?

A

diseases effecting Hgb like Anemia

supplements and high cholesterol levels

liver or kidney issues

184
Q

Goals of Blood Glucose Monitoring

A

Hgb A1c maintained at 7% or less; AACE/ACE criteria is at <6.5% though

Majority of preprandial blood glucose levels 80-120 mg/dL

Bedtime blood glucose levels between 100 and 140 mg/dL

185
Q

What does a 275 mg/dL mean plasma glucose correlate to for A1c? What is normal A1c and Mean Plasma Glucose?

A

275 –> 10% A1c

Normal: 5%; 60-100 mg/dL

186
Q

If we have the mean plasma glucose we can find ___ and vice versa with a chart

A

A1C

187
Q

How did diabetics used to get diagnosed?

A

They tasted urine for sweetness

Urine glucose is almost obsolete because of blood glucose monitoring but it can be used still

188
Q

Urine Tests only reflect what

A

URINE GLUCOSE LEVELS

189
Q

What influences urine glucose levels

A

renal threshold for glucose

fluid intake and urine concentraiton

urine testing methods

drugs

190
Q

ADA recommends testing what in regard to glucose levels?

A

Blood glucose not urine glucose levels (the influencers can give false/skewed results)

191
Q

What is still highly important regarding urine tests, especially for type 1 diabetics?

A

Urine Ketones - these remain important for monitoring diabetic control especially in type 1 who are more prone to DKA

192
Q

Why are Urine Ketones so important?

A

Ketones in the urine is an early sign of diabetic ketoacidosis and can be used for diabetics with high blood sugar to detect imminent danger

DKA can occur quickly so we want to screen for complications by finding ketones early

193
Q

C Peptide Assay

A

Test for diabetes

C peptide is a connecting peptide for proinsulin (inactive) before becoming insulin (active)

C peptide then stays in the blood and we can measure the amount to measure insulin production

194
Q

How does Proinsulin (inactive) turn into Insulin (active)_

A

A and B chains are connected by two sulfide bonds and a C peptide between them - this is the proinsulin

Breaking off the C insulin converts it to active insulin

195
Q

C Peptide Assays are a reliable indicator for..

A

pancreatic beta cell function

196
Q

There is a strong correlation between C peptide levels and …

A

insulin

197
Q

C peptide measurements before and after glucagon stimulation may be valuable for assessing what

A

diabetic insulin therapy

198
Q

What test delineates type 1 from type 2 diabetes?

A

glucagon stimulated c peptide tests

199
Q

C peptide assays can check for diabetes and beta cell function, but also can monitor for …

A

recovery after incision of insulinoma –> rising c peptide levels suggest recurrence or metastasis

200
Q

Insulinoma

A

pancreas tumor that overproduces insulin

201
Q

3 categories/measurements of increased risk for diabetes?

A
  1. Impaired Fasting Glucose (IFG) (From an FPG 100-125 mg/dL)
  2. Impaired Glucose tolerance (IGT) (2 hour PG in OGTT - 140-199 mg/dL)
  3. A1C 5.7 to 6.4%
    * risk extends below the lower limit of the range and is disproportionately greater at the higher ends of the ranges
    * these can also increase risk for cardiovascular disease
202
Q

The three categories/measurements for increased risk of diabetes should be done for …

A

any asymptomatic diabetics or any adult overweight or has one or more risk for diabetes

203
Q

When should the 3 categories of increased risk for diabetes be checked?

A

begin at 45 and be done in 3 year intervals if normal

also in children and adolescents if they have a risk factor or are obese

204
Q

What people are at increased risk for diabetes

A

individuals with higher than normal blood glc levels, but not high enough to be classified as diabetes

Approx 5% of people with prediabetes will progress to diabetes each year

People with weight and lifestyle issues

people with prediabetes have an increased risk for developing type 2 diabetes, heart disease, and stroke

205
Q

Prediabetic A1C range

A

5.7 to 6.5

206
Q

Normal, Pre Diabetic, and Diabetic A1C Levels

A

Normal is below 5.7%

Pre Diabetes is 5.7-6.4

Diabetes is greater than or equal to 6.5%

207
Q

Normal, Pre Diabetic, and Diabetic Fasting BG

A

Normal is <126 mg/dL

Pre Diabetic 100-125 mg/dL

Diabetic is greater than or equal to 126 mg/dL

208
Q

Normal, Pre Diabetic, and Diabetic Oral GTT

A

normal is <92 mg.dL fasting

pre diabetic is 140-199 mg/dL

diabetic is greater than or equal to 200 mg/dL at 2 hours

209
Q

What is diabetic for a random PG/BG

A

greater than or equal to 200 mg/dL with classic symptoms of hyperglycemia

210
Q

What are some testing criteria for diabetes in asymptomatic adults

A

every 3 years starting at 45 regardless of weight:

overweight/obese adults any age AND 1 or more of the following risk factors start earlier:

physical inactivity

1 degree relative with diabetes

high risk ethnicity like in indians and african americans

women: PCOS, infant birth wt > 9#, or GDM

HTN

Dyslipidemia

Cardiovascular disease

history of prediabetes: A1C greater than or equal to .7%, IGT, or IFG

Insulin resistance: severe obesity, acanthosis nigricans

211
Q

Testing Criteria for Diabetic Asymptomatic Children

A

Every 3 years beginning at 10 years or at the onset of puberty - if 2 risk factors are present

Overweight (85th BMI or weight >120% of ideal for height) AND 1 of the following risk factors:

family history of diabetes in 1 degree or 2 degree relative, race/ethnicity, insulin resistance (acanthosis nigricans, HZTN, dyslipidemia, PCOS, SGA, birth weight, maternal hx diabetes or GDM during child’s gestation

212
Q

Recommendations for Asymptomatic Children

A

diabetes self management education and support

psychosocial issues

treatment guidelines for type 2 diabetes in youth

213
Q

Acanthosis Nigricans

A

Skin condition of dark velvety skin

occurs often with diabetes

214
Q

Metabolic Syndrome (“Syndrome X”)

A

Central obesity causes an “apple shape” (waist circumference >102 in men and >88 cm in women)

Fasting serum triglycerides > 150 mg/dL

Low HDL cholesterol (<40 mg.dL in men and <50 in women)

Blood glucose greater than or equal to 130/85

Fasting glucose >110 mg/dL

215
Q

What do you have increased risk for with Metabolic Syndrome (Syndrome X) ?

A

increased risk for:

atherosclerosis

stroke

coronary heart disease

early death

216
Q

Additional Signs and Symptoms associated w/ Diabetes

A

Elevated uric acid levels

fatty liver (especially in concurrent obesity)

progressing to non-alcoholic fatty liver disease

polycystic ovarian syndrome

hemochromatosis (iron overload)

acanthosis nigricans (a skin condition featuring dark patches)

217
Q

How many pregnancies get Gestational Diabetes?

A

7%

218
Q

50% of Gestational Diabetes occurs when what is present?

A

history in the family

history of stillbirth/spontaneous abortion

fetal anomalies or LGA baby

obesity

advanced maternal age (>35 years)

greater than 5 pregnancies

219
Q

Why is management of gestational diabetes critical?

A

there is increased risk of complications

increased mortality

increased fetal abnormalities including macrosomia

hypoglycemia

polycythemia

hyperbilirubinemia

220
Q

Treatment of Gestational Diabetes includes what?

A

Blood glucose monitoring - fasting + postprandial

nutritional guidance –> normoglycemia, proper weight gain, avoid ketosis

221
Q

Macrosomia

A

very large baby (may have fatty heart or kidneys which are metabolically active - could cause hypoglycemia)

can occur from untreated gestational diabetes

222
Q

How does Gestational Diabetes develop?

A

Develops during pregnancy

Type 1 DM discovered during pregnancy and undiagnosed asymptomatic type 2 DM discovered during pregnancy

does NOT include having DM before pregnancy

Must resolve after pregnancy but there is risk of type 2 diabetes

223
Q

How do glucose levels change during gestational diabetes?

A

Normal glucose levels in the first half –> develops relative insulin deficiency during the last half of the pregnancy

224
Q

Risk Assessment for GDM

A

risk assessment for GDM should be undertaken at the first prenatal visit

women with clinical characteristics consistent with a high risk for GDM should undergo glucose testing as soon as feasible

If they are found not to have GDM at that initial screening, they should be retested between 24-28 weeks of gestation

Women of average risk should have testing undertaken at 24-28 weeks of gestation

225
Q

How is a test for GDM done

A

give sugar load of 75 g glucose after fasting for 8 hours then check before glucose, at one hour, and at two hours

226
Q

How does plasma glucose change temporally (over time) for a normal person?

A

Normal levels at night will stay stable and then dips and insulin brings it back to baseline –> you eat and it increases then insulin brings it back down and this occurs for all meals. –> at night it flatlines again

In between meals it lowers back to baseline

227
Q

How does plasma glucose change temporally (over time) for a diabetic?

A

Its similar to regular but the baseline is higher and it takes longer to lower the blood glucose levels

after they eat it shoots up significantly more and then does not drop as much as a normal person

so continuous high bumps occur never coming back down to baseline between meals

At night it very slowly lowers again to baseline

228
Q

Why does alcohol have to dry completely for blood glucose testing?

A

it can cause a false high

229
Q

What kind of blood does a glucometer check for?

A

Capillary blood

venous, capillary, and arterial have different levels so you need the right kind of glucometer for the right area

230
Q

Treatment for Diabetics focuses greatly on …

A

diet and nutrition (but we have gotten away from special diets), medication, and exercise

sometimes pancreatic implant

231
Q

What are the therapeutic goals involving diet treatment for diabetics?

A

Maintenance of near normal blood glc levels (wanna check glycemic index of food)

achieve optimal lipid levels

adequate calories to attain and maintain reasonable weight

prevention and treatment of chronic complications

improvement of overall health through optimal nutrition

232
Q

What kind of foods have higher glycemic index and what kinds are lower?

A

High: Simple Carbs

Low: Fiber, Low Natural Sugar Foods

233
Q

What are there for diabetics rather than specific diets or ADA diets?

A

No, there is rather a dietary prescription based on nutrition assessment and treatment goals

give simple recommendations –> Increased compliance (even from family)

self management ESSENTIAL

Help from registered dieticians is important!

234
Q

How should nutrition therapy be done for Type 1 Diabetics?

A

Based it on individual’s usual food intake

They should be eating at a consistent time sync’d with the action time of their insulin prep use

Need to monitor blood glucose levels and adjust insulin doses for the amount of food they have eaten

insulin regimens should be integrated with lifestyle and adjusted for deviations from usual eating and exercise habits (need to test for both eating and working out)

235
Q

What can give Type 1 Diabetics undergo to allow considerable flexibility in when and what the individual can eat?

A

Intensified insulin therapy, such as multiple daily injections or use of an insulin pump

normal testing occurs 3-6 times a day but an insulin pump gives a basal level every hour for more flexibility

236
Q

How should nutrition therapy be done for Type 2 Diabetics?

A

Hypocaloric diets and weight loss

Moderate caloric restriction and nutritionally adequate meal plan

spacing of meals and spreading carbohydrate intake throughout the day

may require addition of oral hypoglycemics (or insulin)

237
Q

How effective in the long run are hypocaloric diets and weight loss in Type 2 Diabetes treatment?

A

Usually improve short term glycemic levels and have the potential to improve long term metabolic control

BUT, no one proven strategy or method that can be uniformly recommended

238
Q

What things are reduced in moderate caloric restrictions and nutritionally adequate meal plans for Diabetes Type 2?

A

Reduction of total fat, especially saturated fat

decrease as little as 250-300 calories a day

losing 5-7% of weight helps blood sugar level control

239
Q

Why is alcohol moderated in diabetic nutrition?

A

less than 2 drinks a day because it raises blood sugar

240
Q

What nutritional recommendation is lower for people with nephropathy?

A

protein to 10% rather than 10-20%

241
Q

Benefits of using Exercise for Treatment in Diabetes

A

improved glc tolerance

weight loss or maintenance of a desirable body weight

improved cardiovascular risk factors

improved response to pharmacologic therapy

improved energy level, muscular strength, flexibility, quality of life, and sense of well being

242
Q

What are some precautions and considerations when diabetics start exercising?

A

They should start at a low level and gradually increase to avoid injury, hypoglycemia, or cardiac problems

they should self monitor their blood glc level both before and after exercising

a form of sugar should be available in case of emergency

243
Q

What is the best exercise to prescribe for a diabetic?

A

Aerobic activity at 50-70% of maximum oxygen uptake at least 3-4 times a week, and duration of 30-40 minutes/sessions

244
Q

What is the best form of exercise for diabetics

A

aerobic exercises

ex: walking, biking, stationary cycling, lap swimming

245
Q

What is proof of use of glucose available?

A

Weakness during exercise/ after exercise

246
Q

Why is insulin never given orally

A

Insulin is destroyed in the GI tract so it must be administered by injection

247
Q

How is insulin categorized

A

According to onset, peak, duration, and action

248
Q

4 Types of Insulin

A

Rapid

Short

Intermediate

Long Acting

249
Q

What is the only type of insulin that insulin pumps use?

A

Rapid Acting Insulin

250
Q

In order to ensure a diabetic understands how to give themselves insulin what must occur?

A

Injectable protocols need to be taught/return demos

251
Q

What other kinds of medicines can be used for Diabetics other than insulin?

A

Oral Agents

Injectable non-insulin medications

252
Q

Examples of Oral Antidiabetic Agents

A

(just for Type 2 Diabetics)

Alpha Glucoside Inhibitors

Biguanides
Thiazolidinediones

Biguanides

Sulfonylureas
Meglitinides

253
Q

Where and what does Alpha Glucoside Inhibitors do?

A

They act on the gut to block how much glucose is absorbed from food (decreased glucose absorption)

254
Q

Where and what do Biguanides and Thiazolidinediones do?

A

Act on liver - decrease hepatic glucose output (prevents glucose from the liver release)

Act on cells to increase peripheral glucose uptake

255
Q

Where and what do Sulfonylureas and Meglitinides do?

A

Increase insulin production

act on beta cells of the pancreas (must already have working cells for this to work so it does not work in Type 1, only 2)

256
Q

Pancreatic Transplant

A

may be done if beta cells are not working

survival rate is higher for an individual is greater than a graft after 1 and 3 years, but the survival decreases in both over time

Not lifesaving, just increases QOL significantly

257
Q

What is required forever after a pancreatic transplant?

A

Anti Rejection meds for life –> immunosuppression will result because of these

258
Q

Pancreatic transplants are NOT ___ ___, but….

A

not life saving but do improve QOL significantly because this is more convenient than injectable insulin

259
Q

What current research is occurring regarding pancreatic transplants?

A

Transplantation of Islet Cells (Langerhans/Beta Cells) - but for now it does not work well

260
Q

Acute Complications of Diabetes

A

DKA

Hyperosmolar Hyperglycemia non-Ketotic Coma/Syndrome (HHNK, HHNC, HHNS) - mostly for type 2

Somogyi Effect

Dawn Phenomenon

Hypoglycemia

261
Q

Main 3 Signs/Manifestations of Dehydration from Hyperglycemia?

A

Thirst

Increased heart Rate

Warm, dry skin

262
Q

How does Hyperglycemia lead to Dehydration?

A

Increase blood glc –> increased blood osmolarity

increased blood osmolarity –> renal threshold exceeded –> osmotic diuresis –> dehydration

Increases blood osmolatiry –> cellular dehydration (cells shrink) –> dehydration

Dehydration –> thirst, increased HR, warm dry skin

263
Q

One of the first symptoms of hyperglycemia is …

A

Thirst

264
Q

Diabetic Ketoacidosis (DKA)

A

Acute insulin insufficiency with life threatening and dramatic presentation (acute and life threatening)

most typical in Type 1 Diabetes - often the first evidence of the disease

Onset in 1-24 hours - gets bad fast

265
Q

Presenting History of DKA

A

one to several days of polyuria, polydipsia

nausea, vomitting, anorexia, acute abdominal pain

266
Q

Precipitating Factors for DKA

A

failure to take insulin

infection or other illness

trauma or physical stress

emotional stress and extreme anxiety

pregnancy

continuous insulin pump failure

267
Q

Pathophysiology/Progression of DKA

A

Inadequate insulin hinders glc uptake by fat and muscle cells –> glc accumulates in blood –> liver responds by converting glycogen to glucose and releasing into blood –> further blood glc increase –> renal threshold exceeded –> excess glucose excreted in urine

cell starvation –> rapid metabolism of protein for energy –> loss of intracellular K and phosphorus and excessive liberation of amino acids (catabolic process) –> liver converts amino acids to glucose and urea –> blood glc levels grossly elevated –> increased serum osmolarity and glucosuria –> osmotic diuresis leading to dehydration

Conversion of fats into glycerol and FA for energy

268
Q

How does the conversion of fat to glycerol and FA for energy greatly influence DKA pathophysiology?

A

FA end up not being metabolized at the same rate of release so they accumulate in the liver and convert into ketones (ketoacids)

Ketones will accumulate in blood and urine causing acidosis (and build up in liver)

Acidosis leads to more tissue breakdown, more ketosis, more acidosis –> shock, death, coma

269
Q

What is the deadly cycle of DKA?

A

massive fluid loss from osmotic diuresis –> fluid and electrolyte imbalances and dehydration –> water loss exceeds glucose and electrolyte loss –> hyperosmolarity –> perpetuates dehydration

DEADLY CYCLE: Decreased glucose excretion –> further increased blood glc levels –> hyperosmolarity and dehydration –> shock, coma, death

270
Q

Physical Manifestations of DKA

A

Dehydration: Warm dry skin, dry mucous membranes, acute weight loss, tachycardia, weak thready pulse, hypotension

Ketoacidosis: anorexia, nausea, vomiting, acetone breath, abdominal pain, decreased CNS activity leading to lethargy/fatigue/stupor/coma

Compensation (to acidosis): Tachypnea and Kussmaul Respirations

271
Q

Lab Manifestations of DKA

A

serum glucvose 250-600 mg/dL

glucosuria

ketonemia and ketonuria

ABGs: acidosis (pH less than 7.3) and decreased bicarbonate (<15 mEq/L)

Increased BUN d/t dehydration

Potassium levels high, low, or normal depending on degree of dehydration and acidosis, but there is total body depletion of K

272
Q

What is the pathway of cell starvation leading to manifestations of DKA ?

A

No glucose for ATP production –> breakdown of fat and protein stores –> liver produces ketones –> ketoacidosis –> fruity breath, coma, kussmaul respirations

273
Q

Kussmaul respirations

A

deep irregular breathing with pauses in between

274
Q

Acetone Breath

A

sweet fruity breath from the ketones in DKA

275
Q

Treatment for DKA

A

Fluid replacement (deficit of 5-8 L –> give 1-2 L of NS over 1-2 hours)

IV Regular insulin (cont drip or bolus)

K+ replacement once UO re-established (since K+ moves intracellularly)

Bicarbonate (if pH <7.2, but give cautiously b/c of CNS acidosis)

5% dextrose added when glucose <250

276
Q

Why is 5% dextrose given when glucose is <250 in DKA treatment?

A

To prevent a swing in the opposite direction

sudden change in osmolarity can occur when the blood levels are changed to rapidly

277
Q

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNK)

A

relative insulin insufficiency with 50% mortality

DKA does not develop because there is still insulin available

most typical in Type 2 diabetes - often NOT previously diagnosed

278
Q

How is HHNK onset different from DKA onset?

A

HHNK is insidious while DKA is acute and quick

Because of this HHNK is 50% higher in mortality than DKA

279
Q

Presenting History for HHNK

A

polyuria several days to weeks prior

280
Q

Precipitating Factors for HHNK

A

conditions that stress insulin tolerance like peritoneal dialysis, hemodialysis, tube feedings, and TPN

elderly with renal insufficiency

drugs: steroids, diuretics, Dilantin

infection, CVA

281
Q

What manifestations of HHNK are unique and distinctly different from DKA?

A

There are neurologic symptoms and deficits that occur that do not occur with DKA

Because of this, sometimes HHNK is mistaken as a stroke

282
Q

Physical Manifestations of HHNK Syndrome

A

Severe dehydration (dry mucous membranes and extreme thirst)

Neurologic Symptoms

283
Q

What are the neurologic symptoms of HHNK

A

Depressed sensorium lethargy –> coma

deficits: positive babinski’s (ominous), paresis or paralysis, sensory impairment, hyperthermia, hemianopia

seizures

284
Q

Is Dehydration worse in HHNK or DKA

A

HHNK

285
Q

Laboratory manifestations for HHNK

A

serum glucose > 600 mg/dL

serum osmolarity > 300 mosm (high)

glucosuria

increased bun from dehydration (hypovolemia and decreased renal perfusion)

sodium and potassium WNL

decreased bicarbonate due to lactic acidosis from hypovolemia

NO KETOSIS!!!!!!!!!!!!!!

286
Q

Is there ketosis in HHNK

A

No

this is because there is still some insulin present so there is not fat breakdown

287
Q

Treatment for HHNK Syndrome

A

restore intravascular volume with NS

continuous IV insulin

potassium replacement

(RESTORE CIRCULATION VOLUME)

288
Q

What are some other complications from HHNK Syndrome

A

Thrombosis (from hyperosmolar blood that is more sticky due to dehydration)

Embolus

Pneumonia

ARDS

289
Q

Insulin Shock is also known as …

A

Hypoglycemia

290
Q

What levels of glucose signify Insulin Shock

A

<50 mg/dL of glucose in the blood

causes many neurologic issues (ANS response, neuroglycopenia, etc)

291
Q

What is the ANS response of insulin shock (hypoglycemia)

A

PNS: hunger, nausea, hypotension, bradycardia

SNS: anxiety, sweating, vasoconstriction, tachycardia

292
Q

What occurs with the sign/symptom Neuroglycopenia (brain not getting enough glucose) for Insulin Shock

A

Altered cerebral function d/t brain cell starvation
headache

vagueness

decreased problem solving ability (probably cannot self treat at the moment)

slurred speech

emotional lability

convulsions

coma

293
Q

People at risk for Insulin Shock (Hypoglycemia)

A

tight control, pump, or multiple injections

Beta blockers d/t no sympathetic effect

autonomic neuropathy

oral hypoglycemic agents

type 2 with excess insulin secretion

error in insulin dose

increased exercise

not enough food

failure to decrease insulin as infection or other stress resolves

294
Q

How to treat insulin shock?

A

immediate ingestion of carbohydrates (CHOs)

glucagon IV, SQ, IM

295
Q

Glucose levels below 30 can lead to…

A

coma

296
Q

Onset of Hypoglycemia v DKA v HHNK

A

Hypo - Rapid

DKA - Slow

HHNK - Slowest / Insidious

297
Q

Symptoms of Hypoglycemia v DKA v HHNK

A

Hypo - weak, anxious confused

DKA - N/Vm 3 P’s, headache, irritable, coma

HHNK - similar to DKA< stupor, focal motor seizure

298
Q

Skin of Hypoglycemia v DKA v HHNK

A

Hypo - cold moist and pale

DKA - hot flushed and dry

HHNK - very dry

299
Q

Mucous (membranes) of Hypoglycemia v DKA v HHNK

A

hypo - normal

DKA - dry

HHNK - very dry

300
Q

Respirations of Hypoglycemia v DKA v HHNK

A

Hypo - normal

DKA - hyperventilation

HHNK - normal

301
Q

Diabetic types at risk for Hypoglycemia v DKA v HHNK

A

Hypo - both 1 and 2

DKA - 1

HHNK - 2

302
Q

Blood glucose levels in Hypoglycemia v DKA v HHNK

A

Hypo - less than 60

DKA - 300 to 800

HHNK - 600 to 4800

303
Q

Serum Ketones in Hypoglycemia v DKA v HHNK

A

Hypo - none

DKA - high

HHNK - moderate to none

304
Q

Plasma pH in Hypoglycemia v DKA v HHNK

A

Hypo - normal

DKA - acidic

HHNK - normal

305
Q

Treatment for Hypoglycemia v DKA v HHNK

A

Hypo - IV glucose and SQ glucose

DKA - insulin F & E

HHNK - Insulin, crystalloids and colloids

306
Q

Somogyi Effect

A

Unrecog hypoglycemia at night (or when fasting) –> increased catecholamines, glucagon, cortisol, and GH –> hyperglycemia in the morning –> we increase their exogenous insulin –> more hypoglycemia occurs at night –> vicious and dangerous cycle that repeats leading to insulin resistance eventually

307
Q

Somogyi effect often goes together with the …

A

dawn phenomenon

308
Q

What should be done to limit unneeded exogenous insulin regarding the somogyi effect?

A

Take blood sugar in the middle of the night/ at 3 am to note the hypoglycemia

309
Q

Dawn Phenomenon

A

naturally occurring hormonal effect between 3 am and 5 am there there is a pre dawn hyperglycemia (increase) without antecedent hypoglycemia

could be due to changes in circadian rhythm

it is the liver giving you an “early morning snack”

GH is a possible factor in this

310
Q

What type of Diabetic is more likely to experience the Dawn Phenomenon

A

Type 1 Diabetcs

311
Q

What is the different when the dawn phenomenon is alone, versus when it combines with the Somogyi effect?

A

alone –> mild hyperglycemia

in combo –> profound hyperglycemia!

312
Q

When should we check glucose for the dawn effect?

A

always check at night like at 3am, BUT check at 7 am whether at home or in the hospital since you were not hyperglycemic during the night, only now

313
Q

What tissue are MOST affects by elevated blood glucose levels?

A

body cells NOT dependent on insulin to use glucose –> most affected by chronic elevated blood glc levels

  1. RBCs (less oxygen carrying capacity)
  2. Glomerular Cells (kidney damage)
  3. Central and peripheral Nerve cells (neuro deficits)
  4. Blood vessel cells (leads to atherosclerosis)
314
Q

What about diabetes kills diabetics?

A

Not high blood sugar, but the long term damage, dysfunction, and organ failure associated with it

315
Q

What areas have the most long term damage from hyperglycemia?

A

Eye - diabetic retinopathy

Kidney - diabetic nephropathy

Nerves - diabetic neuropathy

Heart and blood vessels - atherosclerosis, hypertension, cardio and cerebrovascular disease

316
Q

Macrovascular Problems (Chronic Complications) of Diabetes

A

These are chronic issues leading to less circulation:

CV Disease
Cerebrovascular Disease
Peripheral Vascular Disease (PVD)

317
Q

Microvascular Problems (Chronic Complications) of Diabetes

A

Issues for Smaller Vessels and Nerves:

Diabetic Neuropathy
Diabetic Nephropathy
Diabetic Retinopathy
Erectile Dysfunction

318
Q

Erectile dysfunction often brings undiagnosed diabetics in, but what may this symptom indicate?

A

May mean the heart is not delivering blood effectively!

319
Q

What/Where are Macrovascular complications from Hyperglycemia

A

Hyper –> Heart –> CAD (Coronary syndrome, MI, CHF)

Hyper –> Brain –> Cerebrovascular accidents (TIA, CVA, Cognitive impairment)

Hyper –> Extremities –> Peripheral Vascular Disease (ulceration, gangrene, amputation)

All of these can lead to death and or disability

320
Q

What/Where are Microvascular complications from Hyperglycemia

A

Hyper –> Eye –> Retinopathy, Cataract, Glaucoma –> Blindness

Hyper –> Kidney –> Nephropathy (microalbuminuria, Gross albuminuria) –> Kidney Failure

Hyper –> Nerves –> neuropathy (peripheral and autonomic) –> amputation

All of these can lead to death and or disability

321
Q

What are some Long Term Complications of Diabetes

A

Cardiovascular (accelerated atherosclerosis - CAD, HTN, CVA, PVD)

Eye - retinopathy, cataracts, glaucoma

Renal - nephropathy and glomerulosclerosis

Nervous - axonal and Schwann cell degeneration; sensory and motor nerve alterations

Bone - charcots changes in joints

Skin and Immune - increased susceptibility to infection and delayed wound healing

322
Q

What are the 2 classifications of peripheral neuropathies?

A

Somatic and Autonomic

323
Q

What are the 2 processes causing Neuropathy in Diabetes?

A
  1. Thickening of vessel walls that supply nutrients to nerves leading to less blood flow
  2. Segmental demyelination affecting schwann cells leading to slower nerve conduction
324
Q

What are some Somatic Neuropathies

A

Polyneuropathies - paresthesias, impaired sensation, diminished reflexes

Mononeuropathies - involvement of a mixed nerve trunk –> motor and sensory nerves affected

Amyotrophy –> muscle weakness and wasting

motor usually bilateral and symmetric and usually occurs first

clawing of the foot

hypersensitivity of light is secondary to retinopathy

325
Q

What are some Autonomic Neuropathies

A

Impaired vasomotor function - postural hypotension

Impaired GI function - gastric atony, diarrhea (from impaired nutrient absorption) (poor gastric tone) (postprandial and nocturnal)

Impaired GU Function - paralytic bladder, incomplete voiding, impotence, retrograde ejaculation

Cranial nerve involvement - extraocular nerve paralysis, impaired pupillary responses, impaired special senses

326
Q

What is the major cause of death for diabetics?

A

Cardiovascular Disease

327
Q

Manifestations of Cardiovascular Disease in Diabetics

A

Accelerated Atherogenesis (onset earlier age, progression more rapid, manifestations of this are more severe in diabetes) (CAD Means that less blood gets to the heart)

Hyperlipoproteinemia (HDLs lower in uncontrolled in DM)

Abnormal platelet function (more clots and bleeding)

*Decreased HDL, increased LDL, increased atherosclerosis, increased total cholesterol, increased triglycerides

328
Q

How to manage Diabetic Cardiovascular Disease

A

management:

Diet

weight loss

exercise

quitting smoking

controlling HTN

329
Q

A 40 year old with diabetes that does not smoke, no HTN, and has normal cholesterol has ___risk of CVD

A

half the risk of CVD

330
Q

CVD increases __x for diabetics with HTN, ___x with high cholesterol, and ___x for smokers

A

2x HTN

8x High Cholesterol

11x Smoking

331
Q

Which type of diabetes has a higher eye disease incidence?

A

type 1 diabetes (5000 new cases a year)

332
Q

___ is the leading cause of blindness

A

retinopathy

333
Q

Retinopathy is ___ and ___ with duration

A

Retinopathy is progressive and worsens with duration

334
Q

2 Types of Retinopathy

A

Non proliferative “background”

Proliferative “neovascularization”

335
Q

Non Proliferative “Background” Retinopathy

A

retinal veins tortuous and dilated

exudates contain lipoproteins

hemorrhages

scarring

retinal detachment

336
Q

Proliferative “Neovascularization” Retinopathy

A

traction on vitreous –> detachment

treatment involves laser surgery to destroy new blood vessels and stop hemorrhaging or a Vitrectomy

337
Q

Glaucoma

A

capillary neovascularization often refractory to treatment

potential retinopathy in diabetics

cataracts are made of sorbitol which is glucose turning into sugar alcohol. It then accumulates to cause glaucoma

damages optic nerve

338
Q

Cataracts

A

retinopathy frequent in diabetics

increased sorbitol (glucose turning into sugar alcohol) in the lenses

cloudy dense lense

treatment involves surgery

339
Q

Blurred Vision

A

retinopathy in diabetic due to osmotic changes –> takes 6-8 weeks to resolve

340
Q

Diabetic eye vascularization …

A

is much more vascularized than in non diabetics

this is proliferative

341
Q

Number one risk for cataracts is ___ and vice versa

A

Galucoma

342
Q

Glaucoma v Cataract as you see it visually

A

Cataracts have a milky opacity

Glaucoma is more increased pressure leading to blindness

343
Q

Nephropathy

A

kidney issues

344
Q

What occurs early versus late stage nephropathy in diabetics

A

Early: Kidney hypertrophies, and GFR increases and albuminuria in new onset type 1 diabetes

Late: Basement membrane changes, proliferation and leakiness

Albumin escapes in the blood and less wound healing occurs and less glomerular filtration rate occurs with potential kidney failure in 5 years

345
Q

Manifestations of diabetic nephropathy

A

proteinuria

progressive decrease in GFR

ESRD in 5 years with persistent proteinuria

AVOID contrast studies (IVPs, angiograms)

346
Q

Treatment for Diabetic Nephropathy

A

dialysis or kidney transplant

347
Q

How to prevent Diabetic Nephropathy

A

ACE inhibitors to protect the kidneys

avoid things hard on the kidneys like contrast studies

*not much can be done genetically, but HTN can be treated

348
Q

How do ACE inhibitors help prevent Nephropathy?

A

ACE = angiotensin converting enzyme inhibitors (these block receptors to lower BP and protect the kidneys)

349
Q

Oncotic Pressure

A

osmotic pressure resulting from the difference between extracellular fluids like protein contents of plasma and interstitial fluids - pressure exerted by proteins on the walls

350
Q

The most common disabler for diabetics is ___

A

neuropathy (lack of sensation)

351
Q

Death is ____ from neuropathy alone BUT ..

A

death is uncommon from neuropathy alone but significant morbidity and decreases in QOL occur

352
Q

The key to stopping neuropathy is ..

A

Prevention !!!

Inspect for trauma, blisters, callouses

assure shoes are a good fit!

353
Q

Common issues due to Neuropathy and causes of neuropathies

A

Gangrene

Underlying Osteomyelitis (Bone Infection)

Vessel ischemia and sorbitol damage to Schwann cells lead to this

Neuropathic ulcers especially on the plantar surface of the foot –> penetrating wounds that a person does not feel occur

354
Q

Common Neuropathic and Lower Extremity issues in Diabetics

A

Diabetic Foot Ulcer of the Heel

Gangrenous Toe

Yellow Nails

Corns

Calluses

Acanthosis Nigricans - darkening of skin

Charcot Foot

Infection

Candidiasis

Diabetic Foot Disease

355
Q

Why does diabetes increase susceptibility for infection?

A

hypoxia

increased glucose to feed microorganisms

decreased WBC delivery through damaged vessels

decreased WBC function –> abnormal chemotaxis and phagocytosis

356
Q

How do insulin requirements change with diabetic infections

A

Insulin requirements increase with infections and decrease with resolution

357
Q

What are some examples of infections for diabetics?

A

Carbuncles and Furuncles

Vaginal Candidiasis

358
Q

Carbuncles and Furuncles

A

Furuncles are infected hair follicles

Carbuncles are groups of furuncles

359
Q

Candidiasis

A

Yeast infection on skin or between digits

common in diabetics

360
Q

Cellulitis

A

red, warm, swelling, and enlarging of the infected subcutaneous tissue

can present, for example, as red lines and blotches on the skin

361
Q

Charcot’s Foot

A

Common in diabetics (neuropathy)

damage to nerves leads to clawing of toes and less padding on the plantar surface of the foot

Decreased sensation and abnormal bone deposition occurs as well

foot cannot be put down correctly

may not feel a broken bone due to lack of sensation

362
Q

Diabetic Foot Disease

A

Issues of the foot due to uncontrolled high blood glucose levels in diabetics

commonly leads to amputation and that may be the only treatment available sometimes

effects are due to neuropathy and vascular disease in the feet

requires a yearly check up for the foot disease

can have gangrene and exposed bone covered with granulation tissue that they do not feel

363
Q

Diabetic Foot Disease accounts for how many amputations a year?

A

20,000 amputations a year - primarily of toes, feet, and legs

accounts for 1/2 of all non traumatic amputations

may be the only treatment for diabetic foot disease infection

364
Q

The most common complication leading to hospitalization for diabetics is …

A

diabetic foot disease

NURS361 - Pathophysiology II (20 decks)

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