Gen Path Exam 2 - Pathology of Diabetes Flashcards

1
Q

Syndrome with disordered carbohydrate metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or to a combo of insulin resistance and inadequate insulin secretion to compensate

A

Diabetes mellitus

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2
Q

Diabetes mellitus affects what % of the US?

A

10%

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3
Q

In the US, ____ million new cases of diabetes are diagnosed each year and ____ million have prediabetes

A

1.2; 86

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4
Q

How many Americans currently have diabetes?

A

30 million

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5
Q

How many Americans will have diabetes in 2050?

A

1 in 3

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6
Q

What is the incidence rate for diabetes in people age 20-44? What about 65-74?

A

20-44 years old = 2%
65-74 years old = 18%

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7
Q

Leading cause of end-stage renal disease, adult-onset blindness, and nontraumatic lower extremity amputations resulting from atherosclerosis of arteries

A

Diabetes

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8
Q

Why were the terms “insulin-dependent diabetes mellitus” and “non-insulin-dependent diabetes mellitus” eliminated by the American Diabetes Association?

A

Bc they are based on pharmacologic rather than etiologic considerations

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9
Q

Due to pancreatic islet beta cell destruction predominantly by an autoimmune process, and these pts are prone to ketoacidosis

A

Type 1 diabetes mellitus

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10
Q

Most prevalent form of diabetes mellitus

A

Type 2 diabetes mellitus

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11
Q

Due to insulin resistance, mainly caused by visceral obesity, with a defect in compensatory insulin secretion

A

Type 2 diabetes mellitus

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12
Q

Used to be termed juvenile-onset diabetes mellitus, or ketosis-prone diabetes mellitus, or insulin-dependent diabetes mellitus

A

Type 1 diabetes mellitus

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13
Q

Used to be termed adult-onset diabetes mellitus,
ketoacidosis-resistant diabetes mellitus or non-insulin-dependent diabetes mellitus

A

Type 2 diabetes mellitus

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14
Q

Known as latent autoimmune diabetes in adults

A

Type 1.5 diabetes

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15
Q

Autoimmune diabetes that begins in adulthood and does not need insulin for glycemic control at least in the first 6 months after diagnosis

A

Type 1.5 diabetes

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16
Q

Shares genetic, immunologic, and metabolic features with both Type 1 and Type 2 diabetes mellitus

A

Type 1.5 diabetes

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17
Q

Some consider it to be a slowly progressive form of Type 1 diabetes mellitus, while others consider it a separate distinct form of diabetes

A

Type 1.5 diabetes

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18
Q

Refers to disorders due to monogenic defects in beta-cell function, with little or no defect in insulin action that was observed in non-obese children, adolescents, and young adults

A

Maturity-onset diabetes of the young

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19
Q

Characterized by carbohydrate intolerance during pregnancy usually resolving after delivery

A

Gestational diabetes mellitus

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20
Q

Diabetes that develop secondary to some other identifiable etiology or acquired disease

A

Secondary diabetes

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21
Q

Pt has hyperglycemia with little or no endogenous insulin secretion

A

Type 1 diabetes mellitus

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22
Q

Onset of disease is abrupt with marked polyuria, polydipsia, polyphagia, weight loss, fatigue

A

Type 1 diabetes mellitus

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23
Q

Highly prone to ketosis; pts frequently present for tx in an intial episode of diabetic ketoacidosis

A

Type 1 diabetes mellitus

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24
Q

Marked sensitivity/brittleness to exogenous insulin administration, particularly with regular insulin

A

Type 1 diabetes mellitus

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25
Q

In Type 1 diabetes mellitus, a prodromal phase of polyuria, polydispia, and weight loss may precede the development of what?

A

Diabetic ketoacidosis

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26
Q

Type 1 diabetes mellitus accounts for what % of diagnosed diabetes cases?

A

5-10%

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27
Q

Type 1 diabetes mellitus incidence most commonly peaks during what times in a person’s life?

A

Middle of first decade
Time of growth acceleration of adolescence

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28
Q

Pts maintain some endogenous insulin secretory capability by pancreatic beta-cells despite the overt abnormalities of glucose homeostasis, including fasting hyperglycemia and/or carbohydrate intolerance

A

Type 2 diabetes mellitus

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29
Q

Pts are NOT absolutely dependent on insulin for life

A

Type 2 diabetes mellitus

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30
Q

Why are pts with Type 2 diabetes mellitus relatively resistant to development of ketosis in the basal state?

A

They have retention of endogenous insulin secretory capabilities

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31
Q

Generally demonstrate marked resistance or insensitivity to the metabolic actions of endogenous as well as exogenous insulin, in part as the result of decreased insulin receptors

A

Type 2 diabetes mellitus

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32
Q

Have a failure of postreceptor coupling and of intracellular insulin action that is also a major cause of insulin resistance

A

Type 2 diabetes mellitus

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33
Q

Can have a long presymptomatic phase, leading to a 4-7 year delay in diagnosis

A

Type 2 diabetes mellitus

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34
Q

Type 2 diabetes mellitus accounts for what % of diagnosed diabetes cases?

A

90%

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35
Q

Type 2 diabetes mellitus occurs most commonly in what people?

A

40 years and older

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36
Q

The incidence of Type 2 diabetes mellitus is increasing more rapidly in what age groups?

A

Adolescents/young adults

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37
Q

Gestational diabetes mellitus develops in what % of pregnancies? What trimester?

A

1-3%; 3rd trimester

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38
Q

Females with gestational diabetes mellitus will exhibit an increased risk for what?

A

Perinatal morbidity and mortality
Developing Type 2 diabetes mellitus later in life

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39
Q

What can greatly reduce the chance of developing over Type 2 diabetes mellitus after having gestational diabetes during pregnancy?

A

Control of weight after pregnancy

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40
Q

What are the causes of secondary diabetes?

A

Genetic defects of Beta cell function
Genetic defects in insulin action
Genetic syndromes
Disease of exocrine pancreas
Drug/chemical induced
Infections

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41
Q

In Type 1 diabetes mellitus, what is increased urination (polyuria) a consequence of? What is this secondary to? What is the result?

A

Osmotic diuresis, secondary to sustained hyperglycemia

Result = loss of glucose, water, electrolytes in urine

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42
Q

In Type 1 diabetes mellitus, what is increased thirst (polydipsia) a consequence of?

A

Hyperosmolar state

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43
Q

In Type 1 diabetes mellitus, what is the initial weight loss due to?

A

Loss of water, glycogen, triglycerides
Reduced muscle mass as AA’s are diverted to form glucose and ketone bodies

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44
Q

A common feature of Type 1 diabetes mellitus is _________ _______, despite normal or increased appetite

A

weight loss

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45
Q

In Type 1 diabetes mellitus, what is postural hypotension a result of?

A

Decreased plasma volume

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46
Q

What is a serious prognostic sign in Type 1 diabetes mellitus?

A

Hypotension in recumbent position

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47
Q

What may be present at the time of diagnosis of Type 1 diabetes mellitus, particularly when the onset is subacute?

A

Paresthesias

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48
Q

In Type 1 diabetes mellitus, what is paresthesias due to?

A

Temporary dysfunction of peripheral sensory nerves

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49
Q

How is temporary dysfunction of peripheral sensory nerves/paresthesia in Type 1 diabetes mellitus usually resolved?

A

Insulin replacement (restores glycemic levels)

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50
Q

What does temporary dysfunction of peripheral sensory nerves/paresthesia in Type 1 diabetes mellitus suggest?

A

Neurotoxicity from sustained hyperglycemia

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51
Q

Why does blurred vision often develop in Type 1 diabetes mellitus?

A

Lenses/retina exposed to hyperosmolar fluids

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52
Q

What does the fruity breath odor of acetone suggest?

A

Diabetic ketoacidosis

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53
Q

Why does a patient’s level of consciousness vary depending on the degree of hyperosmolality in Type 1 diabetes mellitus?

A

Minimal = insulin deficiency slowly develops, sufficient water intake maintained

Stupor or coma = vomiting due to ketoacidosis, dehydration progresses, compensatory mechanisms to maintain osmolarity are inadequate

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54
Q

What type of weight loss are features of more slowly developing insulin deficiency in Type 1 diabetes mellitus?

A

Loss of subcutaneous fat
Loss of muscle

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55
Q

What contributes to muscle wasting and weakness in Type 1 diabetes mellitus?

A

K+ loss
Catabolism of muscle protein

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56
Q

What exacerbates the dehydration and hyperosmolality during Type 1 diabetes mellitus? What is produced that interferes with oral fluid replacement?

A

Diabetic ketoacidosis

Produces anorexia, nausea, vomiting

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57
Q

Which people are typically asymptomatic initially for Type 2 diabetes mellitus?

A

Obese

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58
Q

Patients with Type 2 diabetes mellitus may present with evidence of what complications because of disease present for awhile before diagnosis?

A

Neuropathic
Cardiovascular

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59
Q

What are common initial complaints of women with Type 2 diabetes mellitus?

A

Skin infection
Pruritus (itchy)
Candidal vulvovaginitis
UTIs

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60
Q

Obesity is present in what % of patients with Type 2 diabetes mellitus?

A

80-90%

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61
Q

Where is fat typically found in obese patients with Type 2 diabetes mellitus?

A

Abdomen, chest, neck, face

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62
Q

Mild ________ is often present in obese patients with Type 2 diabetes mellitus

A

hypertension

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63
Q

Type 2 diabetes mellitus is more common in women who have experienced what things in pregnancy?

A

Delivered large babies (>9 lbs)
Polyhydramnios (extra amniotic fluid)
Preeclampsia
Unexplained fetal loss

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64
Q

Lab findings of diabetes mellitus

A

HbA1c >/= 6.5%
Fasting plasma glucose >/= 126
Oral glucose tolerance test w/ plasma glucose >/= 200
Casual/random plasma glucose >/= 200

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65
Q

_______ is useful for diabetes screening and diagnosis in routine clinical practice and this
test is preferred because of ease of administration and reliability

A

HbA1c

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66
Q

The major form of glycohemoglobin is termed ______, which normally comprises only 4 to 6% of the total hemoglobin

A

HbA1c

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67
Q

Glycosylated hemoglobin is abnormally high in diabetics with chronic hyperglycemia and reflects what?

A

Metabolic control

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68
Q

___________ ___________ is produced by nonenzymatic condensation of glucose molecules with free amino groups on the globin component of hemoglobin

A

Glycosylated hemoglobin

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69
Q

The __________ the prevailing ambient levels of blood glucose, the ___________ the level of glycosylated hemoglobin will be

A

higher; higher

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70
Q

Since glycohemoglobins circulate within red blood cells whose life span lasts up to 120 days, they generally reflect the state of glycemia over the preceding ______________

A

2-3 months

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71
Q

When should HbA1c testing be performed in all patients with diabetes?

A

Document degree of glycemic control initially
Continuing care

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72
Q

What is the HbA1c value?
Decreased risk of diabetes mellitus

A

HbA1c < 5.7%

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73
Q

What is the HbA1c value?

Prediabetes: increased risk of diabetes mellitus

A

5.7-6%

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74
Q

What is the HbA1c value?
Prediabetes: higher risk of diabetes mellitus

A

6.1-6.4%

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75
Q

What is the HbA1c value?
Consistent w/ diagnosis of diabetes mellitus

A

6.5% and higher

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76
Q

How is the fasting plasma glucose test confirmed?

A

Repeat testing on a different day

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77
Q

When is an oral glucose tolerance test done?

A

2 hrs after a 75g glucose load

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78
Q

Commonly used to aid in the diagnosis of diabetes mellitus and reflects the rate of absorption, uptake by tissue

A

Oral glucose tolerance test

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79
Q

What are the 3 classic symptoms of hyperglycemia?

A

Polyuria
Polydipsia
Unexplained weight loss

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80
Q

Individuals with glucose levels higher than normal but not high enough to meet the criteria for diagnosis of diabetes mellitus are considered to have what?

A

Prediabetes (aka impaired glucose tolerance)

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81
Q

What is the diagnosis of prediabetes?

A

Fasting plasma glucose: 100-125
Oral glucose tolerance test w/ a plasma glucose: 140-199
HbA1c: 5.7-6.4%

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82
Q

If allowed to persist at high enough levels in the susceptible diabetic, hyperglycemia will progress to what?

A

Diabetic ketoacidosis

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83
Q

What is a less common but complication of hyperglycemia, but has a higher fatality rate?

A

Hyperosmolar hyperglycemic syndrome (HHS)

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84
Q

What are the 4 acute complications of diabetes mellitus?

A

Hyperglycemia
Diabetic ketoacidosis
Hyperosomolar hyperglycemic syndrome (HHS)
Hypoglycemia

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85
Q

T/F: Diabetic ketoacidosis is more commonly seen in patients with Type 2 diabetes mellitus

A

FALSE, more commonly seen in Type 1 diabetes mellitus

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86
Q

Diabetic ketoacidosis results from the inability of the body to metabolize _______ as rapidly as they are produced and the failure of the body to compensate for the decrease in _____ via renal and respiratory mechanisms

A

ketones; pH

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87
Q

Diabetic ketoacidosis usually occurs with a persistently high blood glucose > ____ mg/dL, and is often precipitated by __________

A

250; infection

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88
Q

Signs and symptoms:

Headache
Flushed face
Weakness
Fatigue
Hunger
Confusion
Disorientation
Nausea
Vomiting/abdominal cramps/diarrhea
Dyspnea
Deep, rapid respirations
Fruity breath
Hypotension
Weak pulse
Polydipsia
Polyuria
Polyphagia
Loss of consciousness

A

Diabetic ketoacidosis

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89
Q

What is the mortality rate of diabetic ketoacidosis?

A

5-10%

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90
Q

Diabetic ketoacidosis is responsible for ___% of all deaths in diabetic pts

A

1%

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91
Q

Diabetic-related complication marked by severe hyperglycemia, resultant extreme hypertonic dehydration and absence of significant ketoacidosis

A

Hyperosmolar hyperglycemic syndrome (HHS)

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92
Q

What do patients with Hyperosmolar hyperglycemic syndrome typically present with?

A

Impaired consciousness or coma

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93
Q

Is Hyperosmolar hyperglycemic syndrome more common in Type 1 or Type 2?

A

Type 2 diabetes mellitus

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94
Q

The large number of patients with _______ disease suggests that these patients have a tendency to Hyperosmolar hyperglycemic syndrome because of their decreased ability to compensate for the __________ by excreting glucose

A

kidney; hyperglycemia

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95
Q

In many patients with Hyperosmolar hyperglycemic syndrome, a precipitating acute illness such as what is present?

A

Infection
MI
Stroke

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96
Q

Hyperosmolar hyperglycemic syndrome and diabetic ketoacidosis have a similar pathophysiology.

What is the difference?

A

In HHS:
Hyperglycemia increases osmotic gradient
Water, electrolytes, glucose lost in urine
Causes glycosuria and more severe dehydration
Risk for cardiovascular collapse

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97
Q

What are the 3 symptoms of Hyperosmolar hyperglycemic syndrome?

A

Weakness
Polyuria
Polydipsia

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98
Q

Despite the severe dehydration in HHS, patients may have normal blood pressure, however, many will demonstrate significant ___________ ___________

A

orthostatic hypotension

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99
Q

In HHS, blood glucose values are usually > _____ mg/dL in patients with HHS, and like DKA, HHS is serious and can be fatal, with a ______% mortality rate

A

600; 40-60%

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100
Q

In addition to altered mental status and confusion, other neurologic signs are often present such as hemisensory defects, transient hemiparesis, aphasia or seizures

A

Hyperosmolar hyperglycemic syndrome

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101
Q

What is the most common complication that occurs in pts being treated for diabetes mellitus?

A

Hypoglycemia

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102
Q

Often arises from failure to ingest sufficient foods following insulin administration, exercise w/o sufficient intake of food, over-administration of insulin, sulfonylureas or meglitinides, or presence of infection/other disease

A

Hypoglycemia

103
Q

T/F: The clinical manifestations of hypoglycemia
are nonspecific, vary among persons, and can change from time to time in the same person

A

True

104
Q

Neuroglycopenic symptoms of hypoglycemia result from depriving the brain of its
primary fuel, glucose, and can be divided into what 2 categories?

A

Neurogenic and neuroglycopenic

105
Q

Which symptom of hypoglycemia?

Triggered by the autonomic nervous system

A

Neurogenic

106
Q

Which symptom of hypoglycemia?

Tremulousness, tachycardia, palpitations, anxiety (catecholamine mediated)

A

Neurogenic

107
Q

Which symptom of hypoglycemia?

Diaphoresis, hunger, paresthesias (acetylcholine release)

A

Neurogenic

108
Q

Which symptom of hypoglycemia?

Due to diminished glucose supply to CNS

A

Neuroglycopenic

109
Q

Which symptom of hypoglycemia?

Weakness, dizziness, tingling, difficulty concentrating, blurred vision, confusion, behavioral change, seizure, coma

A

Neuroglycopenic

110
Q

Major cause of death = complications from end-stage renal disease

A

Type 1 diabetes mellitus

111
Q

Major cause of death = macrovascular diseases leading to myocardial infarction and stroke

A

Type 2 diabetes mellitus

112
Q

What are the 10 chronic complications of diabetes mellitus?

A

Macrovascular disease
Microangiopathy
Renal disease
Hypertension
Neuropathy
Ocular
Ulceration/gangrene of feet
Skin/mucous membrane
Oral
Increased risk of infection

113
Q

Diabetes mellitus induces ___________ and a markedly increased predisposition to accelerated _____________ especially in the aorta and large- and medium-sized arteries

A

hypercholesterolemia; atherosclerosis

114
Q

T/F: Except for its greater severity and earlier age of onset, atherosclerosis in diabetics is
indistinguishable from that in non-diabetics

A

True

115
Q

The impact of cardiovascular disease in patients with diabetes mellitus can be gauged from the fact that it accounts for up to ____% of deaths in Type 2 diabetes mellitus

A

80%

116
Q

Diabetics have a 3 to 7.5 times greater incidence of death from __________ causes compared to the non-diabetic population

A

cardiovascular

117
Q

The incidence of myocardial infarction is _____ as high in diabetics as in non-diabetics

A

2x

118
Q

Patients with diabetes have an increased stroke _________ and _________ (primarily due to the accelerated development of cervical carotid artery atheromas)

A

incidence; severity

119
Q

What results in more severe brain injury and a poorer stroke outcome?

A

Hyperglycemia at time of stroke

120
Q

______ atherosclerosis and arteriolosclerosis also constitute part of the macrovascular disease seen in diabetics

A

Renal

121
Q

Microvascular disease caused by ________ changes results in multiple pathologic complications in people with diabetes mellitus

A

capillary

122
Q

A characteristic pattern of wall thickening of small arterioles and capillaries which causes narrowing of the lumen

A

Hyaline arteriosclerosis

123
Q

Widespread; responsible for ischemic changes in the kidney, retina, brain, and peripheral nerves, as well as the vascular lesion associated with hypertension

A

Hyaline arteriosclerosis

124
Q

One of the most consistent morphologic features of diabetes mellitus

A

Microangiopathy

125
Q

What is microangiopathy characterized by?

A

Diffuse thickening of basement membranes

126
Q

Most evident in the capillaries of the skin, skeletal muscle, retina, renal glomeruli, and renal medulla and underlies the development of diabetic nephropathy, retinopathy, and
some forms of neuropathy

A

Diffuse thickening of basement membranes (microangiopathy)

127
Q

Prime targets of diabetes mellitus

A

Kidneys

128
Q

Second to MI as cause of death from diabetes mellitus

A

Renal failure

129
Q

What are the 3 renal lesions seen in diabetes mellitus?

A

Glomerular
Renal vascular (nephrosclerosis)
Pyelonephritis

130
Q

In the kidneys, the characteristic pathologic changes in the glomerulus leads to what?

A

Diabetic nephropathy

131
Q

Where are these important lesions seen?

Capillary BM thickening
Diffuse mesangial sclerosis
Nodular glomerulosclerosis (Kimmelstiel-Wilson)

A

Glomerulus

132
Q

Increase in mesangial matrix associated with mesangial cell proliferation and basement membrane thickening

A

Diffuse mesangial sclerosis

133
Q

Pathognomonic glomerular lesion of DM characterized by ball-like deposits of a laminated matrix in the periphery of the glomerulus

A

Nodular glomerulosclerosis (Kimmelstiel-Wilson)

134
Q

What is diabetic nephropathy characterized by?

A

Persistent albuminuria

135
Q

Kidney excreting more albumin than normal in urine

A

Microalbuminuria

136
Q

Without specific interventions, ~ 80% of patients with T1DM and 20 - 40% of those with T2DM will develop overt _________________ with ______________over the ensuing 10 to 15 years, that is usually accompanied by a relentless decline in _______ and ___________

A

nephropathy w/ macroalbuminuria; GFR; hypertension

137
Q

Difference between microalbuminuria and macroalbuminuria

A

Micro: albumin excretion > 30 but < 300 mg/day

Macro: albumin excretion > 300 mg/day

138
Q

What is the leading cause of chronic renal failure in the US?

A

Diabetic nephropathy

139
Q

What is one of the most significant long-term complications in terms of morbidity and mortality for individual patients with DM?

A

Diabetic nephropathy

140
Q

Hyaline arteriolosclerosis affects both __________ and ________ renal arterioles in patients with DM

A

afferent; efferent

141
Q

An acute or chronic inflammation of the kidneys that usually begins in the interstitial tissue and then spreads to involve the tubules

A

Pyelonephritis

142
Q

One special pattern of acute pyelonephritis, __________ _________, is much more prevalent in diabetics than in non-diabetics

A

necrotizing papillitis

143
Q

What develops with progressive renal involvement?

A

Hypertension

144
Q

____________ and ____________ atherosclerosis is accelerated with hypertension in diabetes mellitus

A

Coronary; cerebral

145
Q

How many adult patients with diabetes mellitus have hypertension?

A

2/3

146
Q

What are the 2 types of diabetic neuropathies?

A

Peripheral (sensory)
Autonomic

147
Q

What are the 2 subtypes of peripheral (sensory) neuropathy?

A

Distal symmetric polyneuropathy
Isolated (peripheral) neuropathy

148
Q

Most common form of diabetic peripheral neuropathy

A

Distal symmetric polyneuropathy

149
Q

Type of neuropathy where defects in nerve function arise in a “stocking-glove” pattern

A

Distal symmetric polyneuropathy

150
Q

In distal symmetric polyneuropathy, sensory involvement usually occurs first and is generally bilateral, symmetric, and associated with dulled perception of __________, ________, and ________, particularly in the _________ extremities

A

vibration; pain; temp; lower

151
Q

Can result also result in hypersensitivity to light touch and occasionally severe “burning” pain and discomfort of the lower extremities, particularly at night; can become physically incapacitating and emotionally disabling

A

Distal symmetric polyneuropathy

152
Q

Long-term complications are insensitivity of the feet, leading to repeated “silent” trauma that predisposes to neuropathic plantar ulcers or bone deformities of the feet secondary to repeated “silent” fractures

A

Distal symmetric polyneuropathy

153
Q

What causes peripheral (sensory) neuropathy in people with diabetes mellitus?

A

Axonal degeneration
Segmental demyelination
Sorbitol accumulation

154
Q

This form of diabetic neuropathy has been attributed to vascular disease/ischemia in blood vessels supplying nerves or traumatic nerve damage

A

Isolated (peripheral) neuropathy

155
Q

Involvement of the distribution of only one nerve (“mononeuropathy”), or of several nerves (“mononeuropathy multiplex”) is characterized by sudden onset with subsequent recovery of all or most of the function

A

Isolated (peripheral) neuropathy

156
Q

Mononeuropathy involving cranial nerves affecting eye movement (III [oculomotor], IV [trochlear], or VI [abducens]) or peripheral nerves can occur

A

Isolated (peripheral) neuropathy

157
Q

What are the 3 clinical disturbances/manifestations of autonomic neuropathy?

A

Cardiovascular
GI
Genitourinary

158
Q

Which clinical disturbance/manifestation of autonomic neuropathy?

Orthostatic/postural hypotension
Tachycardia
Decreased HR variability

A

Cardiovascular

159
Q

Which clinical disturbance/manifestation of autonomic neuropathy?

Esophageal motility abnormalities
Bouts of diarrhea at night
Gastroparesis (decreased in T1DM; increased in T2DM)

A

GI

160
Q

Which clinical disturbance/manifestation of autonomic neuropathy?

Neurogenic bladder (hesitancy, weak stream, dribbling)
Impotence

A

Genitourinary

161
Q

What are the 3 ocular complications in diabetes?

A

Retinopathy
Cataracts
Glaucoma

162
Q

What are the 3 main categories of diabetic retinopathy?

A

Background/simple
Pre-proliferative
Proliferative/malignant

163
Q

Consisting of microaneurysms, hemorrhages,
exudates, and retinal edema

A

Background/simple retinopathy

164
Q

Arteriolar ischemia manifested as cotton-wool spots (small infarcted areas of retina)

A

Pre-proliferative retinopathy

165
Q

Consisting of newly formed vessels

A

Proliferative/malignant retinopathy

166
Q

A leading cause of blindness in the U.S., particularly since it increases the risk of retinal detachment

A

Proliferative/malignant retinopathy

167
Q

Up to 20% of patients with T2DM have
__________ at the time of diagnosis

A

retinopathy

168
Q

__________ ________ occur in diabetic patients and seem to correlate with both the duration of diabetes and the severity of chronic hyperglycemia

A

Premature cataracts

169
Q

What is twice as high in diabetic patients as in age-matched non-diabetic persons and may contribute to the premature occurrence of cataracts?

A

Non-enzymatic glycosylation of lens protein

170
Q

DM raises the risk of __________ glaucoma by ~ 36%

A

open-angle

171
Q

T/F: Closed-angle glaucoma does not have an increased risk associated with DM

A

True

172
Q

What is the leading cause of hospitalization in patients with DM?

A

Foot ulcers

173
Q

Why are patient symptoms with foot ulcers usually less than would be expected from clinical findings?

A

Loss of sensation due to peripheral neuropathy

174
Q

They are usually secondary to a combination of factors, including peripheral vascular insufficiency, repeated trauma (unrecognized because of sensory loss), and superimposed
infection

A

Foot ulcers

175
Q

First step to gangrene and lower extremity
amputation

A

Foot ulcer

176
Q

What has greatly reduced the frequency of gangrene of the foot?

A

Prophylactic foot care

177
Q

Plaque-like reddened areas with a central area
that fades to white-yellow, found on the anterior surfaces of the legs

A

Necrobiosis lipoidica diabeticorum

178
Q

The skin becomes very thin and can ulcerate easily

A

Necrobiosis lipoidica diabeticorum

179
Q

Thickening of skin and epidermis giving skin a “leather-like texture”

A

Scleroderma diabeticorum

180
Q

Typically affects patient with T2DM, mainly on upper back and neck

A

Scleroderma diabeticorum

181
Q

When scleroderma diabeticorum affects the fingers, hands or toes it is sometimes called what?

A

Digital sclerosis

182
Q

The skin on toes fingers and hands become waxy, thick, and tight, with joint stiffness

A

Digital sclerosis

183
Q

A chronic, blistering disease that causes an extremely pruritic rash typically seen on the buttocks and the extensor surfaces of the arms and legs that is most frequently associated with associated with gluten-sensitive enteropathy (celiac disease), but is also seen in some patients with T1DM

A

Dermatitis herpetiformis

184
Q

Associated both T1DM and T2DM and affects skin coloration due to autoimmune reaction to pigmentation

A

Vitiligo

185
Q

The skin in the axilla, groin, and back of neck is hyperpigmented and hyperkeratotic with a typically dark and velvety appearance

A

Acanthosis nigricans

186
Q

It is thought to be associated with significant insulin resistance

A

Acanthosis nigricans

187
Q

Most common cutaneous finding in DM and affects ~50% of diabetics

A

Diabetic dermopathy

188
Q

Presents as shiny round or oval reddish-brown lesions on thin skin of the lower extremity, also known as “shin spots”; usually not painful and do not require tx

A

Diabetic dermopathy

189
Q

Associated with uncontrolled blood sugars and extremely high triglycerides

A

Eruptive xanthomatosis

190
Q

High risk for pancreatitis in patients w/ this finding

A

Eruptive xanthomatosis

191
Q

Can produce erythema and edema of intertriginous areas below the breasts, in the axillas, and between the fingers

A

Candidal skin infections

192
Q

Causes candidal vulvovaginitis in most chronically uncontrolled diabetic women with persistent glucosuria and is a frequent cause
of pruritus

A

Candidal skin infections

193
Q

Name the oral complications of poorly controlled DM

A

Xerostomia
Bacterial, viral, fungal infection
Poor wound healing
Increased incidence/severity of caries
Gingivitis and perio
Abscesses
Burning mouth/tongue

194
Q

Oral findings in patients with uncontrolled DM most likely relate to excessive loss of _______ through urination, altered response to infection, ____________ changes, and possibly, increased _________ concentrations in saliva

A

fluids; microvascular; glucose

195
Q

Why do patients with DM get dry mouth/xerostomia?

A

Increased urine -> decreased extracellular fluid -> decreased saliva secretion

196
Q

What levels are low in the saliva of a person with DM?

A

Ca2+
Phosphate
Fluoride

197
Q

What levels are high in the saliva of a person with DM?

A

Glucose

198
Q

T/F: Adults with uncontrolled DM have more severe manifestations of periodontal disease than do adults without diabetes

A

True

199
Q

What type of DM is perio associated with?

A

Both Type 1 and Type 2

200
Q

What oral lesions are more common in patients with DM?

A

Candidiasis
Traumatic ulcers
Lichen planus
Delayed healing

201
Q

What type of DM are oral lesions associated with?

A

Type 1

202
Q

May lead to oral symptoms of paresthesias and tingling, numbness, burning, or pain caused by pathologic changes involving nerves in the oral region

A

Diabetic neuropathy

203
Q

Abnormal elevation of what can decrease immune function via effect on neutrophil activity, phagocytosis, immunoglobulin, complement function, antigen presentation by monocytes, intercellular adhesion molecules, cytokines, nitric oxide-mediated microvascular relaxation, neutrophil/monocyte sequestration, and generation of oxygen free radicals?

A

Blood and tissue glucose concentration

204
Q

Patients with DM exhibit enhanced susceptibility to infections. Name a few.

A

Skin infections
TB
Pneumonia
Pyelonephritis

205
Q

An autoimmune disease in which destruction of pancreatic beta-cells in the islets of Langerhans in the pancreas are caused primarily by immune effector cells reacting against endogenous beta-cell antigens

A

Type 1 DM

206
Q

In Type 1 DM, after 80 - 90% of the beta-cells are destroyed, ___________ develops and diabetes may be diagnosed

A

hyperglycemia

207
Q

What do patients with Type 1 DM need to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia, and normalize lipid and protein metabolism?

A

Exogenous insulin

208
Q

What is the major factor in the pathophysiology of Type 1 DM?

A

Autoimmunity

209
Q

In Type 1 DM, certain _______ ___________ may stimulate the production of antibodies against a viral protein that trigger an autoimmune response against antigenically similar beta-cell molecules

A

viral infections (mumps, rubella, coxsackie B)

210
Q

Approximately 85% of Type 1 DM patients have circulating ________ _____ ___________, and the
majority also have detectable ____________ ______________ before receiving insulin therapy

A

islet cell antibodies; anti-insulin antibodies

211
Q

The most commonly found islet cell antibodies in Type 1 DM are those direct against what?

A

Glutamic acid decarboxylase

212
Q

Enzyme found within pancreatic beta-cells

A

Glutamic acid decarboxylase

213
Q

The prevalence of Type 1 DM is increased in patients with other autoimmune diseases, such as…

A

Graves disease
Hashimoto thyroiditis
Addison disease

214
Q

A higher prevalence of islet cell antibodies and anti-GAD antibodies have been found in patients with what autoimmune disease?

A

Hashimoto thyroiditis

215
Q

What are the major genetic determinants of Type 1 DM?

A

Polymorphisms of class II human leukocyte antigen (HLA) genes that encode DR/DQ

216
Q

Approximately 95% of patients with T1DM have which genetic polymorphism?

A

HLA-DR3 or HLA-DR4

217
Q

Are heterozygotes or homozygotes at a greater risk for Type 1 DM?

A

Herterozygotes

218
Q

What is a specific marker of Type 1 DM susceptibility?

A

HLA-DQs

219
Q

T/F: Some haplotypes confer strong protection against Type 1 DM

A

True! (ex: HLA-DR2)

220
Q

Which type of DM is a heterogeneous and multifactorial complex disease that involves interactions of genetics, environmental risk factors, and inflammation?

A

Type 2

221
Q

What are the 2 defects that best characterize Type 2 DM?

A

Insulin resistance
Beta-cell dysfunction -> inadequate insulin secretion

222
Q

What must exist for Type 2 DM to occur?

A

Insulin resistance and inadequate insulin secretion

223
Q

In the progression from normal to abnormal glucose tolerance in Type 2 DM, what levels increase first?

A

Postprandial blood glucose

224
Q

What response is unaltered during the induction of insulin resistance in Type 2 DM?

A

Postprandial glucagonlike peptide-1 (GLP-1)

225
Q

What levels are increased during the induction of insulin resistance and glucose intolerance in Type 2 DM?

A

Glucagon
Glucose-dependent insulinotropic polypeptide GIP)

226
Q

Insulin resistance has been attributed to increased levels of what 2 things in plasma?

A

Free fatty acids
Proinflammatory cytokines

227
Q

What does insulin resistance lead to in muscle cells?

A

Decreased glucose transport

228
Q

What does insulin resistance lead to in the liver?

A

Increased glucose produciton

229
Q

What does insulin resistance lead to in fat cells?

A

Increased breakdown

230
Q

What is an essential component in the development of Type 2 DM and does not necessarily follow the stage of insulin resistance?

A

Beta-cell dysfunction

231
Q

Beta-cell function actually ___________ early in the disease process in most patients with T2DM, mainly as a _____________ measure to counter insulin resistance and maintain euglycemia

A

increases; compensatory

232
Q

What is present in approximately 80-90% of T2DM patients at the time of diagnosis?

A

Obesity

233
Q

What is a major risk factor for development of T2DM?

A

Obesity

234
Q

What is the most important environmental factor causing insulin resistance?

A

Obesity

235
Q

____________ plays an important role in the pathophysiology of T2DM, wherein there is an pancreatic islet cell dysfunction in the which the reciprocal relationship between the glucagon-secreting alpha-cells and the insulin-secreting beta-cells is lost

A

Hyperglucagonemia

236
Q

What does hyperglucagonemia lead to?

A

Hyperglycemia

237
Q

Genome-wide association studies of single-nucleotide polymorphisms (SNPs) have
identified a number of genetic variants that are associated with what 2 things?

A

Beta-cell function
Insulin resistance

238
Q

What appear to increase the risk for T2DM?

A

Some SNPs
Over 40 independent loci

239
Q

Susceptibility to T2DM may also be affected by _________ variants involving ________ hormones, which are released from endocrine cells in the gut and stimulate insulin secretion in response to digestion of food

A

genetic; incretin

240
Q

A syndrome of insulin resistance that has been proposed to explain the frequent association of hypertension, insulin resistance, abdominal obesity, hyperlipidemia, and accelerated atherosclerosis

A

Metabolic syndrome

241
Q

Pts with what syndrome are at a high risk for development of T2DM?

A

Metabolic syndrome

242
Q

What are the 3 important morphologic changes that present in the pancreas?

A

Reduced number and size of islets
Leukocytic infiltrates in islets
Amyloid deposition within islets

243
Q

Which morphologic change in the pancreas?

This change most often is seen in T1DM,
particularly with rapidly advancing disease

A

Reduced number and size of islets

244
Q

Which morphologic change in the pancreas?

Principally composed of T-lymphocytes

A

Leukocytic infiltrates in islets

245
Q

Which morphologic change in the pancreas?

Most often seen T1DM at the time of clinical presentation

A

Leukocytic infiltrates in islets

246
Q

Which morphologic change in the pancreas?

Begins in and around capillaries and between
cells

A

Amyloid deposition within islets

247
Q

Which morphologic change in the pancreas?

At advanced stages, the islets may be virtually obliterated; fibrosis also may be observed

A

Amyloid deposition within islets

248
Q

Which morphologic change in the pancreas?

Similar amyloid lesions may be found in older non-diabetics, apparently as part of normal aging

A

Amyloid deposition within islets

249
Q

Which morphologic change in the pancreas?

More often seen in T2DM

A

Amyloid deposition within islets

250
Q

What is the type of amyloid associated with T2DM?

A

Islet amyloid polypeptide

251
Q

What is co-secreted with insulin from pancreatic beta-cells in the ratio of approximately 100:1?

A

Islet amyloid polypeptide

252
Q

What is the precursor of islet amyloid polypeptide?

A

Pro-islet amyloid polypeptide

253
Q

What 2 things have been linked to T2DM and loss of islet beta-cells

A

Islet amyloid polypeptide
Pro-islet amyloid polypeptide