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FDN Week 5 (Block 2) > Diabetes, Peripheral Neuropathy and Metabolic Syndrome > Flashcards

Diabetes, Peripheral Neuropathy and Metabolic Syndrome Flashcards

1
Q

Polyuria

A

Excessive urination

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2
Q

Polydipsia

A

Excessive thirst

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3
Q

Nocturia

A

Urination at night

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4
Q

What does diminished foot arterial pulse indicate?

A

Possible peripheral vascular disease

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5
Q

Why might you order a fasting blood glucose?

A

If you have a peripheral neuropathy, high BMI we need to exclude diabetes.

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6
Q

How do we diagnose diabetes on one visit?

A

Patient presents with ketoacidosis, hyperglycemia, plasma glucose of >200mg/dl

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7
Q

What is the reference interval for glucose?

A

60-99mg/dl

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8
Q

What if we don’t have all the symptoms of diabetes we can only diagnose when?

A

On two separate visits when glucose is >126 fasting, >200 OGTT, >6.5 A1c

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9
Q

HHS?

A

More likely in DMT2, poorly controlled, hyperglycemia and hyperosmolality.

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10
Q

Why do T2DM patient not usually experience ketoacidosis?

A

Even thought they are insulin resistant they produce enough to avoid ketosis.

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11
Q

OGTT?

A

Measure fasting plasma glucose, administer glucose, measure 2 hours later.

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12
Q

What amount of glucose should we use in children and adults for OGTT

A

75mg for adults, weight dependent in children

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13
Q

A1c?

A

A glucose that is added nonenzymatically to hemoglobin - this is glycated hemoglobin. High A1c >6.5 indicates diabetes.

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14
Q

Hemoglobin A1c is an indicator of systemic glycation. What are the physiological effects?

A

When the retina leaks protein it can cause blindness. When in the kidney it is a marker of kidney failure.

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15
Q

With only hyperglycemia on one occasion we can’t diagnose diabetes. How many visits does it take?

A

2 visits with hyperglycemia can lead to a diagnosis of?

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16
Q

What defines elevated glucose but not hyperglycemia?

A

Impaired fasting glucose

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17
Q

What are borderline measurements for predicting increased risk of diabetes?

A

IFG, IGT, A1c predict increased risk.

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18
Q

What is IFG, IGT and borderline A1c called?

A

prediabetes (not diagnosis but description)

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19
Q

IFG

A

Impaired Fasting Glucose

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20
Q

IGT

A

Impaired Glucose Tolerance

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21
Q

What is indicated in pre diabetes?

A

More frequent visits, diet, exercise can reduce risk by 60%

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22
Q

What are symptoms for DMT2?

A

Middle aged, obese, minority, mild hyperglycemia, no ketosis

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23
Q

If a patient presented with complications of diabetes should we test further?

A

Yes, A1c, OGTT, IFG

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24
Q

What percentage of DMT2 patients present with complications?

A

15%

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25
Q

Macrovascular disease (what three vessels)?

A

Coronary artery, Carotid artery, peripheral arteries.

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26
Q

Microvascular disease (what are the manifestations) ?

A

Kidney and eye problems. Neuropathy.

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27
Q

Neuropothy (What are the manifestations)?

A

Peripheral = loss of sensation, glove and sock sensation. Debilitation pain, loss of position sense. Mononeuropathy = Cranial nerve infarction. Autnomic = GUT problems leading to diarrhea, impotence.

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28
Q

TIA?

A

Transient ischemic attack (thrombosis that doesn’t lead to stroke)

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29
Q

Claudication?

A

Pain, fatigue and tiredness in the extremities.

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30
Q

Postural hypertension?

A

Dizziness upon standing - this is due to neuropathy in the autonomic nervous system

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31
Q

What are the causes of complications in diabetes?

A

CVD, retinopathy, nephropathy, neuropathy

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32
Q

What are the risk factors of diabetes?

A

Male, age, hyperlipidemia, hypertension, smoking, obesity

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33
Q

What does hyperglycemia cause?

A

Retinopathy, Nephropathy, Neuropathy

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34
Q

What factors other than hyperglycemia cause nephropathy?

A

Hypertension, familiar diabetic neuropathy, hyperlipidemia

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35
Q

Why does pregnancy increase risks?

A

Growth factors increase vascular growth, increased need for C-Section, increased hypertension and pre-eclampsia

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36
Q

What the increased risk for unborn babies when the mother has diabetes?

A 
Congenital malformations
Fetal Death Inutero
Premature birth
NICU
Hypercalcemia
Hyperbilirubinemia
DMT2 in adulthood
LGA - large for gestation age.
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37
Q

In the first trimester hyperglycemia is a?

A

Teratogen

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38
Q

Dystocia

A

pelvic / cephalo disproportionality

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39
Q

What is the most common cause of death in DMT1?

A

CVD and Renal failure (renal failure has longer to develop)

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40
Q

What is the most common cause of death in DMT2?

A

CVD

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41
Q

What are common secondary causes of hypertension?

A

< 5% of hypertension causes Renal failure, hyperaldosterone

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42
Q

Nephrothapy can be caused by?

A

Diabetes and hypertension

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43
Q

What is small amounts of albumin in the urine an early sign of?

A

Glomerular and endothelial disfunction. THis is a way of evaluating the kidney in someone with diabetes.

44
Q

What is the source of energy in the shortterm in muscle?

A

Creatine phosphate even before or along with ATP

45
Q

How do we test for CVD in a person with diabetes?

A

Lipid panel

46
Q

How do we prevent the complication of diabetes?

A

Good glycemic control. It decreases complications by 50%

47
Q

Etiology of DMT2

A

–> Insulin resistance –>Obesity

48
Q

How does insulin resistance cause hypertension?

A

Na+ Retention
Vasoconstriction (sympathetic tone)
Hypertrophy of vascularity (insulin as growth factor)
Increased Na/K ATPase pump

49
Q

What are the consequences of hyperinsulinism? DMT2

A 
Atherosclerosis
Hypertension
Hypercoagulability
Hyperandrogenism
Hyperuricemia (GOUT)
Acanthosis Nigricans
50
Q

The consequences of inadequate insulinization?

A

Dysglycemia
Dyslipidemia
Nonalcoholic liver disease

51
Q

hyperinsulinism –> insulin resistance =

A

metabolic syndrome

52
Q

What is metabolic syndrome known as?

A

Insulin resistance syndrome

Dysmetabolic Syndrome X

53
Q

What are the characteristics of central obesity?

A

increased circumference
Waste to hip ration
Subcutaneous and visceral fat distribution

54
Q

What fat has the greatest effect on insulin resistance?

A

Visceral fat (hence liposuction doesn’t help)

55
Q

Why is visceral fat more of an impact on insulin resistance?

A

It drains directly into portal drainage and into the liver.

56
Q

How does obesity cause insulin resistance?

A

(1) Increased FFA deposition in liver, muscle and beta cell causes insulin resistance.
(2) Fat throughout the muscle causes increased TNF-alpha and insulin resistance in muscle.
(3) Cortisol increase can cause obesity.

57
Q

ApoB + Insulin =

A

risk increases 11x

58
Q

High ApoB =

A

High LDL

59
Q

Increased glucose –>?

A

(1) Increased inflammation –> fibrinogen –> Fibrin –> Procoagulant
(2) Adipose cells release plasminogen-activator inhibitor
(3) When tissues are injured they release tissue plasminogen activator which is responsible for forming plasmin which breaks down fibrin and break up thrombins.
(4) if we deactivate PAI we turn off the breakdown of clots.

60
Q

Hyperandrogenism pathogenesis?

A

insulin resistance –> hyperinsulinism –> FSH –>LH –> Androgens

61
Q

What are the consequences of Hyperandrogenism?

A

Hirsutism
Polycystic ovary
Dyslipidemia (high amount of lipids in blood)
Hypertension

62
Q

Hyperuricemia (GOUT)

A

Hyperinsulemia –> Increased PCT reabsorbtion of Na+ and decreased uric acid secretion.

63
Q

Acanthosis Nigricans?

A

Thickening, darkening and benign skin in folds

64
Q

What are the consequences of inadequate insulination (not enough insulin action)

A

Dysglycemia
Dyslipidemia
Nonalcoholic liver disease

65
Q

What kind of dyslipidemia is seen in MS

A

Low HDL
Dense LDL
Increased TAG and VLDL
Increased ApoB –> Increased VLDL –>Dense LDL

66
Q

What does a macrophage grab ApoB lipoprotein?

A

It binds to the LD receptor

67
Q

What is non-alcoholic liver disease?

A

Increased FFA delivery to liver

This is due to higher quantities of lipid in the blood.

68
Q

What percentage of adults have MS?

A

25% (and 4% of adolescents)

69
Q

What is the underlying pathophysiology of DMT2?

A

(1) Insulin concentration (2) Tissue sensitivity to insulin. Initial lesion = Insuline resistance, Later lesion = Reduced insulin secretion.

70
Q

Chronic hyperglycemia does what to beta cells?

A

It damages them and reduces insulin secretion.

71
Q

What are the best nonpharmacological ways to manage DMT2?

A

exercise, reduced sugar and carbs in diet, weight loss

72
Q

What drugs stimulate endogenous insulin production?

A

sulfonylureas, Meglitinidines,

73
Q

What drugs stimulate Incretin production?

A

Exenatide

74
Q

What drugs reduces DPP-4?

A

Sitagliptin, Linagliptin

75
Q

What does reduction of DPP-4 do?

A

It inhibits the breakdown of incretin so continued improved insulin release.

76
Q

What are the endogenous incretins?

A

Glucagon-like Peptide (GLP) and Gastric inhibitory polypeptide (GIP)

77
Q

Can insulin be used in treatment of DMT2

A

Remember [insulin] X tissue sensitivity

78
Q

What do thiazolidinediones do?

A

They bind to nuclear receptors and increases insulin resistance by inhibiting transcription of a gene that decreases insulin resistance.

79
Q

How does metformin work?

A

Reduces hepatic output of glucose

80
Q

How does amylin work?

A

Reduces / slows gastric emptying

81
Q

What are the sources of amino acids?

A

Dietary proteins and endogenous (within cells) protein turnover.

82
Q

How do we get nonessential AA’s

A

Via De Novo AA synthesis

83
Q

What are non-protein AA derivatives?

A

Neurotransmitters etc.

84
Q

What are the essential AA’s (ones we must eat)

A

PVT TIM HiLL

85
Q

What are conditionally essential AA’s?

A

They are AA’s we can make if we have enough of the essential AA precursors

86
Q

What enzyme breaks proteins in the stomach?

A

Pepsin

87
Q

What enzymes break proteins in the intestinal lumen?

A

Trypsin and Chymotrypsin

88
Q

What does carboxypeptidase do?

A

Breaks peptides into AA’s

89
Q

How do we get AA’s into the cell?

A

Via a Na+ dependent transporter that is a symporter (secondary active transporter).

90
Q

How is the Na+ Dependent transport powered?

A

By the Na+ / K+ gradient created by the Na+ / K+ ATPAse pump.

91
Q

What is excreted in excess when Gout is present?

A

Uric Acid

92
Q

What are the two pathways for degrading proteins?

A

(1) Acid degradation of protein in lysosome or phagolysosomes
(2) Ubiquitin dependent pathways via proteosomes

93
Q

What are the two nitrogen balances we need to consider?

A

(1) Positive and (2) negative

94
Q

Why do we need positive negative balance?

A

For growing children
Pregnancy
Wound Healing
Recovering adult

95
Q

What are the results of negative balance?

A

Starvation
Malnutrition
Disease

96
Q

What type of AA’s must be consumed?

A

Essential AA’s - the can’t be made de novo

97
Q

What does AA’s in urine mean?

A

It is a sign of illness

98
Q

What is the chief purpose of the urea cycle?

A

To remove excess nitrogen and formation of arginine.

99
Q

What is the purpose of transamination?

A

It is a way to transfer of alpha-amino groups from amino acids to form alpha-keto acids and vice versa. This is a way to form one AA from another.

100
Q

What four amino acids are not transaminated?

A

Proline, hydroxyproline, lysine, threonine

101
Q

What happens with a deficiency of B6 vitamins?

A

You impair transamination and also the production of neurotransmitters.

102
Q

How is GDH regulated?

A

Via allosteric control by ATP and ADP

103
Q

How does ATP regulate GDH?

A

Reduces rate of AA oxidation

104
Q

How does ADP regulate GDH?

A

Stimulates: and glutamate synthesis is increased

105
Q

How does D-Amino Acid Oxidase protect against bacteria?

A

Bacteria requires D-AA for cell walls.

FDN Week 5 (Block 2) (10 decks)

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