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Integrative Nutrition and Pathophysiology > Diabetes 2 > Flashcards

Diabetes 2 Flashcards

1
Q

type 1 diabetes pathophys

A

Results from an autoimmune process that destroys the pancreatic islet cells leaving inadequate levels of insulin production (insulin deficiency)

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2
Q

type 2 diabetes pathogeneis is __
a combo of

A

Pathogenesis is multifactorial, a combination of genetic and environmental conditions

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3
Q

type 2 diabetes leads to
1. defective __ secretion from __ dysfunction leading to relative __
2. __ resistance
3. increased __ production by the liver

A

type 2 diabetes leads to
1. defective insulin secretion from beta-cell dysfunction leading to relative hypoinsulinemia
2. insulin resistance
3. increased glucose production by the liver

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4
Q

3 acute complications of diabetes

A
  1. DKA
  2. HHS
  3. Hypoglycemia
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5
Q

DKA is an __ complication of diabetes characterized by absolute or relative __

A

DKA is an acute complication of diabetes characterized by absolute or relative insulin deficiency

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6
Q

which type is DKA more common in

A

T1DM (but it happens in both)

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7
Q

DKA characterized by

A

biochemical triad

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8
Q

biochemical triad for DKA

A
  1. hyperglycemia
  2. ketonemia: positive serum or urine ketones
  3. anion gap metabolic acidosis
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9
Q

anion gap metabolic acidosis values

A

anion gap > 10
pH < 7.3
serum bicarbonate < 18 mEq/L

Anion Gap Calculation: Sodium-(Chloride + HCO3)

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10
Q

clinical presentation of DKA

A
  1. rapidly evolving (seen within 24-hour period)
  2. hyperglycemia
  3. dehydration
  4. acidosis
  5. hyperosmolarity
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11
Q

causes of DKA

A
  1. forgetting insulin
  2. acute stressors
  3. infection
  4. new onset T1DM
  5. drugs
  6. GI illness
  7. other: MI, CVA, pregnancy
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12
Q

DKA: insulin deficiency leads to __ and a perceived __ state, indirectly activating __ and __

A

DKA: insulin deficiency leads to hyperglycemia and a perceived fasting state, indirectly activating lipolysis and ketogenesis

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13
Q

DKA: counterregulatory hormones promote __, __, and __ which lead to __ and __

A

DKA: counterregulatory hormones promote glycogenolysis, gluconeogenesis, and lipolysis which lead to hyperglycemia and ketogenesis

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14
Q

DKA dehydration

A

Hyperglycemiainduced osmotic diuresis leads to electrolyte loss, decreased glomerular filtration and worsens hyperglycemia

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15
Q

DKA hormone imbalance: too much __
too little (4)

A

DKA hormone imbalance: too much insulin
too little glucagon, cortisol, atecholamines, growth hormone

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16
Q

ways to measure ketone production

A
  1. 3-beta-hydroxybutyrate in blood
  2. acetoacetate in urine
  3. acetone released in lungs (fruity breath)
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17
Q

hyperosmolar hyperglycemic state (HHS) is when you have low or no

A

ketones

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18
Q

HHS characterized by

A

severe hyperglycemia, hyperosmolarity, and dehydration in the absence of significant ketoacidosis

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19
Q

HHS has no (which symptom)

A

ketoacidosis

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20
Q

clinical presentation of HHS resembles __ but is __ severe and takes __ to develop

A

clinical presentation of HHS resembles DKA but is more severe and takes longer to develop

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21
Q

lab findings for HHS

A

Hyperglycemia: typically above 600mg/dl
Hyperosmolarity: serum osmolality > 320 mOsmol/kg
Serum pH >7.3
Absent to mildly elevated ketones

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22
Q

pathophys of HHS
__ deficiency
__regulation of counter-regulatory hormones
__ ketone production
dehydration

A

pathophys of HHS
insulin deficiency
upregulation of counter-regulatory hormones
limited ketone production
dehydration

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23
Q

goal of DKA/HHS treatment

A
  1. Restore intravascular volume with IVF
  2. Correct electrolyte abnormalities
  3. Correct hyperglycemia and acidosis with insulin therapy
  4. Identify and treat any precipitating factors
  5. Provide patient and family education to prevent future recurrent episodes of DKA/HHS
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24
Q

clinical hypoglycemia

A

is a plasma (or serum) glucose concentration low enough to cause symptoms and/or signs, including impairment of brain function.

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25
Q

lower limit of normal fasting glucose:
hypoglycemia symptoms occur at:

A

lower limit of normal fasting glucose: 70 mg/dL
hypoglycemia symptoms occur at: < 55 mg/dL

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26
Q

hypoglycemia can be caused by too much __ or __, too little __, or excessive __

A

hypoglycemia can be caused by too much insulin or oral anti-hyperglycemic agents, too little food, or excessive excessive PA

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27
Q

hypoglycemia is confirmed by __ triad

A

hypoglycemia is confirmed by Whipple’s triad

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28
Q

Whipple’s Triad

A
  1. Symptoms, signs or both consistent with hypoglycemia
  2. Low plasma glucose concentration
  3. Resolution of symptoms/signs after the plasma glucose is raised
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29
Q

hypoglycemia symptoms and signs

A

Autonomic Symptoms (adrenergic): palpitations, tremor, anxiety
Neuroglycopenic symptoms (glucose deprivation in the brain): dizziness, confusion, weakness

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30
Q

why is hypoglycemia so concerning?

A

brain can’t synthesize glucose, so it needs a continuous supply from circulation

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31
Q

counter-regulatory systems to prvent and rapidly correct hypoglycemia

A

Decrease insulin secretion
Increase glucagon secretion ->glycogen breakdown in the liver
Increase epinephrine secretion ->increases hepatic glucose production
Increase cortisol and GH secretion -> enhance hepatic glucose production, increase insulin resistance

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32
Q

hypoglycemia is corrected with __ grams of __

A

hypoglycemia is corrected with 15 grams of fast acting concentrated carbohydrate

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33
Q

hyperglycemia can lead to

A

diabetic tissue damage

34
Q

mechanisms that lead to diabetic tissue damage in hyperglycemia

A

Activation of the polyol pathway
Glycation (AGE’s)
Protein kinase C activation
Increased hexosamine pathway

35
Q

hyperglycemia increases flux through the __ pathway

A

hyperglycemia increases flux through the polyol pathway

36
Q

hyperglycemia and polyol pathway

A

Glucose is normally phosphorylated by the enzyme hexokinase
Hyperglycemia saturates hexokinase → we push to polyol pathway

37
Q

polyol pathway leads to reduced levels of __ and __ –> reduced __ synthesis and increased risk for __ and __

A

polyol pathway leads to reduced levels of NADPH and NAD+ –> reduced glutathione synthesis and increased risk for oxidative stress and damage

38
Q

hyperglycemia leads to the __ complications observed in diabetes

A

hyperglycemia leads to the microvascular complications observed in diabetes

39
Q

other factors such as __ and __ contribute to tissue damage

A

other factors such as genetic determinants and HTN contribute to tissue damage

40
Q

microvascular vs. macrovascular complication

A

Microvascular complications: effect small vessels of body (main focus of today)
Macrovascular complications: large vessels of the body

41
Q

chronic complications of DM

A
  1. microvascular
  2. macrovascular
  3. blindness
  4. kidney damage
  5. nerve damage
  6. amputation
  7. CVD (stroke, heart attack, loss of circulation in arms and legs)
42
Q

diabetic retinopathy is when diabetes causes damage to

A

the capillary endothelial cells of the retina

43
Q

most common DM complication

A

retinopathy

44
Q

main cause of blindness in middle age persons in industrialized nations

A

diabetic retinopathy

45
Q

3 classifications of diabetic retinopathy

A
  1. non-proliferative
  2. proliferative
  3. macular edema
46
Q

non-proliferative diabetic reitnopathy

A

aka background
absence of abnormal new blood vessels
Mild Moderate Severe

47
Q

proliferative diabetic retinopathy

A

presence of abnormal new blood vessels
Mild Moderate Severe

48
Q

macular edema diabetic retinopathy

A

retinal thickening and edema of the macula
Can occur at any stage of diabetic retinopathy

49
Q

characteristics of nonproliferative diabetic retinopathy

A

Exudates: cholesterol deposits in eye
Hemorrhage: bleeding in eye
Microaneurysms: can bleed into eye

50
Q

characteristics of proliferative diabetic retinopathy

A

neurovascularization

51
Q

risk factors for progression of retinopathy

A

Poor glycemic control
Longer duration of DM
Baseline severity
Pre-pubertal onset of Type 1 DM
Pregnancy → additional estrogen is a problem
Sudden improvement in glucose control
HTN
Smoking
Dyslipidemia

52
Q

3 retinopathy treatment options

A
  1. meds
  2. photocoagulation (laser)
  3. vitrectomy
53
Q

meds to treat retinopathy

A

Vascular endothelial growth factor inhibitors are injected into the vitreous eye.
Help stop growth of new blood vessels and decrease fluid build-up

54
Q

photocoagulation to treat retinopathy

A

Burning the blood vessels leads to shrinkage and scar formation
Can stop or slow leakage of blood and fluid in the eye

55
Q

vitrectomy for diabetic retinopathy

A

Tiny incisions are made in the eye to remove blood from the middle of the eye (vitreous)

56
Q

diabetic neuropathy prevalence

A

30%

57
Q

diabetic neuropathy prevalence increases with __ and disease __

A

diabetic neuropathy prevalence increases with age and disease duration

58
Q

other factors contributing to diabetic neuropathy

A

smoking
poor glycemic control

59
Q

clinical symptoms of diabetic neuropathy

A

Distal Symmetrical Polyneuropathies
Autonomic
Radiculopathies (Thoracic and Lumbar)
Micro Neuropathies
Cranial neuropathy
Limb mononeuropathy

60
Q

diabetic nephropathy prevalence

A

T1DM 25-40%
T2 DM 5-40%

61
Q

leading cause of end stage renal disease

A

diabetic nephropathy

62
Q

risk factors fo diabetic nephropathy

A

Poor glycemic control
Genetic susceptibility
HTN
Smoking
Dyslipidemia

63
Q

how to monitor diabetic nephropathy

A

urine protein to characterize degree of progression

64
Q

early phase diabetic nephropathy

A

Hyperfiltration
↑ GFR: from afferent arteriole dilation»>efferent arteriole dilation
↑ Glomerular Pressure
Thickened GBM and mesangial expansion

65
Q

microalbuminuria

A

Dysfunction of the Glomerular Filtration Barrier: podocyte and endothelial damage
Damage may be reversible

66
Q

macroalbuminuria

A

Decreased GFR
↑ BP

67
Q

end stage renal disease

A

Uremia
HD/renal transplant

68
Q

how to prevent diabetic nephropathy

A

yearly screening for urine albumin excretion rate
lifestyle modifications
tight glucose control
hypertension control

69
Q

most common diabetic neurpathy

A

distal symmetric polyneuropathy

70
Q

distal symmetric polyneuropathy

A

Affects 10-50% of patients with DM
Predominantly sensory
“stocking/glove distribution” → hands and feet
Large or small fibers

71
Q

small fiber sensory neuropathy

A

Small = Not covered in myelin
Typically send messages about illness and injury including pain, itch, and temperature discrimination
Pain
Autonomic small fibers also carry messages that control our internal organs
Assess function by testing temperature with a hot and cold test and sensation with a pinprick exam

72
Q

small neuropathy means

A

not covered in myelin

73
Q

large fiber sensory neuropathy

A

Large fiber sensory neuropathy
Thicker fibers covered in myelin
Loss of protective sensation
Loss of sense of position of different parts of the body (proprioception)
Poor balance
Decreased vibration sense
Decreased ankle reflex
May lead to callus, foot ulcers, Charcot foot, amputations

74
Q

how to test for large fiber sensory neuropathy

A

tuning fork
Hit fork, touch bony part of foot
If they say sensation in foot stops vibrating before tuning fork does, they’ve lost a bit of sensation

75
Q

Semmes-Weinstein monofilament

A

Patient closes eyes, touch them in 10 spots
Monofilament always exerts same amount of force
Failing this test is bad bc the patient can’t feel cuts or injuries on their feet (make sure they’re self checking)

76
Q

autonomic neuropathy

A

Affects the sympathetic and parasympathetic system
Responsible for a significant proportion of the morbidity and mortality associated with DM

77
Q

autnomic neuropathy involves which system

A

cardiovascular and GI

78
Q

macrovascular complications of diabetes

A

CVD
skin complications
insulin lipodystrophy

79
Q

acanthosis nigricans

A

Darkening of skin on neck

80
Q

insulin lipodystrophy

A

areas where insulin is injected have fat loss (lipoatrophy) or fibrofatty scar tissue (lipohypertrophy) at injection sites → important because insulin won’t work well if injected into scar tissues

81
Q

if insulin is injected into scarred areas,

A

absorption may be delayed

82
Q

how to prevent diabetes macrovascular complications

A

strict glycemic control

Integrative Nutrition and Pathophysiology (22 decks)

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