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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
lower limit of normal fasting glucose: hypoglycemia symptoms occur at:
lower limit of normal fasting glucose: 70 mg/dL hypoglycemia symptoms occur at: < 55 mg/dL
26
hypoglycemia can be caused by too much __ or __, too little __, or excessive __
hypoglycemia can be caused by too much **insulin** or **oral anti-hyperglycemic agents**, too little **food**, or excessive **excessive PA**
27
hypoglycemia is confirmed by __ triad
hypoglycemia is confirmed by **Whipple's** triad
28
Whipple's Triad
1. Symptoms, signs or both consistent with hypoglycemia 2. Low plasma glucose concentration 3. Resolution of symptoms/signs after the plasma glucose is raised
29
hypoglycemia symptoms and signs
Autonomic Symptoms (adrenergic): palpitations, tremor, anxiety Neuroglycopenic symptoms (glucose deprivation in the brain): dizziness, confusion, weakness
30
why is hypoglycemia so concerning?
brain can't synthesize glucose, so it needs a continuous supply from circulation
31
counter-regulatory systems to prvent and rapidly correct hypoglycemia
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
32
hypoglycemia is corrected with __ grams of __
hypoglycemia is corrected with **15** grams of **fast acting concentrated carbohydrate**
33
hyperglycemia can lead to
diabetic tissue damage
34
mechanisms that lead to diabetic tissue damage in hyperglycemia
Activation of the polyol pathway Glycation (AGE’s) Protein kinase C activation Increased hexosamine pathway
35
hyperglycemia increases flux through the __ pathway
hyperglycemia increases flux through the **polyol** pathway
36
hyperglycemia and polyol pathway
Glucose is normally phosphorylated by the enzyme hexokinase Hyperglycemia saturates hexokinase → we push to polyol pathway
37
polyol pathway leads to reduced levels of __ and __ --> reduced __ synthesis and increased risk for __ and __
polyol pathway leads to reduced levels of **NADPH** and **NAD+** --> reduced **glutathione** synthesis and increased risk for **oxidative stress** and **damage**
38
hyperglycemia leads to the __ complications observed in diabetes
hyperglycemia leads to the **microvascular** complications observed in diabetes
39
other factors such as __ and __ contribute to tissue damage
other factors such as **genetic determinants** and **HTN** contribute to tissue damage
40
microvascular vs. macrovascular complication
Microvascular complications: effect small vessels of body (main focus of today) Macrovascular complications: large vessels of the body
41
chronic complications of DM
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
diabetic retinopathy is when diabetes causes damage to
the capillary endothelial cells of the retina
43
most common DM complication
retinopathy
44
main cause of blindness in middle age persons in industrialized nations
diabetic retinopathy
45
3 classifications of diabetic retinopathy
1. non-proliferative 2. proliferative 3. macular edema
46
non-proliferative diabetic reitnopathy
aka background absence of abnormal new blood vessels Mild Moderate Severe
47
proliferative diabetic retinopathy
presence of abnormal new blood vessels Mild Moderate Severe
48
macular edema diabetic retinopathy
retinal thickening and edema of the macula Can occur at any stage of diabetic retinopathy
49
characteristics of nonproliferative diabetic retinopathy
Exudates: cholesterol deposits in eye Hemorrhage: bleeding in eye Microaneurysms: can bleed into eye
50
characteristics of proliferative diabetic retinopathy
neurovascularization
51
risk factors for progression of retinopathy
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
3 retinopathy treatment options
1. meds 2. photocoagulation (laser) 3. vitrectomy
53
meds to treat retinopathy
Vascular endothelial growth factor inhibitors are injected into the vitreous eye. Help stop growth of new blood vessels and decrease fluid build-up
54
photocoagulation to treat retinopathy
Burning the blood vessels leads to shrinkage and scar formation Can stop or slow leakage of blood and fluid in the eye
55
vitrectomy for diabetic retinopathy
Tiny incisions are made in the eye to remove blood from the middle of the eye (vitreous)
56
diabetic neuropathy prevalence
30%
57
diabetic neuropathy prevalence increases with __ and disease __
diabetic neuropathy prevalence increases with **age** and disease **duration**
58
other factors contributing to diabetic neuropathy
smoking poor glycemic control
59
clinical symptoms of diabetic neuropathy
Distal Symmetrical Polyneuropathies Autonomic Radiculopathies (Thoracic and Lumbar) Micro Neuropathies Cranial neuropathy Limb mononeuropathy
60
diabetic nephropathy prevalence
T1DM 25-40% T2 DM 5-40%
61
leading cause of end stage renal disease
diabetic nephropathy
62
risk factors fo diabetic nephropathy
Poor glycemic control Genetic susceptibility HTN Smoking Dyslipidemia
63
how to monitor diabetic nephropathy
urine protein to characterize degree of progression
64
early phase diabetic nephropathy
Hyperfiltration ↑ GFR: from afferent arteriole dilation>>>efferent arteriole dilation ↑ Glomerular Pressure Thickened GBM and mesangial expansion
65
microalbuminuria
Dysfunction of the Glomerular Filtration Barrier: podocyte and endothelial damage Damage may be reversible
66
macroalbuminuria
Decreased GFR ↑ BP
67
end stage renal disease
Uremia HD/renal transplant
68
how to prevent diabetic nephropathy
yearly screening for urine albumin excretion rate lifestyle modifications tight glucose control hypertension control
69
most common diabetic neurpathy
distal symmetric polyneuropathy
70
distal symmetric polyneuropathy
Affects 10-50% of patients with DM Predominantly sensory “stocking/glove distribution” → hands and feet Large or small fibers
71
small fiber sensory neuropathy
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
small neuropathy means
not covered in myelin
73
large fiber sensory neuropathy
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
how to test for large fiber sensory neuropathy
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
Semmes-Weinstein monofilament
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
autonomic neuropathy
Affects the sympathetic and parasympathetic system Responsible for a significant proportion of the morbidity and mortality associated with DM
77
autnomic neuropathy involves which system
cardiovascular and GI
78
macrovascular complications of diabetes
CVD skin complications insulin lipodystrophy
79
acanthosis nigricans
Darkening of skin on neck
80
insulin lipodystrophy
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
if insulin is injected into scarred areas,
absorption may be delayed
82
how to prevent diabetes macrovascular complications
strict glycemic control

Integrative Nutrition and Pathophysiology (22 decks)

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