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Endocrine Unit Phase 1 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What cells release insulin?

A

beta cells found in the islets of Langerhans of the endocrine portion of the pancreas

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2
Q

What type of disease is type 1 Diabetes Mellitus?

A

Type 4 Hypersensitivity Reaction where pancreatic islet cells undergo autoimmune destruction

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3
Q

What kills the beta cells of the pancreas in type 1 Diabetes Mellitus?

A

Type 4 Hypersensitivity, cell-mediated (CD8+ lymphocytes invade islets, target and kill beta cells) + autoAb against cells

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4
Q

What population is most affected by Type 1 DM?

A

Children

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5
Q

Is type 1 DM associated with genetic mutations? If so, which ones?

A

Mutations in HLA-DR3 and HLA-DR4

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6
Q

Is insulin treatment needed for type 1 DM?

A

Always

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7
Q

Is type 1 DM associated with obesity? Type 2?

A

Type 1, no, then to be thin. Type 2 usually associated with obesity

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8
Q

Is there a genetic predisposition associated with Type 1 and 2 DM? If so, is it weak or strong? How many genes are involved?

A

Yes
Type 1 = weak predisposition, polygenic
Type 2 = strong predisposition, polygenic

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9
Q

Is type 2 DM associated with genetic mutations? If so, which ones?

A

No

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10
Q

What is the glucose intolerance for type 1 diabetes? Type 2? (mild-moderate-severe)

A

Type 1 = severe

Type 2 = mild to moderate

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11
Q

Is insulin treatment needed for type 2 diabetes?

A

Sometimes

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12
Q

What is the pathophysiology of Type 2 DM?

A

insulin resistance (cells cannot properly respond to insulin) + decreased insulin secretion (endocrine pancreas deficient, cannot raise insulin levels to compensate for insulin resistance) + high glucagon levels

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13
Q

What risk factors are associated with Type 2 DM?

A

obesity (especially those w/ excess intra-abdominal fat (visceral fat))
Sedentary lifestyle (low exercise, high triglycerides diet, smoking, alc consumption, sleep duration)
Family hx
Ethnicity (Asian, Hispanic, and African American at higher incidence)
Polycystic Ovary Syndrome
Inflammation + secretion of cytokines by adipocytes

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14
Q

What population is type 2 DM most seen?

A

Obese adults, can still see it in children and non-obese

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15
Q

What is the identical twin concordance rate of getting type 2 diabetes?

A

70-90%

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16
Q

What syndrome is strongly associated with type 2 DM? How can this present?

A

Metabolic syndrome, seen as overweight/obese due to visceral fat

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17
Q

What type of DM is associated with ketoacidosis? Can it be seen with the other type?

A

Type 1 DM, is rare with type 2 DM

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18
Q

How are pancreatic cells affected in type 2 DM?

A

are present but have decreased insulin secretion

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19
Q

What are the serum insulin levels in type 1 DM?

A

Very low or zero

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20
Q

What are the serum insulin levels in type 2 DM?

A

Variable, often high

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21
Q

How many patients in type 1 DM have autoAb against islet cells? What about in type 2?

A

Type 1: 85%-95%

Type 2: 5%-10%

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22
Q

What are the general sxs of diabetes? What are they caused by?

A

Polyuria, Polydipsia, polyphagia –> caused by hyperglycemia

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23
Q

Why do we see polyuria, polydipsia, and polyphagia in DM?

A

hyperglycemia causes increased glucose secretion by the K, results in osmotic diuresis as water follows (polyuria). Increased fluid excretion causes hypovolemia, increased thirst (polydipsia). Although there is hyperglycemia, glucose can’t enter cells = low energy, increased appetite (polyphagia)

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24
Q

What is one short term consequence of hyperglycemia and is seen with diabetes?

A

irreversible glycosylation of Hb, forms Hb A1C

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25
Q

What are the diagnostic tests used for DM?

A

Fasting blood glucose, glycated Hb (HbA1C), random venous blood glucose, and oral glucose tolerance test

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26
Q

What is the cut-off value for diagnosing DM using fasting blood glucose? What should be kept in mind? What about for Hb A1C, random venous blood glucose, and oral glucose tolerance test?

A 
FBG = ≥126 mg/dL, must fast for ≥8 hrs
HbA1C = ≥6.5%, results can be influenced by other conditions
RVBG = ≥200 mg/dL, only use for pts w/ hyperglycemia sxs
OGTT = serum glucose ≥200 mg/dL 2hr after pt ingests glucose
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27
Q

What can affect accuracy of HbA1C test?

A

can be influenced by other conditions such as CKD and hemolytic anemia

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28
Q

What comorbidities are associated with obesity?

A

HTN
Hyperlipidemia = higher incidence of non-alcoholic fatty liver disease + increased fat around neck can cause obstructive sleep apnea

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29
Q

How many of the 4 tests used to dx DM must be abnormal when pt has no hyperglycemic sxs?

A

2 abnormal results of the 4 tests

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30
Q

Which of the 4 tests used to diagnose DM requires pt to show sxs of hyperglycemia?

A

Random venous blood glucose

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31
Q

What is a benefit of HbA1C?

A

tracks glucose levels over the past 3 months

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32
Q

How is HbA1C formed?

A

glucose attaches to Hb via nonenzymatic glycosylation in high glucose environment

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33
Q

Why does HbA1C last for 3 months?

A

Stays in body until RBC turnover (120 days)

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34
Q

What is C-peptide?

A

pt cleaved from pro-insulin as it matures to insulin active form, released with insulin

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35
Q

What can C-peptide tell us?

A

If insulin is made or not

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36
Q

What are the expected levels of C-peptide in type 1 DM? Type 2 DM?

A

Type 1 - no insulin is made, so low or zero C-peptide

Type 2 - insulin levels normal, if a bit low later on so C-peptide will be normal or a bit low

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37
Q

What antibodies can be used to diagnose type 1 DM? Type 2? What do they target?

A

Type 1 = glutamic acid decarboxylase autoAg Ab + Islet cell cytoplasmic autoAg Ab
Type 2 = autoAb only in 5-10% of pts so much less likely

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38
Q

What is the first treatment for DM if it is not life-threatening?

A

lifestyle modifications = Balanced diet high in fiber, low in fat and refined/simple carbs (sucrose, fructose)

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39
Q

When do you give insulin therapy to pts w/ type 1 DM? What about type 2?

A

Type 1 = immediately since can’t produce insulin

Type 2 = only if can’t control w/ diet and multiple oral agents to decrease glucose (metformin)

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40
Q

What is the pathophysiology of Type 1 DM? What is this process called?

A

APC presents Beta-cells with autoantigens to CD4 T cells → release cyk → recruit T and B lymphocytes → direct cytotoxic and Ab-mediated destruction of pancreatic beta cells
= lymphocytic infiltration insulitis

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41
Q

What do they autoAb target in type 1 DM?

A

pancreatic iselt cells and glutamic acid decarboxylase (which controls insulin release from beta cells)

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42
Q

What does the serum glucose level have to be to see polyuria?

A

> 240 mg/dL

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43
Q

What type of DM do you see weight loss associated with? What about weakness?

A

Type 1 DM, cells cannot uptake glucose and use it as food or energy source

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44
Q

What is the common acute complication associated with type 1 DM? What is this caused by?

A

Diabetic Ketoacidosis = hyperglycemia + metabolic acidosis

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45
Q

What clinical presentation can polyuria result in?

A

dehydration, hypotension, dry mucous membranes, increased capillary refill time, decreased skin turgor

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46
Q

What is an acute complication any diabetic pt is at high risk for?

A

fungal (thrush) and candida vaginitis infections

47
Q

What causes the metabolic acidosis often seen w/ type 1 DM? What is the name of this condition?

A

glucose not able to be uptaken so use fat (triglycerides) as fuel –> break it down into free fatty acids via lipolysis –> liver converts them to acidic ketone bodies –> results in systemic metabolic acidosis = Diabetic Ketoacidosis

48
Q

Is there a compensatory mechanism used during diabetic ketoacidosis? If so, what?

A

Kussmaul breathing = deep and rapid breathing to expel more CO2 due to the metabolic acidosis

49
Q

How can DKA be treated? What does it do?

A

IV Insulin: serum glucose should drop <200 mg/dL, then dextrose should be added to prevent hypoglycemia → insulin administration will correct high ketones and hyperglycemia
When ketones no longer in blood, transition pts to subcutaneous insulin
If pt can eat, stop IV insulin and glucose, give short- and long-term insulin

Also, give fluids (normal saline) for volume repletion
add K+ to IV fluids when serum K+ < 5.5 mEq/L
If hypophosphatemia and hypomagnesemia = give phosphate when serum PO3- <1.0 mg/dL and Mg2+ when <2.0 mg/dL

50
Q

What are the chronic complications associated with DM?

A

Microvascular =
Retinopathy, nephropathy, peripheral neuropathy, autonomic neuropathy
Macrovascular = hyperlipidemia + accelerated atherosclerosis

51
Q

What can retinopathy associated with DM lead to? What about Nephropathy?

A

blindness

chronic kidney disease needing dialysis or transplant

52
Q

what symptoms are seen with peripheral neuropathy?

A

numbness, pain, and ulceration of feet

53
Q

What symptoms are seen with autonomic neuropathy?

A

orthostatic hypotension, GI dysfunction (nausea, vomiting, diarrhea), urinary retention/incontinence

54
Q

When do DM patients usually get chronic complications?

A

When have had DM for >5-10 years

55
Q

what does hyperlipidemia increase risk for? What is it associated with?

A

chronic complication of DM, increases risk for stroke, heart disease, and peripheral artery disease

56
Q

What is the normal range value for Hb A1C? Can it be too low or too high?

A

should be ≤7%, shouldn’t try to reach too low, can lead to hypoglycemia. Higher means hyperglycemia

57
Q

What ketone bodies are produced with DKA?

A

beta-hydroxybutyrate and acetoacetate

58
Q

What are beta-hydroxybutyrate and acetoacetate?

A

ketone bodies produced during DKA

59
Q

What do beta-hydroxybutyrate and acetoacetate do?

A

Lower blood pH, results in metabolic acidosis causing DKA

60
Q

How can you see if pt has DKA?

A

Measure serum and urine pH

61
Q

What is the normal range value for C-peptide?

A

0.3-0.6 nmol/L

62
Q

What is the treatment for type 1 DM? Other than lifestyle changes

A

insulin therapy multiple times per day combining short and long-acting + home-monitoring of blood glucose + BP control w/ ACE-I, especially in pts with cardiovascular diseases, retinopathy, or nephropathy + statin therapy for hyperlipidemia

63
Q

When do you give statins? What does it treat?

A

Treats hyperlipidemia, give to all diabetic patients >40 + younger pts w/ elevated LDL

64
Q

What is the most common type of DM in the US?

A

Type 2

65
Q

What types of cells does insulin shift glucose into normally?

A

Mainly liver and muscle cells

66
Q

What causes the insulin resistance in type 2 DM?

A

multiple pre-R, R, and post-R changes → mainly in liver, adipocytes (fat cells), and muscles

67
Q

What does insulin resistance result in initially in type 2 DM? What happens long term?

A

Pancreas tries to compensate by increasing insulin secretion but long-term tires out

68
Q

What is the effect of elevated serum free fatty acids on insulin?

A

Blunts cell’s insulin response

69
Q

What is leptin? How can it play a role in type 2 DM? What levels do we expect to see w/ type 2 DM?

A

leptin signals us to stop eating when full, pts w/ type 2 can have low levels of leptin

70
Q

What is the relationship between glucocorticoid (cortisol) levels and DM?

A

high glucocorticoids can result in type 2 DM

71
Q

What are the traits used to diagnose metabolic syndrome? How many must be present to diagnose it?

A 
3 must be present: 
Abdominal obesity (visceral fat) 
High levels of serum triglycerides
Low levels of serum HDL cholesterol
HTN
Hyperglycemia
72
Q

Are sxs usually present at diagnosis of type 2 DM?

A

No, usually dx w/ labs

73
Q

What is the acute complication associated with type 2 DM?

A

Hyperglycemic Hyperosmolar nonketotic state (HHNS)

74
Q

What sxs are seen with hyperglycemic hyperosmolar nonketotic state (HHNS)?

A

Marked increase in serum glucose > 600
Osmotic diuresis (polyuria, polydipsia)
Electrolyte disorders
Hypotension
weight loss
Volume depletion; skin tenting, dry oral mucosa, low jugular venous pressure, tachycardia, hypotension
Neurologic symptoms: blurred vision, headaches, altered mental status, seizures may be possible → due to hyperglycemia, fluid shifts in brain, H2O leaves b/c of high serum osmolality

75
Q

How does HHNS come about?

A 
Usually brought about by stressor = release of stress hormones catecholamines, cortisol and GH → increase blood sugar levels from storage for “fight or flight”
MI
Stroke
Sepsis
Pancreatitis
Dehydration
Cocaine use
Poor adherence w/ DM meds
Meds such as glucocorticoids, sympathomimetics, high dose thiazides
76
Q

What are the pre-diabetic ranges for Hb A1C, impaired fasting glucose, impaired glucose tolerance test?

A

Hb A1C = 5.7% - 6.4%
Impaired fasting glucose: fasting plasma glucose if 100-125 mg/dL
Impaired glucose tolerance = 2hr plasma glucose value during 75g oral glucose tolerance test of 140-199 mg/dL

77
Q

What are some measures that can be taken to prevent type 2 DM?

A

screen adults 40-70 or younger patients who have BMI>25 and another risk factor, weight loss, stop smoking and other cardiac risk factors, control BP and lipid levels

78
Q

What are the oral hypoglycemic drugs used to treat type 2 DM?

A

Metformin & Sulfonylurea (glyburide and glitazone)

79
Q

What is the tx for type 2 DM? Other than lifestyle modifications?

A

oral hypoglycemic meds (metformin or sulfonylureas - glyburide or glitazone) –> insulin therapy if oral agents don’t work + home-monitoring of blood glucose + BP control w/ ACE-I, especially in pts with cardiovascular diseases, retinopathy, or nephropathy + statin therapy for hyperlipidemia

80
Q

Why is insulin not given immediately for treating type 2 DM?

A

will promote weight gain + more insulin resistance + increase risk of hypoglycemic episodes

81
Q

What is the pathophysiology driving the development of micro- and macrovascular complications associated with DM?

A

nonenzymatic glycation of proteins, nucleotides, and lipids results in formation of advanced glycosylated age products (ex: Hb A1C)
Increase vascular permeability, arterial stiffness, oxidize LDL cholesterol –> retinopathy and neuropathy
Also due to inflammation = increased secretion of cyk (IL-1, IL-6, IL-8, TNF-a) results in T cell activation –> nephropathy and cardiovascular

82
Q

What causes retinopathy and what happens?

A 
Hyperglycemia = retinal blood vessels swell and leak = macular edema
Blood vessels can also close = ischemia of macula
Tiny clots (exudates) can form = affect vision (floaters)
New blood vessels can form in retina in advanced vision - fragile, often bleed into vitreous → floaters and forms scar tissue, can lead to a detached retina

Due to nonenzymatic glycation

83
Q

How do you dx retinopathy?

A

Dx = Fundoscopic exam: see retina, look for changes in vasculature

84
Q

What is the tx for retinopathy?

A

regular follow-up, glycemic control, laser photocoagulation (inhibits blood vessel proliferation) can preserve vision

85
Q

What kind of changes do we see in the K with diabetic nephropathy?

A

glomerular disease = thickening of glomerular basement mb + persistent albumin leaking into urine

86
Q

How can you dx diabetic nephropathy?

A

annual 24 hr urine albumin or spot microalbumin test (urine albumin: urine Cr ratio)

87
Q

What is the tx for diabetic nephropathy?

A

BP control using ACE-I, renal transplant best if at end-stage renal failure, dialysis can also be done

88
Q

What pb (seen via lab test) can be seen with diabetic nephropathy? What is the progression?

A

Begins w/o sxs, only small amts of pt in urine → progresses from microalbuminuria (50-300 mg) to microalbuminuria (>300 mg/24 hrs) to nephrotic range proteinuria (>3500 mg/24 hrs) to progressive renal failure

89
Q

What are the sxs associated w/ peripheral neuropathy? What are you at risk for?

A

foot pain, tingling, numbness + at risk for foot ulcers (can get infected especially if atherosclerotic since narrows arteries).

90
Q

What are measures used to prevent peripheral neuropathy

A

Weekly foot exams - Check for skin changes, poor wound healing, ulcers, sensory deficits (monofilament)

91
Q

What is the tx for peripheral neuropathy?

A

gabapentin, pregabalin, or duloxetine for pain OR alternatives include SSRIs or tricyclic antidepressants (more severe side effects)

92
Q

How do you treat autonomic neuropathy?

A

Orthostatic hypotension: can try exercise, diet changes BUT for very symptomatic pts, drugs to increase vascular tone (midodrine)
Metoclopramide, dimenhydrinate, and ondansetron can be used to treat severe nausea but have side effects which is limiting

93
Q

How do you dx autonomic neuropathy?

A

Hypotension → 1st get ECG and cardiac evaluation
GI sxs → 1st get endoscopy to look for ulcers
Gastroparesis = gastric emptying study (ingested trace radioisotope to follow meal progression) standard for dx
Bladder dysfunction → get cystoscopy

94
Q

What are the sxs of DKA?

A

Nausea, vomiting, diarrhea
Abdominal pain due to ketoacidosis and elevated prostaglandins
Dehydration + polyuria , polydipsia, hypotension
Reflex tachycardia: activation of baroR system due to decrease in blood volume, try to maintain cardiac output
Deep breathing/hyperventilation (Kussmaul breathing due to metabolic acidosis) → get rid of excess CO2
Mental status changes/unconscious due to volume depletion
“Fruity” breath odor, from increased ketone bodies and acetone in blood

95
Q

What are the risk factors for DKA?

A

5 I’s: Infection, Infarction, Insulinopenia (missed doses of insulin), Iatrogenic causes (meds - glucocorticoids), Infant related (pregnancy - increased insulin demand)

96
Q

What electrolyte imbalances do we see with DKA? Why? What sxs does this bring about?

A

Low Na+ due to osmotic diuresis –> hypotension + tachycardia
K+ loss due to osmotic diuresis –> weakness and ECG abnormalities though will present as hyperkalemia since insulin can’t bring K+ into cell, but total body K+ decrease
PO3- loss due to //

97
Q

Why do we see hyperkalemia with DKA (and DM in general)?

A

Insulin needed for cell uptake of K+, not possible so high serum K+ (even though actual amount not changed). However, osmotic diuresis causing loss of K+ so technically losing total body K+

98
Q

What converts the triglycerides to free fatty acids in DKA? What is this process called?

A

Glucagon, via lipolysis

99
Q

What is the action of glucagon in DM?

A

breaks down glycogen in fat cells of the liver + in muscle cells: latter see release of lactic acid (acidosis) and release of prostaglandins (abdominal pain). Also converts triglycerides into free fatty acids

100
Q

What causes the abdominal pain seen in DM?

A

Prostaglandin release from cells due to glucagon

101
Q

What is the role of Cortisol in DM?

A

proteolysis in muscle cells + activates hepatic gluconeogenesis (glucose produced from nonhexose precursors) –> increases serum glucose

102
Q

What are the lab findings for DKA?

A

pH<7.4, low HCO3-, low pCO2 (respiratory compensation)
high beta-hydroxybutyrate and acetoacetate (serum ketone bodies)
Hyperglycemia
Hyperkalemia
Hypomagnesemia and hypophosphatemia
Hyponatremia although serum Na+ > 125 mEq/L and hyponatremic sxs not present b/c serum osmolarity is high
BUN and serum Cr high, w/ BUN/Cr ratio >20 –> prerenal acute K injury w/ DKA b/c of dehydration and low renal blood perfusion

103
Q

What type of metabolic acidosis is seen w/ DKA?

A

high anion gap metabolic acidosis (high levels of unmeasured anions, ketones mainly + lactic acid, in serum)

104
Q

What is the anion gap in DKA?

A

usually >20 in DKA pts (norm 8-12)

105
Q

How will insulin administration affect electrolyte levels in pts w/ DKA?

A

hypokalemia since K+ will be able to taken up by cells

106
Q

What electrolyte may need to be replenished when giving insulin therapy?

A

K+ because although hyperkalemic, will actually have lower total body stores of K+ due to osmotic diuresis. With insulin, K+ will now be able to be uptaken by cells

107
Q

What are the lab values seen w/ HHNS?

A

Extremely high glucose >600, high serum osmolality >320, and absent ketoacidosis (no serum ketones and blood pH >7.3)
Na+ >125 mEq/L, hyponatremia (low serum Na2+) but no sxs since serum osmolality high
Hypokalemia or hyperkalemia depending on insulin levels and degree of dehydration
Total body K+ uniformly decreased so K+ supplementation needed
BUN/Cr elevated b/c of massive dehydration → leads to prerenal acute K injury

108
Q

Does detecting ketone in urine rule out HHNS?

A

No, ketones can be found in any person dehydrated at low but detectable levels

109
Q

How do you treat HHNS?

A

stabilize pt condition = correct volume depletion, hyperglycemia, and stabilize electrolytes
(1) IV 0.9% saline (normal) at 1L/hr = replenish volume
(don’t give >4L in first 4hrs to avoid neurologic damage due to massive fluid shifts)
(2) IV Insulin
Measure glucose levels every hour: once <300 mg/dL = switch to saline w/ 5% dextrose solutionto prevent hypoglycemia
Always start after normal saline to avoid massive fluid shifts
(3) K+; add to IV solution when <3.5 mEq/L, will most likely need IV and oral K+ –> prevent worsening hypokalemia when insulin drives K+ into cells

Treat underlying trigger

110
Q

What can hypokalemia lead to?

A

arrhythmias

111
Q

What are examples of rapid-acting insulin products? Long-acting?

A

rapid acting = lispro, aspart, glulisine

long-acting = detemir, glargine

112
Q

Why give short-acting insulin?

A

For prandial control (food intake)

113
Q

What is amylin? What is its function?

A

peptide secreted alongside insulin from beta cells, 3 functions:
Slows down gastric emptying, inhibits glucagon secretion, acts as satiety agent –> decreases blood glucose

114
Q

What are the 3 most important actions of insulin therapy?

A

Decrease blood glucose, inhibit ketogenesis, and move K+ into cell

Endocrine Unit Phase 1 (5 decks)

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