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Endocrinology > Diabetes Melitus > Flashcards

Diabetes Melitus Flashcards

1
Q

True or False: Insulin is an anabolic hormone?

A

True

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2
Q

What are examples of ketones?

A

acetone, acetoacetate, beta-hydroxybutyrate

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3
Q

Ketogenesis is a result of:

A

Limited other sources of macromolecules to create oxaloacetate and to promote gluconeogenesis.
Beta-oxidation of FAs to produce ketone bodies (influx of acetyl-CoA)

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4
Q

Gluconeogenesis is possible through which molecules:

A

No INSULIN:

  1. Lactate –> oxaloacetate –> phosphoenolpyruvate –> glucose
  2. Lipids –> glycerol –> phospho. –> glucose
  3. Proteins –> AA –> oxaloacetate or pyruvate –> phospho. –> glucose
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5
Q

What is the tool to assess blood glucose control & monitor therapy?

A

HbA1c –> Proportion of glycated Hemoglobin A1 (higher if glucose poorly controlled)

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6
Q

What are the diagnostic values positive for diabetes?

A

FPG ≥ 7.0 mmol/L OR
A1C ≥ 6.5% (in adults) OR
2hPG in a 75 g OGTT ≥11.1 mmol/L OR
Random PG ≥11.1 mmol/L

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7
Q

How to assess positive diabetes diagnostic test for asymptomatic individuals?

A
  1. If random PG test, then repeat with a different test
  2. If other test involved (2hPG in 75 g OGTT, A1c, FPG), repeat same test next day
  3. If two different tests show positive then confirmed
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8
Q

What is the pre-diabetes range for HbA1c?

A

A1c 6.0-6.4%

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9
Q

T1DM is associated with kind of receptor?

A

HLA-DR OR -DQ

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10
Q

Type of antibodies present in T1DM

A

Islet Cell Antibodies (ICA):

  • Glutamic Acid Decarboxylase (GAD)
  • Insulinoma-Associated 2 (IA-2)
  • Zinc-transporter 8 (ZnT8)

Insulin autoantibodies (IAA)

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11
Q

Which antibodies in T1DM are associated with young, and older patients, respectively?

A

GAD -> older

IA-2 and IAA –> young

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12
Q

True or False: most T1DM cases have family history?

A

False: 90% have no family history

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13
Q

Main causes of T2DM?

A

Genetic factors
High fat diet and obesity
Pancreatic dysfunction
Insulin resistance in liver & muscle

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14
Q

How many criteria do you need to meet for a metabolic syndrome?

A 
3 out of 5:
1. Waist circumference (apple-shaped)
2. Elevated TG
3. Reduced HDL-C
4. Elevated BP
5, Elevated FPG
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15
Q

What are the classic symptoms of hyperglycemia?

A

polyuria and polydipsia

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16
Q

Glucose tolerance test (OGTT) is used for screening which type of diabetes?

A

gestational

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17
Q

What type of hypersensitivity reaction is T1DM?

A

Type 4

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18
Q

Diabetic ketoacidosis is related to which type of diabetes and why?

A

T1DM, due to skipping insulin therapy or precipitation of infection/trauma

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19
Q

Describe mechanism of DKA:

A

Low insulin –> high glucagon –> higher gluconeogenesis and lipolysis –> leads to:

–> ketone bodies and urineketones/glucose –> acidosis –> hyperkalemia and decreased GI motility

–> polyuria –> dehydration and loss of phosphates

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20
Q

What does the metabolic acidosis anion gap in DKA lead to?

A

Kussmaul breathing: deep, laboured breathing

Hyperventilation to blow off CO2 and raise pH

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21
Q

Why are ketone bodies created in DKA?

A

Oxaloacetate is depleted because it used up for glucose production and creation of lots of NADH from lipolysis favours conversion of oxalo. to malate

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22
Q

Why is phosphate lost in DKA and what does it lead to?

A

Acidosis shifts phosphate to ECF and then to urine and this leads to loss of ATP –> muscle weakness (resp failure) and heart failure (decreased contractility)

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23
Q

Arrythmias in DKA is a result of….

A

hyperkalemia

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24
Q

True or False: Cerebral edema may result in DKA

A

True

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25
Q

What is a classical complication of DKA and why?

A

Mucormycosis –> fever, headache, eyepain

Due to fungal infection (rhizopus/mucor) that thrive in high glucose and ketoacidosis conditions

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26
Q

What is the treatment for DKA?

A

Insulin –> lowers glucose and puts K+ into cells (must monitor carefully as it may lead to hypokalemia)
IV fluids –> treats dehydration
glucose and potassium may be need to be added while insulin is running

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27
Q

Which shape, apple or pear, is worse for T2DM and why?

A

Apple because it means more visceral fat, and the breakdown of it into FAs not inhibited by insulin. So, FAs used more for fuel over glucose, leading to higher glucose levels.

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28
Q

What is a classic histological finding in T2DM?

A

Amyloid in pancreas (accumulation of amylin peptide)

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29
Q

What is the difference of DKA and hyperglycemic hyperosmolar syndrome (HHS)?

A

HHS:
more common in type 2
high glucose and severe dehydration
few to no ketones (because insulin still available but deficient), no acidosis (no phosphate and K+ imbalance)
very high serum osmolarity –> CNS dysfunction (confusion, coma)

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30
Q

What dermal feature is associated with diabetes insulin resistance? (N)

A

acanthosis nigricans

hyperpigmented regions where skin folds (neck and axillae)

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31
Q

What are the two key underlying mechanism to complications experienced in chronic hyperglycemia? (N)

A

1) non-enzymatic glycation:
leads to cross-linked proteins —> advanced glycosylation end products (AGEs)

2) sorbitol accumulation

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32
Q

What cardiovascular complications results from AGEs? (N)

A

Atherosclerosis:
AGEs trap LDL in large vessels (diabetic macroangiopathy) –> atherosclerosis
This leads to:
1) Coronary heart disease (angina, MI)
2) Stroke/TIA
3) Peripheral vascular disease (arterial ulcers, poor wound healing, gangrene)

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33
Q

What renal complications results from AGEs? (N)

A

Diabetic kidney disease (microangiopathy)
AGEs damage the glomerulus and arterioles due to hyaline arteriosclerosis (cross-linking of collagen):
- afferent –>less renal blood flow (ie. ischemia)
- efferent –> hyperfiltration (albumin in urine)
- basement membrane thickening –> glomerulosclerosis
May lead to end stage kidney disease

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34
Q

What kind of urine screening is done in diabetics?

A

presence of albumin

–> treated by ACE-inhibitors –> reduces hyperfiltration

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35
Q

Which diabetic complications are due to the polyol pathways which creates sorbitol and why? (N)

A

cataracts (sorbitol enters lens) and neuropathy (enters schwann cells) because sorbitol is an osmotic agent that draws a lot of fluid –> osmotic damage

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36
Q

Describe the neuropathy on diabetics: (N)

A
  • stocking-glove sensory loss:
    longest axons affected (feet/legs), worse distally
  • loss of vibration sense, proprioception
  • autonomic neuropathy (postural hypotension, delayed gastric emptying)
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37
Q

How does diabetic retinopathy occur? (N)

A

Pericyte degeration because of osmotic damage via sorbitol accumulation. These cells line the capillaries and damage leads to microaneurysms which causes hemmorrhages if ruptured

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38
Q

True or false: hyperglycemia is a major risk factor for microvascular and macrovascular complications?

A

True: retinopathy, nephropathy, neuropathy, micro/macroalbuminuria

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39
Q

Explain A1C targets:

A
  1. 5 or lower for those in risk of CKD, retinopathy and low risk of hypoglycemia
  2. 0 or lower for most T1DM and T2DM
  3. 1 - 8 functionally dependent
  4. 1 - 8.5 recurrent hypoglycemia, hypoglycemia unawareness, limited life expectancy, frail elderly with dementia

At end of life - A1C is not recommended

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40
Q

To achieve an A1C of 7.0 or lower what pre-, and post-prandial plasma glucose (mmol/L) are required and what if that fails to achieve it?

A

Pre-prandial: 4-7 mmol/L ; post-prandial 5-10 mmol/L

if above fails to achieve A1C of 7 or less then:
Pre-prandial: 4-5.5 mmol/L ; post-prandial 5-8 mmol/L

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41
Q

True or False: glycemic targets should are same for everyone?

A

False: Glycemic targets should be individualized based on the individual’s age, duration of diabetes, risk of severe hypoglycemia, presence or absence of hypoglycemia unawareness, frailty or functional dependence and life expectancy

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42
Q

What are physical activity requirements for diabetics?

A

150 minutes moderate to vigorous with weight training (resistance) per week

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43
Q

What are diet requirements for diabetics?

A

calorie-reduced, low glycemic carbohydrates

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44
Q

What is the initial pharmacotherapy of choice for newly diagnosed T2DM and how often should they be reassessed?

A

metformin, 3-6 mths

45
Q

What happens if a newly diagnosed T2DM has an A1C less than 1.5% over target

A

At the time of diagnosis of type 2 diabetes, healthy behaviour interventions should be initiated. This is new preferred term over “lifestyle modification”. These include nutritional therapy, weight management, and physical activity. This is also an option to start metformin.

If the A1C is less than 1.5% above the patient’s target A1C, if they are not at glycemic target within 3 months of healthy behaviour interventions, metformin should be started or increased.

46
Q

What happens if a newly diagnosed T2DM has A1C more than 1.5% over target?

A

If the A1C is greater than or equal to 1.5% above target A1C, metfomin should be started immediately. A second concurrent antihyperglycemmic agent should be considered.

47
Q

What happens if a newly diagnosed T2DM if they shown symptoms of hyperglycemia?

A

If the patient has symptomatic hyperglycemia and/or metabolic decompensation, insulin should be initiated alone or in combination with metformin. This includes patients with dehydration, diabetic ketoacidosis or hyperosmolar hyperglycemic state (polyuria, polydipsia, weight loss, volume depletion)

insulin is temporary to bring it down

48
Q

If a T2DM patient recently diagnosed is not reaching target A1C within 3 three months (despite being on metformin), what is the next consideration in treatment?

A

If the patient remains not at glycemic target, the first question to ask in choosing the second antihyperglycemic agent is whether the patient has clinical cardiovascular disease. Clinical cardiovascular disease is defined as history of myocardial infarction, coronary artery disease on angiography, unstable angina, stroke, peripheral artery disease)

If the patient has clinical cardiovascular disease, an antihyperglycemic agent with demonstrated CV benefit should be added. This recommendation is based on several cardiovascular safety outcome studies

49
Q

What drugs for T2DM have CV protection effects?

A

GLP-1R agonists:
Empagliflozin (EMPA-REG)
Canagliflozin (CANVAS)
Dapagliflozin (DECLARE-TIMI)

SGLT2 inhibitors:
Liraglutide (Leader)
Semaglutide (Sustain)
Dulaglutide (Rewind)

50
Q

What drugs for T2DM are CV neutral?

A

DPP-4 inhibitors, insulin, thiazoliinediones

51
Q

If T1DM does not have a risk for CVD then what are the considerations for a second pharmaco agent?

A

Drugs that will not induce hypoglycemia, and or weight gain

52
Q

What drugs induce hypoglycemia?

A

insulin, and insulin secretagogues

53
Q

What drugs induce weight gain?

A

insulin, secretagogues and thiazolinediones.

54
Q

Which drug has the best A1C lowering effect?

A

insulin

55
Q

If weight and hypoglycemia are concerns in T2DM wah tagensts should be used in addition of metformin if A1C targets are not met?

A

If hypoglycemia and weight gain are of concern an incretin agent (DPP-4 inhibitor or GLP-1 receptor agonist) and/or an SGLT2 inhibitor are preferred as add on

56
Q

What is the effects of metformin and contraindication?

A

Decreases hepatic gluconeogenesis
Enhances insulin sensitivity (liver and peripheral tissues)
Effective a1c lowing
Potential CV benefit

CKD stage 4-5 and hepatic failure –> contraindication

57
Q

What are the side effects of methformin?

A 
VitB12 deficiency
GI side effects
Lactic acidosis (rare seriousness)
58
Q

What is the mechanism of action of SGLT-2 inhibitors?

A

they inhibit the action of SGLT-2 (ie. the …aglutides), promoting the renal excretion of glucose

59
Q

What are the advantages and disadvantages of SGLT-2 inhibitors?

A 
\+
lowering A1C
very low risk of hypoglycemia
weight loss
lowers BP
renal and cardio protective
-
lower glycemic effect with renal impairment
genital mycotic infections and UTIs
Polyuria
Hypotension
AKI
60
Q

What are the two types of incretins and how do each work?

A
  1. Glucagon-like petptide-1 receptor agonists (GLP-1R) (ie. the …. agliflozins)
    activates the GLP-1 receptors and potentiates the effect of incretins
  2. DPP-4 inhibitors (ie. the …liptins)
    - slows the breakdown of endogenous incretins (ie. GLP-1)
61
Q

What are + and - of GLP-1R drugs?

A

+

  • lowers A1C
  • minimal hypoglycemia chance
  • promotes weight loss
  • CV protection

-

  • costs
  • GI effects
  • injection site rxns
62
Q

What are + and - of DPP-4 inhibitors?

A

+
A1C lowering
minimal chance of hypoglycemia
weight neutral

  • rare pancreatitis, rare severe joint pain
63
Q

What is the mode of action for insulin scretetagogues and what are two categories?

A

Act of K+ channels (closes them and causes depolarization) and increase insulin secretion
Meglinitides
Sulfonylurea (the ..ides)

64
Q

What are the + and - of insulin secretetagogues?

A

+
A1C lowering
affordable

-
risk of hypoglycemia
weight gain

65
Q

What is the mode of action for acarbose?

A

It is a alpha glucosidase inhibitor so it slows down the break down of oligosaccharides to monosaccharides and as a result slows the delivery of glucose to circulation –> prevents post-prandial hyperglycemia

66
Q

What are the + and - of acarbose?

A

+
weight neutral
minimal hypoglycemia
A1C lowering

- 
GI effects (gas so much)
67
Q

What is the mode of action for thiazolidinediones (ie. the ….glitazones)?

A

activates peroxisome proliferator-activated receptor gamma (PPAR), which then enhances sensitivity to insulin (liver and peripheral)

68
Q

What are the advantages and cons to thiazolidinediones?

A

+
A1C lowering
minimal hypoglycemia risk
(weight gain)

-
edema
congestive heart failure

69
Q

What are the importance of basal, and bolus insulin?

A

Basal (ie. intermidate-long acting insulin) prevents hepatic gluconeogenesis, andcontrosl fasting glucose levels)

Bolus (short acting insulin) promotes utilization of gluocose and controls post-prandial glucose levels

70
Q

What are the properties of rapid acting analogs of insulin?

A

Usually are monomers of inuslin (regular tend to associate in hexamers)

71
Q

What are propeties of long/intermediate (basal) inuslin analogs?

A
  • crystalize
  • become into hexamers
  • self-associate to produce dimers
    (all of these extend the time they are in the subcutaneous phase)
72
Q

What should the proportions of basal and bolus insulin for a day?

A

basal: 40-50
bolus: 50-60%

73
Q

How to calculate the daily units of insulin required for a person?

A

weight multiplied by 0.6 units per kg

74
Q

For T1DM, if the pre-pandial PG is above target (ie. 7 mmol/L), what would you do bring it back to A1C targets?

A

use a correction factor of 1 unit for every 3mmol/L above 7

75
Q

What is the result of injecting isulin in the same spot overtime?

A

lipohypertrophy (lipoatrophy sometimes) –> absoption is becomes variable

76
Q

True or false: T2DM require bolus insulin

A

false - only requires bolus if the evening basal does not produce FPG of 4-7 mmol/L in which you have to titrate it with bolus before a meal/each meal

77
Q

Why are diabetics at higher risk for infections?

A
  • hyperglycemia provides glucose for bacteria and yeast
  • diabetes can involve reduced peripheral circulation due to damage which leads to lower immune cells in the affected areas
  • high glucose (above 10 mmol/L) impairs neutrophil function

these can lead to UTIs, foot ulcers, abcesses, gangrene

78
Q

What hormones outweigh insulin in DKA?

A

cortisol, GH, epinephrine, glucagon

79
Q

In DKA what causes changes in LOC?

A

acidosis (high glucose in HHS)

80
Q

True or False: blood perfusion decreases to muscles in DKA

A

True: dehydration leads to hypotension and reduced peripheral perfusion (reduces glucose clearance from blood)

81
Q

What is the purpose of fluids and insulin in DKA?

A

fluids - bring BP up and HR down (first thing to provide to patient)
insulin - to stop gluconeogenesis and acidosis

82
Q

Why restoring fluids important?

A

dilution of glucose, increase perfusion to muscle and kidney

83
Q

T or F: K+ leaks out of cells in acidosis

A

T

84
Q

T or F: insulin will cause a hyponatremia in treatment of DKA

A

F: will cause hypokalemia

85
Q

What are the dignostic tests for DKA?

A 
urinalaysis
plasma glucose
electrolytes (creatinine, bicarb, beta-hydroxybutyrate)
ABG
CBC (ie. for infection)
Chest XR (pnemonia)
ECG (for heart attak and K+ indices)
Troponin (marker for Heart Attack)
Amylase/lipase (for pancreas problem)
  • ketonuria/ketonemia
  • pH less than 7.3
  • serum bicarb less than 15 mmol/L
  • hyperglycemia 14-35 mmol/L
    anion gap more than 14 mmol/L
86
Q

What is euglycemic DKA?

A

normal glucose level while having DKA

- usually with a pregnant or those taking a SGLT-2 inhibitor

87
Q

T or F: giving bicarbonate is a first line treatment

A

F: usually not given unless pH low even after fluids and insulin
- can induce hypokalemia, skin necrosis, and cerebral acidosis

88
Q

What is most common death complication in pediatrics from DKA?

A

Cerebral edema

89
Q

What is common cause of death in elderly from DKA?

A

ARDS - acute respiratory distress syndrome

90
Q

What are some doctor induced (iatrogenic) complications of DKA?

A

hypokalemia –> death

hypoglycemia

91
Q

What are the differences between DKA and HHS?

A

in HHS:

  • insulin is still present
  • osmolarity is high
  • no acidosis or ketones
  • glucose levels are much higher
  • counter hormone levels are pretty much low
  • often with T2DM
92
Q

How to calculate osmolarity and what is the usual?

A

2 x Na + glucose + urea

usually 290 plus/minus 5

93
Q

What is common in DKA and HHS?

A

There is still proteolysis (insulin levels to shut this off stream is higher than lipolysis)

94
Q

What is the glucose level for serious clinically important hypoglycemia?

A

less than 3 mmol/L

95
Q

What are two classes of hypoglycemic symptoms what are they?

A

Adrenergic
shaky, sweaty, hungry, palpitation, anxiety, hunger

Neuroglycopenic
confusion, blurred vision, tired, dizzy, slurred speech, seizures, coma

96
Q

T or F: tightly contrlling glucose fast is eye protective

A

F: leads to retinopathy

97
Q

What may happen due to endothelial damage at the retina?

A

A) blood vessels get blocked leading:

  1. to ischemia –> nerve fibers swollen with fluid –> cotton-wool-spots (non-proliferative)
  2. microaneurysm/microhemmorhages (non-proliferative)
  3. microvascular growth factor (due to ischemia)–> new blood vessels (neovascularization) fragile leading to vitreous hemmorhage –> retinal detachment (proliferative)

B) Blood vessels become leaky –> retina swollen –> changes in visual acuity

Treatment: laser

98
Q

What is the swelling in retina called?

A

macular edema

99
Q

How to manage diabetic retinopathy?

A
  • tight glycemic control
  • tight blood pressure control (esp. ACE-i)
  • lipid lowering (triglycerides - using fibrates)
  • laser photocoagulation (focal or pan retinal)
  • intra-vitreal anti-VEGF (avastin/lucentis) for CSME & Proliferative Retinopathy
100
Q

What are the characteristics of diabetic nephropathy?

A
  • decline in renal function (creatine high urine and GFR falls)
  • albuminuria
  • hypertension
101
Q

Diabetic kidney disease is usually associated with non-profilerative retinopathy: T or F

A

Fasle: associated with proliferative

102
Q

What is a screening test for diabetic nephropathy?

A

albumin to creatinine ratio (2-20 mmol/L microalbuminuria; over 20 macro.)

103
Q

How to manage diabetic nephropathy?

A
  • tight glycemic control
  • tight blood pressure control (esp. ACE-i, ARB)
  • ?SGLT2i in T2DM (??T1)
  • lipid lowering
  • smoking cessation
  • manage CV risk factors, check for other complications (eye, feet)
104
Q

What is the most common presentation of neuropathy in diabetics?

A

foot ulcers (too much pressure leads to swelling and then ulcers due to loss of protective sensation)

105
Q

What consists of peripheral neuropathy?

A

Painful peripheral neuropathy
• burning, tingling, worse at night, symmetrical, feet (and hands)

Distal Symmetrical Sensory Neuropathy
• reduced sensation / numbness
• glove and stocking distribution

106
Q

What are some charateristics of autonomic neuropathy?

A
  • Resting tachycardia
  • Postural hypotension
  • Erectile dysfunction
  • Abnormal sweating
  • Gastroparesis
  • Constipation / diarrhea (PRECAG)
107
Q

What are the differences between neuropathic and ischemic foot ulcers?

A

Neuro:
- painless, plantar, associated with pressure calluses

Ischemic:
- painful, dorsal/lateral, cold, pale, pulseless

108
Q

Charcot Foot

A

Destruction of bony structure due to neuropathy

109
Q

What is hypoglycemia unawareness?

A

A complication of diabetes in which the patient is unaware of a deep drop in blood sugar because it fails to trigger the secretion of epinephrine which generates the characteristic symptoms of hypoglycemia (such as palpitations, sweating, anxiety) that serve to warn the patient of the dropping blood sugar.

Endocrinology (16 decks)

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