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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What lifestyle interventions are proven for diabetes?

A
  1. Diet: DASH/med/whatever is sustainable
  2. Exercise: both activity and focused exercise, including both cardio and strength
  3. Alcohol: less than 1-2/day
  4. Smoking: stop
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2
Q

How does diabetes usually present?

A

1c weight loss/ fatigue

  1. Changes in vision- due to glucose in vitreous humour
  2. Polyuria +polydipsia
  3. May be asymptomatic but have risk factors like metabolic syndrome
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3
Q

What are the monogenic forms of diabetes?

A 
Rare: IPEX (treg) and APS-1 (thymus)
MODY: 
1=lipid profile abnormal 
2=glucokinase mutation 
3=post prandial hyperglycemia
5=renal/uterine development

MELAS: diabetes& deafness

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4
Q

What mutations are linked to type 1 diabetes?

A
  1. Insulin gene mutations (IDDM2)

2. HLA gene mutations (IDDM1)

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5
Q

What environmental triggers in DM1 act via molecular mimicry?

A
  1. Diet (cow’s milk, nitrosamines)

2. Viruses (coxsackie, rubella, mumps)

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6
Q

What environmental triggers in DM1 act via direct destruction?

A
  1. Viruses
  2. Drugs/toxins
  3. Stressors
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7
Q

At what point in DM1 does pre-diabetes occur?

A
  1. Less than 50% beta cell mass
  2. Blunted glucose response
  3. No symptoms
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8
Q

At what point is DM1 official?

A
  1. Less than 10% beta cell mass

2. Symptoms (polyuria, polydipsia, weight loss)

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9
Q

What is a predictor of future progression to DM1?

A
  1. Number of autoantibodies detected

2. During immune attack stage

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10
Q

What are the risk factors for severe hypoglycemia in DM1

A
  1. Adolescents

2. Unable to detect or treat themselves

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11
Q

What causes DKA?

A

Severe and absolute insulin deficiency leading to:
Glycogenolysis
Gluconeogenesis
Lipolysis

Vicious cycle as counter regulatory hormones activated

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12
Q

Presentation DKA

A

Rapid onset, severe acidosis

Osmotic dieresis: polyuria, polydipsia dehydration, decreased LoC

Ketones: vomiting, abdo pain, Kussmaul respiration, fruity breath

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13
Q

Presentation HHS

A

Onset can be insidious

Delirium
Lethargy
Dehydration (osmotic, vomit, not enough drinking)
May have neuro SX: seizures etc

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14
Q

Investigations DKA

A

PH less than 7.3
Bicarb less than 15
High urine and plasma ketones
Anion gap

Apparent hyponatremia
Hypophosphatemia

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15
Q

Investigations HHS

A

Glucose >33

Serum osmolarity >320

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16
Q

Treatment DKA

A
  1. Fluid resuscitation
  2. Give potassium (40mmol/L)
  3. Insulin bolus + infusion, avoid hypoglycemia (0.1 units/kg/hr)
  4. Sodium to avoid dropped plasmolality
  5. Maybe give bicarb if terrible acidosis
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17
Q

Treatment HHS

A
  1. Fluid resuscitation (up to 10L in 24 hours)
  2. Give potassium
  3. Give sodium
  4. Treat underlying cause
    5 maybe insulin i foredeck
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18
Q

What predisposes to HHS?

A 
Type 2 diabetes
Older
Renal insufficiency 
Drugs (steroids)
Endocrine disorders

Precipitated by inadequate fluid intake, severe stress, infection, non compliance

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19
Q

If a child has diabetes before age 1, what should we consider?

A

Monogeneans diabetes like MODY

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20
Q

What are those with type 1 diabetes more at risk for?

A

Other autoimmune diseases like thyroid, celiac, addisons etc

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21
Q

What test is diagnostic of DM in children?

A

Random glucose if they have symptoms

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22
Q

Lipohypertrophy

A

Accumulation of fat following repeated injections at the same site. Can make insulin absorption unpredictable

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23
Q

How should hypoglycemia be treated?

A
  1. Immediate oral glucose (mild/moderate 15g, severe 20g)

2. If unconscious, IM or subcutaneous glucagon

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24
Q

What are the complicAtions of DKA?

A

Thrombotic stroke, dvt, PE
Pancreatitis
Renal failure

Cerebral edema
Seizures from hypoglycemia
Dysrythmias from hypokalemia

25
Q

What effect does the accumulation of intraperitoneal fat have?

A
  1. Releases inflammatory mediators, adipokines, free fatty acids
  2. Contribute to insulin resistance by preferential uptake
  3. Lipotoxicity on beta cells, inhibit GLUT2 transporter
26
Q

Why do microvascular complications of diabetes occur?

A
  1. Hyperglycemia impacts cells that can’t actively transport glucose.
  2. advanced glycation end products (protein dysfunction and ROS generation)
  3. Sorbitol/polyol pathway (increased fructose and decreased glutathione, reducing ROS scavenging)
  4. Protein kinase C (cell signalling, angiogenesis)
  5. Hexosamine pathway
27
Q

How does hyperglycemia affect the endothelium?

A

Leads to chronic vasoconstriction, arterial stiffening, prothrombosis

28
Q

Non proliferation retinopathy

A
  1. Path: leakage of red cells, retinal ischemia

2. Clinical: micro aneurysms, hard exudates, cotton wool spots

29
Q

Proliferative retinopathy

A
  1. New vessel formation, into vitreous humour

2. Highly friable so may have vitreous haemorrhages

30
Q

What pre-conception management should be done for women with diabetes?

A
  1. HBA1C needs to be
31
Q

What is the natural history of DM in pregnancy?

A
  1. Insulin demands increase over pregnancy (baby needs glucose but mother needs normal blood levels)
  2. Insulin resistance increases (see above)
  3. This is triggered by placental growth hormone, so after delivery insulin requirements will drop significantly
32
Q

What are the risks for mother with DM and fetus?

A
  1. Fetal abnormalities
  2. Big baby: nerve palsy from clavicle damage in delivery
  3. Increased fetal hypoxia (risk of polycythemia)
  4. Increased risk of stillbirth
  5. Fetal resp distress, jaundice HYPOglycemia
  6. If DKA, 50% fetal mortality
33
Q

What are the risk factors for gestational diabetes?

A
  1. Family Hx DM, polycystic ovarian disease, previous stillbirth, corticosteroid use, previous large child
  2. BMI>30, acanthosis nigricans, excessive amniotic fluic
34
Q

Gestational diabetes

A

Pregnancy induced diabetes, usually occurs after 20 weeks

35
Q

How is gestational diabetes diagnoses?

A
  1. Oral glucose tolerance test (ideally 24-28weeks)

2. Can do larger tolerance test and if one or more of the testing time values is positive, diagnostic

36
Q

How is gestational diabetes treated?

A
  1. Diet/exercise modification
  2. Insulin (first line)
  3. Metformin (2nd line, can cross placenta)
37
Q

Which anti-hyperglycemic agent causes metabolic acidosis?

38
Q

What is the most common congenital malformation in pregnancy with DM?

A

Caudal regression syndrome

39
Q

What should mom’s with DM do post-partum?

A
  1. Change insulin regime appropriately
  2. Breastfeed if possible
  3. Screen for thyroiditis in T1DM
40
Q

Diabetic Nephropathy

A
  1. Injury to kidneys resulting from high blood glucose
  2. Progressive thickening of basement membrane & proteinuria
  3. Treatment mainstay is EXCELLENT BP control
  4. Have greater CV risk so manage that
41
Q

Autonomic neuropathy

A

Longstanding disease:
reduced sweating
gastroparesis
erectile dysfunction

42
Q

Frequent high morning sugars

A

Suspect night time lows- alter evening basal dose

43
Q

Frequent DKA

A

Suspect missing basal insulin

44
Q

Side effects insulin secretagogues

A
  1. Wight gain
  2. Hypoglycemia (from increased insulin)
  3. Flushing (sulfonylurea)
45
Q

Side effects metformin

A
  1. GI upset
  2. Lactic acidosos
  3. Vitamin B12 deficiency
46
Q

Side effects thiazolidiones

A
  1. Weight gain
  2. Edema
  3. CARDIAC FAILURE!!!
47
Q

side effects Acarbose

A
  1. Flatulence, diarrhea
48
Q

Side effects SGLT-2 inhibitors

A
  1. Weight loss
  2. GU infection
  3. Hypotension
  4. Increased LDL
49
Q

Side effects of incretin based therapies

A
  1. Nausea/vomiting

2. Pancreatitis

50
Q

What OHA is the most effective for decreasnig HBA1C?

A
  1. SGLT-2, GLP-1
51
Q

Contraindications insulin secretagogues

A

Liver disease

52
Q

Contraindications metformin

A

Renal disease
liver disease
CHF

53
Q

Contraindications incretin based therapies

A

DM1, DKA, pancreatitis

54
Q

Best add on to metformin for cardiovascular disease?

A

SGLT-2 inhibitors

55
Q

Which OHA is likely to cause hypoglycemia?

A

Insulin secretagogues (sulfonylurea(aka gly…), meglitinides)

56
Q

Contraindications to tight glycemic control?

A
  1. Hypoglycemia unawareness
  2. MI/CAD (dont want to die in sleep)
  3. Elderly and alone
  4. Terminal illness
  5. Kids
  6. Seizure disorders
57
Q

Early complications of diabetes in pregancy

A

Fetal defects

pregancy loss

58
Q

Late complications of diabetes in pregancy

A

Macrosomia
Placental insufficiency
neonatal hypoglycemia, respiratory distress, jaundice
Pre ecclampisa, HELLP

Endocrine (12 decks)

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