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PEDS ENDO RC TD 2022 > T1DM > Flashcards

T1DM Flashcards

1
Q

Genes associated with T1DM

A

HLA class 2 6p21 (DR3/DR4-DQ8) (OR >6)

Insulin (VNTR)
PTPN22
IL2RA
SH2B3
ERBB3

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2
Q

Risk of T1DM in monozygotic twins?

Siblings?

Gen pop?

A

~40%

~5%

0.5%

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3
Q

Antibodies in T1DM

A

GAD-65
Islet cell antibody (ICA)
Zn T8
Insulin (IAA)

gotta check:
tyrosine phosphatase IA2 (ICA512)
IA2 (insulinoma-associated protein-2)

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4
Q

Type of ketones:
in urine
in blood

Which are older?

A

in urine: acetoacetate
in blood: 3-B-hydroxybutyrate

Urine is older

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5
Q

HHS?
What does it stand for?

BG
pH
HCO3-
Ketonema, ketonuria
Osmolality
Other sympt, features
Treatment

A

Hyperglycemia hyperosmolar state

BG >33
pH >7.3
HCO3- >15

Small ketonuria, +/-mild ketonemia

Serum osmolalilty >320 mOsms/kg

Other sympt, features:
Stupor/coma, seizure, rhabdo, malignant hypertherm

Treatment:
Fluids +/- low insulin:

i) Significant fluid resuscitation (20ml/kg boluses, high fluid rate), also replace urine output
ii) Delay insulin start until BG no longer dropping from fluids alone
iii) Lower insulin rate: 0.025-0.05u/kg/hr

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6
Q

Treatment related consequences of T1DM

A

Lipohypertrophy
Insulin edema

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7
Q

Who should be included in interprofessional team (5)

A

Either a pediatric endocrinologist or pediatrician with diabetes expertise
dietician
diabetes nurse educator
social worker
mental health professional

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8
Q

Education topics that should be included (6)

A
  • Insulin action, administration and dosage adjustment;
  • blood glucose and ketone monitoring;
  • sick-day management and prevention of DKA;
  • nutrition therapy;
  • physical activity;
  • prevention, detection and treatment of hypoglycemia
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9
Q

HbA1C target of T1DM

A

7.5 or less

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10
Q

How to treat hypoglycemia in T1DM?

How to prevent severe hypoglycemias? (Dose)

A

Carbs:

Age
<5 - 5g
5-10 - 10g
>10 - 15g

Glucagon if severe

Prevention: Miniglucagon
A dose of 10 mcg per year of age (the equivalent of 1 unit on the syringe per year of age) (minimum dose 20 mcg (2 units), maximum dose 150 mcg (15 units))
Can give additional doubled dose given if the BG has not increased in 20 minutes

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11
Q

What are causative and associated factors of poor metabolic control in T1DM

A

Depression
Eating disorders
Lower socioeconomic status
Lower family support
Higher family conflict

Additional factors during adolescence:
Physiologic insulin resistance
Depression and other psychological issues
Reduced adherence during a time of growing independence

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12
Q

What is the Reduction in HbA1c with Regular Physical Activity?

A

0.5%

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13
Q

Risk Factors of DKA?
New onset (2)
Known DM (6)

A

New onset:
- Age <3yo
- From areas with low prevalence of DM

Established DM:
- Poor metabolic control or previous episodes of DKA
- Peripubertal and adolescent girls
- Children on CSII or long-acting basal insulin analogues
- Ethnic minorities
- Children with psychiatric disorders
- Those with difficult family circumstances

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14
Q

How to reduce frequency of DKA (5)

A

New onset DM:
Public awareness campaignes about S&S of DM

Established DM:
Education
Behavioural intervention
Family support
Access to 24-hour telephone services or telemedicine for parents of children with diabetes

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15
Q

What is the frequency of cerebral edema in DKA?

A

0.5-1%

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16
Q

What are RF for Cerebral edema in DKA? (10)

A
  • Young age
  • New onset DM
  • Greater severity of acidosis
  • High initial serum urea
  • Low initial pCO2
  • Rapid administration of hypotonic fluids
  • IV bolus of insulin
  • early IV insulin infusion (within 1st hour of admin of IVF)
  • failure of serum Na to rise during tx
  • use of bicarb

2 demographic
3 presentation
5 treatment related

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17
Q

Counselling - points for t1dm? (4)

A
  1. Vaccination (no increased morbidity or mortality from influenza in T1DM , can be more difficult to manage w illness)
  2. Smoking (Significant risk factor for both cardiovascular and microvascular complications of diabetes)
  3. Alcohol and Drugs
  4. Contraception and sexual health (Counsel around avoiding unplanned pregnancy)
    - Pregnancy in adolescent females with T1DM with suboptimal metabolic control may result in higher risks of maternal and fetal complications than in older women with T1DM who are already at increased risk compared to the gen pop
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18
Q

Risk of psych issues in someone w T1DM (5)

A

Diabetes distress
Depression
Anxiety
Eating disorders
Externalizing disorders

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19
Q

Comorbid conditions of T1DM?

A

Clinical autoimmune thyroid disease (AITD)
- Hypothyroidism
- Hyperthyroidism

Addisons disease (unexplained recurrent hypoglycemia and decreasing insulin requirements)

Celiac disease

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20
Q

Comorbid conditions of T1DM?
Screening who, how and when

A
  1. Autoimmune thyroid disease
    - everyone
    - TSH, anti-TPO (don’t repeat TPO if already pos)
    - at dx, q2y
    - if TPO +ve or SX-ic, q6-12m
  2. Primary adrenal insufficiency
    - Sx’ic (unexplained hypoglycemias, decreased need insulin)
    - AM cortisol, Na, K
    - as clinically indicated
  3. Celiac disease
    - Sx’ic (GI sx, poor linear growth, recurrent hypo, poor weight gain, fatigue, anemia, poor control)
    - TTG and IgA
    - as clinically indicated
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21
Q

Complications of T1DM

A

Nephropathy
Dyslipidemia
Retinopathy
Neuropathy
Hypertension

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22
Q

How to screen for nephropathy in T1DM

A

random ACRs (more compliance than first morning)

if abnormal (i.e. >2.5 mg/mmol) require confirmation with a first morning ACR or timed overnight urine collection

confirmed by finding two or all of three samples abnormal over a 3 to 6 month period

only tx if persistent

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23
Q

False positive for proteinuria

A

Transient albuminuria
Benign orthostatic proteinuria
strenuous exercise
infections, nondiabetic kidney disease (i.e., IgA or other types of nephritis),
marked hyperglycemia,
fever, and
menstrual bleeding

24
Q

How to screen for dyslipidemia

A

non fasting lipids
(fine unless TG is high)

25
Q

When to screen in T1DM: Nephropathy

A

Yearly starting age 12y and 5y duration

26
Q

When to screen in T1DM: Retinopathy

A

yearly starting age 15y and 5y duration
can go to 2y if good glycemic control

27
Q

When to screen in T1DM: Neuropathy

A

15y and older if poor metabolic control and 5y duration
yearly

28
Q

When to screen in T1DM: dyslipidemia

A

age 12y and 17y
delay after dx until metabolic control

if <12y, only screen if BMI> 97th %ile, Fh of dyslipidemia or CVD

29
Q

When to screen in T1DM: hypertension

A

all children
q6months

30
Q

Associations w falsely elevated A1C

alternative

A

Any condition that prolongs the life of the erythrocyte or is associated with decreased red cell turnover

iron deficiency
vitamin B-12 and folate deficiency anemias
asplenia/splenomegaly
uremia/chronic renal failure
severe hyperTG
severe hyper bili
chronic alcohol
anemia from blood loss
pregnancy
Vit E ingestion

fructosamine

31
Q

insulin-antagonistic hormones?

A

corticosteroids, catecholamines, glucagon, and GH

32
Q

what is the predominant ketone in DKA?

A

βOHB

33
Q

Indications for the pump

A

i) Under the age of 7 (as per ISPAD guidelines)
ii) Recurrent severe hypoglycemia
iii) Large fluctuation in glucose levels
iv) Suboptimal glycemic control (A1C out of range)
v) Microvascular complications or risk factors for macrovascular complications
vi) Insulin regimen compromises lifestyle
vii) Pronounced dawn phenomenon
viii) Needle phobia
ix) Pregnant adolescents
x) Competitive athletes
xi) Ketosis prone individuals

· Low insulin needs (less than 0.5 units per injection)
· Motivation for a pump
· Wants flexibility
· Gastroparesis
· type 2 diabetes who are not meeting glycemic targets with MDI, oral medication, and lifestyle modifications

34
Q

advantages of the pump

A

· Establishment of a basal profile tailored to patient for better overnight and between meals glucose control
· Easier to manage glycemic excursions that occur with exercise
· Ability to calculate boluses based on glucose reading and carbs easily
· Keeps track of time since last bolus and correction – reduces risk of overcorrecting

35
Q

disadvantages of the pump

A

· Higher risk of DKA due to pump failure given no long-acting insulin
· Costly
· Time demanded of MD and staff in initiating therapy

36
Q

6 pump-specific features that can explain high BG

A

i) Sites are getting placed into areas of lipohypertrophy
ii) Not changing sites regularly
iii) Bolusing after or during eating
iv) Missing boluses
v) Not giving correction boluses
vi) Not putting current BG into pump when bolusing
vii) Basal rates require adjustment
viii) Extended periods with the pump suspended
ix) Outgrown ISF
x) Active insulin time is too long

37
Q

How do you determine basal insulin for pump initiation?

A

TDD x 0.75 divided 2, then divided by 24 hours

38
Q

what is dawn phenomenon

A
  • rise of BG in early morning hours due to spike of counterregulatory hormones
  • can start ~2AM;

often can be managed by increasing basal rate or adding basal about an hour before spike that is higher

39
Q

sns of cerebral edema

A

-New/worsening headache
-Nausea/vomiting
-Cushing’s triad (bradycardia, widened pulse pressure, bradypnea/irregular respirations)
-loss of consciousness
-abnormal pupillary responses
-respiratory failure
-specific focal neurological defects (posturing, cranial nerve palsy)

40
Q

Diagnostic criteria for cerebral edema

A

One diagnostic criterion, two major criteria, or one major and two minor criteria have a sensitivity of 92% and a false positive rate of only 4%.

Diagnostic criteria
● Abnormal motor or verbal response to pain
● Decorticate or decerebrate posture
● Cranial nerve palsy (especially III, IV, and VI)
● Abnormal neurogenic respiratory pattern (eg, grunting, tachypnea,
Cheyne-Stokes respiration, apneusis)

Major criteria
● Altered mentation, confusion, fluctuating level of consciousness
● Sustained heart rate deceleration (decrease more than 20 beats per minute) not
attributable to improved intravascular volume or sleep state
● Age-inappropriate incontinence

Minor criteria
● Vomiting
● Headache
● Lethargy or not easily arousable
● Diastolic blood pressure >90 mm Hg
● Age <5 years

41
Q

how to manage cerebral edema

A

-Elevate head of bed/centre head
-Reduce fluid rate
-Supportive therapy for respiration (ie oxygen)
-Mannitol or 3%NaCl

42
Q

causes of elevated ACR in DM

A

Benign postural proteinuria,
diabetes related nephropathy,
exercise induced proteinuria,
febrile illness, UTI,
acutely elevated glucose
Decompensated CHF
Menstruation
Acute severe elevation in BG
Acute severe elevation in BP

43
Q

how to improve diabetic nephropathy

A

i) Optimizing glycemic control
ii) Blood pressure control (<130/80)
iii) Blocking RAAS – ACEi or ARB (independent of BP)
iv) SGLT2 inhibitor (also has cardioprotection)

44
Q

CF related diabetes - what are factors that cause

A

● Thick secretions plug pancreatic ducts causing a chronic pancreatitis like picture and beta cell damage
● Chronic steroid exposure
● High caloric and often carbohydrate intake
● Insulin resistance from chronic hyperglycemia causing down regulation of GLUT4 transporters
● CFTR channel on beta cells may play a role in insulin secretion
● Tube feeding

45
Q

CF related diabetes
- when to start screening
- how is it different

A
  • 10 yo w OGTT
  • they don’t get microvascular complications
46
Q

Endo d/o that happen in CF

A
  • CFRD
  • osteoporosis
  • short stature
  • male infertility
  • delayed puberty
47
Q

what is the gold standard for assessing insulin sensitivity

A

Euglycemic Hyperinsulinemic Clamp Test

  1. Primed continuous insulin infusion is administered to raise plasma insulin level to a predetermined physiological or pharmacological level
  2. Plasma glucose concentration is measured q5min and variable GIR is administered to maintain the plasma glucose concentration constant at the fasting level
  3. Given that plasma concentration of insulin is steady, the amount of exogenous glucose administered equals the amount of glucose utilized in response to the hyperinsulinemia and provides a direct measure of whole body sensitivity to insulin; can then predict Insulin Sensitivity Index from this value
48
Q

2 tests to measure of insulin insensitivity

A
  1. Homeostasis model of Insulin Resistance (HOMAir): estimates insulin resistance using the formula:
    a. HOMAir (mmol/LxuU/mL) = fasting BG (mmol/L)x fasting insulinuU/mL/22.5 (higher values means increased insulin resistance)
  2. Insulin sensitivity index (ISI) = 10 000/ square root (fasting BGxfasting insulin) x (mean glucose x mean insulin during OGTT) → lower the ISI, the more insulin resistant the subject is
49
Q

Causes of hypoK in DKA

A
  • Shift of K from intracellular to extracellular space in exchange with hydrogen ions that accumulate extracellularly in DKA → shifted K is lost by osmotic diuresis
  • Administration of insulin, leading to intracellular shift of K
  • Secondary hyperaldosteronism due to dehydration leading to excretion of K to hold on to Na/fluid for fluid repletion
  • low total K in body
50
Q

complications of HHS

A

i) Malignant hyperthermia (mechanism unknown)
ii) Rhabdomyolysis due to acute renal failure
iii) Altered mental status (reversible)
iv) Venous thrombosis associated with central venous cath

51
Q

causes of hyperBG and high CPeptide

A

· Type 1 diabetes – in honeymoon phase
· CFRD – there’s not absolute insulin insufficiency
T2DM,
acute renal failure (C-peptide is renally cleared)

52
Q

how does long acting insulin have longer duration of action

A

Has low aqueous solubility at neutral pH; in injection solution, which is pH 4, solution is completely soluble.

Acidic solution is neutralized on injection into SC tissue, leading to microprecipitates, from which small amounts of insulin glargine are released.

Leads to slow release and a constant (peakless) release over time.

53
Q

falsely decreased A1C

A

chronic renal failure
splenomegaly
rheumatoid arthritis

use of erythropoietin iron or B12
reticulocytosis
chronic liver disease

ingestion of aspirin, vit C or Vit E
hemoglobinopathy

hyperTG assay

54
Q

what does glucagon do

A

encourages lipolysis and ketone production in the liver

Binds to receptor on hepatocytes and causes stimulation of glycogen store breakdown

maintains gluconeogenesis (production of glucose from amino acids)

55
Q

iRecommendations for driving with T1DM

A
  1. Consider measuring BG right before driving
  2. Keep meter/testing supplies easily accessible
  3. Keep rapid glucose available to treat low
  4. If driving for long periods, check at least every 4h
  5. Consider a CGM so that you can receive alerts
  6. Consider checking BG more often if at risk of lows ie if have exercised recently, skipped a meal
  7. If recurrent, severe hypoglycemia or hypoglycemia unawareness, must check immediately before driving, at least q2h and/or have a CGM
  8. DO NOT start driving if BG<4; if <4, treat with 15g carbs and wait 40min; before driving, should be >5mmol/L
  9. If hypoglycemia occurs while driving, pull over in a safe spot and take keys out of ignition. Treat and wait 40min after correction to begin driving again
  10. On long journeys, take regular periods for snacks/meals/rest

PEDS ENDO RC TD 2022 (14 decks)

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