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RC Peds Endo 2023 > T1DM > Flashcards

T1DM Flashcards

1
Q

HbA1C target T1DM

A

</= 7.5 % for all

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2
Q

Dose mini glucagon

A

10mcg/year of age = 1u on insulin syringe
min 20mcg
max 150mcg

double if BG not improved in 20 min

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3
Q

Carbs and juice to treat hypoBG

A

<5y
5g, 40ml

5-10y
10g, 85ml

> 10y
15g, 125ml

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4
Q

Causes of poor metabolic control

A

mental health disorder
eating disorder
low SES
Low family support
higher family conflict

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5
Q

Cause of DKA

A

insulin omission
poor sick day management

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6
Q

Increased risk DKA

A

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

Established DM:
poor metabolic control
prev episode of DKA
peripubertal
adolescent girls
CSII
ethnic minorities
psychiatric d/o
difficult family circumstances

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7
Q

Decreased freq of DKA - how?

A

Education
Behavioural intervention
family support
24h telephone service

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8
Q

Risk factors for cerebral edema during tx DKA

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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9
Q

% adolesent females with T1DM w ED

A

10%

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10
Q

Why is ED bad in DKA

A

poor metabolic control
earlier onset and more rapid progression of microvascular complications

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11
Q

Comorbid conditions of T1DM and their %

A

autoimmune thyroid disease - 10%
1ary adrenal insufficiency - rare
celiac disease - 4-9%

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12
Q

Comorbid conditions in T1DM - who to screen, 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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13
Q

Complications of T1DM

A

Nephropathy
Dyslipidemia
Retinopathy
Neuropathy
Hypertension

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14
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

24h urine collection = gold standard

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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15
Q

False positive for proteinuria

A
  • Transient albuminuria
  • Benign orthostatic proteinuria
  • exercise induced proteinuria
  • infections ex UTI
  • nondiabetic kidney disease (i.e., IgA or other types of nephritis)
  • acute marked hyperglycemia
  • acute marked elevation in BP
  • fever
  • menstrual bleeding
  • decompensative CHF
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16
Q

When to screen in T1DM: Nephropathy

A

Yearly starting age 12y and 5y duration

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17
Q

When to screen in T1DM:
Retinopathy

A

yearly starting age 15y and 5y duration
can go to 2y if good glycemic control and <10y duration

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18
Q

Screening for retinopathy

A

7-standard field, stereoscopic-colour fundus photography with interpretation by trained reader (gold standard)

direct ophthalmoscopy or indirect slit-lamp fundoscopy through dilated pupil

digital fundus photography

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19
Q

When to screen in T1DM:
Retinopathy

A

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

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20
Q

When to screen in T1DM: dyslipidemia

A

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

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

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21
Q

How to screen dyslipidemia in T1DM

A

fasting or non fasting:
Total ch
HDL-C
TG
Calc LDL-C

non fasting okay if TG not elevated
if TG >4.5 do fasting (>8h)

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22
Q

When to screen in T1DM:
hypertension

A

all children
q6months

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23
Q

When and how to treat nephropathy in T1DM

A

only if persistent >3 months

confirm not other cause w urine dip and microscopy - cast, blood

ACEi
ARB

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24
Q

Risks for dyslipidemia in T1DM

A

longer duration of DM
microvascular complications or other CV RF (smoking, hon, obesity, fhx premature cvd)

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25
Q

% adolescent w T1DM with hypertension

A

16%

can predict future albuminuria

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26
Q

When and how to initiation transition to adult plan

A

12yo start
education in self care
transition readiness
assessmnets
ID transition goals

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27
Q

Driving w T1DM - medical evaluations

A

q2years

glycemic control
freq/severity of hypoBG
hypoBG awareness
presence of micro- or macrovascular complications (retinopathy, neuropathy, nephropathy, amputation, CV dz) to ID if increased risk MVA

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28
Q

Driving w T1DM - what to do when driving

A

log of BG

always have BG monitoring equipment and rapid carbs within reach

measure BG prior to driving - should be >5
if <4 wait 40 min before driving

measure BG q4h behind wheel or CGM

wear medic alert bracelet

Must refrain from driving immediately if have had severe hypoBG while driving and contact HCP

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29
Q

Driving w T1DM - when to report

A

severe hypoBG while driving in past 12months

more than 1 episode of severe hypoBG while away but not driving in:
- 6m private driver
- 12m commercial driver

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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 hyperbili
chronic alcohol
anemia from blood loss
pregnancy
Vit E ingestion

fructosamine

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31
Q

Associations w falsely lowered 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

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32
Q

3 forms of DM retinopathy

A

1) macular edema
= diffuse or focal vascular leakage at the macula (non-proliferative)

2) progressive accumulation of micro- vascular change that includes microaneurysms, intraretinal hemorrhage, vascular tortuosity and vascular malformation (together known as non-proliferative diabetic retinopathy) that ultimately leads to abnormal vessel growth on the optic disc or retina (proliferative diabetic retinopathy)

3) retinal capillary nonperfusion, a form of vascular closure detected on retinal angiography, which is recognized as a potential complication associated with diabetes that can cause blindness and currently has no treatment

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33
Q

RF for DM retinopathy

A

Longer duration of DM
High A1c
Increased BP
Dyslipidemia
Anemia
Pregnancy (with T1D)
Proteinuria
Severe retinopathy itself

Modifiable:
Glycemic control - ≤7%
Blood pressure control
Statin and fenofibrate – role in preventing development or progression is not established

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34
Q

DM retinopathy

A
  • Laser therapy (i.e photocoagulation to retinal periphery when centre not involved)
  • Intraocular anti-VEGF (first line for centre-involving DME)
  • Vitrectomy – if complicated with non-clearing vitreous bleeding, persistent neovascularization (especially post laser or anti-VEGF)

If visually disabled – refer for low-vision evaluation and rehab

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35
Q

Neuropathy - screening in DM

A

T2D – at diagnosis and annually
T1D - ≥15 y.o, ≥5 yrs diagnosis with poor metabolic control – annual

Assessing loss of sensitivity to the 10g monofilament
loss of sensitivity to vibration at the dorsum of the great toe (with tuning fork)
pinprick or temperature
ankle reflexes

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36
Q

Presentation of neuropathy in DM
- increase risk of what serious thing

A

Peripheral neuropathy (increase risk of foot ulcers and amputation)
- loss of sensation in toes and feet, sharp shooting pains, burning, tingling, throbbing, numbness
The involvement of large fibres may cause numbness, tingling and loss of protective sensation.

Autonomic neuropathy: cardiac auto- nomic neuropathy [CAN]), gastrointestinal tract, genitourinary system, sexual function, pupillary responses and sweating

mononeuropathies/focal neuropathies (median, ulnar, radial, common peroneal nerves), radiculoplexus neuropathy, cranial neuropathies

  • arrhythmias
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37
Q

RF for neuropathy in DM

A

elevated BG
elevated TG
high BMI
smoking
HTN

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38
Q

Treatment of dyslipidemia in DM

target

A

statin
target LDL <2 or 50% reduction from baseline

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39
Q

HHS criteria

A

BG >33
Bic >15
art pH >7.3
ven pH >7.25

Small ketonuria, absent to small ketonemia

Osm >320

Obtundation, combativeness, seizures (50%)

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40
Q

Why is intubation and ventilation high risk in DKA?

A

increase pCOS2 above level the pt had been maintain may cause CSF pH to decrease => worsen cerebral edema

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41
Q

When does eugylcemic DKA happen?

A

partially treated DKA
starvation (anorexia or fasting
low card/high fat diet
SGLT2i

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42
Q

RF for DKA

A

New:
<2yo
minority groups
Low SES

Known DM:
Insulin omission
Poor metabolic control or previous episodes of DKA
Gastroenteritis with persistent vomiting and inability to maintain hydration
Psychiatric d/o (esp eating d/o)
Difficult or unstable family circumstances
Peripubertal and adolescent girls
Binge alcohol consumption
Limit access to medical services

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43
Q

Concerning features for cerebral edema:

A
  • Onset of headache after starting DKA treatment or worsening headache that was already present before starting treatment
  • Inappropriate slowing of heart rate
  • Recurrence of vomiting
  • Change in neurological status – restlessness, irritability, increased drowsiness, confusion, incontinence
  • Increase BP
  • Decrease O2 sat
  • Rapid increase Na conc 🡪 loss of urinary free water as manifestation of DI (from interruption of blood flow to pituitary gland due to cerebral herniation)
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44
Q

What is failure of measured Na to increase or it decreases a sign of in DKA

A

impending cerebral edema

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45
Q

Goals of fluid and late replacement in DKA

A
  • Restore circulating volume
  • Replace Na and extracellular and intracellular water deficits
  • `Improve glomerular filtration and enhance clearance of glucose and ketone from blood
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46
Q

Why does K drop in DKA/tx?

A

1) Major loss is from the intracellular pool – because of transcellular shifts caused by hypertonicity, acidosis, and glycogenolysis & proteolysis due to insulin deficiency

2) K+ is lost from body from vomiting because of osmotic diuresis

3) Volume depletion causes secondary hyperaldosteronism -> urinary K+ excretion

47
Q

what is concern for severe hypophos?

A

hypophos: decreases ATP and 2,3-DPG -> metabolic encephalopathy, impaired myocardial contractility and resp failure (weakness of diaphragm), muscle dysfunction with proximal myopathy, dysphagia, and ileus

Rhabdo if pre-existing severe PO4 depletion

48
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 mmHg
- Age <5 years

49
Q

How to manage cerebral edema

A

Decreased fluids - maintain normal BP (avoid excess, also avoid hypotension)
Head of bed 30 degrees, head midline
Mannitol 0.5-1g/kg over 10-15min
3% saline - 2.5-5ml/kg over 15-30 min
Do not delay tx for imaging!!
Supportive therapy (O2, I&V, etc)

50
Q

How to treat HHS

A

IVF bolus >/= 20ml/kg
(assume 12-15% fluid deficit)

Start insulin when BG no longer drops with IVF alone

0.025-0.05u/kg/h
titrate dose to decreased BG 4-5.5/h

add D2.5/5 if BG dropping too much

want gradual decline in corrected Na and osmolality

replace K as soon as K normal + normal renal fn

replace Mg if severe hypoMg/hypoCa

51
Q

Complications of HHS

A
  • venous thrombosis (from rapid drop in BG/Osm + central venous Cath)
  • rhabdomyolysis (from AKI, severe hyperK, hypoCa, compartment syndrome)
  • malignant hyperthermia (reason unknown)
  • altered mental status (adults - not CE)
52
Q

Risks of baby born to mom w DM

A

LGA
SGA
jaundice
prematurity
still birth
hypoglycemia
NICU
cardiac (transient hypertrophic cardiomyopathy)
skeletal malformations

53
Q

Risk factors for GDM

A
  • > 35yo
  • from a high-risk group (African, Arab, Asian, Hispanic, Indigenous, or South Asian)
  • Corticosteroid medication
  • Obesity (BMI >/= 30 kg/m2)
  • Prediabetes
  • Gestational diabetes in a previous pregnancy
  • Given birth to a baby that weighed more than 4 kg
  • A parent, brother or sister with type 2 diabetes
  • Polycystic ovary syndrome or acanthosis nigricans
54
Q

Screening for GDM

A

If high risk fo T2DM -> screen w HbA1c at first antenatal visit
- If A1c ≥6.5% or FPG ≥7 – have diabetes in pregnancy
- If negative – rescreen at 24-28 weeks

All women screened at 24-28 weeks

50g GCT in nonfasting state - BG 1h later
- BG ≥7.8 mmol/L at 1 h = positive screen and is an indication to proceed to the 75 g OGTT
- BG ≥11.1 mmol/L = diagnostic of gestational diabetes and does not require a 75 g OGTT for confirmation

If GCT screen positive -> 75 g OGTT dx of GDM if 1 of the following:
- Fasting PG ≥5.3 mmol/L OR
- 1 hour PG ≥10.6 mmol/L OR
- 2 hours PG ≥9.0 mmol/L

55
Q

Treatment of GDM

A

MDI insulin

Metformin is alternative but crosses the placenta
- 40% will still need insulin

Glyburide if decline insulin/metformin not tolerated

56
Q

What are the stages of T1DM

A

1) >/=2 Abs - euglycemia
2) >/=2 Abs - hyperglycemia
3) T1DM dx
4) Longstanding

57
Q

Normal Glycemia:

HbA1c

Fasting BG

Oral GTT (2h BG)

Random BG

A

HbA1c<5.7%

Fasting BG <5.6

Oral GTT (2h BG) <7.8

Random BG <11

58
Q

Diabetes:

HbA1c

Fasting BG

Oral GTT (2h BG)

Random BG

A

> /=6.5%

> /= 7

> /= 11

> 11 with symptoms

58
Q

Prediabetes:

HbA1c

Fasting BG

Oral GTT (2h BG)

A

5.7-6.4%

5.6-6.9

7.8-11
(“glucose intolerance)

59
Q

how to prolong honeymoon?

A

Earlier detection

Exercise

Highest safe insulin dose

60
Q

Short acting insulins

A

Regular:
- humulin R
- Novolin Toronto
- Entuzity

61
Q

Rapid actin insulins

A

Aspart:
- Novorapid
- Fiasp

Lispro
- Humalog

Glulisine:
- Apidra

62
Q

Long acting insulins

A
  • Glargine
    ○ Basaglar
    ○ Lantus
    ○ Toujeo
  • Degludec
    ○ Tresiba
  • Detemir
  • Levemir
63
Q

what is the polyol pathway

A

HyperBG -> hexokinase becomes saturated

XS glucose in the cell -> glucose doesn’t get P’d -> gets converted to sorbitol

sorbitol locks it in the cell because it cant cross the membrance
-> it increases AGE on proteins

64
Q

First long term complication in T1Dm?

A

retinopathy

65
Q

Treatment related complications in T1DM

A
  • lipohypertrophy
  • insulin edema
66
Q

Ab in T1DM

A
  • Anti-GAD Ab
  • Anti-islet cell Ab
  • Anti-ZnT8 Ab
  • Anti- insulin
  • Anti-tyrosine phosphatase (IA2)
67
Q

risk of T1DM
DR3/4-DQ8 or DR4/DR4

A
  • Those with DR3/4-DQ8 or DR4/DR4
    ○ with FH: 20%
    ○ w/o FH: 5%
68
Q

Risk of T1DM in :
Monozygotic twins risk
Risk to siblings, children

A

Monozygotic twins risk: ~40%
Risk to siblings, children: ~5%

69
Q

Counselling re: alcohol T1DM

A

Moderate amounts of alcohol can cause BGs to rise
Excess alcohol can cause BGs to fall (competition in liver, glucagon release impeded)

  • Discuss relative alcohol and carb content of diff drinks
  • Recommend eating carb-containing foods before, during and after alcohol consumption
  • Discourage binge drinking (more than 4 drinks)
  • Alternate between alcohol and then a water
  • Avoid sugary alcoholic beverages
  • Check BG more frequently
  • Recommend eating a snack before bed
  • Set alarm to check BG during night to avoid noctural hypoBG
  • Recommend always wearing a medic alert bracelet
  • Discuss if friends would be able to recognize signs of hypoglycemia and intervene if necessary
  • Recommend not taking insulin for the CHO in drinks given that they the alcohol itself can lead to hypoglycemia
  • Glucagon may not work as well because of liver
70
Q

Counselling re: exercise T1DM

A
  • Check BG before, during and after exercise
    • Discuss possible delayed nocturnal hypoglycemia
      ○ Important to check BG overnight
    • Consider temporary basal rate during exercise to avoid hypoBG
    • In not reducing rate, recommend additional carbs before or during runs
    • Do not exercise if hyperBG and ketones >0.5
      Give reduced insulin dose with carbs prior to exercise
71
Q

Who should be in inter professional team for T1DM

A

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

72
Q

HbA1C target for T1DM

A

<7.5%

73
Q

HbA1C target for T2DM

A

<7%

74
Q

Poor control in T1DM - reasons

A

Causative and associated factors:
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

75
Q

How to reduce freq of DKA

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

76
Q

T1DM - risk of what psych d/o

A

Diabetes distress
Depression
Anxiety
Eating disorders
Externalizing disorders

77
Q

Hypothesis why increasing incidence of T1DM

A
  • Hygiene hypothesis – autoimmune hypersensitivity due to a lack of exposure to pathogens
  • Accelerator hypothesis - Increasingly obesogenic environment, which causes insulin resistance (which promotes the development of T1D in people with islet cell autoimmunity – high BG lead to stress and early destruction of beta cells) may account for the rise in incidence of T1D
  • Sunshine hypothesis – Less time spent outdoors (and covered up) leading to Vit D deficiency. Comes from the observation that countries closer to the equator have lower rates of T1D
  • Cows milk hypothesis – exposure to this early antigen (or lack of breastfeeding) disrupts the immune system and increases the risk of T1D

i. v. Environmental triggers – pollution, viruses, toxins, immigrant populations etc.

Genetics

78
Q

Environmental triggers that may cause dvlpt of T1DM

A

Viruses

Dietary factors (all small amount of risk)
○ Breast feeding/cows milk
§ BF- slightly decreases risk
§ Cows milk at young age - slightly increases risk

Low Vitamin D, omega-3 fatty acids

79
Q

% risk with antibodies

A

1 Ab - ~14%
2 or more - 70-80%

80
Q

Phenomena seen in T1DM

A

Dawn phenomenon - overnight spike of counterregulatory hormones (usually ~2am): need to increase basal insulin around time of spike

Simogyi effect - rebound hyperglycemia after a low

81
Q

Improvement of A1c with in Type 1 DM:
- regular physical activity
- CGM
- sensor-augmented pump

A
  • regular physical activity -0.5%
  • CGM -1%
  • sensor-augmented pump -0.5%
82
Q

Specific factors that support the recommendation for insulin pump therapy include:

A
  • Recurrent severe hypoglycemia
  • Wide fluctuations in glucose levels regardless of HbA1c
  • Suboptimal diabetes control (i.e., HbA1c exceeds target of 7.0% or
    TIR is <70%)
  • Microvascular complications and/or risk factors for macrovascular complications
  • Targeted metabolic control but insulin regimen that compromises lifestyle
  • Young children and especially infants and neonates
  • Children and adolescents with pronounced dawn phenomenon
  • Children with needle phobia
  • Pregnant adolescents, ideally preconception
  • Ketosis prone individuals
  • Competitive athletes
83
Q

Pump: % basal v bolus

A

In older children and adolescents expect a 50/50 split
In children <7 years, basal insulin delivery may be 30%–35% of the TDD

84
Q

Unexplained hypo?

A
  • Celiac
  • Addison
  • Taking insulin to cause hypo
  • Incorrectly dosing insulin
  • Muchenhausen by poxy
  • ED
  • Meds - alcohol, ASA, oral hypoglycemic
  • severe illness affecting kidney or liver
85
Q

Risk for severe hypoBG

A
  • history of severe hypo
  • A1C <6%
  • long duration DM
  • adolescence
  • hypoBG unawareness
  • autonomic neuropathy
  • preschool children
86
Q

DKA complications

A
  • hypoK
  • hypoPhos
  • hypoCa
  • hypoMg
  • hypoBG
  • Hyperchloremic acidosis
  • Hypertryglyceridemia → acute pancreatitis
  • cerebral edema
  • VTE/PE
  • aspiration
  • cardiac arrhythmia
  • rhabdo
  • renal failure
  • ARDS
87
Q

% of mothers with GDM go on to develop T2D

A

50%

88
Q

maternal gestational diabetes confers to child:
- risk of T1 and T2

A
  • 6-fold increase in risk of T2D in the child
    1.8-fold increase in risk of T1D in the child
89
Q

Neonatal outcomes of GDM

A

LGA/macrosomia -> shoulder dystocia -> brachial plexus injuries & perinatal asphyxia
Preterm delivery
Stillbirth
Polycythemia
TTN

Hypoglycemia
Hypocalcemia (hypopara)
Hyperbilirubinemia
Polycythemia

MALFORMATIONS:
Hypoplastic left colon,
cardiac malformations (TGA, DORV, VSD, TA),
hypertrophic cardiomyopathy
Sacral agenesis/caudal dysplasia
GI tract anomalies
Neural tube defects

90
Q

What is the Reduction in HbA1c with Regular Physical Activity?

A

0.5%

91
Q

Freq of CE in DKA

A

0.5-1%

92
Q

insulin-antagonistic hormones?

A

corticosteroids, catecholamines, glucagon, and GH

93
Q

what is the predominant ketone in DKA?

A

BOHB

94
Q

DX Criteria 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

95
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

96
Q

how to improve diabetic nephropahy

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)

97
Q

CFRD - 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

98
Q

CF related diabetes
- when to start screening

A
  • 10 yo w OGTT
    (DO NOT DO A1C)
99
Q

Endo d/o that happen in CF

A
  • CFRD
  • osteoporosis
  • short stature
  • male infertility
  • delayed puberty
100
Q

Gold standard for ins sens

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
101
Q

2 reason hypo K 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
102
Q

Diff between mgmt of HHS vs DKA

A
  • Patients may be more dehydrated so expect a larger fluid deficit, may need more boluses
  • Patients with HHS have larger whole body potassium / phosphate / magnesium deficits – monitor for these and replace as needed
  • Monitor CK regularly (every 2-3 hours) for rhabdoymyolysis
  • Use central venous catheters with caution, higher risk of thrombosis
  • Ketosis is usually minimal so early insulin administration is unnecessary. Initiate insulin when blood glucose is no longer falling with fluids alone.
  • may start with lower insulin concentration, 0.025-0.05 U/kg/hr
103
Q

RF for CFRD

A
  • Female
  • More severe disease
  • Pancreatic insufficiency
104
Q

Diff about CFRD

A
  • no DKA
  • no macrovasc comp
    (do get microvasc)
105
Q

Sx of CFRD

A
  • unexplained P&P
  • failure to gain or maintain wt
  • poor GV
  • delayed progression of puberty
  • unexplained decline in PFT
    MAY BE ASX
106
Q

CFRD tx

A

insulin - maybe just basal
no oral antihyperglycemics

107
Q

Eating d/o - signs

A
  • Significant weight loss or weight gain
  • Preoccupation with food content, weight, or dieting
  • Purging behaviors – excessive exercise, laxative/diuretic use
  • Recurrent / frequent DKA
  • Distorted body image
  • Low mood
  • Worsened metabolic control, increased HbA1C
  • Missed or cancelled appointments
  • Changes in school attendanceE
108
Q

Eating d/o - RF

A
  • Female gender
  • Higher BMI
  • Low self esteem
  • History of depression
  • Family history of dieting or eating disorder
109
Q

RF for deterioration in DM control going into adult care

A
  • emotional maturity, teens ability to sustain the daily Tasks of daily therapy
  • loss of parental supervision
  • reduced attendance to DM clinics
  • increased alcohol/substances
  • anxiety, depression
  • disordered eating
  • differing eating patterns as young adults become more independent
  • fear of hypo
  • knowlege gaps
110
Q

Hypo phos - mech in DKA

A
  • Urinary loss from osmotic diuresis
  • Reduced renal tubular reabsorption of phosphate
  • Shift of intracellular phosphate to the extracellular fluid compartment
    result of metabolic acidosis
  • Decreased intake
    (1 coming in, 1 shifting, 2 going out)

Further decrease during tx:
- Dilution from fluid replacement
- Entry of phosphate into cells resulting from insulin treatment
- Continuation of intravenous therapy without food consumption beyond 24 hours is a risk factor for clinically significant hypophosphatemia, although severe hypophosphatemia can also occur earlier in treatment

*Main determinant is degree of acidosis

111
Q

Signs nephropathy is from DM and not renal cause

A

Normal eGFR or not rapidly declining
No family history of nephropathy
Lack of extreme proteinuria >6g/d
Lack of persistent hematuria
Diabetes > 5yrs
Shouldn’t have signs or sx of another systemic disease
other DM comp present too

112
Q

what is lower coefficient of variation associated with?

A

reduced hypo

RC Peds Endo 2023 (17 decks)

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