Case 16: 7yo - DM Flashcards
how to test for Celiac
TTG IgA > 100
Total IgA
(if low total IgA, normal TTG –> false negative)
- endomesial antibody = 100% specificity
gold standard = Biopsy
when can you NOT test for Celiac’s
already gluten free
(can’t get IgA antibodies, or scope/biopsy)
–> need to introduce celiac’s for 4w (1 slice of bread per day)
treatment for Celiac’s
Remove gluten - low FOD-MAP diet
- trend TTG IgA q3-6mo for 1 year (==> takes 1y for antibodies to decrease)
- q1y after that = to test for accidental ingestion
when do you use a genetic test for Celiac’s disease?
1) when gluten-free and don’t want to re-introduce
- useful only when negative
- b/c if positive = 20-30% of population has it
differentiate
= Celiacs
= gluten allergy
= gluten sensitivity
1) Celiac’s = IgA
- sxs: diarrhea, malabsorption
2) gluten allergy = IgE
- sxs: hives, swelling
- exercise induced wheat anaphylaxis = if eat wheat, then exercise within next hour ==> anaphylaxis
3) non-celiac gluten sensitivity
- rule out Celiac’s, rule out glutenallergy
- tx: decrease gluten to tolerable levels
What is the most common age group for significant vomiting
Kids <3yo ==>viral gastroenteritis, dehydration
Why do children have an increased risk of dehydration?
Kids <4yo v. adults
- higher surface areas:body mass ratio == greater relatively area for evaporation
- higher BMR == increased heat, loss of water
- higher % body weight that is water (infants = 70%; children = 65%; adults = 60%)
How do diagnose DM?
Sxs = polyuria, polydyipsia, unexplained weight loss
1) sxs of DM + random BG > 200
2) fasting BG > 126
3) Oral glucose tolerance test: 2-h postload glucose >200
4) HbA1c >/= 6.5%
How to diagnose DKA?
Sxs = vomiting, tachycardia, mental status changes, dehydration
1) random BG > 200
2) venous pH < 7.3 OR serum bicarb < 15
3) moderate/large ketonuria/ketonemia
Diabetic ketoacidosis (DKA)
- epidemiology:
- pathophysiology:
- LABS:
EPIDEMIOLOGY: T1DM»_space;> T2DM
PATHOPHYSIOLOGY: T1DM == relative/abs insulin deficiency (insulin = glucose entry into peripheral tissues; inhibited lipolysis, glycogenolysis, tissue catabolism)
1) HYPERGLYCEMIA: lack of insulin + excess counterregulatory hormones (glucagon, catecholamines, cortisol, GH) –> catabolic state = increased gluconeogenesis, lipolysis, glycogenolysis, inhibited glycolysis
2) KETOGENESIS: increased lipolysis –> mobilized FFAs ==>ketones (acetoacetic, beta-hydroxybutyric acids)
3) METABOLIC ACIDOSIS = increased production of ketones –>decreased Ph
4) + LACTIC ACIDOSIS = dehydration, poor tissue perfusion
5) HYPOVOLEMIA, DEHYDRATION, ELECTROLYTE LOSS (Na, K, PO4) = when BG ~180 –> OSMOTIC DIURESIS
==> further LIPOLYSIS - d/t intravascular volume depletion –>catecholamine release
==>HYPEROSMOLALITY – d/t osmotic diuresis, hyperglycemia
==> RENAL IMPAIRMENT, HYPERGLYCEMIA – d/t dehydration
LABS
- pH(decreased) == metabolic acidosis d/t elevated ketoacids, lactic acid
- serum Na (decreased) == (1) osmotic movement of water into extracelluar space d/t hyperglycemia, hyperosmolarity [dilutional hyponatremia]; (2) renal sodium losses in urine
- serum K (normal) [with total body K decreased] == (1) hyperkalemia d/t acidosis and low insulin driving K out of cells; (2) expected hypokalemia with correction of acidosis and low insulin.
- bicarbonate (decreased) == d/t metabolic acidosis, d/t elevated ketoacids, lactic acid
- creatinine (elevated) ==d/t severe dehydration (prerenal azotemia)
- serum glucose (elevated) == in DM, DKA
- serum, urine ketones (elevated) == d/t increased lipolysis from low insulin
Diabetic ketoacidosis (DKA) - presentation:
PRESENTATION: known T1DM + vomiting = assumed DKA until proven otherwise
- vomiting
- tachycardia
- mental status changes
- dehydration
- weight loss
- SOB
What kinds of potassium can be used during treatment of DKA?
KCl
K acetate
K phosphate == less Cl given; decreased risk for iatrogenic hyperchloremic acidosis; more K and PO4 given (both depleted during DKA)
How to monitor for treatment response in DKA?
- rehydration status
- serum, urine glucose levels
- serum, urine ketone levels
- K levels
Types of dehydration
- causes:
- how to replace the deficit:
- complications of treatment:
==>based on serum Na
1) ISOTONIC/ISONATREMIC (Na nml) == losses: Na and H2O balanced
- causes: acute gastroenteritis, diarrhea
- how to replace the deficit: NS over 12h
- complications of treatment: none
2) HYPOTONIC / HYPONATREMIC (Na < 130) == losses: Na»_space; H2O / dilutional
- causes: pts drink diluted fluids / water in setting of dehydration; adrenal insufficiency (low mineralocorticoids)
- how to replace the deficit (= Na deficit): NS or hypertonic saline over 24h
- complications of treatment: central pontine myelinolysis (d/t rapid correction == rapid shrinking of brain, esp. pons)
3) HYPERTONIC / HYPERNATREMIC (Na>150) == losses: H2O»_space; Na ==>highest mortality
- causes: breastfeeding failure; use of inappropriate rehydration solutions; diabetes insipidus; DKA (osmotic diuresis, hyperosmolarity == although hyponatremic 2/2 hyperglycemia)
- how to replace the deficit (= free water deficit): NS over 48h
- complications of treatment: cerebral edema
Which type of dehydration is associated with the highest mortality?
HYPERTONIC / HYPERNATREMIC (Na>150) == losses: H2O»_space; Na
- breastfeeding failure
- diabetes insipidus
- DKA ==> osmotic diuresis, hyperosmolarity == although hyponatremic 2/2 hyperglycemic
Cerebral edema
- epidemiology:
- timing:
- pathophysiology:
- prognosis:
epidemiology: 0.5-1% of pediatric DKA epiodes
timing: even before
treatment is initiated and up to 24 hours after initiation of treatment.
pathophysiology RFs
- high BUN at presentation
- profound acidosis + hypocapnia
- increased serum Na with treatment
- administration of bicarb
prognosis: 21-24%rate of mortality
T2DM
- epidemiology:
- pathophysiology:
- RFS:
- screening indication
- management
- epidemiology: up to 50% of all new cases of DM; 10x increase in past 20y
- pathophysiology: insulin resistance (nml / high levels of insulin) in peripheral tissues –> hyperglycemia
- RFS: obesity (BMI>95%ile), ethnicity (Native A., African A., Latino A., Asian A.); age (12-16y); female sex; sedentary lifestyle; hyperglycemia over long periods of time
Screening indication: 10yo or puberty, q3y for overweight kids (BMI > 85%ile)
PLUS
- maternal hx of DM or GDM
- Fhx of T2DM in first-degree relative
- race/ethnicity
- signs/conditions of insulin resistance == acanthosis nigricans, HTN, dyslipidemia, PCOS
Management
- insulin for kids with random BG> 250; HbA2c values > 9%
- medical therapy + diet, exercise from time of diagnosis
Adjusted Glasgow coma scale for kids <5yo
A. Adjusted verbal response criteria [v. adult]
5 - Smiles, orientated to sounds, follows objects, interacts [oriented]
4 - Cries but consolable, inappropriate interactions [confused but able to answer questions]
3 - Inconsistently inconsolable, moaning [inappropriate words]
2 - Inconsolable, agitated [incomprehensible sounds]
1 - No verbal response
Others as normal: B. eye-opening response 4 - Eyes open spontaneously 3 - Eyes open to verbal command 2 - Eyes open to pain 1 - No eye opening
C. motor response
6 - Obeys commands
5 - Localizes pain
4 - Withdraws from pain
3 - Abnormal flexion, decorticate posture
2 - Extensor response, decerebrate posture
1 - No motor response, flaccid
What is the threshold for treatment in Glasgow score?
Total score = 15
GCS = 8 –> may require aggressive intervention and management