Zach; Vitamins
B1 Thiamine
- Deficiency
- Early Beriberi (wet – cardiac) (dry- muscle wasting)
- Late Wernicke- Korsakoff
- Malnutrition, AIDS, Alcoholics
- Tx, replete
B2 Riboflavin
- Erythematous lesions, ulceration, mucositis
- Breast fed children, skim milk, pregnant women
- Tx, replete
B3 Niacin
- Pellagra
- 4ds
- Diarrhea, dermatitis, dementia, death
- 4ds
- Alcoholics, aids, IBD, malnutrition
B5 Pantothenic Acid
- Fatigue, headache, muscle weakness, nausea
- Usually deficient with another b vitamin
B6 Pyridoxine
- Dermatologic, dental changes
- Consequence of medicines
- INH, valproic acid, phenytoin, hydralazine, carbamazepine
- Also decreased renal function, autoimmune disease, inborn metabolic errors
B7 Biotin
- Dermatologic and neurologic manifestation
- In pregnant women, IBD, isotretinoin, long term antiepileptics
B9 Folate
- Megaloblastic anemia, glossitis
- Don’t confuse w B12
- Normal MMA, elevated homocysteine
- Elevated in both for B12
- Deficiency, pregnancy, burns, alcoholics
B12 Cobalamin
- Megaloblastic anemia, SCD, neuropathic symptoms
- Old people, vegans, IBD
C
- Scurvy
- Corkscrew hair, gingival hemorrhage, petechiae
- Malnutrition, alcoholics, pirates
Caroline; Hypoglycemia
- <70
- Symptoms generally develop <50-55
- More common in T1DM vs T2DM
- Whipple’s triad
- Do you have low glucose
- Do you have symptoms from low glucose
- Do you get better with glucose
- Mechanisms against hypoglycemia
- Glycogenolysis, gluconeogenesis
- S/Sx
- Adrenergic; anxiety, diaphoresis, hangry, tremor
- Neuroglycopenic; lethargy, confusion, seizures, agitation
- Most commonly in diabetics, usually overcorrection
- Nondiabetics; malnourishment, drugs/alcohol, insulinoma, critical illness, adrenal insufficiency, hypopituitary
- Workup
- POC glucose
- Tx
- Sugar
- Glucagon
- D50 vs D10
- Risk of overshooting w D50
- D50 and be caustic
- Refractory?
- D10 drip
- Consider octreotide
- Has insulin pump?
- Don’t dc pump
- Supportive treatment
- Contact manufacturer to troubleshoot
- Pediatric hypoglycemia
- Often asymptomatic until seizure
- New onset T1DM
- Maternal dm in neonates
- Medicine ingestion; bb, ethanol, sulfonylurea
- Glucose bolus 2ml/kg D10
Lyvers; pediatric endocrine
Hypoglycemia
- Causes
- Fatty oxidation disorder
- Insulin mediated
- Ketotic hypoglycemia
- Disorder of gluconeogenesis
- Other
- Ingestion
- Munchausen
– Obtain critical sample during hypoglycemic <50 episode
– for metabolic disorders
Fatty oxidation
- Can crump quick when glycogen depleted
- Test carnitine
Insulin mediated
Ketotic hypoglycemia
- Glycogen storage disorders
- Hormone deficiency
- hypopit
- Idiopathic (kids grow out of this by 6-8)
Disorders of gluconeogenesis
- Glactosemia
- Fructose disorders
Tx – Rule of 50
- D10 = 5ml/kg
- D50 = 1ml/kg
- Consider steroid
- Glucagon?
- Only helps with insulin mediated diseases bc they need preexisting hepatic stores of glycogen
Hyperglycemia
- DKA
- New onset
- p/w weight loss, polyuria, polydipsia, vomiting
- Look for kussmaul breaths
- Glucose >200
- pH <7.3
- Ketones
- New onset
- Tx
- Correct acidosis, dehydration, glucose
- Fluid resuscitation
- Aggressive
- 10-20 cc/kg bolus LR or NS
- Add potassium due to shifts intracellularly
- <3.5 = bolus
- Defer if >5.5
- Inulin 0.05 – 0.1 ug/kg
- Complications
- Cerebral edema
- Avoid bicarb
- Could be from hypoperfusion from dehydration
- Usually develops first 12hrs
- Tx, mannitol
Shaw; Acid Base
Look at pH (primary disorder) > check for compensation
Respiratory
Metabolic
Metabolic acidosis is usually complicated by compensation
Winters = paCO2 = 1.5 (HCO3) + 8 +- 2
Anion gap = Na – Cl – HCO3
NAGMA = GI vs renal bicarb loss
- Body takes in chloride
MUDPILES
Excess anion gap
- If change in anion gap > change in bicarb then too much bicarb = less acidotic
- AG – 12 + serum bicarb
- >30 =
- <30 = underlying NAGMA (too much Cl)
Use base deficit to predict resuscitation goals
VBG for people that don’t need exact pCO2, pulse ox accurate
ABG for people in shock
R acidosis – minute ventilation
R alkalosis – treat underlying cause
M alk – stop offending agent, consider CA inhibitor
M acidosis – treat underlying cause
Bicarb- need control or respirations to make sure co2 is blown off
- Otherwise benefits are primarily from Na and fluid replacemen t
- Na blocker overdose
Thomas; DKA/AKA
Gluconeogenesis/ glycogenolysis not as efficient glycolysis
Gluconeo breaks down fats and proteins
- Fat breakdown = ketones
- Happens in the liver primarily
Glyco
- No ketones
- Happens in muscle and liver
T1DM no insulin production
T2DM insulin resistance
Insulin = store
Glucagon = burn
T1DM more likely to have DKA
AKA
Wide gap acidosis in chronic drinkers
- Following a binge
- Abrupt stoppage of drinking prior to ED
Due to shift of carb metab due to malnutrition
Alcohol w no glucose
- Fasting state = glucagon secretion > gluconeogenesis (mainly lipolysis)
- If functioning liver
S/Sx
- N/V/abd pain
- Tachycardic, tachypnea
Labs
- Etoh often negative
- Anion gap
- Usually w LFT abnormality
Does not need to be acidotic
- 15% normal ph
- compensation