Endocrine Flashcards
previously diagnosed type 1 DM
est. based on hyperglycemia on multiple ED visits
refer to PCP for insulin dose adjustment
tx of persistent hyperglycemia in T1DM
blood surgery level diary
every dose of insulin administered and type administered
undiagnosed diabetic ER
ER doc makes diagnosis with pt who fits criteria
confirmatory test needed and review of medical hx
tx of undiagnosed diabetic in ER (stable)
12-24 hr f/u with PCP
if this is not possible, admit to tele
t1DM and glucocorticoid
develop hyperglycemia due to steroid tx
warning signs of hyperglycemia, seek close follow up with PCP and monitor glucose free.
add additional prandial doses of insulin )no need to increase basal insulin)
false glucose reading
icodextrin (peritoneal hemodialysis)
increased blood glucose levels with BEDSIDE reading
central lab glucose readings should be the ones that govern management
hypoglycemia value
plasma glucose <50 mg/dL
common in diabetics due to no surge of glucagon
hypoglycemia blunting 2/2
age
BB
neuorpathy
repeat episode = autonomic dysfunction
evaluation of hypoglycemia
history and physical
emphasis on timing and administration of insulin relation to meals
common causes of hypoglycemia
inadequate food intake infection change to regimine OD of medication or insulin BB toxicity renal failure ACS stress
s.s of hypoglycemia
drowsy, confused, dizzy, tired, cant concentrate or speak
tremor, sweating, anxiety, nausea, palpitations, shivering
hunger, weakness, blurred vision
alert pt hypoglycemia tx
glucose containing carbs
unconscious pt hypoglycemia tx
Glucagon 1 mg IV, IM, SC
1 amp of D50 IV
then pt consumes meal or snack
glucagon emergency kit
T1DM family members carry for hypoglycemia
1 mg IM glucagon – 10-15 minutes onset then swallow oral glucose
can cause n/v
hypoglycemia discostino
not on long acting - discharged
on long acting - admitted for monitoring
DKA epidemiology
mc in insulin dependent DM (T1)
higher mortality in elderly and in coma or HoTN
patho of DKA
cellular starvation 2/2 insulin deficiency and counter regulatory hormone excess
causes hyperglycemia, osmotic diuresis, preernal azotemia, ketone formation, wide anion gap metabolic acidosis
insulin fxn
metabolism and storage of carbohydrates , fat, protein
counter regulatory insulin hormones (4)
glucagon
catecholamines
cortisol
growth hormone
hyperglycemia in DKA
due to excess production and underutilization of glucose
counter regulatory hormones DKA cause
MC Glucagon
increased gluconeogenesis
breakdown of fats into free fatty acid and glycerol
proteolysis with increased amino acid level
lipolysis in DKA
free fatty acids that are released are broken down to ketone bodies and cause a metabolic acidosis
osmotic diuresis in DKA
caused by persistently elevated glucose
causes volume depletion and worsened hyperglycemia and increased ketones
this activates RAAS
vasodilation in DKA
despite volume depletion, prostaglandin activation is caused by adipose tissue breakdown
causes of DKA
reduced/skipped insulin injection infection pegnancy hyperthyroidism substance abuse or medication heat CVA GI hemorrhage MI PE trauma or surgery
clinical manifestations of DKA due to
hyperglycemia
volume depletion
adcidosis
clinical features DKA
polyuria, polydipsia increased ventilation HoTN weakness AMS
poor turgor, fruity odor on breath, abdominal pain
ventilation DKA
increased to try to counteract the metabolic acidosis
kussmaul respiration (increased rate and depth)
MC presenting symptoms of DKA
tachycardia
HoTN
these are due to volume depletion
main priority in DKA tx
give NS 1L IV bolus
w.u. of DKA
accucheck UA BMP 12 lead EKG VBG
DKA lab findings
serum glucose >250
anion gap >12
bicarb <15
pH <7.3
hyperkalemia and DKA
due to extracellular shift of K (acidosis)
increased osmolarity due to hyperglycemia
if <3.3 – insulin therapy should not be started until K is managed
insulin will put K back in cell (dysrythma)
ketones in DKA (3)
B-hydroxybutyrate
aceoacetic acid
acetone
priorities of DKA tx
- volume first
- correction of K if needed
- insulin administration
fluid administration DKA
fluids help increase volume and electrolytes and dilute glucose and ketone levels
1 L administered in first 30 (2L administered over 0-2 hrs)
NEXT: 2 L over 2-6 hrs and 2L more over 6-12 hrs
(total 6 L in 6-12 hrs)
if blood glucose is 250 mEq, fluid admin…
5% dextrose in 0.45 NS + 20mEq KCL/L at infusion rate of 250 mL/hr thru second IV line
Potassium and DKA
pts in DKA have potassium DEFECIT but the lab results are high
if initial K is 3.3 or lower (low) then the pt is severely depleted and must replace
life threatening derangement
goals of K replacement DKA
maintain normal ECF K during acute therapy and replace the cell deficit in 24 hrs
if deleted rapidly – cardiac arrhythmia, respiratory paralysis, ileus, rhabdo
DKA tx may cause K to fall bc
insulin promotes reentry into cell
dilution of ECF
acidosis correction
K correction in DKA
serum: >5.3
IV insulin drip with NO supplemental potassium
K correction in DKA
serum: 3.3-4.0
IV insulin drip
IV of 0.45 NS + KCL 40 mq/L at 250 mL/h
K correction in DKA
serum: 4.0-5.3
IV insulin drop
IV 2 of 0.45 NS + KCL 20 mEq/L
K correction in DKA
serum: <3.3
HOLD insulin
0.45 NS at 250 mL/h + 60 mEq/L until K >3.3
insulin drip in DKA
following 1 L of NS and K correction can start
low dose regular insulin drip 0.1 u.kg.hr
once starting to infuse, concentration decreases 50 mg/dL.h
stop once ketonemia and anion gap gone
insulin loading dose in DKA
can be give in adults but NOT IN PEDS (can cause cerebral edema and death)
acute complications of DKA
sepsis
loss of airway
MI
hypovolemic schok
DKA complications related to tx
hypoK hypophosphatemia ARDS cerebral edema hypoglycemia
late DKA complications
recurrent anion gap metabolic acidosis
non anion gap acidosis
vascular thrombosis
fungal infection
DKA and pregnancy
triggered at lower serum glucose levels
pregos have more vomiting and UTI –> triggers of DKA
leading cause of fetal loss (30% mortality)
DKA prego patho
mom hyperglycemia - fetal hyperglycemia and death
maternal acidosis = fetal acidosis, decreased blood flow and oxygenation
maternal hypoK = arrhythmia in fetus and death
pt population most likely to get HHS
debilitated pt with poorly controlled T2DM or undiagnosed T2DM
HHS precipitated by
limited access to water
medical event/stressor
development of HHS is attributed to 3 main factors
- insulin resistance and/or deficiency
- increased hepatic gluconeogenesis and glyconeolysis
- osmotic diuresis and dehydration
HHS patho
increased serum glucose causes water in vascular space and GFR increase
kidneys unable to reabsorb glucose = osmotic diuresis
pt is unable to replace fluid loss = water deficit and profound volume depletion
history of HHS
elderly w/comorbidities start to develop mental status changes
medical conditions that predispose a patient to HHS
PNA
UTI
non compliance with DM meds
PE, hear related illness, mesenteric ischemia, MI, burn, renal, CVA, rhabdo
diagnosis of HHS
severe hyperglycemia (>600 mg glucose) with negative ketones
elevated osmolality of >315 mOSM/kg
arterial pH > 7.3
serum osmolality in HSM
> 300 (>320- lethargy)
HHS tx
correction of hypovolemia
ID and tx precipitating causes
correction of electrolyte abnormalities, hyperglycemia, osmolarity
complications of HHS
cerebral edema UNCOMMON
limit volume rate to <50 ml/kg in first 4 hrs
potential for hypoglycemia, hypokalemia and pulmonary edema if rapid fluid admin
alcoholic ketoacidosis
acute cessation of alcohol consumption after chronic abuse
N/V and GI complaints
drinking + vomiting then decreased food and alcohol changes
alcoholic ketoacidosis s/s
tachycardia, tachypnea, abdominal tenderness
n/v, abdominal pain
diagnostic criteria for alcoholic ketoacidosis
serum glucose low-slight elevated binge drinking ending in n/v/decreased intake wide anion gap metabolic acidosis positive serum ketone wide anion gap metabolic acidosis
tx of alcoholic ketoacidosis
hydration (5% dextrose)
carbohydrates to reverse ketoacitosis (increase insulin and suppress glucagon release)
thiamine supplementation
replace electrolytes
