hypoglycemia Flashcards
What are the diabetes classifications
Prediabetes (A1c 5.7% - 6.4%)
Type 1
Type 2 (insulin secretion defect/decreased sensitivity)
Gestational
Other (dz of exocrine pancreas, like CF; drug/chemical induced; monogenic diabetes syndromes)
What is the pathophysiologic difference between Type 1 and Type 2 diabetes
Type 1: pancreas fails to produce insulin
Type 2: pancreatic cells fail to respond properly to insulin
What do pancreatic cells produce
alpha cells: produce glucagon
beta cella: produce insulin and amylin
islet cells involved in endocrine
acini cels involved with exocrine
What is a whipple
removal of pancreas and part of the duodenum (because it is so in contact with the pancreas)
What is the epidemiology of T1DM
MC in non-hispanic white kids/teens in the US
Bimodal distribution; peak at 4-6 and 10-14 y/o
F=M
Family risk factor
Environment plays a role
What are RF for T2DM
Modifiable: physical inactivity, high body fat/weight, high BP, high cholesterol
Non-mod: Hx of gestational DM, race, 45+, FHx
What is Immune Mediated T1DM
Beta cell autoimmunity; 2/2 genes HLA DR3 and DR4 and environmental causes
MC in Scandinavian and northern European
What is Idiopathic T1DM
related to PAX-4- a transcription factor that is essential for the development of pancreatic islets
MC in asian or african origin
What can a study of first degree relatives with T1DM tell you
persistent presence of 2+ auto-antibodies is an almost certain predictor of clinical hyperglycemia and diabetes
What happens to bets cells with time if you have Immune mediated T1DM
beta cell destruction steadily declines, until the “honeymoon phase” (AKA clinical diabetes) where beta cells become overactive in a last ditch effort- after this, they poop out way faster
What are the T1DM autoantibodies
Islet cells (ICA); Insulin (IAA) also glutamic acid decarboxylase 65 (GAD65)- tyrosine phosphatase (ICA-512)- zinc transporter (ZnT8)
Presence of antibodies facilitates the screening of
siblings of the patient
adults with atypical features of T2DM
What tests can you get to diagnose T1DM
C peptide: low C peptide + low insulin= T1DM
Glutamic acid decarboxylase autoAb: Abs against specific enzyme in B cells
Insulin Abs:
Insulinoma associated-2 auto Ab: Abs against specific enzyme in B cells
Islet cell cytoplasmic autoAb: not often used
Zinc transporter 8 Ab: new, targets enzyme specific to B cells
What is the C peptide test
quantitative blood test for connecting peptide that’s cleaved before insulin is formed
AKA- C peptide levels usually match insulin level
low C-peptide means insulin is not being made
(can check in the presence of exogenous insulin)
What is the Islet cell cytoplasmic autoantibody test
Islet cells sense blood glucose levels and release insulin accordingly
test for rxn between islet cell Abs in humans and islet cell proteins from animal pancreas
What happens to antibodies as the disease progresses
they decrease, because pancreatic cells die so they need less antibodies
What is Hgb A1c
test measure of average blood glucose in the past 2-3 months- no need for fasting!
Diagnostic levels are 6.5% or higher
GOAL (if <19): <7.5%
-But this alone is not a diagnostic test, blood glucose is preferred to dx T1DM if Sx
When is srceening for T1DM with an antibody panel recommended
if a first degree family member has T1DM
if for a clinical research study
Define Pre-Diabetes levels
FPG: 100-125
2h PG from OGTT: 140-199
A1c: 5.7-6.4%
What are essentials for T1DM diagnosis
-polyuria, polydipsia, & weight loss associated with random plasma glucose 200+
-PG of 126+ after overnight fast, 2+ times
-Ketonemia, ketonuria, or both
Islet autoAbs frequently present
What are essentials for T2DM diagnosis
(many pts >40 and obese; w/ HTN, dyslipidemia, and atherosclerosis)
-Polyuria and Polydipsia
-Candida vaginitis in females
-PG >126 after overnight fast, 2+ times; and, PG>200 2 hrs after OGTT
-Hgb A1c >6.5%
(ketonuria and weight loss NOT common at time of dx)
S/Sx of T1DM are
Hyperosmolality and hyperketonuria (2/2 accumulating circulating lgucose and FA breakdown)
Polyuria/polydipsia (2/2 sustained hyperglycemia causing osmotic diuresis)
Loss of glucose as free water and lytes (2/2 diuresis)
Blurred vision (2/2 lens exposure to hyperosmolar fluids)
-Kussmaul breathing, n/v/abd pain, weight loss, fruity breath, lethargy, stupor)
What are symptoms present in T1DM that are absent in T2DM
polyphagia with weight loss
nosturnal enuresis
Total estimated cost of fiagnosed DM is
245 billion!
176 in direct medical costs, 69 in reduced productivity
What is your T1DM treatment plan (with each type of provider)
PCP: refer to endocrine (if not sick) or ED if needs immediate Tx
Dietician: carb, fat, protein meal planning
Nursing: draw insulin- injection instruction or pen device
Pharm: SMBG, ketone monitoring, med education, hypoglycemia management
Behavioral: discharge planning, etc.
Pharmacotherapy for T1DM is…..
INSULIN BITCH
also ASA from primary prevention
What are the types of insulin for T1DM treatment
Rapid acting: Novolog (insulin aspart) 3-6 hr
Short acting: Humilin R U-100, or, Novolog R (regular) 0-12 hr
Intermediate acting NPH: Humilin N, or, Novolin N 0-18 hr
Long acting: Latus (insulin glargina), or, Levemir (insulin detemir) 0-24 hr
What diabetic patient should be on ASA
if high risk CVD;
men >50
women >60
+1: HTN, HLD, smoking, FHx, albuminuria
Though rarely needed, what are your transplant options for T1DM
Pancreas transplant w/ or w/o kidney transplant (better with kidneys for some reason)
Islet cell transplant (injected in liver, but you need a LOT)
-but T1DM cant receive pancreatic islet auto- transplant
T1DM treatment that can be happening in the future
Ultrafast insulin to maintain euglycemia
fully closed loop system (glucose monitoring + insulin pumps with glucagon)
artificial pancreas
vaccines
better transplants
What is the MC T1DM complication
Neuropathy
(MC GI complication is gastroparesis
What lipoprotein abnormalities are mainly present in T1DM
Slight LDL elevation- but levels normal out when hyperglycemia is corrected
Other diabetes complications include
diabetic foot ulcers
gangrene of the feet
optic neuropathy
Coronary atherosclerosis, MI, PVD, CVA
How do you classify hypoglycemia
level 1 (mild): <70, can be treated with fast acting carbs (bread, crackers, juice, etc.) level 2 (mod): <54 level 3 (severe): severe cognitive impairment, external assistance for recovery
What can cause hypoglycemia
too much insulin, too much EtOH, post exercise
loss of glucagon response, sympatho-adrenal response
Gastroparesis, ESRD
hypopituitarism
addison’s disease. myxedema
liver failure
GI surgery
Insulinoma (high insulin, high c-peptide)
Symptoms of hypoglycemia include
shaky tachy sweaty blurry vision weak, tired headache hungry anxious
What meds can cause hypoglycemia
*Beta Blockers Sulfonylureas Gatifloxacin and Levofloxacin ACE-I Salicylates Quinine Pentamidine
How can you treat hypoglycemia
glucose tab/juice
give carbohydrate 15g, wait 15 min
-Parenteral emergency glucagon kit (1mg injection)
-50mL of 50% glucose solution by rapid IV infusion
What os Somogyi effect
when you have nocturnal hypoglycemia leading to a surge of hormones causing pre-breakfast hyperglycemia (high BG by 7am)
-Eliminate dose of intermediate insulin at dinnertime; give a lower dose at bedtime/increase food at bedtime
What is plasma osmolality
number os solutes in a solution/kg (norm 275-295)
2xNA + glu/18 + bun/2.8
-predominating factor is sodium!
What happens to osmolality in hyperglycemia
You have more glucose in the vessels, attracting more water into the vessel; but the sodium in the vessels stays the same. So in hyperglycemia, you get a falsely low sodium level
What can cause hyperosmolality
advanced renal failure
alcohols (mannitol, ethanol, glycerol, isopropanol)
hypertonic hyponatremia
hyperglycemia
What is HHA (hyperglycemic hyperosmolar state)
Hyperglycemia without ketones! MC in T2DM
BG >600 w/ serum osmolality >310
NO acidosis (pH >7.3)
Bicarb >15 (not ridiculously low)
Normal anion gap, min to no ketonuria/ketonemia
S/Sx of HHS include
profound dehydration
non-ketotic
polydipsia, polyuria
+/- neuro changes (nystagmus-coma)
HHS labs will show
plasma glucose 800-2400
BUN >100
How do you treat HHS?
FLUIDS!!
Insulin
Potassium
Phosphate
When treating HHS, where should blood glucose levels be maintained
250-300; reduces the risk of cerebral edema
when BG reaches 250, can give insulin subQ
Explain fluid treatment in HHA
restore UOP 50ml+
if w/ hypovolemic Sx: 0.9% NS
maintenance: 0.45% saline
When blood glucose gets to 250, give 5% dextrose in water, 0.45% NS, or 0.9% NS
Explain insulin treatment in HHS
can be delayed, mainly bc fluid replacement usually decreases BG = increase GFR and renal excretion of glucose
If in ketonemia: insulin infusion at 0.5 units/kg/hr (no bolus)- goal is lower BG 50-70/hr
Explain potassium treatment in HHS
K+ declines rapidly (insulin drives K+ intracellularly)- eventually, it increases! so monitor closely
Give KCl liberally, unless in CKD or w/ oliguria
Explain phosphate treatment in HHS
If severe hypophosphatemia (<1mg) during insulin therapy, give to ketoacidotic patients at 3 mmol/hr
What is DKA
severe insulin deficiency, MC in T1DM (often first manifestation! people get first diagnosed after this event)
Develops rapidly (w/in 24 hrs)
Marked elevation of glucagon, cortisol, GH, Epi, and NE
*Preventable by SBGM and blood or urine ketones
What are precipitating factors of DKA
Infection
insulin omission, pancreatitis, MI, stroke, drug use, glucocorticoids
AKA- the 6 I’s (insulin deficiency, iatrogenic, infection, inflammation, ischemia/infarct, intoxication)
In insulin deficiency, you can go three ways (algorithm)
hyperventilation = low PaCO2 = metabolic acidosis (pH <6.8)= death from diabetic coma
increased glucose production= polyuria/polydipsia= dehydration= death from diabetic coma
decreased protein synthesis= fatigue
S/Sx of DKA are
*N/V, abdominal pain, hyperventilation
polydipsia, polyuria, enuresis, fruity acetone breath, Kussmaul breathing, tachy/orthostasis (hypovolemia), AMS, coma
What labs should you get for a patient in DKA
ABC's CBC (infection?) BMP (glucose, AG, bicarb, K, Na) ECG UA + dipstick (ketones) Plasma osmolality serum ketones ABG if HCO is low amylase will be high w/o pancreatitis
Diagnostic criteria for DKA vs HHS
DKA: BG>250, pH <7.3, HCO3 <18, moderate ketonuria or ketonemia
HHS: BG >600, pH >7.3, HCO3 >15, min-no ketonuria or ketonemia
What are abnormal lab findings in DKA
MET acidosis (2/2 high ketoacids)
K and Phosphate: labs normal/high, but body actually depleted (mag as well)
occasionally BG can be <250 if in starvation, EtOH, or pregnancy
How do you treat DKA
determine hydration status first!
Hypovolemia: 0.9% NS
Mild dehydration: eval corrected serum Na
Cardiogenic shock: hemodynamic monitoring and vasopressors
-High or normal serum Na: 0.45% NS
-Low Na: 0.9% NS
What are therapeutic goals in DKA
restore plasma volume and tissue perfusion decrease BG and osmolality correct acidosis replenish electrolyte losses ID and treat precipitating factors
when treating DKA, when do you give insulin
AFTER addressing K+
monitor K+ frequently!!
