hypoglycemia Flashcards

(61 cards)

1
Q

What are the diabetes classifications

A

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)

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2
Q

What is the pathophysiologic difference between Type 1 and Type 2 diabetes

A

Type 1: pancreas fails to produce insulin

Type 2: pancreatic cells fail to respond properly to insulin

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3
Q

What do pancreatic cells produce

A

alpha cells: produce glucagon
beta cella: produce insulin and amylin
islet cells involved in endocrine
acini cels involved with exocrine

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4
Q

What is a whipple

A

removal of pancreas and part of the duodenum (because it is so in contact with the pancreas)

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5
Q

What is the epidemiology of T1DM

A

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

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6
Q

What are RF for T2DM

A

Modifiable: physical inactivity, high body fat/weight, high BP, high cholesterol
Non-mod: Hx of gestational DM, race, 45+, FHx

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7
Q

What is Immune Mediated T1DM

A

Beta cell autoimmunity; 2/2 genes HLA DR3 and DR4 and environmental causes
MC in Scandinavian and northern European

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8
Q

What is Idiopathic T1DM

A

related to PAX-4- a transcription factor that is essential for the development of pancreatic islets
MC in asian or african origin

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9
Q

What can a study of first degree relatives with T1DM tell you

A

persistent presence of 2+ auto-antibodies is an almost certain predictor of clinical hyperglycemia and diabetes

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10
Q

What happens to bets cells with time if you have Immune mediated T1DM

A

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

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11
Q

What are the T1DM autoantibodies

A
Islet cells (ICA); Insulin (IAA)
also glutamic acid decarboxylase 65 (GAD65)- tyrosine phosphatase (ICA-512)- zinc transporter (ZnT8)
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12
Q

Presence of antibodies facilitates the screening of

A

siblings of the patient

adults with atypical features of T2DM

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13
Q

What tests can you get to diagnose T1DM

A

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

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14
Q

What is the C peptide test

A

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)

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15
Q

What is the Islet cell cytoplasmic autoantibody test

A

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

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16
Q

What happens to antibodies as the disease progresses

A

they decrease, because pancreatic cells die so they need less antibodies

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17
Q

What is Hgb A1c

A

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

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18
Q

When is srceening for T1DM with an antibody panel recommended

A

if a first degree family member has T1DM

if for a clinical research study

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19
Q

Define Pre-Diabetes levels

A

FPG: 100-125
2h PG from OGTT: 140-199
A1c: 5.7-6.4%

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20
Q

What are essentials for T1DM diagnosis

A

-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

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21
Q

What are essentials for T2DM diagnosis

A

(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)

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22
Q

S/Sx of T1DM are

A

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)

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23
Q

What are symptoms present in T1DM that are absent in T2DM

A

polyphagia with weight loss

nosturnal enuresis

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24
Q

Total estimated cost of fiagnosed DM is

A

245 billion!

176 in direct medical costs, 69 in reduced productivity

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25
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.
26
Pharmacotherapy for T1DM is.....
INSULIN BITCH | also ASA from primary prevention
27
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
28
What diabetic patient should be on ASA
if high risk CVD; men >50 women >60 +1: HTN, HLD, smoking, FHx, albuminuria
29
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
30
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
31
What is the MC T1DM complication
Neuropathy | (MC GI complication is gastroparesis
32
What lipoprotein abnormalities are mainly present in T1DM
Slight LDL elevation- but levels normal out when hyperglycemia is corrected
33
Other diabetes complications include
diabetic foot ulcers gangrene of the feet optic neuropathy Coronary atherosclerosis, MI, PVD, CVA
34
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 ```
35
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)
36
Symptoms of hypoglycemia include
``` shaky tachy sweaty blurry vision weak, tired headache hungry anxious ```
37
What meds can cause hypoglycemia
``` *Beta Blockers Sulfonylureas Gatifloxacin and Levofloxacin ACE-I Salicylates Quinine Pentamidine ```
38
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
39
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
40
What is plasma osmolality
number os solutes in a solution/kg (norm 275-295) 2xNA + glu/18 + bun/2.8 -predominating factor is sodium!
41
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
42
What can cause hyperosmolality
advanced renal failure alcohols (mannitol, ethanol, glycerol, isopropanol) hypertonic hyponatremia hyperglycemia
43
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
44
S/Sx of HHS include
profound dehydration non-ketotic polydipsia, polyuria +/- neuro changes (nystagmus-coma)
45
HHS labs will show
plasma glucose 800-2400 | BUN >100
46
How do you treat HHS?
FLUIDS!! Insulin Potassium Phosphate
47
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
48
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
49
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
50
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
51
Explain phosphate treatment in HHS
If severe hypophosphatemia (<1mg) during insulin therapy, give to ketoacidotic patients at 3 mmol/hr
52
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
53
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)
54
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
55
S/Sx of DKA are
*N/V, abdominal pain, hyperventilation | polydipsia, polyuria, enuresis, fruity acetone breath, Kussmaul breathing, tachy/orthostasis (hypovolemia), AMS, coma
56
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 ```
57
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
58
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
59
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
60
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 ```
61
when treating DKA, when do you give insulin
AFTER addressing K+ | monitor K+ frequently!!