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Summer FDTN Exam 2 > hypoglycemia > Flashcards

hypoglycemia Flashcards

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
Q

What is your T1DM treatment plan (with each type of provider)

A

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
Q

Pharmacotherapy for T1DM is…..

A

INSULIN BITCH

also ASA from primary prevention

27
Q

What are the types of insulin for T1DM treatment

A

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
Q

What diabetic patient should be on ASA

A

if high risk CVD;
men >50
women >60
+1: HTN, HLD, smoking, FHx, albuminuria

29
Q

Though rarely needed, what are your transplant options for T1DM

A

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
Q

T1DM treatment that can be happening in the future

A

Ultrafast insulin to maintain euglycemia
fully closed loop system (glucose monitoring + insulin pumps with glucagon)
artificial pancreas
vaccines
better transplants

31
Q

What is the MC T1DM complication

A

Neuropathy

(MC GI complication is gastroparesis

32
Q

What lipoprotein abnormalities are mainly present in T1DM

A

Slight LDL elevation- but levels normal out when hyperglycemia is corrected

33
Q

Other diabetes complications include

A

diabetic foot ulcers
gangrene of the feet
optic neuropathy
Coronary atherosclerosis, MI, PVD, CVA

34
Q

How do you classify hypoglycemia

A 
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
Q

What can cause hypoglycemia

A

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
Q

Symptoms of hypoglycemia include

A 
shaky 
tachy
sweaty 
blurry vision 
weak, tired 
headache 
hungry 
anxious
37
Q

What meds can cause hypoglycemia

A 
*Beta Blockers
Sulfonylureas 
Gatifloxacin and Levofloxacin 
ACE-I 
Salicylates 
Quinine
Pentamidine
38
Q

How can you treat hypoglycemia

A

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
Q

What os Somogyi effect

A

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
Q

What is plasma osmolality

A

number os solutes in a solution/kg (norm 275-295)
2xNA + glu/18 + bun/2.8
-predominating factor is sodium!

41
Q

What happens to osmolality in hyperglycemia

A

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
Q

What can cause hyperosmolality

A

advanced renal failure
alcohols (mannitol, ethanol, glycerol, isopropanol)
hypertonic hyponatremia
hyperglycemia

43
Q

What is HHA (hyperglycemic hyperosmolar state)

A

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
Q

S/Sx of HHS include

A

profound dehydration
non-ketotic
polydipsia, polyuria
+/- neuro changes (nystagmus-coma)

45
Q

HHS labs will show

A

plasma glucose 800-2400

BUN >100

46
Q

How do you treat HHS?

A

FLUIDS!!
Insulin
Potassium
Phosphate

47
Q

When treating HHS, where should blood glucose levels be maintained

A

250-300; reduces the risk of cerebral edema

when BG reaches 250, can give insulin subQ

48
Q

Explain fluid treatment in HHA

A

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
Q

Explain insulin treatment in HHS

A

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
Q

Explain potassium treatment in HHS

A

K+ declines rapidly (insulin drives K+ intracellularly)- eventually, it increases! so monitor closely
Give KCl liberally, unless in CKD or w/ oliguria

51
Q

Explain phosphate treatment in HHS

A

If severe hypophosphatemia (<1mg) during insulin therapy, give to ketoacidotic patients at 3 mmol/hr

52
Q

What is DKA

A

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
Q

What are precipitating factors of DKA

A

Infection
insulin omission, pancreatitis, MI, stroke, drug use, glucocorticoids
AKA- the 6 I’s (insulin deficiency, iatrogenic, infection, inflammation, ischemia/infarct, intoxication)

54
Q

In insulin deficiency, you can go three ways (algorithm)

A

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
Q

S/Sx of DKA are

A

*N/V, abdominal pain, hyperventilation

polydipsia, polyuria, enuresis, fruity acetone breath, Kussmaul breathing, tachy/orthostasis (hypovolemia), AMS, coma

56
Q

What labs should you get for a patient in DKA

A 
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
Q

Diagnostic criteria for DKA vs HHS

A

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
Q

What are abnormal lab findings in DKA

A

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
Q

How do you treat DKA

A

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
Q

What are therapeutic goals in DKA

A 
restore plasma volume and tissue perfusion 
decrease BG and osmolality 
correct acidosis 
replenish electrolyte losses 
ID and treat precipitating factors
61
Q

when treating DKA, when do you give insulin

A

AFTER addressing K+

monitor K+ frequently!!

Summer FDTN Exam 2 (11 decks)

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