E: Medical Nutrition Tx For Diabetes

Front 1

What is the hierarchy of nutrition?

Back 1

nutrient --> food --> meal --> diet pattern

Front 2

What are the lifestyle goals for preventing diabetes?

Back 2

- sustained >7% WL.
- <25% of diet = fat
- 1200-1800 kcal/day
- >150min per week of physical activity.

Front 3

What has shown (in the DPP) to have the larger impact on pt BW, metformin or lifestyle changes?

Risk reduction (...I don't know if this is RRR.... hmmm... take w/ a grain of salt) in incidence of diabetes?

Back 3

lifestyle changes, though both were more effective than placebo.

lifestyle (58%) > metformin (31%)

Front 4

Is there a "diabetic diet?"
- what is the primary thing modified to control daily blood G management?

Back 4

No.
- total CHO intake.

Front 5

What is the average minimum requirement for CHO daily intake?
- should insulin tx "cover" dietary CHO intake @ meals and snacks?

Back 5

130 g/day.
- yes.

Front 6

What is a common insulin:CHO ratio?
- what is one serving of CHO?

Back 6

1:15

15grams.

Front 7

What is Glycemic index (GI)?

Glycemic Load (GL)?

Are they the bee's knees for diabetic nutrition?

Back 7

G excurison due to ingestion of CHO containing food relative to a standard (white bread or oral G)

GI, accounting for total CHO intake.

No, they *may* provide a modest benefit over that observed when total CHO is considered alone. ... plus, there are some major problems w/ the index.

Front 8

Is peak blood sugar from a meal typically longer or shorter when the meal is high in fat?

Back 8

longer.

Front 9

What is the euglycemic diet?
- for what is it indicated?

Back 9

- jovanovic diet: goal is to reduce caloric intake to just above the ketonuric threshold; reduce CHO to <40% total cal (min 175g a day); breakfast is small and low in CHO to counter dawn effect.

gestational diabetes.

Front 10

What are the points of MNT that have an "E" consensus?

Back 10

minimize transfat intake
<200mg/day cholesterol.
<1-2 drinks/day (F-M EtOH)

drink w/ dinner to \noct hypoG i/ pts w/ insulin or secretogogues

Chromium supplementation is NOT recommended.

Front 11

What is the definition of diabetic ketoacidosis?
- what are some possibilities for arbitrary lvls that might help ya remember how severe these things have to be?

Back 11

presence of hyperglycemia, ketosis, and acidosis SIMULTANEOUSLY.
- blood glucose > 250 mg/dL, arterial pH < 7.30, bicarbonate < 15 mmol/L, serum osmolality variable, and moderate ketonemia present

Front 12

Is DKA fatal w/o tx?

What is more common, HyperG hyperosmolar state or DKA?

Can DKA be the presenting sx of new onset t1dm?

Back 12

yes.

DKA.

yes.

Front 13

20 yo WF, type 1 diabetes since age 12
2 days of fever, cough, shortness of breath
Blood sugars 200s-300s; usually 70s-160s
VS: T 102.1 RR 26 BP 88/50 HR 122 BG 360 mg/dL
Na 132, K 5.8, Cl 100, HCO3 12, BUN 24, Cr 1.5; AG = 20; serum/urine ketones (+); arterial pH = 7.1
CXR: RLL pneumonia

Wha's goin' on?

Back 13

DKA

Front 14

68 yo AAM, no history of diabetes
2-week prednisone course for asthma
Thirsty, urinating more, blurred vision
Wife brings him in for confusion, dizziness
VS: BP 80/46 HR 130 “Drowsy”
Na 144, K 3.1, Cl 107, HCO3 25, BUN 32, Cr 2.8
BG = 710 mg/dL; AG = 12; serum osm = 327

What's goin' on?

Back 14

Hyperglycemic hyperosmolar state (HHS)

Front 15

What are some common causes of DKA among pts having established t1dm?

Back 15

inadequate or mistakenly missing insulin tx

increased insulin req due to infection or other illness.

Front 16

DKA and HHS are "points along a spectrum."
- Both are caused by what?
- what characterizes each?

Back 16

- insufficient insulin
- DKA: high BG and acid formation; HHS: v.high BG/Osm and *dehydration.*

Front 17

Dose insulin have acute metabolic effects or slower, mitogenic effects?
- what are the acute metabolic effects, if any?

Back 17

both.
- anabolic (promotes creation of large-molecule storage forms of energy); anti-catabolic (prevents breakdown of large-molecule storage forms of energy into fuel).
-

Front 18

When insulin is present, energy is converted into storage forms, e.g., glucose --> glycogen, FFA & ketones --> TriG. W/o insulin, what happens?
- what about in DKA?

Back 18

The storage forms are broken down i/ a controlled manner in the fasting state.
- this process is unregulated.

Front 19

In whom is DKA typically seen?

Back 19

- usually established t1dm, sometimes new onset.
- less common in t2dm
- any age
- short time presentation; rapid development of sx.

Front 20

High glucagon, GH, cortisol and catecholamines can lead to what re: insulin requirement?

Back 20

increased insulin requirement

Front 21

What does the unchecked hyperG lead to in DKA? unchecked ketogenesis?

Back 21

osmotic diuresis --> dehyrdation --> electrolyte loss

ketosis --> high anion gap metabolic acidosis.

Front 22

What are the body's defense mechanisms against acidosis?

Back 22

- ketone bodies are excreted & buffered in the urine; kidney initially regenerates bicarb.
- serum bicarb, bone, and intracellular proteins buffer the H+ ions
- acidosis stim hyperV in the lung --> blows off CO2.

Front 23

Can ketones initially be present in the urine and the blood w/o a fall in arterial pH?
- what happens once the characteristic picture is finally seen?

Back 23

yes, due to the body's mulitiple defense mechanisms.
- low bicarb, low pCO2, low arterial pH w/ high AG met. acidosis (the unmeasured cations in this case are the ketone bodies)

Front 24

What is the best indicator of DKA severity? How about while tracking treatiment?

Why wouldn't we use bicarb lvls?

Why wouldn't we use ketone lvls?

Back 24

Anion gap, both cases.
Best indicator of successful treatment [I.e. “closing” or normalization of the anion gap]

we tx w/ normal saline for volume expansion --> commonly leads to hyperchloremic acidosis --> may persist after ketoacidosis has cleared.
- results in a normal AG acidosis.
- thus, closing of the AG is the best sign of recovery.

they're estimated by the nitroprusside rxn, which detects only acetone (not an acid) and acetoacetate. i/DKA, B-hydroxybutyrate predominates. Ketone lvls can also be confusing during recovery because the B-hyd gets converted back into acetoacetic acid.

Front 25

Can B-hydroxybutyrate be measured w/o a special meter or a sendout lab?

Back 25

no.

Front 26

Even though ketones aren't the best marker in DKA, if they're not strongly positive in diluted serum, but the AG is high, what alternative dx should be considered?

Back 26

lactate, alcohol, salicylate, renal failure.

Front 27

Tachycardia, hypotension, orthostasis, dry mucous mem., poor skin tugor, Kussmaul respirations, fruity breath, and relative hypothermia.... sx of what?

Back 27

DKA.

Front 28

On history, thirst, polyuria, profound weakness, abdominal pain, and nausea/vomiting... features of what?

Back 28

DKA

Front 29

What is the definition of HHS?

Back 29

hyperG w/ high osmolality
- absent or small ketones and near-normal pH.

Front 30

features of pts presenting with HHS?

Back 30

- older
- known t2dm or unrecognized/untx t2dm
- longer pre-coma phase than DKA
- insidious development
- greater severity of obtundation @ presentation
- dehydration presenting w/ shock-like state
- occasional misdx of stroke.

Front 31

What types of medications can precipitate HHS?

Back 31

corticoS, Thiazides, phenytoin.

Front 32

What is the pathogenesis of HHS?

Back 32

severe hyperG leads to losses of water, Na, Cl, K, and Phosphorus. Clinical dehydration, hyperosmolality, hypotension.

Front 33

dehydration, hyperG, hyperNa, hyperosmolality are worse in DKA or HHS?

Back 33

HHS.

Front 34

The likelihood of obtundation in HHS relates to severity of what?

Back 34

severity of hyperG/hyperO; NOT severity of acidosis.

Front 35

What treatment differences exist between DKA and HHS?

What can complicate the clinical course of HHS?

Back 35

HHS: more free water and greater V replacement; K replacement is REQUIRED.

seizures or vascular thromboses and embolism.

Front 36

What are the elements of tx for HHS and DKA?

Back 36

- fluids, including NaCl, eventually free water, eventually G
- IV insulin until AG closes
- Postassium
- occasionally phosphate

Front 37

Should you give K during tx of DKA and HHS?

What other electrolytes can drop precipitously during tx?

Back 37

yes, both.

Life-threatening hypokalemia can develop during insulin treatment
Potassium re-enters cells under the influence of insulin therapy
The small extracellular compartment experiences a precipitous drop of potassium concentration
Anticipatory replacement during treatment of DKA is almost always required

phosphorous can, but it's uncommon.

Front 38

Absolute insulin deficiency is associated with (DKA/HHS)?

Relative insulin deficiency?

Back 38

DKA
HHS

Front 39

68 yo AAM, no history of diabetes
2-week prednisone course for asthma
Thirsty, urinating more, blurred vision
Wife brings him in for confusion, dizziness
VS: BP 80/46 HR 130 “Drowsy”
Na 144, K 3.1, Cl 107, HCO3 25, BUN 32, Cr 2.8
BG = 710 mg/dL; AG = 12; serum osm = 327

- dx?
- how should you tx?

Back 39

HHS

IV fluids, S Osm <320 by day 2, mentation improved. Aggressive K, Mg replacement. D/c on SQ insulin. Prednisone stopped. Transitioned to orals and diet therapy.