Clinical Aspects of Diabetes Mellitus

Question 1

Fingerstick glucose (FSG), Bedside glucose (BSG), Accucheck, Home glucose monitoring (HGM), glucose self-monitoring (GSM), etc. are all names for _______ glucose monitoring

Answer 1

Capillary

Question 2

Difference between basal vs. bolus insulin

Answer 2

Basal is LONG-acting insulin to achieve more steady-state glucose control (to mimic baseline levels in non-diabetics)

Bolus insulin can be adjusted at mealtime and is based on FSG (“sliding scale”) +/- carb count anticipated

Question 3

3 possible presentations that should make you include DM in differential diagnosis

Answer 3

Mental status changes

Abd pain

Dehydration

Question 4

AEIOUTIPS mnemonic for mental status change DDx

Answer 4

Alcohol
Epilepsy w/ seizures
Infection
Overdose
Uremia
Trauma
INSULIN (HIGH/LOW BG)
Poisoning/Psychosis
Stroke

Question 5

BAD GUT PAINS mnemonic for abdominal pain DDx

Answer 5

Bowel obstruction
Appendicitis, adenitis (mesenteric)
Diverticilitis, DKA, dysentery, diarrhea, drug withdrawal

Gastroenteritis, gallbladder dz
UTI
Testicular torsion, toxin (lead, black widow spider bite)

PNA/pleurisy/pancreatitis/perforated bowel/peptic ulcer/porphyria

Abdominal aneurysm

Infarcted bowel/infarcted myocardium/incarcerated hernia/inflammatory bowel dz

Splenic rupture/infarction/sickle cell crisis

Question 6

Etiology of DKA

Answer 6

Inadequate insulin administration

Infection (PNA, UTI, gastroenteritis, sepsis)

Infarction (any location — coronary, cerebral, mesenteric, peripheral)

Surgery

Drugs (cocaine)

Question 7

Initial and progressive sxs of DKA

Answer 7

Initially: anorexia, N/V, polyuria, polydipsia

Progresses to abdominal pain, altered mental function, coma

Question 8

Clinical signs of DKA

Answer 8

Kussmaul respirations (rapid/deep)

Acetone (fruity) breath odor

Dry mucous membranes

Poor skin turgor

Tachycardia

Hypotension

Fever

Abdominal tenderness

Question 9

Lab findings in DKA (including glucose levels, ketone levels, acid/base status, sodium, potassium, and lipids)

Answer 9

Hyperglycemia

Ketosis

High anion gap metabolic acidosis

Measured (not corrected) Na+ is low secondary to hyperglycemia

Serum K+ may be normal or somewhat high (result of acidosis) but there is actually a total body deficit

Hypertriglyceridemia

Hyperlipoprotenemia

Hyperamylasemia

Leukocytosis

Question 10

MUDPILES mnemonic for HAGMA DDx

Answer 10

Methanol
Uremia
DKA
Paraldehyde
Isopropyl Alcohol, Iron, INH
Lactic acidosis
Ethylene glycol
Salicylates

Question 11

DKA is usually monitored in the ICU with frequent monitoring of general status, vital signs, glucose (qh), fluid I/O, and other labs — acid-base status, renal function, potassium and other electrolytes (q2-4 hrs +/- ABG). What is the approach to fluid replacement in DKA?

Answer 11

“1-2-3 method”

2-3 L NS (0.9%) over first 1-3 hours

Then, 0.45% saline at 150 ml/hr

When glucose reaches 250 mg/dL, switch to 5% dextrose and 0.45% saline at 100-200 mL/hr

Question 12

What is the fluid deficit in DKA vs. NKHS?

Answer 12

DKA: fluid deficit often 3-5 L

NKHS: fluid deficit often 8-10 L

Question 13

Initial insulin administration in DKA pt

Answer 13

10-20 units IV or IM

Then, 5-10 units/hr continuous IV

Increase if no response in 1-2 hrs (orders can be written with guidelines to titrate)

Question 14

What are some important tests to run on a DKA pt to evaluate for underlying causes of their current condition?

Answer 14

Blood cultures

EKG

CXR

Drug screen

Seek additional hx from family, or from pt has mental status improves

Question 15

When should K+ replacement be considered in DKA?

Answer 15

When serum K < 5.5 mEq/L

[when supplementing K+, keep in mind: renal function, baseline EKG and continuous cardiac monitoring for changes, verify urinary output and measure hourly — may need foley]

Question 16

DKA tx goals are to increase the rate of glucose utilization in insulin-dependent tissues, reverse ketonemia and acidosis, and correct depletion of water and electrolytes. What is the glucose goal when caring for a DKA pt?

Answer 16

150-250 meq/dl

Question 17

When caring for a DKA pt, when can you start intermediate or long-acting insulin?

Answer 17

When pt is able to eat (mental status improved, no N/V, no abd pain, anion gap normalized)

Allow overlap timing of IV with SQ insulin — usually by 30-60 mins

Question 18

Etiologies of NKHS

Answer 18

Insulin deficiency

Inadequate fluid intake

Osmotic diuresis induced by hyperglycemia

Precipitating factors include sepsis, MI, glucocorticoids, phenytoin, thiazide diuretics, impaired access to water

Question 19

Symptoms of NKHS

Answer 19

Polyuria

Polydipsia

Altered mental status

Question 20

What symptoms are present in DKA that are ABSENT in NKHS, and thus can help differentiate the two?

Answer 20

N/V, abd pain, and kussmaul respirations are typically ABSENT in NKHS

Question 21

Lab findings in NKHS (including acid/base status, ketones, and sodium)

Answer 21

Lactic acidosis in NKHS may produce a MILD increase in anion gap

Moderate ketonuria from starvation

CORRECTED serum sodium is usually increased

Question 22

Tx of NKHS in the ICU includes frequent monitoring of general status, vital signs, glucose, acid/base status, renal function, K+, and other electrolytes. What is the procedure for fluid replacement in NKHS?

Answer 22

2-3 L NS (0.9%) over 1-3 hrs

When glucose reaches 250 mg/dL, switch to 5% dextrose and 0.45% at 100-200 ml/hr

Question 23

Insulin administration protocol for NKHS

Answer 23

Regular insulin:
5-10 units IV bolus (or IM), then 3-7 units continuous infusion

Transition when eating as with DKA

[also similar to DKA is to monitor and replace K+ as needed, and investigate/address underlying causes of NKHS]

Question 24

Similarities between DKA and NKHS

Answer 24

Insulin deficiency (absolute or relative)

Glucagon excess (absolute or relative)

Volume depletion

Mental status changes

Question 25

Long term complications of diabetes mellitus

Answer 25

Retinopathy

Neuropathy

Heart disease and widespread vascular disease

Nephropathy (autonomic and peripheral)

Question 26

Major cause of mortality in T2DM

Answer 26

Cardiovascular disease [risk increases with poor control]

Question 27

What is the HbA1c?

Answer 27

3-4 month average of blood glucose [based on glycosylation of RBCs; hemoglobinopathies or recent transfusions alter results]

Less than 7 is considered satisfactory control; also important to consider glucose “spread” or range of values — if broad range that is not good control

Question 28

Describe effect of autonomic neuropathy of DM on the GI tract — and how this affects diabetic control

Answer 28

Autonomic neuropathy leads to delayed gastric emptying — causes BG to drop because exogenously administered insulin begins working right away, then BG spikes later when the insulin is no longer active

Question 29

Creatinine clearance tends to decline more quickly in which type of diabetes?

Answer 29

Type 2

Question 30

T/F: standard urine dipstick is highly sensitive to proteinuria

Answer 30

False — the standard urine dipstick only senses proteinuria of >300 mg/24 hrs

A better screening for proteinuria is microalbumin/creatinine ratio — which corrects for variations d/t urine concentration [microalbuminuria = 30-300 mg]

Question 31

What is the purpose of a 24 hr urine collection in a diabetic pt?

Answer 31

For protein and creatinine clearance — used to quantify large amounts of protein in urine (e.g., nephrotic range proteinuria), can be done in the same specimen but need to obtain SERUM creatinine at the same time to determine creatinine clearance

Problematic because it is difficult for pts to remember to save ALL urine, dexterity is required to get it into container, leaks may occur, etc.

Question 32

What is included in quarterly vs. annual diabetes monitoring appts?

Answer 32

Quarterly: HgbA1c, Review Self-glucose monitoring, Foot inspection for ulceration, etc.

Annual: dilated eye exam, urine protein screening (microalbumin/creatinine ratio), monofilament testing