Clinical Aspects of Diabetes Mellitus Flashcards
Fingerstick glucose (FSG), Bedside glucose (BSG), Accucheck, Home glucose monitoring (HGM), glucose self-monitoring (GSM), etc. are all names for _______ glucose monitoring
Capillary
Difference between basal vs. bolus insulin
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
3 possible presentations that should make you include DM in differential diagnosis
Mental status changes
Abd pain
Dehydration
AEIOUTIPS mnemonic for mental status change DDx
Alcohol Epilepsy w/ seizures Infection Overdose Uremia Trauma INSULIN (HIGH/LOW BG) Poisoning/Psychosis Stroke
BAD GUT PAINS mnemonic for abdominal pain DDx
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
Etiology of DKA
Inadequate insulin administration
Infection (PNA, UTI, gastroenteritis, sepsis)
Infarction (any location — coronary, cerebral, mesenteric, peripheral)
Surgery
Drugs (cocaine)
Initial and progressive sxs of DKA
Initially: anorexia, N/V, polyuria, polydipsia
Progresses to abdominal pain, altered mental function, coma
Clinical signs of DKA
Kussmaul respirations (rapid/deep)
Acetone (fruity) breath odor
Dry mucous membranes
Poor skin turgor
Tachycardia
Hypotension
Fever
Abdominal tenderness
Lab findings in DKA (including glucose levels, ketone levels, acid/base status, sodium, potassium, and lipids)
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
MUDPILES mnemonic for HAGMA DDx
Methanol Uremia DKA Paraldehyde Isopropyl Alcohol, Iron, INH Lactic acidosis Ethylene glycol Salicylates
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?
“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
What is the fluid deficit in DKA vs. NKHS?
DKA: fluid deficit often 3-5 L
NKHS: fluid deficit often 8-10 L
Initial insulin administration in DKA pt
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)
What are some important tests to run on a DKA pt to evaluate for underlying causes of their current condition?
Blood cultures
EKG
CXR
Drug screen
Seek additional hx from family, or from pt has mental status improves
When should K+ replacement be considered in DKA?
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]
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?
150-250 meq/dl
When caring for a DKA pt, when can you start intermediate or long-acting insulin?
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
Etiologies of NKHS
Insulin deficiency
Inadequate fluid intake
Osmotic diuresis induced by hyperglycemia
Precipitating factors include sepsis, MI, glucocorticoids, phenytoin, thiazide diuretics, impaired access to water
Symptoms of NKHS
Polyuria
Polydipsia
Altered mental status
What symptoms are present in DKA that are ABSENT in NKHS, and thus can help differentiate the two?
N/V, abd pain, and kussmaul respirations are typically ABSENT in NKHS
Lab findings in NKHS (including acid/base status, ketones, and sodium)
Lactic acidosis in NKHS may produce a MILD increase in anion gap
Moderate ketonuria from starvation
CORRECTED serum sodium is usually increased
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?
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
Insulin administration protocol for NKHS
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]
Similarities between DKA and NKHS
Insulin deficiency (absolute or relative)
Glucagon excess (absolute or relative)
Volume depletion
Mental status changes
Long term complications of diabetes mellitus
Retinopathy
Neuropathy
Heart disease and widespread vascular disease
Nephropathy (autonomic and peripheral)
Major cause of mortality in T2DM
Cardiovascular disease [risk increases with poor control]
What is the HbA1c?
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
Describe effect of autonomic neuropathy of DM on the GI tract — and how this affects diabetic control
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
Creatinine clearance tends to decline more quickly in which type of diabetes?
Type 2
T/F: standard urine dipstick is highly sensitive to proteinuria
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]
What is the purpose of a 24 hr urine collection in a diabetic pt?
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.
What is included in quarterly vs. annual diabetes monitoring appts?
Quarterly: HgbA1c, Review Self-glucose monitoring, Foot inspection for ulceration, etc.
Annual: dilated eye exam, urine protein screening (microalbumin/creatinine ratio), monofilament testing
