Endocrine Flashcards
When a patient presents with unexplained weight loss, what should always be on your differential?
Endocrine cause
- uncontrolled DM 1
- adrenal insufficiency
- pheochromocytoma
- hyperthyroidism
Malignancy (esp in elderly)
Diabetes Mellitus
a syndrome of disordered metabolism and inappropriate hyperglycemia due either to a deficiency of insulin secretion, or to a combination of insulin resistance and inadequate insulin secretion to compensate
Type 1 DM: causes
Causes: pancreatic islet B cell destruction predominantly by an autoimmune process
-90% are related to autoimmune attack on islet cells associated with certain HLA genes
-the other 10% are idiopathic - no islet cell destruction
islet autoantibodies are often present
Type 2 DM: causes
Caused by either tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/or impaired insulin production
Type 1 DM: treatment
eucaloric diet
preprandial rapid acting insulin plus basal intermediate or long acting insulin
Type 2 non-obese DM: treatment
eucaloric diet alone
OR
diet plus oral agents
Type 2 obese DM: treatment
weight reduction
hypocaloric diet plus oral agents and insulin
metformin: mechanism
acts on the liver to reduce gluconeogenesis and causes a decrease in insulin resistance
- lowers basal and postprandial glucose levels
metformin: advantages
Not associated with weight gain
Low risk of hypoglycemia
Reduces LDL, triglycerides
No effect on BP
Inexpensive
metformin: disadvantages
-increased risk of GI side effects
-risk of lactic acidosis increased for people with stable or acute heart failure, liver disease, alcoholism, or recovering from major surgery
-increased risk of vitamin B12 deficiency
-less convenient dosing
Discontinue 1-2 days before receiving iodinated radio contrast medium; may cause lactic acidosis (BLACK BOX WARNING)
Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin): mechanism
Inhibits DPP-4 from degrading GLP-1, increasing its blood concentration which causes increased insulin to be released from beta cells
Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin): advantages
weight neutral
fewer GI side effects
rarely causes hypoglycemia
Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin): disadvantages
expensive
Glycosurics (canagliflozin) (SGLT-2 inhibitors): mechanism
block the re-uptake of glucose in the renal tubules, promoting loss of glucose in the urine
Glycosurics (canagliflozin) (SGLT-2 inhibitors): advantages
mild weight loss
mild reduction in blood sugar levels
minimal risk of hypoglycemia
Glycosurics (canagliflozin) (SGLT-2 inhibitors): disadvantages
vaginal candidiasis
UTI
GLP agonists (Liraglutide): mechanism
bind to a membrane GLP receptor, causing increased insulin to be released from beta cells
Reduce glucagon
Slow gastric emptying
GLP agonists (Liraglutide): advantages
significant weight loss
low risk for hypoglycemia
GLP agonists (Liraglutide): disadvantages
-increased risk of pancreatitis
increased risk for thyroid cancer (BLACK BOX WARNING
DKA: mechanism
Lack of insulin + elevated glucagon –> increased levels of glucose by the liver
Glucose spills over into the urine, taking water and solutes (Na+ and K+) along with it
This leads to polyuria, dehydration, polydipsia
Absence of insulin –> release of FFAs from adipose tissue, which are converted into ketone bodies and cause metabolic acidosis
Initially, the body buffers the change with the bicarbonate buffering system, but this is quickly overwhelmed and other mechanisms must work to compensate for the acidosis
DKA: labs/Dx
Essentials of diagnosis:
-Hyperglycemia >250mg/dL
-Acidosis with venous pH <7.3 (arterial pH <7.25)
-Serum bicarbonate (15mEq/L) low
-Serum positive for ketones (beta-hydroxybutane >1.5)
Hyperkalemia
BUN/Cr elevated
Anion gap >15
Hct elevated
Leukocytosis
Low pCO2
Elevated serum osmolality (>330 mosm/L)
Ketonemia, ketonuria
Glycosuria
DKA: Treatment
Unable to protect airway or comatose: intubate immediately
- Restore fluid deficit: 20-40cc/kg boluses
- 1 L NS in the first hour, then 500 ml/hr
- If glucose >500, use 1/2 NS after first hour
- When glucose <250mg/dL, D5 1/2NS to prevent hypoglycemia - Treat hypokalemia before giving insulin
- Treat hyperglycemia: Regular insulin
- 0.1 units/kg IV bolus
- 0.1 units/kg/hr IV gtt- insulin gtt titrated hourly according to delta glucose
- If glucose does not fall by at least 10% after the first hour, repeat bolus
- insulin gtt titrated hourly according to delta glucose
- Acidosis
- if pH <7.1, start bicarb drip 44-48 mEq in 900 ml 1/2 NS until pH >7.1
-overcorrection can lead to hypokalemia d/t transcellular shift of K+ when the pH changes too fast
Identify and treat underlying infection
ICU
HHNK
Hyperglycemic/hyperosmolar non-ketotic state
State of greatly elevated serum glucose, hypoerosmolality, and severe intracellular dehydration without ketone production
Patients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion
Similar to DKA (develops d/t insulin deficiency) but usually occurs over days to weeks
More common in type 2 diabetes rather than type 1
HHNK is often precipitated by
non-compliance
infection
MI
stroke
surgery
steroid administration
HHNK: essentials of diagnosis
Hyperglycemia >600mg/dL
elevated BUN/Cr
serum bicarb >15mEq/L
elevated Hb A1c
serum osmolality >310mosm/L
no acidosis, pH >7.3
normal anion gap, <14
no ketosis, b-hydroxybutyrate <0.5
HHNK: treatment
Protect the airway
Dehydration:
- Isotonic IV fluids (6-10L NS) within the first 24 hours
- 1 L in the first hour, then 500 ml/hr
- if glucose >500 mg/dl, use 1/2 NS after the first hour
- when glucose <250 mg/dl, change to D5 1/2 NS to prevent hypoglycemia
Insulin
- Less insulin is usually required- glucose usually decreases with fluids alone so a relatively normal insulin regimen can be given
- 0.1 u/kg regular insulin IV bolus
- 0.1 u/kg/hr gtt
- if glucose does not fall by at least 10% after the first hour, repeat bolus
Hypoglycemia treatment: overdose of metformin
octreotide 75mcg SC/IM
Feed the patient
Observe for 12-24 hrs
Hypoglycemia treatment: if there has not been any obvious error made and hypoglycemia persists
Consider:
-insulinoma: will require endocrine consult
-beta blocker overdose
-factitious disorders
Type 1 DM is strongly associated with which antigens?
human leukocyte antigens (HLA)
Type 1 DM: presentation
-polyuria
-polydipsia
-polyphagia
-weight loss
-nocturnal enuresis
-weakness, fatigue
-serum glucose >200mg/dL
-ketonemia, ketonuria, or both
Type 2 DM: presentation
-age >40
-insidious onset of hyperglycemia
-polyuria
-polydipsia
-women: recurrent vaginitis
-late: peripheral neuropathies, blurred vision
-chronic skin infections, including pruritis
-often associated with HTN, HLD, atherosclerotic disease
-high levels of insulin to prevent ketosis
Type 1 and Type 2 DM: labs/Diagnosis
At least one:
-Serum fasting (>8 hrs) BG >126 mg/dl on more than one occasion
-Random plasma glucose >200 mg/dl with signs of hyperglycemia (e.g. polyuria, polydipsia, weight loss)
-plasma glucose >200 mg/dl measured 2 hours after a glucose load of 1.75 g/kg (max dose 75g) in an oral glucose tolerance test
-glycated hemoglobin (A1C) >6.5
Somogyi Effect and treatment
Seen in Type 1 DM
Nocturnal hypoglycemia develops after stimulating a surge of counter regulatory hormones with raise blood sugar
-hypoglycemic at 3am but rebounds with an elevated blood glucose at 7am
Treatment: reduce or omit the bedtime dose of insulin
Dawn Phenomenon and treatment
Seen in Type 1 DM
Results when tissue becomes desensitized to insulin nocturnally
-blood glucose becomes progressively elevated throughout the night, resulting in elevated glucose levels at 7am
Treatment: add or increase the bedtime dose of insulin
Risk factors for Type 2 DM
waist circumference >40 in in men and >35 in in women
BP >130/85
Triglycerides >150
FBG >100
HDL <40 in men and <50 in women
DKA: S/Sx
CNS depression or coma
Kussmaul’s breathing
Hyptension
Tachycardia
Parched mucous membranes
Abdominal pain, NV
polyuria, including nocturia
polydipsia
weakness/fatigue
fruity breath
orthostatic hypotension with tachycardia
poor skin turgor
HHNK: S/Sx
polyuria
weakness
changes in LOC
hypotension
tachycardia
poor skin turgor
What condition is associated with recurrent nephrolithiasis?
hyperparathyroidism
pheochromocytoma
Adrenal mass
pheochromocytoma: risk factors
females > males
foods high in tryamine (alcohol, certain cheeses)
Pheochromocytoma: S/Sx
headache
diaphoresis
hypertension
orthostatic hypotension
tachycardia
leukocytosis
Thyroid tests for screening
TSH: most sensitive test for primary hypothyroidism and hyperthyroidism
Free thyroxine (FT4): quite sensitive for hypothyroidism, as T4 is the product of the thyroid itself
Thyroid testing for nodules
Fine-needle aspiration: best diagnostic method for thyroid cancer
123I uptake and scan: “Cold” spots usually indicate a more malignant hypofunctioning nodule
99mTc scan: vascular (more worrisome) vs avascular (less worrisome) nodules
Ultrasound:
-assist in FNA
-cystic lesions are of low-suspicion for cancer
-solid lesions are of high suspicion for cancer
What to do if you find thyroid nodules
Check TSH and T4
More suspicious nodules should be referred for FNA
Less worrisome thyroid nodules
High TSH, low FT4
older women
cystic appearance on ultrasound
family history of goiter
How does 131I work
It is taken up by the remaining thyroid tissue after thyroidectomy and the isotope destroys it
It renders the patient radioactive for a period of time and the patient must quarantine
Hypothyroidism: symptoms
fatigue
cold intolerance
constipation
weight gain
depression
menstrual problems
hoarseness
“puffy” appearance to the face, pale complexion, under-eye edema and hyperpigmentation, tongue enlargement, eyebrow thinning
extreme weakness
arthalgias
cramps
dry skin
hair loss
brittle nails
bradycardia
slowed DTRs
hypoactive bowel sounds
Hypothyroidism: labs
TSH: high in primary, low in secondary
T4: low
resin T3 uptake: decreased
hyponatremia
hypoglycemia
T3 is not a reliable test
myxedema
late hypothyroidism, can result in myxedema coma
myxedema coma
Occurs when an already hypothyroid patient is placed under physiologic stress (e.g. infection)
Often results and coexists with acute adrenal insufficiency
myxedema coma: Symptoms
decreased LOC
hypothermia
hyponatremia
hypoglycemia
hypotension
hypoxia/hypercapnia
bradycardia
myxedema coma: labs
TSH: very high
FT4: very low
random cortisol: low (reflects adrenal insufficiency)
myxedema coma: treatment
Protect airway
Fluid replacement as needed
levothyroxine 400mcg IV once, then 100mcg IV daily
If adrenal insufficiency is present: hydrocortisone 100mg IV, then 25-50mg IV q8h
support hypotension
slow rewarming with blankets, avoid circulatory collapse
symptomatic care
hyperthyroidism: symptoms
tachycardia
tremor
sweating
weight loss, increased appetite
anxiety
loose stools
heat intolerance
irritability
fatigue
menstrual problems
exophthalmos, lid lag
hyperreflexia
smooth, warm, moist velvety skin
fine/thin hair
increased incidence of AFib
hyperthyroidism: labs
TSH: very low
FT4: high
T3: high
thyroid resin uptake: high
ANA: positive (no evidence of SLE or other collagen diseases)
hyperthyroidism: treatment
propranolol: symptomatic relief
Thiourea drugs for patients with mild cases, small goiters, or fear of isotopes
-methimazole (Tapazole) 30-60mg/day until FT4 levels return to normal
- propylthiouracil 300-600mg daily in 4 divided doses
131I to destroy the thyroid, then thyroid hormone replacement therapy for life
Thyroid surgery (must be euthyroid pre-op)
Lugol’s solution 2-3 got PO daily x10 days to reduce vascularity of the gland
thyroid storm
results from untreated hyperthyroidism
can be mistaken for acute mania or psychosis
thyroid storm: presentation
Fever
Marked tachycardia
Mental status changes
GI disturbances
Profuse diaphoresis
Hyperglycemia
thyroid storm: treatment
arrhythmias (AF/RVR is the most common): digoxin
propylthyiouracil 150-250mg Q6h OR
methimazole (Tapazole) 15-25mg every 6 hours WITH the following in 1 hour:
-Lugol’s solution 10 gets TID
OR
-sodium iodide 1 g slow IV with:
-propanolol 0.5-2g IV Q4h or 20-120 mg PO q6h with
-hydrocortisone 50mg Q6h with rapid reduction as situation improves
behavioral: benzos
destroy thyroid: 131I or thyroidectomy
Subclinical hypothyroidism: labs
TSH elevated
Subclinical hyperthyroidism: labs
TSH low
unbound T4 normal
Graves disease: labs
TSH low
T3 elevated
T4 elevated
Graves disease: presentation
Age of onset typically 20-40
More prevalent in females
Goiter
Ophthalmopathy
Fatigue
Heat intolerance
Anxiety
Palpitations
Neck swelling
Eyelid retraction
Exophthalmos
Periorbital edema
Thyroid gland firm and enlarged
hyperthyroidism: cause/incidence
More common in women (8:1 ratio)
Onset most commonly between 20-40 years old
Graves’ disease is the most common presentation
Other causes:
-toxic adenoma
-subacute thyroiditis
-TSH secreting tumor of the pituitary
-high dose amiodarone
hypothyroidism: cause/etiology
Most common cause: Hashimoto’s thyroiditis
Primary disease of the thyroid gland
Pituitary deficiency of TSH
Hypothalamic deficiency of thyrotropin-releasing hormone (TRH)
Iodine deficiency
Idiopathic causes
Damage to the thyroid
hypothyroidism: management
Levothyroxine 50-100 mcg daily, increasing dosage by 25 mcg every 1-2 weeks until symptoms stabilize
- decrease dosage >60 years of age
- initial hair loss may occur
parathyroids
4 tiny glands within the thyroid that:
-sense levels of calcium in the blood
-secrete parathyroid hormone
4 jobs of parathyroid hormone
-increasing osteoclastic activity in the bones, which increases delivery of calcium and phosphorous to the bloodstream
-increasing renal tubular reabsorption of calcium
-inhibiting the net absorption of phosphorous and bicarbonate in the renal tubule
-stimulates the synthesis of 1,25-dihydroxycholecalciferol (the active metabolite of vitamin D) in the kidney
These all have the net effect of a rise in the serum ionized calcium
Most common cause of hypoparathyroidism
accidental injury or removal of the parathyroids during thyroidectomy
hypoparathyroidism: symptoms
tetany
parasthesias
carpopedal spasms
abdominal cramping
hypoparathyroidism: labs
serum Ca: low
ionized Ca: low
urine Ca: low
serum Mg: low
PO4(3-): high
alk phos: normal
hypoparathyroidism: treatment
calcium salts
vitamin D
acute hypoparathyroid tetany: treatment
intubation/mechanical ventilation if needed
calcium gluconate IV slowly until tetany ceases, then gtt to maintain serum Ca between 8-9 mg/dL
Calcitrol IV daily
transplant cryopreserved parathyroid tissue that was removed during surgery if it was preserved by the surgeon
hyperparathyroidism: cause
caused by hypersecretion of parathyroid hormone, most often by a parathyroid adenoma
hyperparathyroidism: symptoms
often asymptomatic but patients often have frequent kidney stones
hyperparathyroidism: labs
serum Ca: high
urine Ca: high
urine phos: high
serum phos: low to normal
alk phos: normal to high
hyperparathyroidism: treatment for acute hypercalcemia
fluids
bisphosphonate
hyperparathyroidism: treatment for mildly symptomatic disease
surgical excision of the affected parathyroid if it can be identified
bisphosphonates to counteract the elevated PTH’s effect on osteoclasts
calcimimetics (Cinacalcet) “fools” the parathyroid into thinking the calcium is very high, thereby lowering the PTH secretion
Addison’s Disease: causes
caused by destruction or dysfunction of the adrenal glands, resulting in a deficiency of:
- cortisol
- aldosterone
- adrenal androgens (e.g. dehydroepiandrosterone)
Usually caused by
-autoimmune attack of adrenal cortices
-metastatic cancer
-bilateral adrenal hemorrhage (e.g. with anticoagulants)
-pituitary failure resulting in decreased ACTH
cortisol
increases blood glucose by gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbs
aldosterone
essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon
plays a central role in the homeostatic regulation of BP, Na+, and K+ levels
Addison’s disease: Symptoms
weakness
easy fatiguability
anorexia
weight loss
N/V/D
amenorrhea
Hyperpigmentation in buccal mucosa and skin creases
Diffuse tanning/bronxzing and freckles
Orthostasis and hypotension
Scant axillary and pubic hair
acute:
-Rapid worsening of chronic signs and symptoms
-fever
-altered LOC
Addison’s disease: labs/Dx
hypoglycemia
hyponatremia
hyperkalemia
neutropenia
AM serum cortisol levels: low or fail to rise after being given corticotropin (exogenous ACTH)
elevated ESR
lymphocytosis
Cosyntropin stimulation test to r/o Addison’s
When should you consider acute Addisonian crisis?
Known Addison’s disease or patients on chronic steroids who present with
- hypotension
- hypothermia
- hypoglycemia
- hyperkalemia
Cushing’s disease: cause
excessive cortisol that is a result of:
- excessive ACTH secretion by the pituitary in the case of a pituitary adenoma
- chronic glucocorticoid use
- adrenal hyperfunction
- adrenal tumors
Cushing’s disease: S/Sx
moon face
buffalo hump
central obesity
hypertension
muscle wasting
thin skin
purple abdominal striae
acne
poor wound healing
hirsutism
weakness
amenorrhea
impotence
headache
polyuria and thirst
labile mood
frequent infections
Cushing’s disease: labs/Dx
hyperglycemia
hypernatremia
hypokalemia
glycosuria
leukocytosis
elevated serum cortisol in AM
dexamethasone suppression test to differentiate cause
serum ACTH
Cushing’s disease: management
If caused by chronic glucocorticoid therapy
- attempt to slowly wean from them if possible
If not caused by glucocorticoids, measure ACTH
- low = adrenal tumor
- CT scan to locate tumor. If it cannot be found, the adrenals should be resected and patient should be placed on hydrocortisone for life
- high = pituitary adenoma
- brain MRI; excise adenoma
pheochromocytoma
rare condition where a tumor forms (usually in the adrenal glands) that secretes catecholamines (norepinephrine and epinephrine) inappropriately
pheochromocytoma: presentation
“attacks” of headache, perspiration, palpitations, nausea, chest pain, tremor
often hypertensive and tachycardic
- hypertensive crisis
- ventricular arrhythmias may occur
pheochromocytoma: labs and imaging
TSH: normal
FT4: normal
24 hour urine: metanephrines, catecholamines, vanillylmandelic acid
CT of adrenals to confirm and localize tumor
PET scan
pheochromocytoma: management
Surgical removal
Alpha adrenergic medications pre-op
-Phentolamine (Regitine) 1-2mg IV Q5 min until controlled, then 1-5 mg IV every 12-24 hrs
-Convert to PO asap: phenoxybenzamine (Dibenzyline)
Post-op watch for:
-hypotension (d/t depleted catecholamines)
-adrenal insufficiency
-hemorrhage
Addison’s disease: outpatient management
specialist referral
glucocorticoid and mineralocorticoid replacement
-hydrocortisone
-fludrocortisone acetate (Florinef)
Addison’s disease: inpatient management
Hydrocortisone 100-300mg IV initially with NS
Replace volume with D5NS at 500 ml/hr x4 hrs
Vasopressors usually ineffective
Treat underlying cause, often infection
SIADH: causes/etiology
Release of ADH occurs independent of osmolality or volume dependent stimulation
Inappropriate water retention
Tumor production of ADH
CNS disorder: stroke, trauma, infection, psychosis
Chronic lung issue
SIADH: S/Sx
Neuro changes d/t hyponatremia: mild HA, seizures, coma
Decreased DTRs
Hypothermia
Weight gain/edema
N/V
Cold intolerance
SIADH: labs/Dx
Hyponatremia
Decreased serum osmolality (<280 mOsm/kg)
Increased urine osmolality (>100 mOsm/kg)
Urine sodium >40 mEq/L
SIADH: management
Treat underlying cause
Na+ >120 mEq/L: 1000 ml/day fluid restriction and monitor
Na+ 110-120 mEq/L without neuro symptoms: 500ml/day fluid restriction and monitor
Na+ <110 mEq/L or neuro symptoms present, isotonic or hypertonic saline and furosemide at 1-2 mEq/h
-Monitor K and Na losses hourly and replace
Diabetes Insipidus: causes/etiology
excessive urination and extreme thirst from an inadequate output of the pituitary hormone ADH or the lack of normal response by the kidney to ADH
Central DI: causes/etiology
Related to pituitary or hypothalamus damage resulting in ADH deficiency
-idiopathic causes
-damage to hypothalamus or pituitary
-surgical damage
-accidental trauma
-infections
-metastatic carcinoma
Nephrogenic DI: causes/etiology
Due to a defect in the renal tubules resulting in renal insensitivity to ADH
-familial X-linked trait
-Acquired due to pyelonephritis, K+ depletion, sickle cell anemia, chronic hypercalcemia, medications (e.g. lithium, methicillin, etc)
DI: S/Sx
thirst/cravings for water (fluid intake 5-20 L/day)
Polyuria (2-20L/day) and nocturia
Weight loss
Fatigue
Changes in LOC
Dizziness
Elevated temperature
Tachycardia
Hypotension
Poor skin turgor, dry mucous membranes
DI: labs/Dx
Hypernatremia
Elevated BUN/Cr (BUN fluctuates d/t dehydration)
Serum osmolality >290 mOsm/kg
Urine osmolality <100 mOsm/kg
Urine spec grav low <1.005
Vasopressin (Desmopressin) challenge test - 0.05-0.1 ml nasally or 1 ug SQ or IV with measurement of urine volume
-Central DI: positive
-Nephrogenic DI: negative
If no apparent cause, MRI to rule out mass/lesion
DI: management
IV fluids:
- Na+ >150: give D5W to replace half of volume deficit in 12-24 hrs (rapid lowering of Na+ can cause cerebral edema)
- When Na+ <150, switch to 1/2NS or NS
DDAVP 1-4 mcg IV/SQ every 12-24 hours for acute situations
- Maintenance dose of DDAVP is 10 ug Q12-24 hrs intranasally
How to evaluate for primary aldosteronism
Hold diuretics
Add 1 teaspoon of salt to daily diet for 5 days, then collect 24-hour urine sample for creatinine, sodium, and aldosterone to determine if elevated aldosterone is secondary to dietary salt restriction
primary aldosteronism: essential feature
elevated and inappropriate aldosterone
acromegaly
clinical syndrome that occurs as a result of excessive growth hormone secretion
acromegaly: clinical findings/ presentation
growth stimulation in connective tissue, cartilage, bone, skin
thickening of skin and coarse facial tissues
enlarged thyroid with/without hyperthyroidism
LVH, cardiomyopathy
hypertension
sleep apnea
adult onset
Which drugs can block or mask early signs of hypoglycemia
beta blockers
target A1c for patients >65 years old with significant comorbidities
<8.0%
Comorbidities:
-cancer
-CHF
-depression
-falls
-HTN
-stage 3 or worse CKD
-stroke
Earliest marker for diabetic nephropathy
microalbumin
can be detected before the patient is symptomatic
-Gold standard: urine albumin concentration from an early morning urine sample
When to discontinue metformin in a patient with CKD
GFR <30 mL/min (risk of lactic acidosis)
Oral hypoglycemic agent that should be avoided in elderly patients due to susceptibility to dehydration and AKI, and thus hypoglycemia
sulfonylureas (glyburide)
When transitioning from an insulin infusion to subcutaneous basal insulin, when should you stop the insulin drip?
1-2 hours after the basal insulin is given
Anion gap should be normal to <12 mEq/L
How to manage insulin while a patient is NPO and hyperglycemic
Long acting insulin
Correctional (basal) insulin
Hold prandial insulin
