Endocrine Emergencies Flashcards
Physiology of metabolism in starvation:
_________________ are made as byproduct of fatty acid metabolism and used as energy source especially by the __________________.
The two major ketones are _________________ and ______________.
Ketone production is typically tightly regulated to prevent excessive ketoacid production and _______________.
ketones, brain
acetoacetone and B hydoxybutyrate (BHB)
metabolic acidosis
Pathologic ketonemia
ketones build as acids and spill them out as urine, this increases the anion gap
What is the patho of DKA?
IT MAINLY OCCURS IN DM TYPE I. As levels of insulin decrease, fuel stores are mobilized during fasting, resulting in __________________. Despite the presence of intravascular glucose, in the absence of insulin, counter regulatory hormones take over and cells are unable to use glucose as fuel source > breakdown adipose and muscle (catabolic)
Free fatty acids are converted to _______________ which are ________________ and _____________________ which is converted to __________________.
___________________ is falsely NORMAL due to _________________ from osmotic diuresis
As adipose tissue is broken down, prostaglandins ____________ and ____________ are produced > ________________________ occurs despite profound levels of volume depletion
insulin released which is triggered by glucose ingestion > stimulates liver to take in glucose and store as glycogen > increases lipogenesis > stimulates mm to take up amino acids
HYPERGLYCEMIA
ketones
BHB and acetoacetic acid which is converted to acetone
Potassium, volume depletion
I2 and E2
paradoxical vasodilation
______________ is the primary reason that causes DKA aside from missing an insulin injection.
infection
What are the clinical features of DKA?
the metabolic alterations of DKA tend to evolve within 24 hours.
symptoms:
polyuria and polydipsia
vomiting and abdominal pain
alterations in consciousness
signs:
tachy, orthostasis, hypotension, poor skin turgor, dry mucous membranes
kussmaul respirations
fruity odor on the breath
temporal wasting
How is DKA diagnosed?
You want to be aware of euglycemic ketoacidosis which is glucose ___________________
- blood glucose > 250 mg/dl
- an anion gap > 10 to 12 mEq/L
- a bicarb level <15 mEq/L
- pH <7.3 and indicating metabolic acidosis
- moderate ketonuria or ketonemia
divided into mild, mod, severe states
<250
What is the workup for DKA?
CBC, CMP, note potassium and calcium, phosphate, magnesium, serum osm
assume total body K depletion
assume NA is higher
urinalysis
ABG
ketones-serum vs urine
EKG changes induced by hypo/hyperkalemia
What is the treatment of DKA?
- volume repletion is most important
- correction of electrolyte and acid-base imbalances
potassium-rapid development of severe hypokalemia which is the most life threatening electrolyte derangement during the treatment if DKA (insulin action on K)
- if > 5.2 - cleared to start insulin
- if 3.3 < K < 5.5 and urine output then add 20 to 30 mEQ/L to IV fluids PLUS insulin for at least 4 hours to keep K between 4 and 5 meq/L
- if K < 3.3 hold insulin until replace K > 3.3 - Reversal of metabolic consequences of insulin insufficiency > given insulin
Resolution of DKA =
Avoidance of complications:
K > arrythmia. decrease ____________ and ___________
a serum bicarb level > 15
a venous pH > 7.3 and or a normal calculated anion gap
phos and mag
DKA is triggered at low sugar levels in _________________ so the provider should recognize signs and symptoms of DKA and check a serum ________________ level
pregnancy
BHB
What is the goal of treatment for DKA?
glucose < 200
bicarb greater than or equal to 18
venous pH > 7.3
How to manage DKA in a patient with an insulin pump
assume a problem with the pump, disconnect the pump before starting insulin infusion
if DKA resolves in ED and pump works, then restart pump therapy approx 1 hour before the IV insulin drip instead of SC insulin
In very young children, new onset diabetes and adolescents with DKA, _________________ remains the most common and feared cause of (high rate) mortality. It develops within ___________ hours of treatment
Tx: _____________
cerebral edema
4-12
IV mannitol
________________ occurs in alcoholic patients who enter a period of fasting after a dramatic period of ethanol binging. This results in __________________ and ______________. N/V, abdominal pain, and constitutional complaints are common. Ketosis favors __________ due to ___________ depletion from alcoholism.
Tx:
Improvement will see an increase in ______________
alcoholic ketoacidosis
metabolic acidosis and dehydration
BhB, NADH
Tx: IV fluids, replenish electrolytes, supplemental dextrose
urine ketones
Hyperosmolar hyperglycemic state (HHS) is a progressive _________________ and __________________ found in pts with poor controlled or undiagnosed ______________________ commonly it is a ____________________ illness. It is present mostly in _____________.
hyperglycemia and hyperosmolarity
DM Type II
precipitating
elderly
What are the 3 main underlying factors of hyperosmolar hyperglycemic state (HHS)
insulin resistance/ deficiency
inflammatory state + stress hormones = increased hepatic glucogenesis and glycolysis
osmotic diuresis followed by impaired renal excretion of glucose
What is the clinical presentation of someone with hyperosmolar hyperglycemia?
The exam in these patients is mostly from _________________. _____________ has linear relationship to serum osmolality
- typically elderly and often institutionalized with baseline cognitive impairment and comorbid illnesses.
- vital signs, lab results and or mental status have evolved over days to weeks
- symptoms are often nonspecific and may include malaise, weakness, anorexia, fatigue, vomitinig, and cognitive impairment
- may have no prior history of DM and present with acute illness such as stroke, MI, pneumonia, abdominal emergencies, and sepsis also precipitated by new medication.
volume depletion
coma
HHS diagnosis
it is important to recognize the potential for a variety of mixed acid-base patterns in patients with HHS
serum glucose usually >600
elevated plasma osmolality of > 315
serum bicarb > 15
arterial pH > 7.3
serum ketones that are negative to mildly positive
order labs: CBC, CMP, mag/phosphate, serum and urine osm, lactate, BhB, bloor/urine cx, trop, CPK, VBG, TSH, etc etc
What is the treatment for HHS?
once glucose decreases to <300, change the IV solution to 5% dextrose in half-normal saline and reduce insulin infusion from 0.02 to 0.05 until serum osmolality is <315 and glucose is between 200-300
- start IV fluids- alone may decrease glucose by 35-70
- replete K with IV fluids before insulin is started
In HHS, the complications are
1. changes in serum osmolality > ________________. Start head CT or MRI is indicated.
2. venous and arterial thrombosis > patients should receive prophylactic anticaogulation
osmotic demyelination syndrome.
What is the treatment for hyperglycemia?
low dose of regular or rapid acting insulin 1 unit SC for every 30-50 mg/dL above glucose of 250-300)
a long acting insulin should be given in the ED to prevent DKA
What is the treatment for patients without severe and symptomatic hyperglycemia
regular or rapid acting insulin can be given to reduce glucose to 250 > discharged with prescription of metformin > see doc within 24 hrs
What is the treatment for hyperglycemia in patients using insulin pumps?
no guidelines- treat the same as patients who are on multiple daily doses of insulin
Hypoglycemia is plasma glucose ________________. T1DM is more prone to hypoglycemia because the surge of________________ is absent and ___________________ secretion may be blunted due to neuropathy, age or autonomic dysfunction from prior hypoglycemic episodes.
< 70
glucagon
epinephrine
What is the treatment for hypoglycemia ?
15 to 20 grams of glucose which can be repeated if hypoglycemia persists after 15 minutes.
glucagon emergency kits stimulated glycogenolysis and is effective in 10 to 15 minutes
recall long acting potential of sulfonylureas
Myxedema crisis/hypothyroidism is a state of metabolic and multiorgan decompensation characterized by:
1.
2.
3.
- uncorrected hypothyroidism
- AMS/coma
- hypothermia usually < 95.9 F
Myxedema crisis/hypothyroidism is precipitated by a number of conditions:
infection, anesthetic agents, cold exposure, trauma, MI, CHF, stroke, GI, hemorrhage, surgery, burns, medications, thyroid medication noncompliance
In myxedema crisis/hypothyroidism, _______________ is the most common presentation.
Half of the patients present with ________________. High mortality rate.
hypothermia
hypotension, systolic <100
The clinical presentation of hypothyroidism and myxedema crisis is ….
What is the diagnostic clue?
bradycardia, hypotension, hypothermia, hypoventilation, AMS/coma.
You also see hypoglycemia, pleural effusions, hyponatremia, hypercapnea
increase TSH, decrease T4 and T3 (primary) OR decrease TSH, T4 and T3 (secondary)
What is the treatment for myxedema crisis/hypothyroidism?
ABCs, oxygen, IV access, cardiac monitoring
IV therapy: dextrose for hypoglycemia, water restriction for hyponatremia
Vasopressors if indicated
hypothermia: treated with passive rewarming
steroids: hydrocortisone due to increased metabolic stress
IV thyroid replacement: IV levothyroxine preferred
Hyperthyroid/thyroid storm is excessive thyroid hormone which leads to…
1.
2.
3.
4.
increasing metabolic rate
heart rate
ventricle contractility
muscle and CNS excitability
What lab values confirm primary hyperthyroidism?
low TSH, increase free T4
Thyroid storm is an acute, severe, life threatening hypermetabolic event caused by _______________________________ or ____________________________
excessive release of thyroid hormone causing adrenergic hyperactivity
OR
increase peripheral response to thyroid hormone in response to one or more precipitants (graves disease being most common)
The order of therapy for a thyroid storm is VERY important…..
- obtain pregnancy test
- supportive care - IV fluids, dextrose
- inhibit peripheral adrenergic effects- reduce afterload and heart rate (propanolol, esmolol, reserpine)
- inhibit thyroid gland synthesis of new thyroid hormone with a thionamide
- inhibit release of thyroid hormone (at least 1 HR after previous step) form of iodine
6.Prevent peripheral conversion of T4 to T3 with hydrocortisone or dexamethasone - Prevention of free thyroid hormones reabsorption - choletyramine
- DEFINITIVE THERAPY IS RADIOACTIVE IODINE ABLATION THERAPY OR SURGERY
Adrenal crisis:
Primary adrenal insufficiency or addison’s disease is due to intrinsic adrenal gland dysfunction and results in decrease
1.
2.
3.
The patient will present with
1.
2.
3.
4.
- cortisol
- aldosterone
- gonadotropin
- hyperpigmentation
- hyponatremia
- hyperkalemia
- hypoglycemmia
Secondary adrenal insufficiency is due to ________________ dysfunction which means no __________ or _______________ therefore, ONLY _____________ deficiency
hypoglycemia
hypothalamic-pituitary dysfunction
ACTH, CRP
cortisol
When does adrenal crisis occur?
when an increased demand fails to increase hormone production and is life threatening. The crisis is usually precipitated by an event like infection, surgery, trauma, burns
In adrenal crisis, what does the lack of cortisol affect?
- heart
- water excretion
- electrolytes
- metabolism
- immune system
- growth/development
Patients with adrenal crisis will present with…..
You want to consider adrenal crisis in patients with unexplained hypotension esp in patients with a history of chronic glucocorticoid therapy; those with acquired immunodeficiency syndrome, TB, autoimmune disease or severe head trauma.
severe hypotension to refractory vasopressors
also GI, CNS sx
What is the treatment for adrenal crisis?
What do you NOT want to use in someone with known adrenal insufficiency?
IV fluids if hypotensive
Hydocortisone bolus to treat underlying condition
vasopressors only after steroid therapy in pts unrespnsive to agressive fluid resuscitation
etomidate
