Endocrine Metabolic Emergencies Flashcards
Diabetic Ketoacidosis (DKA)
-MC in which type of DM?
-pathophys
-
MC type is DM1
Pathophys:
- bodys response to cellular starvation
- relative insulin deficiency with excess glucagon
- Acidosis:
- -insulin deficiency; not enough to drive glucose into cells, leads to cellular starvation. the cell requires something other than glucose for energy now so lipolysis with subsequent fatty acid transport to hepatocytes where they are turned into ketoacids. This results in ketonuria, anion gap metabolic acidosis with compensatory tachypnea and vomiting.
- dehydration:
- -relative insulin deficiency leading to increased serum level of glucose increasing osmotic load and spills into urine. Water drawn out of cells via oncotic pressure resulting in impaired consciousness and shock.
- hypotension:
- -initially there is an increase in volume in vasculature compartment (hyperglycemia pulling fluid from cells into serum) but as glucose begins to spill into the urine there is massive osmotic diuresis resulting in cellular hydration and vasculature depletion.
DKA
- presentation
- treatment & management
Presentation:
- hyperglycemia (polydipsia, polyuria)
- Acidosis from ketoacids (tachypnea, fruity odor of breath)
- volume loss (dehydration signs such as dry memebranes, poor skin turgor, delayed capillary refill, mental confusion.
Treatment:
-AGGRESSIVE fluid therapy (volume repletion)***
- reversal of metabolic consequences of insulin insufficiency
- correct electrolytes; K+ replacement if indicated by labs.** (development of severe hypokalemias the most life threatening electrolyte derangement during tx of DKA)***
- treat underlying cause
- 0.1units/kg/hr insulin after initial fluid bolus***
- monitor, large bore IV with NS running
- bedside glucose, urine dipckstick, EKG
- CBC, electrolytes
- ABG
- blood cultures
DKA:
- complications
- causes of DKA in a pt who is not a new onset diabetic?
Complications:
- hypoglycemia
- cerebral edema
- hypokalemia
- hypophosphatemia
- ARDS
Cause:
- compliance issues
- d/c insulin therapy
- insults to the body such as infection, MI, PE, etc.
Hyperosmolar Hyperglycemic State:
- aka
- occurs in which type of DM?
- characterized by what 3 features?
- what is the usual serum glucose in these patients?
- what is the usual plasma osmolality?
- what is ususal bicarb and pH?
- shared labs/sx w/ DKA?
THIS IS AN EMERGENCY
aka; nonketotic hyperosmolar state of hyperosmolar hyperglycemic nonketotic syndrome (HHNS)
-occurs in those with DM2 (poorly controlled or undiagnosed)
Characterized by:
- severe hyperglycemia
- hyperosmolality
- LACK of ketonemia
Serum glucose greater than 600mg/dL
plasma osmolality greater than 315mOsm/kg
Bicarb greater than 15
pH greater than 7.3
labs/sx: hyperglycemia, hyperosmolality, severe volume depletion, electrolyte disturbances,, and ***Sometimes acidosis.
What is the lab value in each of the following between DKA and HHNS?
- plasma glucose
- arteial pH
- serum bicarb
- urine ketone
- serum ketones
- serum osmolarity
- anion gap
- alteration in sensoria or mental obtundation
DKA:
- glucose greater than 250
- pH: less than 7.3
- bicarb less than 18
- urine ketones: positive
- serum ketones: positive
- osmolarity: variable
- anion gap: greater than 10
- mentation: alert to stupor/coma depending on the severity.
HHNS:
-plasma glucose: greater than 600
- arterial pH: greater than 7.3
- serum bicarb: greater than 15
- urine ketone: small
- serum ketones: small
- serum osmolarity:greater than 320
- anion gap: less than 12
- alteration in sensoria or mental obtundation: stupor/coma
Hyperosmolar hyperglycemic (nonketotic) state:
- whos at greatest risk of this?
- pathophys
greatest risk: inability to access water
-often occurs in a nonambulatory nursing home pt.
pathophys:
- uncontrolled DM leading to hyperglycemia, attraction of water from intracellular space initially increasing intravascular volume, but then the increasing serum glucose spills into the urine pulling water with it (profound osmotic diuresis), decreased GFR leading to further decrease glucose excretion worsening hyperglycemia.
HHNS:
- presentation
- tx
Presentation:
- elderly, usually referred by caretaker for abnormalities in VS and/or mental status.
- precipitated by acute illness such as PNA or UTI
- weakness, anorexia, fatigue, cough, dyspnea, or abd pain
Tx:
- volume repletion
- correct electrolyte abnormalities
- identify and tx precipitating cause
- gradual correction of hyperglycemia
Hypoglycemia:
-signs and sx
Signs and Sx:
- neurogenic:
- -sweating
- -pallor
- -tachycardia
- -palpitation
- -tremor/shaking
- -nervousness/anxiety
- -tingling, paresthesias (mouthand fingers)
- neuroglycopenic:
- -HA
- -drowsiness
- -lightheadedness/syncope
- -mental dullness/confusion
- -amnesia
- -seizures
- -coma
Hypoglycemia thresholds:
- at what plasma glucose level does each of the following occur?
- -secretion of insulin counter-regulatory hormones glucagon and epi
- -neurogenic sx
- -neuroglycopenic
Define hypoglycemia unawareness? who is most at risk for this?
Management of hypoglycemia
65-68mg/dL counter regulatory hormones are released
54mg/dL neurogenic sx
47mg/dL neuroglycopenic sx
Hypoglycemia unawareness: development of low serum sugar values without physiological ability to react.
Greatest risk for this are extremes of age, comorbidities, medications (beta blockers)
Hypglycemia management:
-15-20g of glucose; effects should be apparent in 15 minutes
-retest glucose in 15mins to see if you need to give glucose again
-alter insulin regimen or dosage
…and now another slide has management that says:
-initially 1g/kg of body weight dextrose as D50W in adults which can then be followed by infusion of D10W at a rate to maintain serum glucose above 100mg/dL.
-repeat glucose check q30min x2hrs
-PO replacement (300g carbs)
-glucagon 1mg IM or IV
-octreotide (somatastatin analogue) can be given after initial glucose therapy
Adrenal Medulla:
- controlled by what?
- secretes which hromones?
Adrenal cortex:
-secretes which hormones?
Medulla:
- controlled by the nervous system
- secretes E andd NE
Cortex: GFR;
- glomerulosa: mineralocorticoids…aldosterone
- fasciculata: glucocorticoids…cortisol
-reticularis: sex hormones
Salty, sugar, sex.
Describe the feedback mechanisms of ACTH
Hypothalamus secretes corticotropin releasing hormone whereby the anterior pituitary then releases ACTH which tells the adrenal cortex to secrete cortisol. Cortisol stimulates gluconeogenesis, protein mobilization, fat mobilization, stabilizes lysosomes, andd relieves stress.
Cortisol can also have a negative feed back on both the anterior pituitary and the hypothalamus.
Adrenal Insufficiency vs Crisis:
-describe the differences
What are the two types of adrenal insufficiency?
Adrenal insufficiency is the failure of adrenal glads to produce essential basal secretion of steroids. (addisons)
Adrenal crisis is the failure to respond to the increased demands caused by stress of sudden inability to secrete essential steroids,
Adrenal insufficiency:
- Primary = addisons, result from destruction or dysfunction of the adrenal cortex
- secondary = results from inadequate stimulation of adrenal cortex by ACTH.
Please review feedback mechanisms on slides 48 & 49 of adrenal insufficiency feedback loops.
.
Primary Adrenal Insufficiency:
- what are the causes of decreased blood pressure?
- why do these pts get increased HR?
- why do these patients have a low blood glucose?
- why do they have hyperkalemia? hyponatremia?
Decreased blood pressure:
-decreased cortisol( cortisol up-regulates alpha-1 adrenergic receptors on vascular smooth muscles causing vasoconstriction) so a decreased amount would lead to vasodilation.
-decreased aldosterone (aldosterone increases Na reabsorption by renal cells leading to an increase in extracellular fluid volume and blood volume, venous return, cardiac output and arterial pressure, SO a decrease in aldosterone decreases BP.
increased HR:
-it is a compensatory mechanism of the decreased BP/volume.
Decreased blood glucoses:
-decreased cortisol ( cortisol increases blood glucose concentration by promoting gluconeogenesis and decreasing glucose uptake by the tissues, therefore a decrease in cortisol would decrease blood sugar.
Hyperkalemia: decreased aldosterone; aldosterone stimulates K secretion by renal principal cells, so with decreased aldosterone we get a build up of K+.
Hyponatremia:
-decreased aldosterone; aldosterone increases Na reabsorption by renal principal cells, So if we have decreased aldosterone we will have decreased Na reabsorption into the blood.
Adrenal Crisis:
- what is the primary manifestation?
- tx
- who ususally get this?
This is an emergency
primary manifestation is hypotension.
Tx:
- hypotension is resistant to catecholamine and IV fluid adminstration.
- missing cortisol must be replaced or else =death.
Who;
- undiagnosed pt with primary adrenal insufficiency who has been subject to serious infection or acute, major stress.
- in pt w/ known primary adrenal insufficiency who does not take more glucocorticoid during an acute infection
