Flashcards in DKA Vignette II Deck (20)
_______ derangements are also common and dangerous for patients with DKA
As the patient fights dehydration, the body compensates by holding onto _______ more avidly
Increased _______ conservation in the distal convoluted tubule and cortical collecting duct of the nephron is mediated by aldosterone, which stimulates an antiport mechanism whereby _______ is retained at the expense of _______ loss in the urine. Therefore, patients in DKA are depleted in their total body _______
Increased sodium conservation in the _______ and _______ is mediated by aldosterone, which stimulates an antiport mechanism whereby sodium is retained at the expense of potassium loss in the urine.
-distal convoluted tubule
-cortical collecting duct of the nephron
Increased sodium conservation in the distal convoluted tubule and cortical collecting duct of the nephron is mediated by _______, which stimulates an antiport mechanism whereby sodium is retained at the expense of potassium loss in the urine.
Acidosis leads to influx of _______ ions into the cells, leading to a charge neutral efflux of _______. Therefore, the acidosis can cause an excess of _______ despite the overall depletion.
-extracellular potassium (hyperkalemia)
a patient in DKA may present with _______ but will manifest _______ needs than most other patients you encounter
as you treat this patient, you must continue to watch _______ levels and be prepared to make adjustments to the _______ content of IV fluids in order to prevent severe _______ and severe _______, both of which can lead to death.
_______ is the “lethal” part of the three drug lethal injection cocktail used by the majority of the 32 states with the death penalty.
_______, occurring in about 0.15-0.3% of all cases of pediatric DKA, is the leading cause of morbidity and mortality, with a death rate ~24%. A further 20% of patients with _______ suffer long term neurologic outcomes
Cerebral edema, Cerebral edema
Acidosis leads to dysregulated _______ blood flow and perhaps even disruptions at the level of the blood brain barrier. Part of the process can be _______ as we rehydrate the patient with relatively _______ fluids.
we aim to replace fluid losses more slowly than you would in cases of non-diabetic dehydration, preventing _______ and slowing the rate of _______
-decreases in blood sodium concentration
-decrease of blood glucose
Overly rapid rehydration and hypotonic IV fluids can precipitate _______, which manifests as: _______
-mental status changes; headache; Cushing’s triad (hypertension, bradycardia, irregular respirations); or fixed, dilated pupils.
Treatment for cerebral edema includes
elevating the head of the bed, hyperventilating the patient (if intubated) [N.B. Rapid decrease in serum CO2 constricts cerebral arteries and therefore decreases cerebral blood flow], and giving IV mannitol or hypertonic saline.
Given via IV, _______ serves to raise the effective osmolality of the blood and pull water back from the brain in order to decrease swelling.
Be able to identify straightforward DKA
- Ill appearance, rapid breathing, nausea/vomiting/belly pain, dehydration
- Hyperglycemia, Ketones in blood/urine, acidosis (low pH and HCO3-)
Describe the major metabolic disturbances in DK
-High blood sugar (>200 mg/dL)
-Acidosis (low pH and HCO3-)
-Potassium may be high or low (typically normal to elevated blood levels early on, but with risk of falling potassium during treatment)
Describe the stimulus for insulin release:
Glucose enters the beta cells in the pancreas --> increased ATP/ADP ratio --> closes a channel to cause rising intracellular potassium --> increasing intracellular potassium depolarizes the membrane --> Calcium ions influx --> leads to insulin exocytosis
Describe at least three target-site actions of insulin
-Liver – store glucose (as glycogen) and lipid, stop lipid and glycogen breakdown
-Muscle – store glucose, make protein
-Adipose – store glucose and triglyceride (incorporated into chains of fats)