DKA and HHS Flashcards

1
Q

what does insulin do in the fed state?

A

as always it is the anabolic hormone so it causes uptake of glucose into cells, thus decreasing glucose concentration in the blood. translocation of the GLUT4 receptor. stimulates storage of glucose in the lover as glycogen. promotes synthesis of ffatty acid stimulates the uptake of amino acids. increases permeability of potassium, phosphate and magnesium

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2
Q

which tissues do not depend on GLUT4?

A

brain and liver

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3
Q

what happens to insulin secretion as the glucose concentration declines?

A

it decreases. cells become unable to take up glucose and rely on alternative metabolisms

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4
Q

what does glucagon do?

A

increases the breakdown of glycogen. lipolysis, gluconeogenesis also occur

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5
Q

what is the role of ketones?

A

they are used in prolonged fasting to preserve the body muscle.

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6
Q

what is the pathophysiology of DKA and HHSq

A

relative insulin deficiency. increase in the amount of counter regulatory hormones (due to infection, stress, medication) volume depletion (5-12 liters).

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7
Q

what are the counter regulatory hormones>

A

glucagon, cortisol, epinephrine, growth hormone.

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8
Q

what is the pathogenesis of DKA?

A

decreased relative insulin causes increased glucagon/regulatory hormones. this causes reliance on alternative metabolism: lipolysis, ketosis and hyperglycemia (lack of use, lack of insulin to push it into cells, etc). formation of ketones to keep tissues happy, excessive diuresis due to glucose leads to dehydration and thirst.

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9
Q

HHS pathogenesis

A

relative decrease in insulin leads to hyperglycemia, osmotic diuresis and dehydration. however there is enough insulin to keep lipolysis and ketogenesis away, but not enough to increase glucose utilization.

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10
Q

DKA presentation

A

T1DM, generally young, abdominal discomfort, vomiting, kussmaul respirations, vascular shock, mental status changes.

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11
Q

HHS presentation

A

T2DM, generally elderly, debilitating disease, volume contraction, without ketosis. mental status changes.

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12
Q

how many patients have overlap between ketosis and HHS

A

1/3

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13
Q

what is the triad of DKA

A

hyperglycemia, metabolic acidosis, ketone production.

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14
Q

what is the triad of HHS

A

hyperglycemia, hyperosmolarity, dehydration. there is absence of significant ketosis.

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15
Q

best treatment plan for HHS/DKA

A

take insulin even when not eating, increase the frequency of testing and titrate insulin, drink fluids, monitor urine ketone. if continuously high glucose or vomit call MD.

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16
Q

what is meticulous treatment? 14 things

A

fluids, insulin, potassium, bicarbonate, sodium, ketones, acidbase, phosphate, creatinine, lactic acid, leukocytosis, amylase, liver function, hypertriglyceridemia.

17
Q

when to give bicarbonate?

A

impaired myocardial function, cerebral vasodilation, pulmonary vasoconstriction, coma, GI compilcations. ONLY IN SEVERE acidosis (pH 6.5

18
Q

why not give bicarb?

A

too much causes hypokalemia, decreased tissue oxygenation, cerebral edema, paradoxical CNS acidosis.

19
Q

what lab to follow to see if treatment is working?

A

do not follow ketones because they move slower than glucose. follow anion gap and the glucose.

20
Q

what are some complications of HHS/DKA

A

hypoglycemia (may need to start dextrose), hypokalemia (monitor and replace), hypechloremic non anion gap metabolic acidosis (occurs during recovery phase of DKA/usually self limited with few clinical consequences). cerebral edema (usually fatal or has serious neurological sequelae).

21
Q

what is the cause of cerebral edema in DKA?

A

unknown. too fast fluid correction, excessive bicarb, hyponatremia, too rapid glucose correction?

22
Q

which has a higher mortality? HHS/DKA

A

HHS.