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ABBEY MSII Unit 5 > Pharm DKA & HHS > Flashcards

Pharm DKA & HHS Flashcards

1
Q

normal food metabolism in fed state

A
  1. decreases blood glucose concentration
  2. spares muscle and fat from fuel metabolism
  3. increases permeability of cells to potassium, magnesium, and phosphate

INSULIN in ANABOLIC STATE

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2
Q

how does insulin decrease blood glucose concentration

A
  1. facilitates entry of glucose into tissues via GLUT4 transporter
  2. stimulates storage of glucose in the liver as glycogen
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3
Q

GLUT4 what does it do and where is it present?

A

transporter for glucose into tissues - not present on brain and liver

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4
Q

how does insulin spare muscle and fat from fuel metabolism?

A
  1. promotes synthesis of fatty acids (lipoproteins) in the liver
  2. inhibits adipose tissue breakdown
  3. stimulates uptake of amino acids
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5
Q

normal fuel metabolism in fasting state

A
  1. insulin secretion decreases as glucose levels decline
  2. glucagon increases

CATABOLIC state

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6
Q

what happens as glucose levels decline?

A

insulin secretion decreases so cells are unable to take up glucose and change to alternative fuels

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7
Q

what does glucagon do?

A
  1. stimulate gylcogenolysis (glycogen breakdown into glucose)
  2. gluconeogenesis (glucose production from amino acid precursors)
  3. lipolysis
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8
Q

what happens in a prolonged fasting state?

A

ketones produced for energy to conserve protein

-ketonemia causes metabolic acidosis

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9
Q

pathophysiology of DKA and HHS

A
  • absolute or relative insulin deficiency
  • increase in counter-regulatory hormones (stress, infection, medications)
  • volume depletion (5-12L)
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10
Q

flatbush diabetes

A

ketosis-prone type 2 diabetes (african, blacks, hispanic patients)

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11
Q

what are the counter-regulatory hormones?

A

glucagon, cortisol, growth hormone, epinephrine

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12
Q

glucagon effects on liver, muscle, adipose tissue

A

liver: + glycogenolysis, + gluconeogenesis, + ketogenesis
muscle: minimal action
adipose tissue: minimal action

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13
Q

cortisol effects on liver, muscle, adipose tissue

A

liver: +glycogenolysis, + gluconeogenesis
muscle: - amino acid uptake, + proteolysis, - insulin action
adipose tissue: + lipolysis, - insulin action

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14
Q

growth hormone effects on liver, muscle, adipose tissue

A

liver: + gluconeogenesis, + IGFs/IGFBP
muscle: + amino acid uptake, - glucose uptake
adipose tissue: +lipolysis, - glucose uptake

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15
Q

epinephrine effects on liver, muscle, adipose tissue

A

liver: +glycogenolysis, +gluconeogenesis, +ketogenesis
muscle: +glycogenolysis, - insulin action
adipose tissue: + lipolysis, - insulin action

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16
Q

precipitating factors for DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A
  1. infection
  2. insulin
  3. infarct
17
Q

volume depletion effects on body

A
  1. hyperglycemia (low insulin and elevated counter-regulatory)
  2. renal threshold for glucose surpassed (threshold is 160-190, any more and osmotic diuresis causing electrolyte loss)
  3. severe water loss (polyurea, dehydration, increased thirst, polydipsia)
18
Q

pathogenesis of DKA (diabetic ketoacidosis)

A

-decreased effective insulin concentration and increase in counter-regulatory hormones causing ketosis and hyperglycemia, lipolysis of adipose tissue (causing increased FFA), and unrestrained hepatic fatty acid oxidation to ketone bodies

19
Q

what is hyperglycemia in DKA due to?

A
  • increased gluconeogenesis
  • increased glycogenolysis
  • impaired glucose utilization by peripheral tissues
20
Q

what is transient insulin resistance in DKA due to?

A

hormone imbalance (counter-reg hormones) and elevated FFA concentrations

21
Q

pathogenesis of HHS

A

less well understood than DKA

  • relative insulin deficiency –> hyperglycemia –> osmotic diuresis –> dehydration
  • enough insulin to prevent lipolysis and ketogenesis but not enough to facilitate glucose utilization
22
Q

similarities between DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A

hyperglycemia (glycosuria (osmotic diuresis), loss of water and electrolytes, dehydration, impaired renal function)

23
Q

differences between DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A 
DKA = hyperlipidemia and ketoacidosis (causing acidosis) d/t absolute insulin deficiency
HHS = hyperosmolarity with absent/minimal ketogenesis due to relative insulin deficiency
24
Q

clinical presentation of DKA (diabetic ketoacidosis)

A
  • Type 1 DM
  • young
  • abdominal discomfort
  • vomiting
  • kussmaul respirations
  • vascular shock
  • mental status change
25
Q

clinical presentation of HHS

A
  • Type 2 DM
  • elderly
  • debilitating disease
  • volume contraction
  • without ketoacidosis
  • mental status changes
26
Q

what are the three diagnostic criteria of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A

DKA: 1. hyperglycemia, 2. metabolic acidosis 3. ketone production
HHS: 1. hyperglycemia (more than DKA), 2. hyperosmolality 3. dehydration

27
Q

treatment of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A
  1. fluids
  2. insulin (continuous regular insulin preferred) - add dextrose once glucose reach 200-300
  3. potassium (give before insulin if less than 3.2 to avoid hypokalemia which causes ventricular arrhythmias)
  4. bicarbonate (controversial - needed in severe acidosis or severe hyperkalemia)
28
Q

serum osmolality equation

A

Na (mmol/L) X 2 + urea (mg/dL) / 2.8 + glucose (mg/dL) / 18

29
Q

ketones

A
  • alternative fuel source
  • present under normal circumstances (starvation, alcohol, pregnancy)
  • acetoacetic acid, beta-HBA forms, and acetate forms
30
Q

how to test ketone levels

A
  • ames acid test measures acetoacetic acid in blood and urine (purple color change) - does not directly test beta-HBA
  • now use beta-hydroxybutyrate directly
31
Q

ketone levels: normal, DKA, starvation

A

AMES: normal: less than .15; starvation: 4-6; DKA: 3-30

Beta-hydroxybutyrate: normal: .02-.27; fast: .5; DKA: 2

32
Q

resolution of DKA

A

glucose less tahn 200, bicarbonate greater than 15, venous pH greater than 7.3, calculated anion gap less than 12

33
Q

resoluation of HHS

A

normal osmolality, normal mental status

34
Q

complications of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A
  • hypoglycemia (start dextrose when glucose less than 200),
  • hypokalemia,
  • hypercholoremic non-anion gap metabolic acidosis (during recovery phase)
  • cerebral edema
35
Q

mortality with DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A

DKA: less than 1%
HHS: 5-20%

36
Q

poor prognostic factors DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A

hypotension, azotemia, deep coma, associated illness

37
Q

leading cause of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)

A

MI and infection (esp pneumonia)

ABBEY MSII Unit 5 (8 decks)

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