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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
clinical presentation of HHS
- Type 2 DM - elderly - debilitating disease - volume contraction - without ketoacidosis - mental status changes
26
what are the three diagnostic criteria of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)
DKA: 1. hyperglycemia, 2. metabolic acidosis 3. ketone production HHS: 1. hyperglycemia (more than DKA), 2. hyperosmolality 3. dehydration
27
treatment of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)
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
serum osmolality equation
Na (mmol/L) X 2 + urea (mg/dL) / 2.8 + glucose (mg/dL) / 18
29
ketones
- alternative fuel source - present under normal circumstances (starvation, alcohol, pregnancy) - acetoacetic acid, beta-HBA forms, and acetate forms
30
how to test ketone levels
- 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
ketone levels: normal, DKA, starvation
AMES: normal: less than .15; starvation: 4-6; DKA: 3-30 | Beta-hydroxybutyrate: normal: .02-.27; fast: .5; DKA: 2
32
resolution of DKA
glucose less tahn 200, bicarbonate greater than 15, venous pH greater than 7.3, calculated anion gap less than 12
33
resoluation of HHS
normal osmolality, normal mental status
34
complications of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)
- hypoglycemia (start dextrose when glucose less than 200), - hypokalemia, - hypercholoremic non-anion gap metabolic acidosis (during recovery phase) - cerebral edema
35
mortality with DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)
DKA: less than 1% HHS: 5-20%
36
poor prognostic factors DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)
hypotension, azotemia, deep coma, associated illness
37
leading cause of DKA (diabetic ketoacidosis) and HHS (hyperosmolar hyperglycemic state)
MI and infection (esp pneumonia)

ABBEY MSII Unit 5 (8 decks)

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