DM, DKA, HHS

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94 Terms

1
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what is the underlying cause of diabetic ketoacidosis (DKA)?

a profound underlying deficiency of insulin

2
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what four hallmark features characterize DKA?

hyperglycemia, ketones, acidosis, and dehydration

3
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in which type of diabetes does DKA most commonly occur?

Type 1 DM

4
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what are some precipitating factors for DKA?

illness, infection, inadequate insulin dosage, undiagnosed type 1 DM, poor self-management, lack of education/resources, or neglect

5
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why does fat breakdown occur in DKA?

because glucose cannot enter cells without insulin, so the body uses fat as an alternate energy source

6
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what are ketones and why are they significant in DKA?

acidic by-products of fat metabolism that cause metabolic acidosis when present in excess

7
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what happens when ketones are excreted in urine (ketonuria)?

electrolytes are lost along with ketones, leading to imbalances

8
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How does insulin deficiency affect protein metabolism?

it impairs protein synthesis, increases protein breakdown, and causes nitrogen losses

9
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What role does gluconeogenesis play in worsening DKA?

amino acids are converted to glucose in the liver, adding to hyperglycemia

10
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what are the consequences of osmotic diuresis in DKA?

severe dehydration, polyuria, polydipsia, and electrolyte depletion.

11
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What major electrolytes are depleted in DKA if untreated?

sodium, potassium, chloride, magnesium, and phosphate

12
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how can vomiting worsen DKA?

it increases fluid and electrolyte losses

13
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What complications occur if DKA is not treated?

hypovolemia —> shock —> renal failure —> worsening acidosis —> coma —> death

14
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Why does polyuria and polydipsia occur in DKA?

high glucose pulls fluid into urine (osmotic diuresis), leading to dehydration and thirst

15
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What is the normal pH range for arterial blood?

7.35-7.45

16
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what happens to the pH in DKA?

it decreases (<7.35) indicating metabolic acidosis

17
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What is the normal PaCO₂ range?

35-45 mm Hg

18
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What happens to PaCO₂ in DKA?

it decreases (<35 mmHg) due to due to Kussmaul respirations (respiratory compensation)

19
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what is the normal HCO₃⁻ range?

22-26 mEq/L

20
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What happens to HCO₃⁻ in DKA?

it decreases (<22 mEq/L) because bicarbonate is consumed buffering acids

21
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what glucose level is typically seen in DKA?

blood glucose level >250 mg/dL

22
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Besides lab values, what physical assessments are important in suspected DKA?

skin turgor, dry mucous membranes, intake & output, vital signs

23
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what are some signs of dehydration in DKA?

poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension

24
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What type of respirations are often seen in DKA?

Kussmaul respirations (deep, rapid breathing to blow off CO2)

25
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why is DKA considered a serious condition?

because it proceeds rapidly and must be treated promptly

26
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can DKA always be treated in the hospital?

No. If fluid/electrolyte imbalances are not severe and glucose levels can be safely monitored at home, DKA can be managed on an outpatient basis

27
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What factors determine if a DKA patient needs hospitalization?

presence of fever, nausea, vomiting, diarrhea, altered mental status, cause of DKA, and ability to communicate to the HCP every few hours

28
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Why do patients with DKA and infections (e.g., pneumonia or UTI) usually need hospitalization?

because infection worsens illness severity and complicates management

29
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What is the first therapeutic goal in managing DKA?

establish IV access and begin fluid and electrolyte replacement

30
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What IV fluids are typically used first for DKA patients?

IV infusion of 0.45% or 0.9% NaCl at a rate that raises BP and restores urine output to 30-60 mL/hr

31
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When glucose levels approach 250 mg/dL, what is added to IV fluids?

5%-10% dextrose, to prevent hypoglycemia and sudden glucose drop that can cause cerebral edema

32
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Why is rapid rehydration with hypotonic solutions dangerous in DKA?

it can cause cerebral edema

33
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What is the aim of fluid and electrolyte therapy in DKA?

to replace extracellular and intracellular water and correct deficits of sodium, chloride, bicarbonate, potassium, phosphate, and magnesium

34
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What special monitoring is needed in patients with kidney or heart disease receiving fluids for DKA?

monitoring for fluid overload

35
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Why must serum potassium be checked before starting insulin therapy in DKA?

because if a patient is hypokalemic, insulin will further decrease potassium levels, leading to life threatening hypokalemia

36
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Why can initial serum potassium be misleading in DKA?

it may appear normal or high but rapidly decrease once insulin therapy begins (insulin drives K+ into cells)

37
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What type of insulin therapy is given in DKA?

IV insulin (regular) therapy to correct hyperglycemia and hyperketonemia

38
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Why must serum glucose not be reduced too rapidly in DKA?

rapid drops can cause cerebral edema

39
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What is the safe target rate for glucose reduction with insulin in DKA?

36-54 mg/dL per hour

40
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How does insulin therapy affect potassium and fluid balance?

insulin allows water and potassium to enter the cell with glucose, leading to possible vascular volume depletion and hypokalemia

41
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What must be closely monitored during insulin therapy in DKA?

the patients fluid balance and potassium levels

42
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What GI-related symptoms are seen in DKA?

ABD pain, n/v, dry mouth, and thirst

43
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What neurological symptoms can occur in DKA?

restlessness, confusion, and lethargy

44
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What vital sign and cardiovascular changes are seen in DKA?

rapid, weak pulse and possible fever

45
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What lab findings are typical in DKA?

serum glucose >250 mg/dL, glucosuria, and ketonuria

46
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What is Hyperosmolar Hyperglycemia Syndrome (HHS)?

life-threatening complication of diabetes in which patients produce enough insulin to prevent ketoacidosis but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion

47
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Which type of diabetes is HHS most commonly associated with?

Type 2 DM

48
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Who is most at risk for developing HHS?

patients over 60 years of age with type 2 DM

49
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What are common causes of HHS?

UTIs, pneumonia, sepsis, acute illness, and newly diagnosed type 2 DM

50
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what factors often contribute to the development of HHS?

impaired thirst sensation or functional ability to replace fluids

51
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what is a typical history in patients with HHS?

inadequate fluid intake, increasing mental depression or impaired cognition, and polyuria

52
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What is the main pathophysiologic difference between HHS and DKA?

HHS has enough insulin to prevent fat breakdown and ketoacidosis, so ketones are absent or minimal

53
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Why can HHS go undetected longer than DKA?

HHS has fewer early symptoms, allowing glucose levels to climb extremely high before recognition 

54
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What neurological manifestations are common in HHS due to high serum osmolality?

somnolence, coma, seizures, hemiparesis, and aphasia

55
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Why can HHS be misdiagnosed as a stroke?

Neurologic symptoms such as hemiparesis and aphasia closely mimic stroke.

56
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What is the critical step in differentiating HHS from stroke?

immediate determination of blood glucose level

57
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What are the laboratory findings in HHS?

blood glucose (>600 mg/dL)

increased serum osmolality

absent or minimal ketones in blood and urine

58
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Why does HHS not cause metabolic acidosis?

because there is enough circulating insulin to prevent fat breakdown and ketone formation

59
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Which condition is more likely to cause severe dehydration: DKA or HHS?

HHS, because it progresses more slowly and patients often go longer without treatment

60
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What is the mortality risk of HHS?

HIGH = MEDICAL EMERGENCY

61
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What is the primary management strategy for HHS?

Immediate IV insulin administration and fluid replacement with 0/9% or 0.45% NaCl

62
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How does fluid replacement differ between DKA and HHS?

HHS usually requires larger fluid volumes, given slowly and carefully to prevent overload.

63
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Why must fluid replacement be done cautiously in HHS?

patients are often older with cardiac or renal compromise, increasing risk of fluid overload

64
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When should IV dextrose be added in HHS management?

when blood glucose levels fall to 250 mg/dL (13.9 mmol/L) to prevent hypoglycemia.

65
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how does potassium imbalance differ between DKA and HHS?

Hypokalemia is less significant in HHS but fluid losses may cause mild deficits requiring replacement.

66
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What assessments are crucial during HHS management?

vital signs, intake/output, skin turgor, cardiac monitoring, renal function, mental status, and serum osmolality

67
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Why is cardiac monitoring important in HHS treatment?

Insulin therapy causes potassium to shift into cells, risking hypokalemia that affects cardiac function.

68
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What signs may indicate potassium imbalance in HHS?

ECG changes, tachycardia, hypovolemic shock, altered respirations

69
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Once the patient is stable, what should care focus on?

identifying and correcting the underlying cause of HHS

70
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What must nurses closely monitor in hospitalized patients with DKA or HHS?

Glucose, urine output, urine ketones, and laboratory data to guide care.

71
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What are the three key treatment priorities nurses must monitor in DKA and HHS?

  1. IV fluids (to correct dehydration)

  2. insulin therapy (to reduce glucose and ketone levels)

  3. electrolyte replacement (to correct imbalances)

72
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Which body systems should be assessed related to hydration and electrolyte balance?

renal status and cardiopulmonary status

73
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Why is it important to monitor level of consciousness in DKA/HHS patients?

Altered mental status may signal worsening metabolic imbalance or cerebral edema.

74
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Why are DKA/HHS patients at risk for potassium imbalance?

Low insulin and osmotic diuresis cause potassium loss, and insulin therapy shifts potassium into cells, leading to hypokalemia.

75
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How does potassium movement during insulin therapy affect the body?

Potassium rapidly moves into cells, which can cause dangerous hypokalemia and affect cardiac function.

76
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What tool is useful for detecting changes in potassium levels in DKA/HHS patients?

continuous ECG monitoring

77
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Which vital signs and symptoms should be assessed frequently in DKA/HHS?

fever, hypovolemic shock, tachycardia, and Kussmaul respirations

78
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What are the common causes of hypoglycemia in diabetes?

  • too little food

  • too much insulin

  • too much exercise without enough food

  • insulin taken at the wrong time

  • alcohol use without food intake

79
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What blood glucose level defines hypoglycemia?

glucose less than 70 mg/dL

80
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what skin finding is commonly seen in hypoglycemia?

cold, clammy skin

81
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What sensory symptoms may occur in hypoglycemia?

numbness of fingers, toes, and mouth

82
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What cardiovascular sign may occur with hypoglycemia?

tachycardia

83
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What emotional or behavioral changes may appear with hypoglycemia?

Emotional changes such as irritability or mood swings.

84
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What neurological symptoms may occur in hypoglycemia?

headache, nervousness, tremors, faintness, dizziness, unsteady gait, slurred speech, changes incision, seizures, or coma

85
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What symptom of hunger is common in hypoglycemia?

intense hunger

86
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What is the initial nursing action when hypoglycemia is suspected?

check glucose

87
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After correcting low glucose, what should be determined?

the cause of hypoglycemia

88
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what is the immediate treatment for a conscious patient with hypoglycemia?

Have the patient eat or drink 15–20 g of quick-acting carbohydrate (e.g., 4–6 oz regular soda, 5–8 LifeSavers, 1 Tbsp syrup or honey, 4 tsp jelly, 4–6 oz orange juice, or commercial dextrose product).

89
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how long after giving carbohydrates should blood glucose be checked again?

15 minutes

90
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If glucose is still <70 mg/dL after the first treatment, what should be done?

have the patient eat or drink another 15-20g of carbohydrate

91
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Once blood glucose is stable, what additional food should be given if the next meal is more than 1 hour away or the patient is active?

a carbohydrate plus protein or fat (crackers with peanut butter or cheese)

92
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What should be done if hypoglycemia symptoms do not improve after 2–3 doses of quick-acting carbohydrate?

notify the HCP or emergency services immediately 

93
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What is the treatment for a worsening or unconscious patient with hypoglycemia?

give 1 mg glucagon SQ or IM, or IV administration of 20-50 mL of 50% glucose

94
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Why should an unconscious hypoglycemic patient be turned onto their side?

to prevent aspiration