Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

TBL 1 > NIHMS: DKA > Flashcards

NIHMS: DKA Flashcards

1
Q

what does HHS stand for?

A

hyperglycemic hyperosmolar state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does DKA stand for?

A

diabetic ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

in what kind of patients does HHS and DKA occur in?

A

both DKA and HHS can occur in patients type I and II diabetes

DKA is more common in young people with T1D

HHS is more common in adult & elderly patients with T2D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

is DKA or HHS more common?

A

DKA frequency has increased 30% in the last decade with more than 140,000 hospital admissions

HHS accounts for <1% of all diabetes-related admissions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are both DKA and HHS characterized by?

A

insulinopenia and severe hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the general treatment for both DKA and HHS?

A
  • agressive rehydration
  • insulin therapy
  • electrolyte replacement
  • discovery/treatment of underlying precipitating events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what’s a hallmark of diabetic comas?

A

Kussmaul rapid breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the two types of diabetic coma?

A
  1. Kaussmaul breathing and positive ketones
  2. unusal, in older well-nourished individuals - severe hyperglycemia and glycosuria but without Kaussmaul breathing, fruity breath odor or positive urine acetone test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the typical symptoms of diabetic coma?

A
  • polydipsia (thirst)
  • polyuria (lots of dilute urine)
  • glucose in urine
  • declined mental status
  • high acetoacetic acid and BHB acid in urine
  • preceding deep and frequent respiration and severe dyspnea = Kussmaul breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when was the first diabetic coma reported?

A

1828

august W. von stosch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when was Kaussmaul breathing discovered?

A

1874

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

when was insulin discovered?

A

1921

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what was the DKA mortality rate before insulin?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which individuals are at higher risk for DKA?

A
  • high HbA1C
  • longer diabetes duration
  • adolescents (18-25 years)
  • girls
  • T1D
  • ethnic minorities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

does HHS or DKA have a higher mortality rate?

A

HHS (5-16% which is 10x DKA %)

HHS occurs most commonly in older patients with T2D with an intercurrent illness like infection, surgery or ischemic events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is usually the cause of mortality in DKA and HHS patients?

A

usually not from metabolic complication of hyperglycemia or metabolic acidosis

usually due to severe dehydration and advanced age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the leading cause of death for children and young adults with T1D?

A

DKA

accounts for 50% of all deaths in diabetic patients <24 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the DKA mortality rate?

A

<1% in the US

it’s higher with elderly patients with life-threatening illnesses

> 10% in countries with limited acute care resources

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what increases DKA mortality?

A

recurrent DKA admissions vs. 1 DKA admission

23.4% vs 5.2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does the outcome of patients HHS depend on?

A

severity of dehydration, presence of co-morbidities and advanced age

hospitalization and multiple HHS episodes increase mortality risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how much is spend on treatment of hyperglycemic crises?

A

$2.4 billion

it’s a severe economic burden

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the most common precipitating causes of DKA in USA?

A

41-60% poor adherence to treatment = #1 cause! aka discontinuing insulin

17-24% newly diagnosed diabetes mellitus (insulin deficiency or resistance) - people find out they have diabetes because they go into DKA

14-16% infection

10-18% other (malfunctioning insulin pump)

3-4% unknown

*in other countries, infection is usually the highest cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is a psychological risk factor in DKA?

A

depression and eating disorders

reported in up to 20% of recurrent episodes of DKA in young patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are common causes of HHS?

A
  • UTIs
  • pneumonia
  • acute cardiovascular events

any illness that causes dehydration or reduced insulin activity can lead to HHS

poor aberrance to medical treatment and new diabetes onset are less common causes of HHS than DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which medications can cause DKA and HHS to develop?

A

SGLT2 inhibitors

  • glucocorticoids
  • B-blockers
  • thiazide diuretics
  • certain chemotherapeutic agents
  • atypical antipsychotics (olanzapine and resperidone)

SGLT2 inhibitors cause DKA and ketosis in T1D and T2D (mostly T1D)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is euglycemic DKA?

A

only mild to moderate elevations in blood glucose

an atypical presentation of DKA that can lead to delayed recognition and treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are potential mechanisms that would cause SGLT2 inhibitors to lead to ketosis and DKA?

A

SGLT2 inhibitors lower plasma glucose by inhibiting proximal tubular reabsorption of glucose in the kidney

  • higher glucagon levels
  • reduction of daily insulin requirement = decreased suppression of lipolysis and ketogenesis
  • decreased urinary excretion of ketone
28
Q

what are the two most pathophysiological mechanisms for DKA and HHS?

A
  1. significant insulin deficiency
  2. increased concentration of counter-regulatory hormones like glucagon, catecholamines, cortisol and growth hormone

these lead to increased hepatic glucose production due to increased hepatic gluconeogenesis and glycogenolysis as well as reduced glucose utilization in tissues

low insulin leads to activation of hormone-sensitive lipase which accelerates triglyceride breakdown to FFA - in the liver, FFA are oxidized to ketone bodies due to increased glucagon/insulin ratio

29
Q

what does the increased glucagon/insulin ratio in DKA and HHS cause?

A

lowers the activity of malonyl CoA which modulates movement of FFA into hepatic mitochondria where FA oxidation takes place

30
Q

what leads to metabolic acidosis in DKA?

A

increased production of ketone bodies (acetoacetate and BHB which are strong acids) leads to reduction of bicarbonate and metabolic acidosis

31
Q

do HHS patients have high ketone bodies? why?

A

no

due to:

  1. higher levels of insulin (most important)
  2. lower levels of counter-regulatory hormones and FFA
  3. inhibition of lipolysis by the hyperosmolar state
32
Q

hyperglycemia and ketoacidosis result in what immune response?

A
  1. an inflammatory state characterized by an elevation of pro-inflammatory cytokines
  2. increased oxidative stress markers

increased inflammatory response, oxidative stress, and ROS production can lead to capillary perturbation and cellular damage of lipids, membranes, proteins and DNA

33
Q

what are some pro-inflammatory cytokines? when are they produced? what do they do?

A

during hyperglycemia

macrophages produce pro-inflammatory cytokines:

  • tumor necrosis factor-alpha (TNFα)
  • interleukin (IL)-6
  • IL-1β
  • C-reactive protein

lead to impaired insulin secretion and reduced insulin sensitivity

34
Q

what do increased FFA levels cause?

A

increases insulin resistance

impaired NO production

35
Q

what are the signs and symptoms of DKA?

A
  • fatigue
  • GI complaints: nausea, vomiting, ab pain
  • Kussmaul respiration
  • fruity breath (acetone)
  • hyperglycemia symptoms: polyuria, polydipsia, weight loss
  • dehydration: dry mucous membranes, poor skin turgor, tachycardia, hypotension
36
Q

what’s the triad of things that happens with DKA?

A

hyperglycemia
ketonemia
metabolic acidosis

DKA classifies by degree of acidosis, decrease in bicarbonate and altered sensorium

37
Q

what are the characteristics of mild DKA?

A

> 250 blood glucose

bicarbonate between 10-18

pH < 7.3

high ketones in urine or blood

increased anion gap metabolic acidosis >12

38
Q

in what patients does euglycemic DKA happen?

A

it’s DKA but blood sugar is <250

  • pregnancy
  • prolonged starvation
  • alcohol intake
  • SGLT2 inhibitor use
39
Q

what test is used to diagnose DKA?

A

high anion gap metabolic acidosis >12

nitroprusside test in urine or serum which estimates acetoacetate and acetone levels - can underestimate severity of ketoacidosis because it doesn’t recognize BHB

40
Q

what are the symptoms of HHS?

A

plasma glucose > 600 mg/dl

efective osmolality > 320 mOsm/kg

absence of ketoacidosis

pH > 7.3

bicarbonate > 18

increased anion gap metabolic acidosis as the result of concomitant ketoacidosis and/or increase in serum lactate levels or renal failure

41
Q

what are the leukocyte counts for a patient in DKA?

A

significant leukocytosis = WBC count in 10-15,000 range

attributed to stress, dehydration

42
Q

what are sodium serum levels for a DKA patient?

A

low serum Na because of the osmotic flux of water from the intracellular to extracellular space in the presence of hyperglycemic

increase in serum Na in the presence of severe hypoglycemia indicates a profound degree of dehydration and water loss

43
Q

what are potassium serum levels for a DKA patient?

A

serum K+ levels are usually elevated in DKA and HHS

happens because of a shift of K from the intracellular to the extracellular space due to insulin deficiency and hypertonicity and academia in DKA

during insulin treatment and fluid administration, K+ levels decrease due to a shift back to intracellular space which can result in hypokalemia

44
Q

what are serum phosphate levels in DKA patients?

A

elevated serum levels

phosphate shifts from intracellular to extracellular space due to insulin deficiency, hypertonicity and catabolic state

dehydration can also increase total serum protein, albumin, amylase and creatinine phosphokinase concentrations

45
Q

what is starvation ketosis?

A

patients rarely have serum bicarbonate concentration less than 18 because of the slow onset of ketosis that allows increased ketone clearance and enhanced kidney ability to excrete ammonia to compensate for the increased acid production

46
Q

how do you treat hyperglycemic crisis?

A

fix:

  • dehydration
  • hyperglycemia
  • hyperosmolality
  • electrolyte imbalance
  • increased ketonemia

monitor fluid administration, insulin dosage, urine output, lab measurement of glucose/electrolytes/venous pH/bicarbonate/anion gap every 2-4 hours

47
Q

where in the hospital do DKA patients get treated?

A

ED or step-down units

ICU not necessary

48
Q

where in the hospital do HHS patients get treated?

A

ICU

because they have altered mental status and significant higher mortality rates than DKA

49
Q

how does fluid therapy help with hyperglycemic emergencies?

A

IV fluids:

  • expand intravascular volume
  • restore renal perfusion
  • reduce insulin resistance by decreasing circulation counter-regulatory hormone levels

isotonic saline @ 500-1000 mL/hour initially

200 mL/hour after volume depletion is corrected

once glucose is 200, fluids should contain dextrose to allow continued insulin administration until ketonemia is correctected while avoiding hypoglycemia

50
Q

how does potassium therapy help with hyperglycemic emergencies?

A

metabolic acidosis and insulin deficiency lead to extracellular movement of potassium = total body depleted of K+ even if serum K levels are normal or elevated in DKA

insulin therapy lowers serum K levels by promoting movement back into intracellular compartment

insulin administration in patients with admission hypokalemia & with really low K levels could result in severe hypokalemia so you need to replace K at a lower rate and insulin administration needs to be delayed till K levels get higher

acute or chronic renal failure patients need lower doses of K

51
Q

how does bicarbonate therapy help with hyperglycemic emergencies?

A

only recommended in patients with life threatening acidosis (pH<6.9)

bicarbonate therapy can increase the risk of hypokalemia and cerebral edema

52
Q

what is the main treatment for DKA?

A

continuous IV insulin administration:
- it lowers serum glucose by inhibiting endogenous glucose production and increasing peripheral utilization

-it also inhibits lipolysis, ketogenesis and glucagon secretion = decreases production of ketoacidosis

subcutaneous and intramuscular injections of insulin can also be used if needed but not recommended for patients with hypotension, severe DKA or with HHS

53
Q

under what conditions is DKA considered resolved?

A

<250 mg/dl

venous pH >7.3

normal anion gap

serum bicarbonate > 18 mEq/L

54
Q

under what conditions is HHS resolution considered resolved?

A

serum osmolality < 310 mOsm/kg

glucose < 250 mg/dL

recovered mental alertness and mental status

55
Q

what are some types of subcutaneous basal insulin? when should they be used?

A

NPH, (insulin analogs: glargine, deter, degludec)

should be given at least 2 hours before discontinuing IV insulin because abruptly stoping IV insulin could result in hyperglycemia, ketogenesis and metabolic acidosis rebound because the half-life of insulin is only 10 minutes

56
Q

what’s the preferred insulin regimen for patients with T1D and DKA? (and for most HHS patients)

A

multi-dose insulin regimens with basal insulin and prandial rapid-acting insulin analogs

57
Q

what’s the most common complication of DKA?

A

hypoglycemia

lack of frequent monitoring, failure to reduce insulin infusion rate, or to use detrox-containing solutions when blood glucose levels hit 200 can cause hypoglycemia during insulin treatment

most hypoglycemic patients don’t exhibit adrenergic manifestations (sweaty, nervous) so you have to monitor glucose levels every 1-2 hours

58
Q

what are side effects of hypoglycemia?

A

seizures, arrhythmias, cardiovascular events

59
Q

what is the second most common complication during DKA and HHS treatment?

A

hypokalemia

even though admission serum K is usually elevated, during insulin treatment plasma K will decrease due to increased cellular K uptake in peripheral tissues

to prevent hypokalemia, replacement with IV K+ when concentration <5.2 is needed

60
Q

what is the third complication with DKA?

A

cerebral edema (rare)

not really understood but we think it has to do with disruption of the blood-brain barrier

degree of edema formation during DKA correlates with degree of dehydration and hyperventilation at presentation but it doesn’t correlate with initial osmolality, osmotic changes during treatment or rate of fluid/Na+ administration

61
Q

what are signs of cerebral edema?

A

4-12 hours after treatment has started but as late as 24-48 hours after treatment

altered consciousness, abnormal motor or verbal response to pai, cranial nerve palsy, abnormal respiratory pattern

62
Q

what’s the treatment for cerebral edema?

A

administer mannitol

or hypertonic saline if there’s no response to mannitol

then get a CT scan to rule out other causes of neurological deterioration like thrombosis and cerebral infarction, hemorrhage, or dural sinus thrombosis

corticosteroids and diuretic therapy don’t help

63
Q

what is the fourth complication of DKA?

A

rhabdomyolysis

in DKA patients but more commonly HHS patients

results in increased risk of acute kidney failure

symptoms: myalgia, weakness, dark urine

need to monitor creatine kinase levels

64
Q

how do you prevent hyperglycemic emergencies?

A

medication-noncompliance is leading cause of DKA due to inability to afford medication or get transportation to pharmacy

can reduce hospitalization rate by developing assistance programs to provide insulin to patients and reduce lapses in treatment

also providing diabetes educators in close contact with and easily accessible to patients reduces number of hospitalizations related to hyperglycemic emergencies

65
Q

why are DKA and HHS patients dehydrated?

A

High blood sugar causes further dehydration as your kidneys attempt to unload glucose and ketones by producing large amounts of urine

Increased dehydration causes higher blood sugars, which in turn cause further dehydration

TBL 1 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions