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Flashcards in Dibetic Emerg IN CLASS Deck (40)
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1
Q

Insulin promotes absorption of glucose from the blood to:

A

skeletal muscles and fat tissue.

Normally insulin allows glucose transport into the cells for energy or storage as glycogen. Also stimulates protein synthesis and free fatty acid storage in adipose tissue

2
Q

Is pancreatitis always a result of alcohol use?

A

Pancreatitis can result from leaky gall bladder (autodigestion) – don’t assume pacnreatitis is result of alcohol

3
Q

Diabetes is risk factor for what conditions?

A

MI, stroke, renal failure, retinopathy, peripheral and autonomic neuropathy and peripheral vascular disease

4
Q

Type 1 DM. When does it usually occur?

How is it managed?

A

usually occurs before age 30 (can occur at any age)

Patient is usually thin and requires exogenous insulin and dietary management to achieve control

5
Q

Type 2 DM
Who gets it?
Tx?

A

Common in overweight adults over 40
Treated with exercise, meal planning and anti diabetic drugs, may include insulin
Increasingly diagnosed in adolescents and young people

6
Q

What’s more common, type 1 or 2 DM?

A

type 2

7
Q

Cause of Type II DM?

A

may result from impaired insulin secretion, peripheral insulin resistance, increased basal hepatic glucose production obesity, hormonal contraceptives, pregnancy, insulin antagonists i.e. phenytoin over the counter regulatory hormones

From class: body may just be too big, [pancreas can’t produce enough insulin for it}
Contraceptives + pregnancy affects sugar levels

8
Q

Type I cause?

A

autoimmune disease strongly associated with leukocyte antigens DR3 and DR4. May be associated with certain viral infections

9
Q

T/F Glucagon secretion is inhibited by increasing glucose levels with or without insulin

A

F - ONLY when insulin is present

DKA and HHS occur in environment where there is a lack (relative or absolute) of insulin so that glucagon cannot be turned off thereby increasing the blood glucose further.

10
Q

How do DKA + insulin differ in terms of insulin secretion + how does this affect acid involved?

A

DKA – no insulin therefore gluconeogenesis and lipolysis
Production ketone bodies (acetone breath) and ketoacidosis (can be severe)

HHS – insulin still present therefore gluconeogenesis and lipolysis mainly inhibited
Ketones mild/absent and pH normal/mild

11
Q

Is pH abnormal in HHS? How is fluid loss affected?

A

no ketones and normal pH but typically greater fluid loss

12
Q

Causes of DKA/HHS?

A

Usually a stressful event that causes the release of glucagon, cortisol and catecholamines:

  • Infection
  • MI
  • Treatment errors with insulin
  • Diarrhea and vomiting
  • Stroke
  • Trauma
  • Pancreatitis
  • Unknown etiology
13
Q

How does stress r/t glucose levels?

A

Acute Stress –> hormone release including counter regulatory hormones (corticosteroids, catecholamines)
All attempt to increase glucose further to deal with the stress –> fight or flight) –> All worsen an already high blood glucose level

14
Q

Signs + symptoms of DKA?

A

acetone breath, ketones in urine, acidosis, confusion/coma all from ketone production
Kussmaul breathing (deep rapid breathing) and abdominal pain from metabolic acidosis
polyuria from high glucose (osmotic diuresis) glc in urine
polydipsia and tachycardia from dehydration
sodium may be increased/ decreased or normal
Hypotension from dehydration

Polyuria, Polydipsia, Blurred vision, Weakness, Headache, Orthostatic hypotension, frank hypotension (volume depletion),anorexia, nausea, vomiting, abd pain, acetone breath, hyperventilation, mental status changes

15
Q

S+S of HHS

A

HHS – negative ketone breath and ketone in urine because no ketone bodies produced
stupor/coma from hyperosmolar state
fluid imbalance dehydration, high sodium
polyuria from high glucose (osmotic diuresis) glc in urine
polydipsia and tachycardia from dehydration
Hypotension from dehydration

16
Q

What is Kussmaul breathing?

A

KUSSMAUL RESPS = trying to blow off CO2; DEEP and FAST breathing

17
Q

How is K+ level in blood changed in acidemia?

A

K+ inc in blood as H+ ions move into the cells

18
Q

T/F Severity of DKA always increases with inc blood glucose levels

A

no

severity of DKA is not necessarily related to blood glucose

19
Q

WHy low bicarb levels in DKA?

A

Are compensating (H+ binds with HCO3- to get to CO2 so can blow off?)

20
Q

Diagnostics seen in DKA?

A

Elevated bld Glucose – severity of DKA is not necessarily related to blood glucose
Low Bicarb levels
Accumulation of ketones (bld and urine)
Electrolyte levels (K+, Na+)
Elevated Creatinine, BUN, hgb, hct (post rehydration continued elevation present in the pt with renal insufficiency

21
Q

Blood glucose levels seen in DKA + HHS?

A

HHS > 33.3 mmol/L

DKA: > 13.9 mmol/L

22
Q

HHS S+S?

A

Hypotension, profound dehydration, (dry mucus membranes, poor skin turgor) , tachycardia, varying neurological signs

23
Q

What is the mortality rate in HHS?

A

ranges 10% to 40%

DKA < 5 %

24
Q

Diagnostics in HHS?

A

Bld, glucose, lytes, BUN, Complete bld count, serum osmolality, ABGs
- will look at extended lytes (P, Mg, etc)

25
Q

What is the leading cause of death in children with T1DM

What aspect of this condition is generally fatal?

A

DKA

Cerebral edema accounts for ½ of DKA related deaths

26
Q

Guidelines for when bicarb may be used in DKA tx?

A

If acidosis pH < 7, may use bicarb to alkanize blood otherwise it tends to cause problems when used at higher pH

27
Q

Expected diagnostics + lab tests in DKA/HHS?

A

CBC, 660,
amylase/lipase (may be up but not pancreatitis but it could be cause for increased Glc),

troponin (look at renal function before determine why it is elevated – use in conjunction with ECG),
urinalysis (ketones and glucose; also WBC could mean UTI so infection was source of stress), ECG (to r/o MI), Chest Xray to r/o pneumonia; blood cultures and lactate to r/o sepsis if suspected; cardiac monitoring if concerned of arrhythmias

28
Q

How much fluid may be required for DKA?

What is used?

A

Rehydration: may require 6 to 10 l of IV fluids to replace losses (polyuria, hyperventilation, diarrhea and vomiting

Normal Saline at a rapid rate for 2 to 3 hours.
NS(0.45%) may be used for HTN or Hypernatremia

29
Q

What is the main electrolyte of concern during restroration of DKA? How would you see levels of this change?

A

the major electrolyte of concern is K+. Initial plasma conc. of K+ may be low, normal or even high – but there are major losses of body stores. se K+ levels drop throughout treatment as K+ re-enters the cell

30
Q

What aspects of tx changes in K+ plasma levels during DKA tx?

A

Rehydration leads to:
Increased plasma volume = decreased conc of se K+
Increased urinary excretion of K+
Insulin Administration: enhances K+ movement back into the cell.

31
Q

Main concern for risks of K+ changes in DKA?

A

Cautious K+ replacement is vital to avoiding dysrhythmias caused by low se K+

32
Q

What aspect of tx in DKA reverses acidosis?

A

Ketones accumulate as a result of fat breakdown. In DKA this process is reversed with insulin, which inhibits fat breakdown = stopped acid build-up

33
Q

Key nursing interventions during tx of DKA?

A
Monitor: intake and output, electrolytes, blood glucose
Administer intravenous fluids
Administer insulin, potassium
Administer – other medications
    (dependant on underlying cause)
Monitor: fld overload, adequate 
renal function (hyperkalemia,)
ECG: monitored for dysrthymia
V/S, ABGs
Documentation
34
Q

What med might be given to pt who is intubated during tx of DKA?

A

May get ventolin as well if intubated

If caused by infection, will use broad spectrum abx quickly

35
Q

What on the ECG shows risk of arrhythmia?

A

On ECG: peaked T is classic of risk for arrhythmia (refractory period shortened)

36
Q

What kind of line is commonly set up for DKa?

A

Not uncommon to have arterial lines (taking regular ABGs)

37
Q

How does recovery of DKA + HHS differ in terms of length?

A

DKA usually have quite quick recovery. HHS slower.

38
Q

If neurological symptoms are present in HHS, how long will it take to clear these?

A

may take 3 -5 days to clear

39
Q

Nursing care in HHS? (looks same as DKA for most part…?)

A
Monitor: intake and output, electrolytes, blood glucose
Administer intravenous fluids
Administer insulin, potassium
Administer – other medications
    (dependant on underlying cause)
Monitor: fld overload, adequate 
Renal function (hyperkalemia, creatinine, BUN,GFR)
ECG: monitored for dysrthymia
V/S, ABGs
Careful assessment: CVS, pulmonary etc (related to aging)
Documentation
Education when recovered
40
Q

Teaching that needs to be done for pt’s during times of illness:

A

From CDA website (this is under slides)
Test your blood glucose levels every two to four hours;
Continue to take your diabetes medication;
Drink plenty of extra sugar-free fluids or water; try to avoid coffee, tea and colas as they contain caffeine, which may cause you to lose more fluids.
Replace solid food with fluids that contain glucose, if you can’t eat according to your usual meal plan;
Try to consume 15 grams of carbohydrate every hour;
Call your doctor or go to an emergency room if you vomit and/or have had diarrhea two times or more in four hours;
If you are on insulin, be sure to continue taking it while you are sick. Check with your healthcare team regarding guidelines for insulin adjustment during illness.
Rest.

The Jerreat article:
Avoid sugar containing cough medicine
Continue to eat/drink carbohydrates as not consuming them may make ketosis worse
Stay hydrated
If one cannot tolerate liquid carbs and is vomiting, seek medial attention
Continue insulin and you may need to check blood glucose more frequently as stress from illness could increase insulin requirements