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NURS232 > Complications of DM > Flashcards

Complications of DM Flashcards

(54 cards)

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1
Q

2 Acute complications related to Hyperglycemia

A

Diabetric Ketoacidosis
Hyperosmolar hyperglycemic nonketotic syndrome (HSS)

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2
Q

Diabetic Ketoacidosis mostly a problem for DM 1 or 2

A

Type 1

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3
Q

Nonketotic

A

No ketones involved

The primary differentiator bw HSS (No ketones) and DKA (Keotones)

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4
Q

Good ______ reduces DM complications

A

Glucose control

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5
Q

Hypoclymia is acute or slow acting

A

Acute

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6
Q

Hyper or hypoglycemia more dangerous

A

Hypoglycemia

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7
Q

Hypoglycemia caused by

A
  1. Mismatch in the timing of food intake and the peak action of insulin or PO hyperglycaemic agents
  2. Excessive insulin or PO hypoglycaemic agents
  3. Ingestion of insufficent carbs
  4. Excessive exercise
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8
Q

S/S of Hypoglycemia

A

Adrenergic: Epinephrine release
(Sympathetic NS response): Diaphoresis (Sweating), tremors, hunger, nervousness, anxiety, pallor and palpitations

Neuroglycopenic (Not enough glucose for brain): Irritability, visual disturbances, difficulty speaking, confusion, coma

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9
Q

Untreated Hypoglycemia

A

Loss of Consciousness, coma, seizure

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10
Q

Fuel for the brain is

A

Glucose enables us to think clearly

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11
Q

Hypoglycemic unawareness

A

Asymptomatic hypoglycemia
- A person does not expereicne the usual ANS s/s associated with hypoglycemia (often related to neuropathy that interfere with warning signs)

My occur with sudden drop in BG

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12
Q

Homeostatic mechanism used to counteract hypoglycemia

A

Low BG triggers sympathetic NS, releasing Epinephrine which targets glucagon release to make glucose available to the body

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13
Q

Treatment of Hypoglycemia (According to CPG)

A

Check BS; treat if BS , 4 mmol/L

Provide dextrose tabs according to CPG associated with specific level of BS

Once BS higher than 4, provide longer acting starch and sugar

Once stable, provide ducation and prevention

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14
Q

DKA

A

Profound deficiency of insulin - hyperglycemia and dehydration

Fats are metabolized in absence of insulin (For alternate energy source) - ketosis and acidosis (Body reacts to lack of glucose in cell)

Seen most often in DM Type 1

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15
Q

Ketosis

A

The big problem in DKA

Body breaks down fats, fats break down into ketones, acitones is one

Acitone body results in fruity breath

Beta hydroxibuderate (

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16
Q

Beta hydroxibuderate

A

ketone that is tested for) - Releases hydrogen ions that contirbute to the metabolic acidosis

As body compensates for acidosis

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17
Q

Metabolic Events leading to DKA and D-Coma

A

Islet beta cell destruction
Resulting in Insulin deficiency
Leads to decreased tissue glucose utilization
Liver release glucose (Glucogon broken down)
- Compounds problem
Adipose tissue is targeted to break down fat into ketones
Liver contributes in breaking down ketones

Excess glucose results in increased vascular fluid to match the solutes (and flush them out)

Kidneys pass this excess fluids
- Poluria
- Glucose in urine

Results in cellular starvation
- Polyphagia, cannot be satisfied

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18
Q

What causes acidosis

A

The body likes to remain slightly basic

H+ ions are acidic, too many are circulating

Body compensates by pulling these cations into the cells

Causes K+ ions to be pulled out (Intercellular potassium depletion occurs) - high levels of intravascular levels

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19
Q

Blood potassium levels in DKA are

A

Normal or high since H+ Ions replace Potassium in cells, kicking them into bloodstream

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20
Q

Potassium is most important for

A

Impact in stability of cardiac membrane (electrical conduction)

If potassium is not bw 3.5-5 mmol/L in blood it can cause cardiac abnormalities

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21
Q

Causes of DKA (6)

A

Illness (stress)
Infection (Stress)
Inadequate insulin doses to shift adequate glucose into cells
Insulin omission
Undiagnosed DM type 1
Poor self diet management

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22
Q

S/s of DKA

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A

Polyuria, Polydipsia
Dehydration

Early symptoms - lethargy and weakness
Later - Poor skin turgor, dry mucous mems, tachycardia, Ortho HOTN, sunken eyes

N/V

Abdom pain

Rapid Resp Rate

Fruity breath odour

BG > 14mmol/L, pH < 7.35

Ketones in blood and urine

23
Q

Treatment in DKA

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A

Food & Electrolyte replacement
Prioritizing according to ABCs (BS under D)

Two IVs (Large bore)

IVF (Usually Bolus dose NaCl) - isotonic (Will decrease BS bc of dilution) until urine output is > 30mL/h

Bloodwork (arterial blood gas, betahydroxate buterate level, electrolytes)

Deal with pH (Introduce basic solution into vascular system i.e Sodium Bicarb)

Fix electrolyte levels

BS levels monitered every hour

Small bolus of insulin followed by insulin infusion of 1unit/mL

24
Q

What is the problem with introducing insulin to a DKA

Study These Flashcards
A

Shifts the electrolyte balance as BS comes down

25
When treating DKA, once BS drops to around 14 mmol/L what is given?
Dextrose, to prevent them from becoming Hypoglycemic Maintenance solution containing Potassium will be given to slowly fix their state
26
Hyperglycemic, Hyperosmolar, nonketotic, Syndrome Occurs in
Clients able to produce enough insulin to prevent DKA, but not enough to prevent sever hyperglycemia, osmotic diuresis, and ECF depletion DKA does not occur LESS COMMON than DKA Often occurs in older adults with DM type 2 (impaired thirst, funcitonal inability to replace fluids) Higher mortality than DKA Glucose in blood creates osmosis of water to dilute the intravascular hypertonic hyperglycaemia leading to dehydration
27
Why is HHS so deadly
Because it takes awhile to develop, often alongside comorbidities. By the time they have S/S they are very sick Treatments must be more cautious bc of comorbidies
28
Can HSS Pt secrete insulin
Usually there is some ability, therefore Non-ketotic
29
Is DKA slower than HSS
No HSS is slower, more difficult to reverse quickly
30
HSS S/S
Fewer symptoms than DKA in early stages Neruo: Often issues BG >34 mmol/L Ketone bodies are absent in blood and urine Less marked and extreme S/S than DKA
31
Tx for HSS
Similar to DKA but SLOWER IV Fluids Insulin bolus +/- insulin infusion Once 14.0 mmol/L, QID Sliding Scale insulin Monitor and replace electrolytes (normally smaller deficit than DKA) Monitor Response to treatment
32
Caution with fluid replacement in HSS
T2 Pts often have multiple comorbidieis and/or are elderly Often more is necessary, but occurs slower
33
Example of macrovascular coplications of DM
Coronary artery disease (atherosclerosis), stroke, hypertension, peripheral vascular disease
34
Examples of Microvascular Complications of DM
Complications are not reversible Retinopathy Nephropathy (Glomuruli, Bowmans capsule) Neuropathy - Sensory - Autonomic
35
Neuropathy Sensory
Tingling, numbness in extremities, can be MORE sensitive at the begining Most common form is distal symmetrical Paresthesias Hyperesthesia Complete or partial loss of sensitivity to touch & temperature Pain described as burning or shooting , cramping, crushing, or tearing (unusual)
36
Neuropathy - Autonomic
Affecting nearly all body systems can lead to hypoglycemia unawareness GI: GERD, N+V, gastroperesis CV: Silent MI, ortho HOTN, Increased resting HR ED Neruogenic Bladder
37
Macrovascular complication prevention (behaviour)
Behaviour mods: - Healthy eating - Increase Physical Activity - Quit Smoking - Weight modification
38
Macrovascular complications treatment/prevention through Prophlactic and pharm therapy
ACE inhibitors (ie Ramipril) Anti-platelet therapy (ie ASA) Anti-cholesterol agents (ie Lipitor Prevent CV and renal disease. Target BP= 130/80
39
Retinopathy
Earliest + most treatable changes  no changes in vision. Regular dilated eye exams IMPORTANT. Best treatment is prevention: Maintain good glycemic control Control BP
40
Nephropathy
Damage to small BVs that supply the glomeruli of kidneys Risk similar for T1 and T2 DM Best treatment is prevention (Good glycemic control, BP control, annual screening
41
Leading cause of end stage renal disease in Canada is
Nephropathy
42
The only treatment for diebetic neuropathy
Control of BG Effective in many but not all Pharm management outside of BG Foot care Specific NCPs
43
What causes necrotic toes in DMs
Decreased circulation
44
Necrosis and poor blood flow often lead to
Infections
45
Why is foot care really important
Because just a scratch can turn into a wound that can result in amputation
46
Foot care includes
Basic to advanced Always wearing protective shoes Inspect foot daily Not removing corns or calluess Identify high risk clients by checking protective sensation + vascular status Recognizing and treating wounds promptly Maintainting good nutrition Cessation of smoking HTN control Depride wound Antibiotic use Bed rest Prevent edema Offload feet MRi to see bone involvement
47
How can you know CV status of feet
Colour (white, pale, inflamed are bad signs), temp, cap refill (<3)
48
Monitering Diabetes
Self management of Blood glucose All pt should self moniter if on medications Self Monitering before meals Keep accurate record of trend information (High and low BG) All DM pt should have urine dipsticks in home (Checking for glucose and ketones)
49
Secondary Prevention of DM in population
Screening every 3 yrs for people over 40 OR high risk people Screen earlier and more frequently in those with more risk factors Screening for Type 2 includes - FPG test and /or A1C test
50
Important FACTORS in DM pt assessments
Neuro - A+Ox3, GCS, Vision changes + PERRLA RESP: Are they smokers? (Nicotine Replacement Therapy) CVS: HR/ BP (130/80 is goal) CWMS, Cap Refill, Feet check (periph circ) GI: Last Bowel Movement (Assessing status of bowel peristalsis) GU: Fluid intake, urine routines Overall - ANY evidence of infection
51
What is BP goal
130/80
52
Adrenergic Signs of Hypoglycemic
Fight or flight response
53
Neuroglycopenic signs of hypoglycemia
Decreased O2 to brain
54
Do we treat DKA or HSS with rapid therapy?
DKA, HSS need more gradual treatment

NURS232 (27 decks)

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