Class notes

With Surg Midterm #2 Content

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Course
NURS2810 (NURS2810)

Institution
University Of Windsor (U Of W )

Everything you need to know about content weeks 5-8 in Adult Health and Health Alterations. Including complications of diabetes (DKA, HHNS, hypo and hyperglycemia, musculoskeletal, acid-base imbalances).

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Uploaded on December 18, 2024
Number of pages 16
Written in 2024/2025
Type Class notes
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Contains All classes

diabetes
diabetes complications
hhns
dka
acid base imbalance
acidosis
alkolosis
trauma
fractures
orthopedic surgery
musculoskeletal assessment

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Med-Surg Fall 2024 Midterm #2 Review
Week Five: Diabetes, Acute and Long-Term Complications
Unstable blood sugars-> need to be on tight control. Unstable meaning 8, 21, 16 throughout the day.
Can be cardiac, renal, and vascular complications
Hypoglycemia -> under 4 mmol/L
Hyperglycemia -> over 6 mmol/L
HYPOGLYCEMIA
Too much insulin in relation to glucose availability.
Coincides with peak action of insulin/oral agents.
Brain NEEDS glucose, hypogly brain might die.
This occurs in all diabetics.
Causes: Meals, medication, activity. You will see CNS effects for sure because your brain needs glucose to
function.
Clinical Manifestations: HIWASH
-> CNS symptoms (confusion, irritability, speech)
-> SNS stimulation-> sympathetic nervous system (FIGHT/FLIGHT)
->Untreated will lead to LOC, seizures, coma, death.
Hypoglycemia unawareness: no warning signs, this is very bad, you will lapse into severe hypoglycemia.
Autonomic neuropathy interferes with counter regulatory hormones (glucagon, cortisol, growth hormone)
-> Controls BP, temp, digestion, blood function. When you have damage to nerves, they will not sense drops in
blood sugar, leads to unawareness.
-> Patients on Beta Blockers, they B-blockers mask the symptoms of hypoglycemia, and are thought to be issue
with med and not actually anything else.
Treatment of Hypoglycemia:
-15-20 simple carbs (fruit juice, soft drink), 3-4 glucose tabs.
-Avoid sweets with fat, it will slow sugar absorption, delays response to treatment.
-Repeat blood glucose every 15 minutes
-Eat your regular meal 60 minutes later
- Carb + protein = good!
If they are unconscious…
1 mg glucagon IM/SubQ
*watch out for rebound hypoglycemia…
patient must eat complex carbs once alert.
IV DEXTROSE 20-50 mL over 1-3 mins

HYPERGLYCEMIA

,Clinical Manifestations
3 P’s -> polyuria, polydipsia, polyphagia, glycosuria, blurred vision, fatigue, headache, weight loss.
Causes:
-Increase food intake, decreased meds, infection (stress on body = increased BG), stress of the hospital,
corticosteroid use.
-Illness + infection -> increased stress -> increased counterregulatory hormones -> increased blood glucose
Treatment:
-Monitor blood glucose
-Check for urinary ketones
-Increase fluids to look for dehydration.
-Continue oral hypoglycemia agent, may need to increase the original dose.
Prevention:
-Adherence to sick day rule
-> continue taking insulin / oral meds when you are throwing up, but ensure you are taking
BG every 2-4 hours.
Patients CAN NOT make their own correction scale
Medications must be taken on time. Check blood sugar when needed, maintain diet.
DIABETIC KETOACIDOSIS (DKA)
Blood glucose is around 20 mmol/L or more, periods of time, it is cyclical. There is usually an underlying
illness, stress psychological/physiological will cause this.
Typically we will see this in Type I but can be Type II.
Causes:
-Stopping insulin (sick day rule), inadequate insulin dosage because they were ill, undiagnosed diabetes
Ketoacidosis: fats are metabolized in fact cells in blood. This is the key difference between DKA and HHNS.
-> Ketones will spill into urine.
Pathophysiology: continuation of effects of insulin deficiency.
-severe metabolic acidosis (ketone breakdown, not enough insulin uses fats instead).
-Severe dehydration which can lead to shock.
-Severe electrolyte imbalance
POTASSIUM:
Insulin promotes K entering cells. When insulin is low, you have more K moving out of the cell, nothing is
keeping that K in there. This causes increased polyuria and you lose your potassium in urine. Osmotic dialysis
ketone breakdown in urine, no insulin, leaves in urine, polyuria 1-3 prior to clinical manifestations. Ketones in
the urine can be an early sign.

Clinical Manifestations:
-Dehydration (increased heart rate due to low fluid volume, increased BP, poor turgor, dry mucous membranes).

, -Kussmual’s breathing. This is a compensatory mechanism. It is rapid deep breathing you are trying to blow off
CO2 to become less acidotic.
-Fruity breath, because of acetone almost. This is due to break down of ketones and this tells you it is not
HHNS.
-Abdominal pain, N/V, cardiac dysrhythmias (remember caused by too high or too low potassium).
Treatment:
Note that we are NOT giving insulin first! This would be bad. K for cardiac.
1. Replace fluid and electrolytes (potassium shift happens, hypokalemia)
-> Start in 0.9NS or 0.45NS (potentially add in glucose because of rebound hypoglycemia) be prepared, fluid
replacement therapy goal is to replace extra and intracellular water.
->Too rapid of IV fluid will lower serum glucose (drop too aggressively) and can cause cerebral edema, you are
flushing out the glucose, add the hypertonic feature and the hypoglycemia, that is bad for the brain. You want to
get them to a 14. If they are 22 you do not want to drop them to a 7, this drop is traumatizing on the body your
brain NEEDS that glucose, and if you suck it all out, your brain is looking for it and will cause cerebral edema.

2. Insulin administration (IV bolus, then infusion), DO NOT jump to this first always rehydrate!
Potassium must be 3.3, so it can be pulled into cell before you give insulin. Anything lower do not give insulin.
3. Identify and correct the underlying cause (ex. Infection)
You may have increased counterregulatory hormones which are working against insulin, we don’t have insulin
we can’t help that potassium back into the cell. Hyperkalemia is bad, you will die.

HYPEROSMOLAR HYPERGLYCEMIC STATE (HHNS)
Blood glucose is going to be 34 mmol/L or greater.
Occurs in Type II diabetes, often elderly because of their poor fluid/diet intake.
Strongly associated with impaired thirst sensation or inability to replace fluids.
You will see fewer symptoms with this, you can tell from the blood glucose level (periods of time, it is also
cyclical).
The difference here is you get DKA because you don’t have insulin/good insulin production. In HHNS, you still
have some insulin production, there is enough insulin to prevent ketosis, this is why this is NON-KETOTIC.

Similar to DKA, there will be just enough insulin to prevent hypoglycemia. Extreme hyperglycemia will cause
intracellular dehydration because of the movement of water from cells. Since there are lack of symptoms, you
notice neurological symptoms due to such high blood sugar.
Clinical Manifestations:
Dehydration, weakness, polyuria, polydipsia due to impaired thirst sensation, solemnize. No fruity breath, no
hypokalemia because you still have some insulin. You need to monitor closely because of the lack of symptoms.
Treatment: Rehydrate, 0.9 or 0.45 NS, insulin therapy depends after rehydration.
DIABETES MELLITUS- CHRONIC COMPLICATIONS
Macrovascular

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