Diabetes Flashcards

1
Q

S and S of Hypoglycemia

A
BG more then 4.0 mmol/L
•  Confusion – change in LOC 
•  Sweating
•  Rapid pulse
•  Tremors
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2
Q

S and S of Hyperglycemia

A
•  BG > 7.0 mmol/L (11 is VIHA)
•  Polyuria – excessive urination
•  Polyphagia – increased hunger
•  Polydipsia – increased thirst
•  Glucosuria – high levels of glucose in the urine
•  Weight loss 
•  Fatigue

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3
Q

Review…

Effects of Insulin

A

Normal response to High BG

Simulates glucose uptake into cells and storage of glucose as glycogen in the liver and muscles.

Also stimulates protein synthesis and free fatty acid storage in adipose tissue.

Inhibits gluconeogenesis and lypolysis

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4
Q

Review

Effects of Glucagon

A

Normal response to low BG. Stimulating Gluconeogenesis and breakdown of glycogen

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5
Q

Diabetes is…

And is a major risk factor for….

A

Characterized by disturbances in carbohydrate, protein and fat metabolism

Ineffective insulin production, poor insulin sensitivity.

A major risk factor for MI, stroke, renal failure, retinopathy, peripheral and autonomic neuropathy and peripheral vascular disease

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6
Q

Cause of type 1 vs type 2

A

Type I: autoimmune disease strongly associated with leukocyte antigens DR3 and DR4. May be associated with certain viral infections. Beta-cells destroyed

Type 2: 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

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7
Q

Why is glucagon not inhibited when those with DKA or HHS.

A

Inhibition of glucagon requires insulin. Signal for more glucose (glucagon stim) is coming from cells, who are glucose starved. Insulin is required to get glucose into cell and stop the signalling.

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8
Q

How do DKA and HHS differ in the aspect of insulin levels?

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

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9
Q

Major problems of HHS and DKA

A

DKA- Hyperglycemia, Acidosis, Osmotic diuresis (dehydration)

HHS- Hyperglycemia, Osmotic Diuresis (Worse then DKA)

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10
Q

What sort of events might cause DKA or HHS and why

A
Reduced insulin admin (DKA)
OR
Stress events:
Infection
MI
Diarrhea and vomiting 
Stroke
Trauma
Pancreatitis 
Unknown etiology 

Acute Stress -> hormone releas glucagon, corticosteroids, catecholamines)

All attempt to increase glucose further to deal with the stress (fight or flight)
All worsen an already high blood glucose level
ANY trauma will bring stress response

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11
Q

S and S of DKA

A

Can develop quickly ( 13.9 mmol/L

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

AND… Blurred vision, Weakness, Headache, Orthostatic hypotension, frank hypotension (volume depletion), anorexia, nausea, vomiting, and pain (r/t acidosis), , mental status changes. Hyperkalemia (before Tx)

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12
Q

Main S and S of HHS

A

Develops more slowly than DKA (days to weeks)

Blood glucose > 33.3 mmol/L

No ketone breath and ketone in urine

Stupor/coma from hyperosmolar state

Profound Dehydration -> high sodium,
polyuria from high glucose (osmotic diuresis)  glc in urine

Hypotension- Polydipsia and tachycardia from dehydration

Higher mortality then DKA 10-40%

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13
Q

COMPARE those at risk of DKA and HHS

A

DKA - Type 1 (Can be Type 2)

HHS- Occurs predominantly in type II diabetics (some cases of type 1)

Older people with no history of diabetes or mild T2DM

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14
Q

Key Requirements of Patient with DKA

A

Insulin
Hydration
Electrolytes replacement

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15
Q

Diagnostics common in DKA patient

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 (ARF)

(post rehydration continued elevation present in the pt with renal insufficiency

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16
Q

Diagnostic for a HHS patient

A

++ high Blood glucose, lytes (Na+), BUN (hypovolemia), Complete bld count (stress), serum osmolality (BG and Dehydration), ABGs (normal)

17
Q

What age group is at risk if they develop DKA?

Why is it common?

Complications?

A

Pediatrics.

Newly Diagnosed Type 1. 
Omission of insulin: when child or caregiver fails to comply 
Delivery failure
Infection
Type 2 Diabetes can present as DKA

1/2 die from cerebral edema during rehydration

18
Q

Common interventions

Complications

A

ABCS- LOC (NG or Airway)
Reverse Hyperglycemia
Reverse Dehydration- losses
Restore Electrolytes balance- K and Na

Prevent complications: Cerebral edema, ARF, Pottasium, pH, Thromboembolic events, ARDS.

19
Q

What concerns might we check with Diagnostics?

A
CBC and lytes- The obvious and Infec.
Amylase/lipase- Pancreas r/t insulin
Troponin and RFT's- 
Urinalysis- Infect, Ketones?, 
ECG- MI and arrythmias
Chest xray- ?Pneumonia
ABG's - Acidosis?
20
Q

Why does K need to be watched carefully with treatment of DKA and HHS

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.

… Avoid Tx causing low K

21
Q

What part of Tx reverses Acidosis in DKA

A

Insulin Admin- Deals with underlying problem of ketone production.

22
Q

What teaching might be helpful for diabetic experiencing sickness.

A

Inc BG testing
Don’t stop meds
Drink lots of Fluids
If you can;t eat, drink fluids containing glucose
See physician if regularly vomiting or Diarrhea

23
Q

Two key hormones released during stress response

A

Catecholamines – including adrenaline and noradrenaline

Glucocorticoid hormones –
including cortisol

24
Q

What kind of insulin will be administered with DKA or HHS

A

IV Insulin “regular” Short acting Humalin-R

25
Q

In HHS Tx, BG is not going down despite fluids and insulin? Potential problem?

A

Even with insulin, blood glucose levels in HHS patients may not decline initially; this usually suggests renal impairment or inadequate fluid resuscitation rather than insulin resistance

26
Q

Renal threshold for glucose?

A

Blood glucose levels that exceed the renal threshold (10–12mmol/litre) can precipitate an osmotic diuresis, leading to life-threatening dehydration.

27
Q

Warning signs of cerebral Edema?

What to Monitor

A
Headache.
Return of vomiting.
Behavioural changes.
Reduced level of consciousness.
Elevation in blood pressure and fall in pulse rate. Decreased oxygen saturation.

Consider Monitoring
Heart rate, respiratory rate, blood pressure. Neurological observations (at least hourly). Strict fluid input and output.
Capillary blood glucose.
Urinary ketones.
Blood ketones on fingerstick. Electrocardiogram.

28
Q

What is Metformin

A
  • Antidiabetic
  • Management of type 2 diabetes mellitus; may be used with diet, insulin, or sulfonylurea oral hypoglycemics.
  • Decreases hepatic glucose production. Decreases intestinal glucose absorption. Increases sensitivity to insulin.
  • Side Effects: Largely GI: Abdominal bloating, diarrhea, nausea, vomiting.
  • Watch for renal impairment (might need to be discontinued)