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Endocrinology > Diabetic Emergencies > Flashcards

Diabetic Emergencies Flashcards

1
Q

What are the 3 life-threatening diabetic emergencies?

A

Diabetic ketoacidosis (DKA)

Hyperosmolar hyperglycaemic state (HHS)

Hypoglycaemia

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2
Q

Which type of hyperglycaemic emergency is most common in type 1 and type 2 diabetes? Why is there are difference?

A

Type 1= DKA

Type 2= HHS

Difference due to type 1 having ABSOLUTE insulin deficiency whereas type 2 only has relative insulin deficiency
I.e. even small amount of insulin can act to inhibit ketogenic processes

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3
Q

What are the 4 biochemical consequences of insulin deficiency and how are they related to the symptoms of hyperglycaemic emergency?

A
  1. Increased glycogenolysis + gluconeogenesis
    - increased serum glucose leads to osmotic diuresis and consequent dehydration and loss of electrolytes (Na+ and K+)
  2. Increased proteolysis
    - increased serum AA= glucogenic and ketogenic
  3. Lipolysis
    -increased glycerol and FA= ketogenic and glucogenic
    I.e. alternative energy source due to lack of glucose uptake into cells
  4. Increased ketogenesis
    - induces metabolic acidemia i.e. ketone bodies lead to acidosis
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4
Q

What is the triad of DKA?

A

Hyperglycaemia

Ketonaemia

Metabolic acidosis

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5
Q

What are the 2 basic causes underlying the pathophysiology of DKA and why do they lead to DKA?

A
  1. Insulin deficiency
  2. Increased counter-regulatory hormones (can be released in response to stress causes by illness)

Consequences:
-increased hepatic gluconeogenesis and glycogenolysis which leads to HYPERGLYCAEMIA

-induces lipolysis which increases the concentration of free FA which induces KETOGENESIS AND KETOACIDOSIS

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6
Q

What complications of DKA can result in death?

A

Hypovolemic shock due to acidosis inducing collapse of vessels

MI

CVA

Mesenteric arterial occlusion

Acute pancreatitis

Infection i.e. pneumonia

Cerebral oedema

ARDS (pulmonary oedema)

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7
Q

What are possible precipitating factors of DKA?

A

Infection i.e. UTI or pneumonia

Treatment errors i.e. missing insulin or insufficient dose

New diagnosis of T1DM

Stress

Alcohol

Pregnancy

MI

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8
Q

What is important advice/steps that T1DM patients need to be given to help prevent DKA?

A

Sick day rules= more insulin required when unwell

Monitor blood glucose and ketones when ill

Check that pen/pump working

Don’t miss a dose (even if not eating due to illness)

Stay hydrated

Avoid strenuous activity

Keep same diet

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9
Q

What are the clinical features of DKA?

A 
Hyperglycaemia:
Excessive thirst 
Polyuria 
Weight loss
Abdominal pain 
Nausea 
Blurred vision 
Ketonaemia:
Rapid breath (Acidotic respiration)
Headache 
Confusion 
Acetone breath (pear drops) 
Hot dry skin (inappropriate vasodilation)
Hypothermic (“”)
Circulatory collapse (“”) = tachycardia + hypotension 
Drowsiness 
Coma
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10
Q

Why does vasodilation occur in DKA patients and what are the clinical signs of this?

A

Acidosis induces vasodilation

Signs:

  • hot dry skin
  • hypothermic
  • circulatory collapse = hypotension and tachycardia
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11
Q

What are the 3 diagnostic criteria for DKA?

A

Glucose:
>11mmol/L or known diabetic
Lab glucose

Ketones:
Capillary blood showing ketonaemia i.e. >=3 mmol/L
Urinary test showing ketonuria i.e. >2+ on dip stick

pH:
<7.3 (venous)
HCO3 <15mmol/L

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12
Q

What other tests are important outside the diagnostic criteria and why is this?

A

Other tests can be used to assess for any precipitating factors which can them help to guide treatment

Eg:

  • U+E ie assess renal impairment to indicate level of dehydration
  • FBC and cultures= infection markers
  • ECG= evidence of MI
  • ABG to assess acid-base status= can see if acidosis has been compensated for i.e. decreased CO2
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13
Q

What happens to ureas and sodium and potassium levels in DKA and why?

A

Raised Urea= due to dehydration
Low sodium= electrolyte i.e. increased Na loss in hyperglycaemia
Low potassium= osmotic diuresis

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14
Q

What 2 forms of management should be done immediately in DKA and why?

A

Fluid replacement

  • replace circulatory volume + correct hypotension
  • clear ketones
  • correct electrolyte imbalance
Insulin = fixed rate IVII (0.1 units/kg/h)
-suppression of ketogenesis 
-reduction of blood glucose 
-correct electrolyte imbalance 
NOTE: continue normal insulin
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15
Q

What are the different things which need to be monitored in a DKA patient?

A

Blood glucose
Ketones
Blood gas for pH and HCO3
Potassium

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16
Q

What are possible complications which can arise whilst managing DKA?

A

Hypoglycaemia

Potassium derrangment

Fluid overload

17
Q

What is rebound ketosis and why does it occur? What can be done to avoid this in DKA?

A

Ketosis induced by allowing glucose levels to reach hypoglycaemic range and therefore inducing counter-regulatory hormones which induced ketosis

Give 10% glucose infusion when blood glucose falls <14mmol/L

18
Q

Why do potassium levels need to be monitored once DKA treatment has begun? When and how can it be replaced if necessary?

A

Insulin can induce fall in potassium due to activating Na+/K pump which promotes movement of K+ into cells

If fall <5.5mmol/L= 0.9% NaCl solution with potassium 40mmol/L

19
Q

How can fluid overload by managed in DKA?

A

Manage fluid balance i.e. monitor how much IV fluid going in vs how much fluid going out

Catheterise to monitor urine output

20
Q

Why might thromboprophylaxis be given in DKA? What type is given?

A

Increased risk of thromboembolism in DKA

LMWH

21
Q

What is the criteria for DKA to be classified as resolved? What are the measures taken after DKA resolution? How does this differ depending on whether px eating and drinking?

A

Blood ketone <0.3 mmol/L
Venous pH >7.3

If E+D:

  • convert to SC insulin
  • stop IVI

If not E+D:

  • move to variable rate IV insulin infusion
  • continue IVI
22
Q

What is the pathophysiology relating to HHS?

A

Hyperglycaemia causes osmotic diuresis
Osmotic diuresis causes excess water and electrolyte loss
Water moves out of intracellular compartment== cellular dehydration

23
Q

Why don’t HHS patients become ketoacidotic?

A

Insulin NOT completely absent- some present to suppress lipolysis and ketogenesis

Hyperosmolarity also inhibits lipolysis

Decreased FFA which leads to decreased induction of ketogenesis

24
Q

What are the characteristic features of patient presenting with HHS?

A

Hypovolaemia

Hyperglycaemia (>30mmol/L)

Lack of significant kyperketonaemia and acidosis

Osmolality >320 mosmol/Kg

Dehydration= 10-15% weight water deficit

Altered mental state= associated with >330mosmol/kg

Thrombotic complications

25
Q

What are possible precipitants of HHS?

A

Dehydration or poor intake associate with illness
Infection
MI
Stroke
Steroids
Diuretics
Poor compliance with diabetes regimen or poor control

26
Q

What is required for a diagnosis of HHS?

A

Serum osmolality >320 = HYPEROSMOLAR

Glucose > 30mmol/L = HYPERGLYCAEMIA

HCO3 >15mmol/L

PH > 7.3

Blood ketones <3.0 mmol/L

27
Q

What is the aim of HHS treatment?

A

Normalise osmolality

Replace fluid and electrolytes

Normalise BG

Treat underlying causes

Prevent complications i.e. A or V thrombosis/ cerebral oedema/seizures/central pontine myelinolysis

28
Q

A patient with history of T2DM presents to A+E with increased urinary frequency, increased thirst, nausea and vomiting. What is the top differential? How can this be confirmed and how should they be managed?

A

HHS

Serum osmolality of >320

Glucose >30mmol/L

not evidence of acidosis or ketosis

Managed:

  1. fluid replacement:
    - 0.9% normal saline
  2. Insulin
    - only if not dropping by 5mmol/L/h with saline alone
    - fixed rate IVII 0.05 units/kg/h
  3. Potassium
    - only if not w/i 4-5mmol/L target with resusitation alone
  4. Thromboprophylaxis (LMWH)
  5. Foot protection
29
Q

HHS patient is given fluid replacement but is not presenting with hypernatraemia. Why has this happened? How can this be avoided?

A

Fluid replacement gradually lowers osmolality which can cause shift in water into intracellular space
Leads to increase in serum sodium== hypernatraemia

Monitor osmolality and electrolytes regularly and adjust rate of saline accordingly

30
Q

What is the difference in treatment between HHS and DKA?

A

Insulin NOT given as standard in HHS unless it is not falling by 5mmol/L/h

31
Q

What is Whipple’s triad?

A

Symptoms of hypoglycaemia

Plasma glucose conc <4mmol/L

Resolution of symptoms after plasma glucose concentration raised

32
Q

What is the biochemical definition of hypoglycaemia?

A

<4.0 mmol/L

I.e. four= floor

33
Q

What occurs between 3.5-3.8mmol/L glucose in hypoglycaemic patient?

A

Stimulates increase in counter-regulatory hormones which act to try and increase blood glucose but also contribute to the symptoms associated with hypoglycaemia

Hormones:

  • Ad
  • NAd
  • Autonomic activity
  • Glucagon
  • GH
  • ADH
  • Cortisol
34
Q

Symptoms associated with hypoglycaemia can fit into 2 categories? What are these categories and what are the associated symptoms? What blood glucose level do they typically present?

A

3.2 mmol/L

Autonomic (due to increased Ad and NAd)

  • sweating
  • pallor
  • tachycardia
  • tremor
  • tingling
  • hunger

Neuroglycopenic

  • confusion
  • odd behaviour
  • drowsiness
  • in coordination
  • slurring
  • diplopia
  • dizziness
  • headache
35
Q

What are the possible causes of hypoglycaemia?

A 
Excess insulin or SU 
Insufficient food 
Exercise 
Alcohol/drugs 
-impaired glucogenesis 
-loss of warning and can be mistaken for drunkenness 
Strict glycaemic control 
Long duration of diabetes 
Hypoglycaemia unawareness 
-elderly or children 
-nocturnal episodes 
Hot weather 
Renal failure
36
Q

A patient presents to A+E with hypoglycaemia. They are conscious. How are they treated? How would this change if they were unconscious?

A

15-20g rapid acting carbohydrate

Recheck BGL after 10-15 mins
-repeat with carbs if still below 4 (can repeat max of 4 times)

Consider 1mg IM glucagon

IV glucose if still <4= 200ml of 10% over 15 mins

20g long acting carbohydrate AFTER BGL >4 + recovered

Unconscious:

  • ABCDE
  • IV glucose 100ml of 20% for 15mins
  • 1 mg IM glucagon
  • recheck BGL after 10 mins and repeat IV if <4
  • 20g long acting carbs after >4 + recovered
37
Q

What are examples of 15-20g rapid acting carbs?

A 
200ml pure orange juice
4-6 glucose tablets 
20g glucose gel 
59ml bottle of glucose juice 
150ml coke 
4 jelly babies
38
Q

What can be given for 20g LA carbs?

A

2 plain biscuits
One slice of bread
200-300ml milk

Endocrinology (18 decks)

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