Hyperglycemia Flashcards

1
Q

Diabetes mellitus

A

Etiopatho
- Chronic metabolic disease characterized by
hyperglycemia as a cardinal biochemical feature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophysiology of DM

A

Pathophysio
- Insulin inhibits glycogenolysis, gluconeogenesis,
lipolysis and ketogenesis.
- Hunger in the midst of plenty: hyperglycemia without
cellular uptake of glu because of receptor resistance or
hyposensitivity.
- Reactivation of counterregulatory hormones (in order
of activation): glucagon –> epinephrine –> cortisol –>
GH
- Patient remains hyperglycemic despite poor oral intake
and increased losses because of counterregulatory
hormone effect, causing lipolysis and ketogenesis = net
effect is hyperglycemia, ketoacidosis, and
hyperthyroidisemia
- Kidney max glu 180mg/dL, beyond that result to
glucosuria resulting to polyuria and hypotension,
ketonuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical manifestations of DM

A

CM
Mnemonic: 3P’s+weight loss/ 4T’s: Toilet, Thirsty, Tired, Thinner
1. Polydipsia, polyuria, nocturia
2. Unexplained weight loss
3. Glucosuria, ketonuria
4. Monilial vaginitis – among F with chronic glucosuria
5. Polyphagia/ Hyperphagia
6. BOV, mood changes, skin infections, oral thrush,
abdominal pain
7. Ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diagnostics

A

Impaired fasting glucose Tolerance
Fasting glucose: 100-125 mg/dl (5.6-7.0 mmol/L)
2-hr Plasma glucose (OGTT):
≥140mg/dL but <200 (≥7.8 mmol/L)
HBA1C: 5.7-6.4%

Diabetes Mellitus
≥126 mg/dL (7.0mmol/L)
2hr Plasma glucose (OGTT): ≥200 mg/dL (≥11.1mmol/L)
HBA1C: ≥6.5%
others: symptoms of DM + random blood glucose ≥200mg/dL (≥11mmol/L)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Management

A

Mgt
1. Glycemic control – gycohemoglobin (HbA1c)
monitoring
- Reliable index of long-term glycemic control
- Reflects the ave blood glu concentration of the
preceding 2-3 months
- For known diabetics:
o 6-7.5%: good diabetic control
o 7.6-9.9%: fair
o >10%: poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Rapid acting

A

Aspart
Glulisine
Lispro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Short acting

A

regular Humulin R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Intermediate

A

NPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Long-acting

A

Detemir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the “honeymoon period”?

A

reduced exogenous insulin needs shortly
after starting tx due to residual B-cell function. Usually fades
within a few months reflected as steady increase in insulin
requirements and wider glu excursions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the usual regimen?

A

Usual regimen:
- 4 injection regimen: basal bolus regimen at night that
is slow-onset, long duration for between mean glucose
control (glargine/detemir) (40-50% of total dose) +
rapid-onset insulin at each meal (Lispro/aspart) (50-
60% of total dose div by 3)
- 3 injection regimen: NPH + rapid analog bolus at
breakfast à rapid-acting bolus analog at supper à
glargine at bedtime
- Insulin pump therapy/ continuous SC insulin infusion
(CSII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Other medications for DM?

A

Metformin – insulin sensitizer; usual starting dose 500mg OD, may
be inc to 1500-2500mg/d BID-TID
- AE: GI disturbance, lactic acidosis. Avoid in hepatic or
renal impairment
Sulfonylureas – occasionally used when metformin monotx
unsuccessful or contraindicated
- 1st gen: Acetohexamide, Chlorpropamide, Tolbutamide
- 2nd gen: Glipizide, Glyburide, Glimepiride
2. To ensure N growth (height and weight)
- CHO counting: allows patients to adjust insulin dosage
to their mealtime CHO intake
- Exercise. WOF hypoglycemia post workout
3. To prevent acute complications – DKA, cerebral edema
4. To prevent long-term vascular complications –
retinopathy, nephropathy, CAD, CV ds, neuropathies
- Diabetic retinopathy: leading cause of blindness
- Diabetic nephropathy: leading known cause of ESRD
5. Refer to endo/multidisciplinary specialists (ophtha,
nephro, cardio, neuro)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is dawn phenomenon?

A

Elevated blood glu early morning before breakfast:
Dawn phenomenon – due to overnight GH secretion à inc insulin
clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Somogyi phenomenon?

A

Somogyi phenomenon – theoretical rebound from late-night or
early-morning hypoglycemia (exaggerated counterregulatory
response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is etiopathogenesis of DKA?

A

Etiopatho
- End result of metabolic abN due to severe deficiency of
insulin or severe insulin ineffectiveness
- Effects of insulin deficiency:
o Glu utilization by muscle and fat decreases
o Excess glu production via glycogenolysis and
gluconeogenesis –> leading to
hyperglycemia
o Resultant osmotic diuresis produces
polyuria, urinary losses of e’ and
dehydration
o Combination of insulin deficiency + elevated
counterregulatory hormones = accelerated
lipolysis and impaired lipid synthesis
o Increased plasma cholesterol and FFA –>
leads to ketone body formation
(acetoacetate & beta-hydroxybutyrate) à
resulting in metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical manifestations of DKA?

A

CM
1. Abdominal discomfort or pain, nausea, emesis
2. Tachypnea, tachycardia
3. Fruity breath odor – from acetone
4. Kussmaul respiration – deep, heavy, nonlabored rapid
breathing
5. Dehydration with continuing polyuria
6. Diminished neurocognitive function, confusion,
drowsiness, possible coma
7. Progression of sx may be accelerated during
illness/trauma

17
Q

Diagnostics

A

Dx
Biochemical Criteria for DKA
a. Hyperglycemia blood glu >200 mg/dL or >11
mmol/L
b. Venous pH <7.3
c. serum bicarbonate <15mmol/L
d. Ketonemia (blood beta-hydroxybutyrate) >3
mmol/L or moderate/large ketonuria (>2+)
- All 4 criteria should be met
- Metabolic acidosis

18
Q

Classification of DKA

A

MILD
oriented, alert or fatigued
venous pH: 7.25-7.35
serum HCo3: 16-20 mEq/L

MODERATE
Kussmaul respiration, fruity breath odor, oriented by sleepy, arousable
venous pH: 7.15-7.25
serum HCO3: 10-15 mEq/L

SEVERE
Kussmaul or depressed respiration, sleepy to depressed sensorium, comatose
venous pH: <7.15
serum HCO3: <10 mEq/L

19
Q

Other diagnostics

A
  1. Serum Hgt
  2. VBG/ABG (pH, HCO3, PCO2) – metabolic acidosis
  3. Serum Na, K, ketones
  4. ECG/cardiac monitor – WOF peaked T waves, ST
    depression, widening QRS (hyperK), flattened T waves,
    arrhythmia, u waves (hypoK)
  5. BUN, Crea, Osm
  6. CBC – an elev WBC count in response to stress is
    characteristic of DKA and is not indicative of infection
  7. HbA1c
  8. Urine ketones
20
Q

Management

A

Mgt
1. Refer to Endo/PICU
2. Fluids
- 1st hr = Resuscitation fluids:
o If volume depleted but not in shock:
10mL/kg IV 0.9% PNSS over 30-60min (more
rapidly if with poor tissue perfusion)
o Shock: 20mL/kg isotonic saline boluses.
Additional bolus of 10ml/kg may be needed
to be administered cautiously 1-2x
o Shock must be adequately treated before
proceeding due to volume depletion
- Subsequent fluid mgt:
o 0.45% NaCl, 0.9% NaCl, or LR (depends on
hydration status, serum Na, and Osm)
o Give M fluid requirement + replace
estimated fluid deficit over 24-48h
§ 5-7% deficit in moderate DKA
§ 7-10% deficit in severe DKA
o Dehydration should be slowly corrected over 48h
3. 2nd hr = Mgt of hyperglycemia – insulin infusion
(human regular insulin 0.05-0.1 U/k/h) at least 1 h
after fluid replacement tx
- Addition of glucose to avoid hypoglycemia:
o 5% solution when blood glucose <300 mg/dl
o 10% solution when blood glu <200mg/dL
- When CBG <250mg/dL. May add 5% glu: change IVF to
D5NSS
- 100 mg/dl/h = target rate of insulin decrese
4. K replacement – if hypokalemic: start K replacement
before insulin tx
- If hyperkalemic: defer K replacement until UO
documented
- If N: start K replacement tx after initial volume
expansion, concurrent with insulin Tx
- 20-40 mmol K/L IVF
5. Bicarbonate Tx – rarely needed
- May increase risk of hypokalemia and cerebral edema
- Administer 1-2 mmol/kg over 60 min only if with:
o Life-threatening hyperkalemia
o Severe acidosis (venous pH <6.9)
6. Supportive Tx
- Mannitol: for cerebral edema
- Secure airway and continuous NGT suction to
decompress stomach
- Oxygen support for patients with circulatory
impairment or shock
- Hook to cardiac monitor: r/o hyper/hypokalemia
- Urinary catheterization prn
7. Monitoring – VS, neuro status, fluid I&O, CBG q1h or
more frequently prn
- E’ and ABG q2-4h or more frequently prn
- Q1 blood glu
- Q1 I&O
- Repeat e’s after start of IVF
8. Transition care – transition to oral intake and SC insulin
upon resolution of DKA:
a. HCO3 > 15 mEq/L
b. pH > 7.30
c. Na 135-145 mEq/L
d. No emesis

21
Q

What are the complications?

A

Complications
1. Cerebral edema – most dreaded complication of DKA
- Warning signs: headache and slowing of HR, change in
neurological status (restlessness, irritability, inc
drowsiness, incontinence), specific neurological signs
(CN palsy), rising BP, dec O2 sat
- Mgt: treat urgently
o Reduce rate of IVF by 1/3
o Mannitol 0.5-1 g/kg IV over 20 mins, repeat
if there is no initial response in 30min to 2h
o Hypertonic saline (3%) 5ml/kg over 30 min
as alternative tx
o Elevate head of bed by 30-45 degrees
o Intubation – impending respiratory distress
o Cranial CT scan – r/o other intracerebral causes of neuro deterioration: thrombosis, hemorrhages)
2. Hypoglycemia – due to overaggressive tx, or poor
monitoring
- Sweating, trembling, dizziness, mood changes, hunger,
headache, BOV, extreme tiredness, paleness, sz
- Mgt:
o Uncomplicated: immediate source of glu= juice/ milk
o Glucagon (n/a)
o Dextrose infusion (D50-50)

22
Q
A