Endocrine 6 Flashcards

(33 cards)

1
Q

Compared to type 1 DM, choose the statements that MOST accurately describe type 2 DM (select 2).
a. peripheral sensitivity to insulin is reduced
b. it is more likely to cause hyperglycemia hyperosmolar syndrome
c. is usually associated with a thin body habitus
d. it is usually caused by an autoimmune response

A

a. peripheral sensitivity to insulin is reduced
b. it is more likely to cause hyperglycemic hyperosmolar syndrome

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2
Q

_________ and _________ don’t need insulin for glucose uptake

A

The brain and liver

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3
Q

With DM, although glucose is present in the bloodstream, it is

A

unable to enter many of the cells that require it which shifts metabolism towards protein catabolism and lipid oxidation

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4
Q

Type 1 DM is characterized by

A

a lack of insulin production (beta cell destruction)

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5
Q

Type 2 DM is characterized by

A

a relative lack of insulin+ insulin resistance

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6
Q

__________ describes a group of characteristics that are common to patients with DM or to those who are at higher risk of developing DM

A

Metabolic syndrome

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7
Q

Diagnostic criteria of metabolic syndrome includes

A

at least three of the following:
fasting plasma glucose >100-110 mg/dL
abdominal obesity (>40 in in men and >35 in women )
serum triglyceride level >150 mg/dL
serum HDL <40 mg/dL in men and <50 mg/dL in women
BP >130/85 mmHg

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8
Q

_____________ is more common with type 1 DM

A

diabetic ketoacidosis

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9
Q

Diabetic ketoacidosis is usually caused by

A

infection

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10
Q

Treatment of DKA includes

A

volume resuscitation, insulin, and potassium after acidosis subsides

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11
Q

_____________ is more common with type 2 DM

A

Hyperglycemic hyperosmolar state

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12
Q

Hyperglycemic hyperosmolar state is usually caused by

A

insulin resistance or inadequate insulin production

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13
Q

With HHS, glucose is typically

A

higher than DKA and metabolic acidosis is mild if present

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14
Q

Treatment of HHS includes

A

volume resuscitation, insulin, and electrolyte correction

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15
Q

Criteria for diagnosis of DM includes

A

fasting plasma glucose >126 mg/dL
random glucose level >200 mg/dL + classic symptoms
two hour plasma glucose >200 mg/dL during an oral glucose tolerance test
hemoglobin A1C> 6.5%

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16
Q

Classic symptom triad of DM is

A

polyuria
polydipsia
dehydration

17
Q

Treatment of type 1 DM includes

A

insulin (always required)

18
Q

Treatment of type 2 DM includes

A

weight reduction
dietary changes
oral hypoglycemic agents
insulin

19
Q

Symptoms of DKA may include

A

Kussmaul’s respirations d/t metabolic acidosis & acetone causes fruity-smelling breath

20
Q

The following factors can mask the signs of intraoperative hypoglycemia EXCEPT:
a. general anesthesia
b. propranolol
c. diabetic autonomic neuropathy
d. hydrochlorothiazide

A

d. hydrochlorothiazide

21
Q

_________ suggests an increased risk of difficult intubation in the DM patient

A

The prayer sign

22
Q

The DM patient may have reduced range of motion of the

23
Q

DM patients are at risk of

A

aspiration
hypothermia
orthostatic hypotension

24
Q

___________ impairs the patient’s ability to mount a sympathetic response to hypovolemia & the cardio-depressant effects of anesthetic drugs

A

Diabetic autonomic neuropathy

25
Hypoglycemia can be masked by
General anesthesia or beta-blockers
26
When should surgery be scheduled for the Dm patient?
early in the day to prevent interruption of nutrition and hypoglycemic therapy
27
Peripheral neuropathy usually begins in a
"stocking and glove" distribution
28
Peripheral neuropathy is treated with
NSAIDs, antidepressants, and anticonvulsants
29
Osmotic diuresis leads to
fluid and electrolyte abnormalities
30
This fluid could cause hyperglycemia
Lactate in LR can be converted to glucose
31
The DM patient should be assessed for
renal dysfunction
32
Hyperglycemia worsens neurologic outcome after
ischemic brain injury
33
Diabetic dysfunctions include
risk of dysrhythmias reduced vagal tone-- tachycardia painless myocardial ischemia diarrhea & constipation regional anesthesia can worsen neurologic defects in the patient with diabetic polyneuropathy