Endocrine Flashcards
1
Q
What is the cut off value to define hypoglycemia
A
< 70 mg/dl
2
Q
in general, is hypoglycemia more common in type I or type 2 diabetics
A
type 1 diabetics
3
Q
management of asymptomatic hypoglycemia
A
- defensive actions
- repeating measurement in near future
- avoid critical tasks (driving)
- ingest carbs
- adjusting tx regimen
4
Q
management of symptomatic hypoglycemia (able to swallow)
A
-
15-20 g oral carbohydrate
- 3-5 glucose tablets/hard candies
- 1/2 c juice
- sufficient to raise blood sugar to a safe level without inducing hyperglycemia
5
Q
management of symptomatic severe hypoglycemia (unable to swallow)
A
-
subcutaneous or intramusclar injection of 0.5 to 1.0 mg of glucagon
- recovery in 15 min
- may be followed by N/V
- 25 g of 50% glucose (dextrose) IV
6
Q
25 g of 50% glucose (dextrose) IV should be followed with
A
- subsequent glucose infusion or if mental status allows, food should be given
7
Q
tx of hypoglycemia caused by a sulfonylurea
A
patient must be admitted because half-life of drug is so long that condition will certainly reoccur
8
Q
what is equation for anion gap? what is the normal range?
A
- Na - Cl + HCO3
- normal < 10
9
Q
List causes of elevated anion gap metabolic acidosis (mneumonic)
A
MUDPILES
- Methanol
- Uremia (renal failure)
- Diabetic, alcoholic, or starvation ketoacidosis
- Paracetamol, propylene glycol, paregoric
- Inborn errors of metabolism: iron, ibuprofen, isoniazid
- Lactid acid
- Ethylene glycol
- Salicylates
10
Q
clinical presentation
- hyperglycemia
- hypotension
- hyponatremia
- hypokalemia
- hyperventilation
- elevated serum keytones
- dehydration
- AMS
- diffuse abd pain
- acidosis
- elevated anion gap
A
diabetic ketoacidosis
11
Q
hyperglycemic crisis in DM (diabetic ketoacidosis and hyperosmolar hyperglycemic state) are both precipitated by what conditions
A
- infection (think UTI or pna)
- trauma, surgery
- MI
- Insulin omission
12
Q
DKA signs/symptoms tend to develop over what time period
A
hours/days
13
Q
What is commonly the presenting sign of diabetes in type I diabetics
A
DKA
14
Q
describe the physics behind why DKA occurs
A
-
insulin deficiency -> relative glucagon excess
- increase in lipolysis -> glycerol + FFA
- glycerol -> inc gluconeogenesis -> hyperglycemia
- FFA -> ketogenesis
- hypergycemia -> osmotic diuresis
- dehydration
- Metabolic acidosis
- hypergycemia -> osmotic diuresis
- increase in lipolysis -> glycerol + FFA
15
Q
what diagnostics must be present to diagnose someone with DKA
A
- hyperglycemia: generally > 250 mg/dl
- Keytones: urine and serum positive
- Bicarbonate: Low
- Anion gap: elevated
- ABG: acidosis
16
Q
What electrolyte must you watch for when you give insulin in a patient with DKA
A
- Potassium
- insulin causes potassium to enter cells -> significant K+ deficit
17
Q
List therapeutic goals of DKA
A
- restore circulatory volume
- correct serum osmolarity
- clear serum keytones
- reducing blood glucose is last
18
Q
Treatment of DKA
A
- isotonic saline IV: give fluids aggressively
- correct electrolyte disorders
- follow K+ closely
- reverse acidosis and ketogenesis
- control blood glucose
- continuous IV insulin infusion
19
Q
would you use bicarbonate to treat patients in DKA
A
- general rule: bicarbonate should NOT be used to tx patients in DKA even when there is a severe acidosis present
- however, approprate to administer bicarb when significant hyperkalemia is present
- bicarb will push potassium into cells
20
Q
what are adverse effects of administering bicarbonate
A
-
paradoxical CSF acidosis
- -> severe cerebral edema and brain damage
21
Q
When should the insulin infusion be stopped when treating patients in DKA
A
- If there is still an elevated anion gap, insulin administration must continue
- presence of insulin will stop lipolysis
22
Q
Hyperosmolar Hyperglycemic State is mainly seen in type I or type 2 diabetics
A
type 2
23
Q
signs/symptoms of Hyperosmolar Hyperglycemic State present in what time period
A
- days to weeks
24
Q
clinical presentation
- altered state of consciousness
- weakness: both generalized and focal
- polydipsia and polyruia
- dehydration
A
Hyperosmolar Hyperglycemic State
25
what plasma osmolarity is seen in Hyperosmolar Hyperglycemic State
plasma osmolarity \> 320
26
is there acidosis in Hyperosmolar Hyperglycemic State
* **No acidosis** due to **relative** insulin deficiency
* amount of insulin present is insufficient to prevent hyperglycemia but sufficient to prevent lipolysis and ketogenesis
27
treatment of Hyperosmolar Hyperglycemic State
* **fluid and electrolyte replacement**
* insulin IV if fluid replacement alone is inadequate
* **treat underlying problem**
28
who gets thyroid storm
* can develop in patients with long standing untreated hyperthyroidism
* BUT often is precipitated by an acute event
* surgery, trauma, infection, acute iodine load, post-partum
29
Diagnostic criteria for thyroid storm includes what categories
* thermoregulatory dysfunction
* CNS effects
* GI-hepatic dysfunction
* cardiovascular dysfunction
* heart failure
* precipitant history
30
PTU and methimazole are examples of
Thionamides
31
In thyroid storm treatment, what is given first to control tachycarida
beta blocker
32
List treatment steps of thyroid storm
1. beta blocker
2. PTU or methimazole
3. **1 hr after** thionamide is given, administer iodide solution
4. give glucocorticoids and bile acid sequestrants simultaneously
33
function of PTU
* decreases thyroid hormone synthesis AND blocks the conversion of T4 to T3
* results in lower serum T3 levels and thus may be preferred
34
function of Methimazole
decreased thyroid hormone synthesis
35
function of glucocorticoids in tx of thyroid storm
* reduce T4 to T3 conversion
* promote vasomotor stability
* possibly treat an associated relative adrenal insufficiency
36
function of bile acid sequestrants in tx of thyroid storm
decrease enterohepatic recycling of thyroid hormones
37
if patient is allergic to or has a contraindication to the use of thioamides, what is the treatment of choice
thyroidectomy
38
What is Myedema coma
* severe deficiency in thyroid hormones leads to encephalopathy
39
causes of Myedema coma
1. culmination of severe, long-standing hypothyroidism
2. precipitated by an acute event
40
what are the cardinal features of Myedema coma
* Hypothermia
* CNS depression/coma
41
who is at the highest risk for Myedema coma
* elderly
* women
42
clinical presentation
* nonpitting edema with abnormal deposits of mucin in the skin and other tissues
* puffiness of hands and face
* thickened nose
* swollen lipds
* enlarged tongue
Myedema coma
43
Pretibial myxedema is commonly seen in what condition
hyperthyroid state: graves disease
44
mortality associated with Myedema coma
30-40%
45
Treatment of Myedema coma
1. administer thyroid hormone: **T4**
2. glucocorticoids-hydrocortisone- given until adrenal insufficiency is ruled out
3. recovery is slow
46
primary adrenocortical insufficiency
* adrenal gland is damaged/not functioning and cannot produce glucocorticoids or mineralocorticoids
* addisons disease
47
secondary adrenocortical insufficiency
* defect of the pituitary gland inhibiting proper release of ACTH
48
tertiary adrenocortical insufficiency
* suppression of hypothalamic-pituitary-adrenal function
49
most common cause of tertiary adrenocortical insufficiency
abrupt withdrawal of chronic administration of high doses of glucocorticoids
50
what are mineralocorticoid levels affected in tertiary adrenocortical insufficiency
* mineralcorticoid secretion is nearly normal because this function depends mostly on renin-angiotensin system rather than on ACTH
51
common symptom associated with acute adrenal crisis
profound hypotension
* think of adrenal criss when shock is othewise unexplained and inadequatly responsive to vasopressors and volume replacement
52
what is Waterhouse-Friderichsen syndrome
* adrenal infarction due to meningococcemia
* think of this with
* fever
* mental status changes
* purpura
53
managment of adrenal crisis
* administer hydrocortisone and mineralocorticoid
