Exam 4 - Endocrine Flashcards
(90 cards)
1
Q
The ____ is the primary source of glucose production via glycogenolysis & gluconeogenesis
A
Liver
2
Q
____ of the glucose released by the liver is freely metabolized by tissues in the brain, GI tract, and red blood cells
A
75%
3
Q
After eating, when does glucose usage exceed availability?
A
2-4 hours
4
Q
Glucagon plays a primary role in regulating blood glucose by?
A
- Stimulating glycogenolysis
- Simulating gluconeogenesis
- Inhibiting glycolysis
5
Q
____ is the most common endocrine disease affecting ____ in 10 adults
A
Diabetes
1 in 10
6
Q
What is Type 1a DM?
A
an autoimmune destruction of pancreatic β cells, leading to minimal or absentinsulin production
7
Q
What is type 1b DM?
A
a rare, non-immune disease of absolute insulin deficiency
8
Q
What is Type 2 DM?
A
- non-immune, and results from defects in insulin receptors and signaling pathways
- accounts for 90% of DM
9
Q
What happens in Type 1 DM before onset of symptoms?
A
- A long period (9-13 yrs) of B-cell antigen production
- At least 80-90% B cell function is lost
10
Q
Disease progression in Type 2 DM?
A
- In initial stages, tissues become desensitized to insulin, leading to ↑secretion
- Over time, pancreatic function decreases & insulin levels become inadequate
11
Q
What 3 main abnormalities are seen in DM2?
A
- Impaired insulin secretion
- ↑hepatic glucose release c/b a reduction in insulin’s inhibitory effect on liver
- Insufficient glucose uptake in peripheral tissues
12
Q
Causes of insulin resistance?
A
- Abnormal insulin molecules
- Circulating insulin antagonists
- Insulin receptor defects
13
Q
Hgb A1c percentages for normal, prediabetic, and diabetic?
A
- Normal < 5.7%
- Prediabetic 5.7-6.4%
- Diabetic >6.5%
14
Q
ADA criteria for diagnosis of diabetes?
A
- A1C > 6.5%
- FPG > 126 mg/dL
- 2 hr glucose > 200 mg/dL durting OGTT
- w symptoms of hyperglycemia - random glucose > 200 mg/dL
15
Q
Initial treatment for DM2?
MOA?
A
- Metformin
- Enhances glucose transport into tissues
- ↓TGL & LDL levels
16
Q
Sulfonylurea MOA?
A
- Simulates insulin secretion
- Enhances glucose transport to tissues
17
Q
Sulfonylurea adverse effects?
A
- Sulfonylureas not effective long term d/t diabetic progressive loss of B cell function
- hypoglycemia, weight gain & cardiac effects
18
Q
What treatments are most effective at lowering A1c?
A
Lifestyle changes, metformin, sulfonylureas: ↓ by 1-2%
Insulin: ↓ by 1.5-3.5%
GLP-1 antagonist: ↓ 0.5-1.5%
19
Q
What drugs/substances can exacerbate hypoglycemia?
A
ETOH, metformin, sulfonylureas, ACE-I’s, MAOI’s, Non-selective BB’s
20
Q
What is hypglycemia unawareness?
Treatment?
A
- Pt becomes desensitized to hypoglycemia and doesn’t show autonomic sx
- Neuroglycopenia ensues→fatigue, confusion, h/a, seizures, coma
- Tx: PO or IV glucose (may give SQ or IM if unconscious)
21
Q
Onset, peak, and duration of the short acting insulins?
A
22
Q
Onset, peak, and duration of the intermediate acting insulins?
A
Onset: 1-2 hours
Peak: 6-10 hours
Duration: 10-20 hours
23
Q
Onset, peak, and duration for glargine (lantus)?
A
Onset: 1-2 hr
Peak: none
Duration: 24 hours
24
Q
Patho of DKA?
A
- DKA more common in DM1, often triggered by infection/illness
- High glucose exceeds the threshold for renal reabsorption
- Creates osmotic diuresis & hypovolemia
- The liver overproduces of ketoacids
25
Lab findings for DKA?
26
DKA treatment?
* IV volume replacement
* Regular Insulin: Loading dose 0.1u/kg + low dose infusion @ 0.1u/kg/hr
* Correct acidosis: sodium bicarb
* Electrolyte supplement: k+, phos, mag, sodium
27
Why is important to correct sodium with glucose?
Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema
28
What is HHS?
* When blood glucose exceeds renal glucose absorption, massive glucosuria occurs
* Severe hyperglycemia, hyperosmolarity & dehydration
29
Symptoms and treatments for HHS?
Sx: polyuria, polydipsia, hypovolemia, HoTN, tachycardia
Tx: fluid resuscitation, insulin bolus + infusion, e-lytes
30
At what point do the kidneys no longer clear K+?
GFR < 15-20
31
What drug slows the progression of proteinureia and GFR decrease in DM?
ACE-i's
32
Definition of peripheral neuropathy?
How does it progress?
* Distal symmetric diffuse senorimotor neuropathy
* Starts in toes and progesses proximally
33
What is autonomic neuropathy?
Treatments?
- Affects any part of the ANS
- CV: orthostatic hypotension, dysrhytmias
- GI: gastroparesis
- TX: glucose control, small meals, prokinetics
34
DM preop anesthesia concerns?
- Assess hydration status, avoid nephrotoxins, and preserve RBF
- Gastroparesis may ↑aspiration rx, regardless of NPO status
* PO diabetic drugs should be held to avoid hypoglycemia
35
What is an insulinoma?
Who is at greater risk?
* Benign insulin-secreting pancreatic tumor
* Occurs 2x more in women than men, normally in 50s-60s
36
How is an insulinoma diagnosed?
Whipple triad:
* Hypoglycemia w/ fasting
* Blood glucose < 50 w/sx
* Sx relief w/glucose
37
What drug should be given preop to someone with an insulinoma?
Insulinoma treatment?
* Diazoxide, which inhibits insulin release from B cells
* Surgery is curative
38
The thyroid gland is innervated by which system?
Both adrenergic and cholinergic nervous systems
39
What is production of thyroid hormones reliant on?
Exogenous iodine
40
How does iodine become thyroid hormones?
- Transported into thyroid fallicular cells after GI absorption
- Iodide binds to thyroglobulin and yields inactive monoiodotyrosine and diiodotyrosine
- These undergo coupling w/ thyroid peroxidase to form thyroxine (T4) and triiodothyronine (T3)
41
T4/T3 ratio?
10:1
42
Hypothalamus role in thyroid regulation?
The hypothalamus secretes Thyrotropin-releasing hormone (TRH), which signals the anterior pituitary to release thyrotropin-stimulating hormone (TSH)
43
Role of TSH in regulation of T3 and T4?
* TSH binds to thyroid receptors and enhances the synthesis/release of T3 & T4
* TSH is also influenced by plasma levels of T3 & T4 via a negative feedback loop
44
Best test to assess thyroid activity?
TSH assay
45
Normal TSH level?
0.4-5.0 milliunits/L
46
What test is used to test pituatary function and TSH secretion?
TRH stimulation test
47
What test can determine if a thyroid lesion is cystic, solid, or mixed?
Ultrasound
48
3 causes of hyperthyroidism?
- Graves (leading cause)
- Toxic goiter
- Toxic adenoma
49
Symptoms of hyperthyroidism?
- Anxious
- Flushed
- Exopthalmos
- Increased DTR
- Emotional instability
- Tachycardia, hyperdynamic
50
Patho of graves disease?
Lab findings?
- Autoimmune, c/b thyroid-stimulating antibodies, stimulating growth, vascularity, and hypersecretion
- +TSH antibodies, low TSH, high T3 & T4
51
Graves disease treatments?
- 1st line: methimazole or propylthiouracil (PTU)
- BB relieve symptoms (propanolol impairs peripheral conversion of T4 to T3)
- Subtotal thyroidectomy
52
What is thyroid storm?
Triggers?
Lab findings?
* Life-threatening hyperthyroid exacerbation
* Triggered by stress, trauma, infection, medical illness, or surgery (inadequate treatment after emergency)
* Thyroid hormone levels in thyroid storm may not be much higher than basic hyperthyroidism
53
1st and 2nd most common cause of hypothyroidsim?
1st - thyroid gland ablation
2nd - idopathic, likely autoimmune (hashimoto's thyroiditis)
54
Hypothyroidism symptoms?
- Fatigue
- Apathy
- Pale, cool skin
- Decreased CO
- Decreased ECG amplitude
55
Hypothyroidism treatment?
Levothyroxine
56
What is myxedema coma?
* Rare, severe form of hypothyroidism characterized by delirium, hypoventilation, **hypothermia**, bradycardia, HoTN, and dilutional hyponatremia
* Medical emergency
57
Myxedema coma treatments?
* IV hydration w/glucose solutions, temp regulation, e-lyte correction, and supportive care
* Mechanical ventilation is frequently required
58
Causes of goiter?
- Lack of iodine
- Ingestion of goitrogen
- Hormone defect
59
What may the patient need if both layrngeal nerves are damaged?
Tracheostomy d/t AW obstruction (vocal cords close)
60
How may hypoparathyroidism present after thyroid surgery?
Hypocalcemia within 48 hours
61
What does the adrenal cortex synthesize?
glucocorticoids, mineralocorticoids (aldosterone), and androgens
62
What is the pathway for adrenal secretion of substances?
- Hypothalamus sends corticotropin-releasing hormone (CRH) to the anterior pituitary, which stimulates release of corticotropin (ACTH)
- ACTH stimulates the adrenal cortex to produce cortisol
- Cortisol helps convert NE to EPI, and induces hyperglycemia
63
What is pheochromocytoma?
Catecholamine-secreting tumor that originates from chromaffin cells
64
Where do pheochromocytomas occur?
* 80% occur in the adrenal medulla
* 18% in organ of Zuckerkandle (glands)
* 2% neck/thorax
65
How do pheochromocytomas change epi and norepinephrine secretion?
NE:EPI ratio 85:15, the inverse of normal adrenal secretion
66
Diagnosis for pheochromocytoma?
- 24h urine collection for metanephrines and catecholamines
* CT & MRI
67
Drugs used to treat pheochromocytoma?
* **Phenoxybenzamine**- (most frequent) - noncompetitive α1 antagonist with some α2-blocking properties
* **Prazosin** & **Doxazosin**- pure α1 blockers, shorter acting w/ less tachycardia
* CCB
68
Why should you never give a nonselective BB before an alpha blocker to someone with a pheochromocytoma?
Blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises
69
What are the 2 forms of Cushings (hypercortisolism)?
ACTH-*dependent* Cushings: high plasma ACTH stimulates adrenal cortex to produce excess cortisol
ACTH-*independent* Cushings: excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH (adrenocortical tumors)
70
Symptoms of Cushings?
sudden weight gain - usually central w/ ↑facial fat (**moon face**), ecchymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia
71
Treatment for Cushings?
- transsphenoidal microadenomectomy if resectable (1st choice)
- Ant. pituatary resection
- Adrenalectomy for adenoma or carcinoma
71
Anesthesia concerns for hypercortisolism?
* Manage BP
* Cosider osteoporosis in positioning
72
What are the two forms of Conn Syndrome (hyperaldosteronism)?
**Primary hyperaldosteronism**: Excess secretion of aldosterone c/b tumor (aldosteronoma) - decreased renin
**Secondary hyperaldosteronism**: c/b elevated renin levels
73
Hallmark symptom of hyperaldosteronism?
Spontaneous HTN w/hypokalemia
74
What can mimic hyperaldosteronism?
Long-term ingestion of licorice
75
Treatments for hyperaldosteromism?
* Aldosterone antagonist (Spironolactone)
* K+ replacement
* antihypertensives
* diuretics
* tumor removal
* possible adrenalectomy
76
Hallmark symptoms for hypoaldosteronism?
Treatment?
* Hyperkalemia in the absecene of renal insufficiency
* Commonly have hypercholremic metabolic acidosis
* Increased Na+ intake and daily fludrocortisone
77
What are the 2 types of adrenal insufficency?
**Primary (Addison dz)**: Autoimmune adrenal gland suppression (>90% of the glands must be involved before signs appear)
**Secondary**: hypothalamic-pituitary suppression leading to a lack of CRH or ACTH production - only gluccocorticoid deficency
These patients lack pigmentation
78
Diagnosis for adrenal insufficency?
Treatments?
- Baseline cortisol < 20 μg/dL and remains < 20 μg/dL after ACTH stimulation
- Tx: steroids
79
How many PT glands are there?
What causes PTH release or inhibition?
- 4, behind the thyroid gland
- Hypocalcemia stimulates release
- Hypercalcemia stimulates inhibition
80
What causes primary hyperparathyroidsim?
* benign parathyroid adenoma (90%)
* carcinoma (< 5%)
* parathyroid hyperplasia
81
Symptoms and treatment for hyperparathyroidism?
Sx: lethargy, weakness, n/v, polyuria, renal stones, PUD, cardiac disturbances
TX: surgical removal of abnormal portions of the gland
82
What is secondary hyperparathyroidism?
compensatory response of the parathyroid glands to counteract a separate disease process involving hypocalcemia (CKD)
83
What is pseudohypoparathyroidsim?
Disorder where PTH is adequate, but the kidneys are unable to respond to it
84
Labs for hypoparathyroidism?
Anesthesia concerns?
Treatments?
Labs: ↓PTH, ↓Ca++,↑phos
Anesthesia concerns: Acute hypocalcemia s/a after accidental parathyroid removal may cause inspiratory stridor or laryngospasm
Tx: Tx: Calcium replacement, Vitamin D
85
What hromones are secreted by the anterior and posterior pituatary?
Anterior: GH, ACTH, TSH, FSH, LH, prolactin
Posterior: vasopressin and oxytocin
86
What is acromegaly?
Treatments?
- Excessive growth hormone (insulin-like growth factor 1), most often seen with anterior pituitary adenomas
- Causes overgrowth of soft tissues (airway obstruction)
- Tx: removal of pituatary adenoma or somatostatin analouges
87
What are the 2 types of DI (vasopressin deficiency)?
Central/Neurogenic DI: destruction/dysfunction of the posterior pituitary
Nephrogenic DI: failure of kidneys to respond to ADH
88
How can you treat DI?
Neurogenic DI: DDAVP
Nephrogenic DI: low-salt, low-protein diet, thiazide diuretics, and NSAIDs
89
What is SIADH?
Symptoms and treatment?
* Excessive vasopressin
* hyponatremia, ↓serum osmolarity, ↑urine sodium and osmolarity
* Tx: fluid restriction, Na+ tabs, loop diuretics, ADH antagonists (Demeclocycline)
