Endocrine Flashcards

1
Q

What are the 7 hypothalamic hormones?

A

Luteinizing hormone
Corticotropin hormone
Thyrotropin
Prolactin releasing
Prolactin inhibiting
Growth hormone inhibiting
Growth hormone stimulating

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

Where is the pituitary gland located?

A

Sella turcica

Anterior - adenohypophysis
Posterior - neurohypophysis

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

Which hormones are released from the anterior pituitary?

A

FLAT PiG

Follicle
Luteinizing
Adrenocorticotropic
Thyroid stimulating
Prolactin
Growth

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

What does the follicle stimulating hormone do?

A

Germ cell maturation and follicle growth in females

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

What does the luteinizing hormone do?

A

Testosterone production in males and ovulation in females

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

What does the adrenocorticotropic hormone do?

A

Adrenal hormone release

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

What does the thyroid stimulating hormone do?

A

Thyroid hormone release

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

What does prolactin do?

A

Lactation

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

What does growth hormone do?

A

Cell growth

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

What two hormones are from the posterior pituitary ? What are their functions?

A

Antidiuretic - water retention
Oxytocin - uterine contraction and breast feeding

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

Anesthetic complications for acromegaly?

A

Everything is large + glucose intolerance

Large face, teeth, epiglottis, narrowing of cords, turbinate’s

Increased risk of CAD, HTN, rhythm disturbances

Muscle weakness

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

Differentiate T3 to T4, source?

A

T4 - thyroid

T3 - extrathyroid conversion of T4 to T3

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

Differentiate T3 to T4, highest concentrations?

A

T4 - in the blood (T4 delivers T3)

T3 - In the target cell

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

Differentiate T3 to T4, protein binding?

A

T4 - more

T3 - less

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

Differentiate T3 to T4, potency?

A

T4 - Less

T3 - more

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

Differentiate T3 to T4, half life?

A

T4 - 7 days
T3 - 1 day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does iodine deficiency affect T3 and T4?

A

Iodine is a substrate that the thyroid needs to make T3 an T4

without it, NO T3 or T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does the thyroid affect cardiac function?

A

Increases

Chronotropy
Inotropy
Lusitropy
Number of beta receptors

Decreases
SVR
Number of muscarinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does the thyroid affect respiratory function?

A

Increases CO2, O2 and Minute ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does the thyroid affect MAC?

A

Has NO effect

BUT

hyperthyroidism can have a slower induction time
hypothyroidism can have a faster induction time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Most common cause of hyperthyroidism?

A

Graves

also

MG
Carcinoma
Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis

Also

iodine deficiency
Neck radiation
Thyroidectomy

Amiodaron can effect both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How are T3 and T4 affected by hyper/hypothyroidism?

A

Hypo - Low TSH and High T3+T4

Hyper - High TSH and Low T3+T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Myxedema coma vs cretinism?

A

Myxedema coma - end stage hypothyroidism that leads to coma

Cretinism - neonatal hypothyroidism -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What three thioamides can treat hyperthyroidism ?

A

PTU, Methimazole, Carbimazole

Block iodine

Need 6-7 weeks to work and are only PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why are beta blockers used in hyperthyroidism?

A

Reduce SNS stimulation and inhibit peripheral conversion of T4 to T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Contraindications to radioactive iodine?

A

Pregnancy

Breast feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When can surgery be done in patients with hyper/hypothyroidism?

A

Hyper - Do not proceed with elective, for emergency - give beta blockers, potassium iodine, glucocorticoid, PTU

Hypo - okay if mild or moderate disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Best way to secure an airway with a goiter?

A

Awake intubation

or a technique that maintains spontaneous ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which drugs should be avoided in hyperthyroidism?

A

Sympathomimetics
Anticholinergics
Ketamine
Pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a thyroid storm?

A

Stressful in hyperthyroid and euthyroid and occurs 6-18 hours after surgery

S/sx
Fever > 38.5
Tachycardia
HTN
CHF
Shock
Agitation
Can mimic MH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How manage a thyroid storm?

A

Block synthesis (methimazole, carbimazole, PTU, potassium iodide)

Block release ( radioactive iodine, potassium iodide)

Block T4 to T3 (PTU, propranolol, glucocorticoids)

Block beta receptors (Propranolol, esmolol)

Support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How can you assess the RLN?

A

Have the patient say E or Moon

Can also look under DL, and use a NIM tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What happens if the parathyroid is resected?

A

Hypocalcemia at least 6-12 hours after surgery

S/sx of hypocalcemia

Muscle Spasm
DELAYED GASTRIC EMPYTING (increased risk for aspiration)
Laryngospasm
Hypotension
Prolonged QT
Paresthesia
Chvostek’s sign
Trousseau’s sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3 layers of the adrenal cortex?

A

GFR

G- Mineralocorticoids (aldosterone) salt
F- Glucocorticoids (cortisol) sweet
R- Androgens (dehydroepiandrosterone) sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is released from the adrenal medulla?

A

Catecholamines

Epi - 80%
Norepi - 20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where is angiotensinogen made?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where is ang 1 made?

A

systemic

39
Q

Where is ang 2 made?

A

lung

40
Q

How much cortisol is produced in a day?

A

15-30mg/day with a normal level of 12 mcg

Stress can create 100mg/day

41
Q

How does cortisol affect cardiovascular function?

A

Improves it by increasing the number of beta receptors

Also helps vasculature respond to vasoconstriction

42
Q

Which steroids have no glucocorticoid effects?

A

Aldosterone

43
Q

Which steroids have no mineralocorticoid effects?

A

Dexamethasone
Betamethasone
Triamcinolone

44
Q

Unique side effects of epidural triamcinolone?

A

Used to treat lumbar disc disease

Muscle weakness
Sedation
Anorexia

45
Q

What is Conn’s syndrome?

A

Too much aldosterone

Primary - from adrenal gland
Secondary - from renin secreting tumor

s/sx of increased mineralocorticoids

-HTN from Na and water
-Hypokalemia from wasting
- Metabolic alkalosis from H wasting

46
Q

High intake of what food resembles hyperaldosteronism?

A

Long term licorice ingestion (glycyrrhizic acid)

47
Q

Treatment for Conn’s?

A

Aldosterone antagonists (spironolactone or eplerenone)

Potassium supplementation

Na restriction

Removal of aldosterone secreting tumor

48
Q

Cushing’s syndrome vs Cushing’s disease?

A

Syndrome - too much cortisol
Disease - too much ACTH

49
Q

** What are glucocorticoid effects?

A

Hyperglycemia
Weight Gain
Infection
Osteoporosis
Mood disorder
Muscle weakness

50
Q

** What are mineralocorticoid effects?

A

-HTN from Na and water
-Hypokalemia from wasting
-Metabolic alkalosis from H wasting

51
Q

** What are androgenic effects?

A

Women become masculinized (hirsutism, thin hair, acne, amenorrhea)

Men become feminized (gynecomastia, impotence)

52
Q

How does Cushing’s present?

A

Will present with excess of all three groups

Mineral
Gluco
Androgenic

53
Q

Which endocrine disorder can occur after resection of pituitary gland?

A

DI ( too little ADH )

54
Q

Presentation of adrenal insufficiency?

A

Addisons

Low electrolytes except for Hyperkalemia
Muscle weakness
Anorexia
Acidosis
N/V
Hyperpigmentation

55
Q

Treatment for addisons?

A

Steroids

56
Q

What is acute adrenal crisis? Treatment?

A

From stress - medical emergency

Fever
Hemodynamic instability
Hypoglycemia
Impaired mental state

Steroids (hydrocortisone)
Fluids (D5NS)
Supportive

57
Q

What is the stress response in patients with chronic steroid therapy?

A

Suppresses the ACTH so the patient will not be able to increase their cortisol

58
Q

Graph for who needs steroids?

A
59
Q

What are the 4 hormones produced by the pancreas which cells produce them?

A

Alpha - Glucagon
Beta - Insulin
Delta - Somatostatin
PP - Pancreatic polypeptide

60
Q

Which conditions increase insulin release?

A

Anything that increases glucose

SNS
PNS
Glucagon
Catecholamines
Cortisol
Growth Hormone
Beta agonists

61
Q

Which conditions decrease insulin release?

A

Anything that decreases glucose

Insulin
Volatile anesthetics
Beta antagonists

62
Q

What factors stimulate glucagon release?

A

Anything that uses glucose will stimulate glucagon

Hypoglycemia
Stress
Trauma
Sepsis
Beta agonists

63
Q

What factors inhibit glucagon release?

A

Insulin
Somatostatin

64
Q

Other uses for glucagon?

A

Increases contractility, HR, AV conduction by increasing intracellular cAMP.

Beta-blocker overdose
CHF
Low CO after MI or CPB
Improving MAP after anaphylaxis
Relaxes biliary sphincter

65
Q

What is somatostatin?

A

Regulates endocrine hormone output from islet cells and released by delta cells

Growth inhibiting hormone
Inhibits glucagon and insulin
Inhibits splanchnic blood flow, gastric motility, and gall bladder contraction

66
Q

What is the pancreatic polypeptide?

A

Inhibits exocrine hormone secretion, gallbladder contraction, gastric acid secretion, and gastric motility

67
Q

What is the classic triad of diabetes?

A

Polyuria
Dehydration
Polydipsia

68
Q

Type 1 vs 2 diabetes? Causes?

A

1 - no insulin production (autoimmune)
2 - lack of insulin plus resistance (obesity)

69
Q

What is DKA? More common?

A

Usually caused by an infection in type 1

Not enough insulin puts the body into ketosis

Patient is hyperglycemia but cells are staved

Metabolic acidosis causes Kussmaul respirations

Acetone causes fruity breath

70
Q

Treatment for DKA?

A

Volume
Insulin + potassium

71
Q

What is HHS? More common?

A

Type 2 with hyperglycemia > 600

Metabolic acidosis, dehydration, hypovolemia

NO ANION GAP

72
Q

Long term side effects of DM?

A

Neuropathy
Retinopathy
Nephropathy
CAD
PAD
Cerebrovascular disease
Stiff joints
Poor wound healing
Cataracts
Glaucoma

73
Q

How does DM affect the ANS?

A

Painless MI
Reduced vagal tone
Dysrhythmias
Orthostatic hypotension
Delayed emptying
Impaired thermoregulation
Diarrhea

74
Q

What is the prayer sign?

A

DM cause glycosylation of joints which causes stiff joints

Increased difficult intubation

75
Q

MOA of biguanides? Example? Key facts?

A

Metformin - Inhibits gluconeogenesis

Does not cause hypoglycemia
Risk of metabolic acidosis
Used in polycystic ovarian disease

76
Q

MOA of sulfonylureas? Example? Key facts?

A

Stimulate secretion of insulin from beta cells

Glipizide, glimepiride, glyburide

Risk of hypoglycemia, avoid in sulfa allergies

77
Q

MOA of meglitinides? Example? Key facts?

A

Stimulate secretion of insulin from beta cells

Repaglinide, Nateglinide

Risk of hypoglycemia

78
Q

MOA of thiazolidinediones? Example? Key facts?

A

Decrease insulin resistance

Rosiglitazone, Pioglitazone

Does not cause hypoglycemia

BLACK BOX WARNING FOR CHF

79
Q

MOA of glucagon like peptide 1 receptor agonists? Example? Key facts?

A

Increases insulin from beta cells, decreases gastric emptying, decreases glucagon from alpha cells

Liraglutide, exenatide

Risk for hypoglycemia

80
Q

MOA of dipeptidyl-peptidase-4 inhibitors? Example? Key facts?

A

Increases insulin from beta cells, decreases glucagon from alpha cells

Suffic - liptin

Risk for hypoglycemia

81
Q

MOA of amylin agonists? Example? Key facts?

A

decreases gastric emptying, decreases glucagon from alpha cells

Pramlintide

N/V
Hypoglycemia
Does not alter insulin levels

82
Q

Insulin Table

A
83
Q

Risks, presentations, and treatment of hypoglycemia

A

highest risk if insulin given during fasting

S/sx : SNS stimulation

Hard to diagnose

Possible delayed emergence

Rebound hyperglycemia

D50 or glucagon

84
Q

Association between insulin and allergic reactions?

A

Not as common now

*NPH AND FISH ALLERGY MAY SENSITIZE PATIENT TO PROTAMINE

85
Q

Which drugs counter hypoglycemia effect of insulin?

A

Epi
Glucagon
Cortisol

86
Q

Which drugs extend or enhance hypoglycemia of insulin?

A

MAOI
Salicylates
Tetracyclines

87
Q

What is carcinoid syndrome?

A

Secretion of vasoactive substances from enterochromaffin cells

GI tract or lungs

Release - histamine, serotonin, kinins, kallikrein

88
Q

Carcinoid tumor

A
89
Q

Most common s/sx of carcinoid tumor?

A

Flushing and diarrhea

90
Q

Most common s/sx of carcinoid crisis?

A

tachycardia
Hyper.hypotension
Flushing
Abd pain
Diarrhea

91
Q

How is carcinoid crisis treated?

A

Somatostatin
Antihistamines
5-HT3 antagonists
Steroids
Phenyl or vaso

92
Q

Which should be avoided in carcinoid crisis?

A

Histamine releasing drugs
Succ
Exogenous catecholamines
Sympathomimetic agents (ketamine, ephedrine)

93
Q
A