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PANCE review COPY > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Cushing’s disease vs Cushing’s syndrome

A

The disease is the most common cause of Cushing’s syndrome

Disease is ACTH-secreting pituitary adenoma that causes increase in cortisol

Syndrome is hypercortisol state

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2
Q

Causes of Cushing’s Syndrome

A

Cushing’s disease (pituitary adenoma, most common cause)
Chronic steroid use
Adrenal tumor
Ectopic production by ACTH-secreting tumor (often small lung cell carcinoma)

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3
Q

Patients most commonly affected by Cushing’s Syndrome

A

premenopausal women

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4
Q

Hallmark findings of Cushing’s Syndrome

A 
buffalo hump
moon face
proximal muscle weakness
pigmented striae
obesity - centrally located with skinny limbs
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5
Q

Best lab to dx Cushing’s Syndrome

A

24 hr urine for free cortisol

> 125 is diagnostic

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6
Q

How does overnight dexamethasone suppression test help dx Cushing’s Syndrome?

A

Distinguishes pituitary vs ectopic cause of cortisol elevation

Patient gets 1 mg of dexamethasone at 12pm. 8am plasma ACTH measured

Pituitary tumor (Cushing's Disease) - low ACTH; negative feedback
Ectopic tumor - no ACTH change
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7
Q

How is Cushing’s Disease treated?

A

transsphenoidal resection with hydrocortisol replacement, but if tumor cannot be removed chemo or radiation therapy useful

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8
Q

How is Cushing’s Syndrome treated?

A

Metyrapone and Ketoconazole may suppress hypercortisolism

Parenteral octreotide may suppress ACTH

Often patients treated for Cushing’s syndrome will go into cortisol withdraw and require steroid tapering therapy with hydrocortisone or prednisone

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9
Q

Clinical findings of Addison’s Disease

A

Sparse axillary and pubic hair
Hyperpigmentation of skin, esp. creases or pressure areas (waist band/bra line)
Hypotension and small heart

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10
Q

What chemicals/lytes are low in Addison’s Disease? which are elevated?

A

Low – Na and glucose

Elevated – K+, Ca2+ and BUN

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11
Q

Diagnostic lab test for Addison’s disease

A

low plasma cortisol and aldosterone with elevated ACTH

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12
Q

Treatment of Addison’s disease

A

Replacement with oral hydrocortisone or prednisone

Fludrocortisone also useful for sodium retention

DHEA may also be given

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13
Q

Difference between pathophysiology of primary and secondary hyperthyroidism

A

Primary hyperthyroidism: problem with thyroid

Secondary hyperthyroidism: problem with pituitary

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14
Q

___________ is the most common cause of hyperthyroidism. It is an autoimmune disease in which the body creates antibodies that bond to the TSH receptors and force excessive T3/T4 production.

A

Graves’ disease

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15
Q

20-40% of patients with Grave’s disease have what findings that can distinguish from other hyperthyroid issues?

A

conjunctivitis
exophthalmos (bulging of eyes)
pretibial myxedema (non-pitting edema of knee)
thyroid bruit

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16
Q

Some of the many symptoms of hyperthyroidism

A

Eyes: stare, lid lag, diplopia
CV: Tachycardia, A-fib, palpitations, chest pain
Skin: Fine hair, warm/moist skin, onycholysis
Mental changes: irritability, Nervousness, fatigue
Heat intolerance, sweating
Weight loss, increased appetite
Hyperreflexia
Goiter

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17
Q

What is a thyroid storm?

A

very rare but severe form of hyperthyroidism

risk factors include stressful illness, thyroid surgery, radioactive iodine treatment

symptoms: fever, tachycardia, vomiting/diarrhea, dehydration, muscle weakness, confusion

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18
Q

How does hyperthyroidism affect TSH, T3, T4

A

TSH decreased (primary) or elevated (secondary)
T4 elevated
T3 elevated

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19
Q

What is specifically elevated in Graves’ disease?

A

anti-TSH receptor antibodies

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20
Q

Radioactive iodine uptake scan results of Graves disease

A

thyroid has increased iodine uptake

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21
Q

First line treatment for acute hyperthyroidism and thyroid storm? Long term control?

A

Acute: beta blockers (especially propanol)

Long term: Methimazole and propylthiourcial (PTU)

Definitive tx: Radioactive iodine ablation

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22
Q

How to treat A-fib of hyperthyroidism?

A

Digoxin

Warfarin to prevent possible clotting

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23
Q

Pathway of T3/T4 production from hypothalamus signaling

A

Hypothalamus → thyroid releasing hormone → pituitary → thyroid stimulating hormone → thyroid → T3 and T4

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24
Q

Why might a patient have hypothyroidism?

A

Thyroiditis
Patient doesn’t have thyroid
Meds: amiodarone, lithium, PTU & Methimazole
Iodine deficiency

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25
Q

Some of the many hypothyroidism symptoms:

A

cold intolerance, puffy face, fatigue, pale/cool skin, thin brittle nails, depression, dementia, weakness, anorexia, constipation, weight gain, bradycardia, hyporeflexia
+/- Goiter

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26
Q

TSH, T3, and T4 levels in hypothyroidism

A
  • TSH elevated (primary) or decreased/normal (secondary)
  • T4 decreased
  • T3 may be normal
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27
Q

Treatment of hypothyroidism

A

Thyroid hormone replacement: Levothyroxine (synthetic T4)

Treatment is for life
Thyroid levels checked yearly
Watch for signs of hyperthyroidism

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28
Q

thyroid storm : hyperthyroidism

__________ : hypothyroidism

A

myxedema

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29
Q

Patients with myxedema will have symptoms of hypothyroid as well as what?

A 
mental changes ranging from confusion to coma
convulsions
hypotension
hypothermia
hypoventilation
rhabdomyolysis and AKI
hyponatremia
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30
Q

Treatment of myxedema

A

IV levothyroxine
intubation prn
slow warming with warm blankets prn

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31
Q

What is Hashimoto’s thyroidits?

A
  • Autoimmune disease causing partial or complete impairment of thyroid gland; hypothyroid sx’s
  • Typically occurs with other autoimmune problems like Sjorgren’s, MG, DM-I, celiac disease, Addison’s, etc.
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32
Q

Clinical presentation of thyroiditis

A

enlarged, firm, nodular thyroid
dysphagia
+/- pain

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33
Q

What condition has increased anti-thyroperoxidase and anti-thyroglobulin antibodies?

A

Hashimoto’s thyroiditis

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34
Q

What imaging is used to differentiate thyroiditis from nodular goiter or malignancy?

A

Thyroid U/S

Radioiodine uptake scan

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35
Q

Why is a fine needle aspiration done for patients with Hashimoto’s or thyroid nodule?

A

significant risk of thyroid cancer

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36
Q

Why is a fine needle aspiration done for patients with suppurative thyroiditis?

A

suppurative thyroiditis is likely bacterial infection, so FNA can be helpful for gram stain and culture

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37
Q

How is postpartum thyroiditis treated?

A

self-limiting

symptomatic treatment prn

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38
Q

How is subacute thyroiditis treated?

A

Aspirin first line for pain and inflammation
Propranolol for hyperthyroid sx’s
Levothyroxine for hypothyroid sx’s

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39
Q

How is Hashimoto’s thyroiditis treated?

A

If patient hypothyroid -> Levothyroxine
If patient has large goiter -> Levothyroxine in effort to shrink goiter

Otherwise monitor for hypothyroid

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40
Q

Which thyroiditis is due to a bacterial infection?

A

Suppurative thyroiditis

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41
Q

How can you tell if Hashimoto’s thyroiditis has Sjogren’s as well?

A

dry eyes
dry mouth

** 33% of Hashimoto’s will also have Sjogren’s syndrome

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42
Q

You believe a patient presenting to you has relatively severe hypothyroidism. You send off a thyroid panel as well as CBC and BMP. What abnormality do you expect to find on BMP?

A

decreased sodium

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43
Q

Different types of thyroiditis

A 
Hashimoto’s - autoimmune issue (most common)
Suppurative - bacterial infection 
Subacute/ de Quervain's - viral
Riedel - fibrous infiltration
Postpartum
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44
Q

3 hormones that regulate calcium levels in the blood?

A

PTH and Vit D increase calcium

Calcitonin decreases calcium

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45
Q

Primary hyperparathyroidism typically caused by what?

A

adenoma in 1 of 4 parathyroid glands

could also be from hyperplasia or carcinoma

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46
Q

What is secondary hyperparathyroidism caused by what?

A

overstimulation of parathyroid glands

  • Chronic renal failure and poor Vit D production which decreases calcium
  • Malignant tumor (breast, lung, pancreas)
  • Calcium deficiency
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47
Q

“moans, (abdominal) groans, stones, and bones” =

A

hyperparathyroidism

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48
Q

What lab value differentiates primary and secondary hyperparathyroid?

A

serum phosphate low in primary and elevated in secondary

both have elevated serum PTH

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49
Q

Because serum calcium is high in hyperparathyroid, what is low?

A

Vit D

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50
Q

Possible XR findings of hyperparathyroid

A

demineralization
subperiosteal bone resorption, especially fingers
cysts of jaw
salt and pepper skull

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51
Q

What is the recommended definitive treatment for symptomatic and some asx hyperparathyroidism?

A
  • parathyroidectomy (94% success rate)

- monitor complications of hypocalcemia with Ca2+ supplements and hyperthyroidism with propranolol

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52
Q

How can one acquire hypoparathyroidism?

A 
*Post thyroidectomy
Heavy metal damage
Low magnesium
Granulomas
Infection
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53
Q

Congenital cause of hypoparathyroidism

A

DiGeorge Syndrome (chrom 22 defect) and other genetic disorders

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54
Q

Acute hypoparathyroid symptoms

A

Irritability
Tetany - involuntary contractions
Carpopedal spasms
Tingling (circumoral, distal extremities)

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55
Q

Chronic hypoparathyroid symptoms

A 
Lethargy
Parkinsonism
Mental retardation
Anxiety
Cataracts
Dry skin, brittle nails
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56
Q

What is Trousseau sign?

A

blood pressure cuff placed around arm and inflated to pressure > systolic BP and held in place for 3 min to occlude brachial artery -> spasm of hand and forearm

observed in patient’s with low calcium

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57
Q

What is Chvostek sign?

A

sign of existing tetany seen in hypocalcemia

facial muscles contract when facial nerve tapped at masseter

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58
Q

What do a positive Trousseau and Chvostek signs indicate?

A

hypocalcemia

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59
Q

What labs values are low in hypoparathyroidism?

A

Serum and urinary Ca
PTH
Magnesium

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60
Q

ECG findings of hypocalcemia

A

prolonged QT

T wave abnormalities

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61
Q

Emergency treatment of hypoparathyroidism

A

Airway maintenance

IV calcium gluconate

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62
Q

How is hypoparathyroidism managed long term?

A

Calcium and Vit D supplements
Magnesium if appropriate
Close monitoring of calcium

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63
Q

What is pseudohypoparathyroidism?

A

patient makes enough PTH, but receptors don’t respond

presents just like hypoparathyroidism except PTH is elevated

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64
Q

Non-surgical treatment of hyperparathyroidism and high calcium

A

Fluids!!!! (1st line if extremely high Ca levels)
IV Bisphosphonates
Cinacalcet (calcimimetic)
Vit D
Estrogen to decrease Ca in postmenopausal woman
Propranolol to protect heart from elevated Ca

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65
Q

What is the most common and least aggressive type of thyroid cancer?

A

papillary carcinoma (80%)

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66
Q

What is the second most common thyroid cancer that is more aggressive and may secrete enough T4 to cause thyroid storm?

A

Follicular thyroid cancer

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67
Q

Thyroid cancer that may be associated genetics or MEN type 2

A

Medullary thyroid cancer

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68
Q

What characteristics of thyroid suggest malignancy?

A

single palpable nodule
painless neck swelling

may cause dysphagia, hoarseness, dyspnea, or hyperthyroid sx’s

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69
Q

How are suspicious thyroid nodules diagnosed?

A

Fine needle aspiration

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70
Q

TSH and T4 are normal in all thyroid cancers except for _______.

A

follicular cancer; produces excess T4 which suppresses TSH

71
Q

Best to image metastasis in lungs with _____ and metastasis in bone with _____.

A

CT

MRI

72
Q

Treatment of thyroid cancer

A

Total or near total thyroidectomy
Neck dissection and lymph node removal if indicated

Post op:
Levothyroxine (synthetic T4) if thyroidectomy
Radioactive iodine ablation for residual dz, metastatic dz and to prevent recurrence

Monitor with whole body radioactive iodine scans and monitor TSH for levothyroxine dose

73
Q

Which type of thyroid cancer is least common but most aggressive?

A

anaplastic

74
Q

How is thyroid cancer remission defined?

A

Two consecutive negative whole body radioisotope scans

75
Q

Leading cause of blindness in U.S.

A

diabetes

76
Q

Type I DM is secondary to autoimmune disease affecting what in body?

A

islet beta cells of pancreas, so patient can’t produce enough insulin

77
Q

What gene is a risk factor for DM-I?

A

HLA

78
Q

Signs of DKA

A

N/V
polyuria and polydipsia
change in mental state
fruity breath

79
Q

Clinical findings of Type 1 DM

A 
Signs of ketoacidosis
Weight loss despite normal diet
Blurry vision
Poor wound healing
Acanthosis nigricans
Neuropathy
80
Q

Ways to dx diabetes

A

1) fasting blood glucose levels >126 mg/dL on more than one occasion
2) non-fasting blood glucose of >200 mg/dL
3) oral glucose tolerance; fasting patient consumes 75 g oral glucose and 2 hrs later glucose level > 200 mg/dL

81
Q

What is hemoglobin A1c? What is normal?

A

indicates sugar levels over previous 3 months and is used for monitoring glucose control

Normal is 3.8-6.3%

82
Q

Diet and Education for diabetes management

A

Increase fiber and complex carbs
Monitor carb intake
Monitor glucose
Eat snacks and meals at regular intervals

83
Q

Examples of rapid acting insulin

A

Lispro, Humalog, Novolog

84
Q

Onset, peak, and effective duration of rapid acting insulin?

A

Onset: 5-15 minutes
Peak: 1-1.5 hours
Duration: 3-4 hours

85
Q

Examples of short acting insulin

A

Human Regular

86
Q

Onset, peak, and effective duration of short acting insulin?

A

Onset: 30-60 minutes
Peak: 2 hours
Duration: 6-8 hours

87
Q

Examples of intermediate acting insulin

A

Human NPH (Neutral protamine hagedorn) and Lente

88
Q

Onset, peak, and effective duration of intermediate acting insulin?

A

Onset: 2-4 hours
Peak: Flat
Duration: about 24 hours

89
Q

Examples of long acting insulin

A

Lantus, Ultralente

90
Q

Onset, peak, and effective duration of long acting insulin?

A

Onset: 30-180 minutes
Peak: Lantus no peak, Ultralente 10-20hrs
Duration: 20-36 hrs

91
Q

Which type of insulin is used before meals?

A

Short acting insulin, Human Regular

92
Q

Which insulin is typically two doses daily and used in conjunction with a short acting insulin?

A

Intermediate acting insulin, Human NPH

93
Q

What are routine exams all diabetic should have?

A

Regular visits to podiatrist for foot care

Regular diabetic eye exams

94
Q

How many units of regular or Lispro insulin should be used based on carbs eaten?

A

1 unit for every 10-15 grams

95
Q

How does DM-2 present differently than DM-1?

A 
dx'd later in middle age or later
insidious onset (usually asx)
abdominal obesity
functioning pancreas that produces insulin, but receptors and tissues do not respond (insulin resistance)
96
Q

Type of neuropathy in diabetes

A

stocking-glove distribution

97
Q

What races are more susceptible to DM-2?

A

African American, Hispanic, Pima Indians

98
Q

Lipid panel changes in DM-2?

A

Elevated triglycerides 300-400 mg/dl

Low HDL

99
Q

Most common drug class used to stimulate insulin secretion

A

sulfonylureas (glypburide, glipizede, glimepiride)

100
Q

First line therapy for DM-2

A

Metformin

101
Q

Meds that lower glucose? How?

A

Metformin – reduces hepatic glucose production

alpha-Glucosidase inhibitors (Acarbose)– decrease carb absorption from intestines

102
Q

Thiazolidinediones MOA for treating DM-2

A

increase tissue sensitivity to insulin

ex: rosiglitazone and pioglitazone

103
Q

Treatment of DM-1

A

NEED INSULIN

104
Q

Treatment of DM-2

A

1) Diet and exercise to improve insulin resistance
2) Oral meds: Metformin 1st line; others are sulfonylureas, alpha-glucosidase inhibitors, thiazolidinediones
3) Insulin therapy

105
Q

Patients with metabolic syndrome are at higher risk for what?

A 
DM 2
Elevated triglycerides
Lower HDL
Elevated LDL
HTN
Blood clots
Atherosclerosis
106
Q

What is clinical definition of metabolic syndrome?

A

3 or more of following:

BP > 130/85
Fasting glucose > 100
Waist circumference
- M > 40 inches
- W > 35 inches
Low HDL
- M less than 40
- W less than 50
Triglycerides > 150
107
Q

What is postprandial hypoglycemia?

A

blood sugar drop after eating

Early = 2-3 hours after
Late = 3-5 hours after
108
Q

Causes of hypoglycemia

A 
Exogenous insulin overdose
Insulinoma
Addison’s disease (hypopituitarism) 
Renal failure
Liver problem
Glycogen storage
Alcohol related
109
Q

How can alcohol cause hypoglycemia?

A

Liver problems
Alcohol inhibits gluconeogenesis
N/V – gastritis

110
Q

How does Addison’s disease cause hypoglycemia?

A

hypopituitarism -> adrenal insufficiency -> low cortisol

no cortisol to break down glycogen in liver into glucose and no cortisol to convert fats, proteins, and carbs into glucose

111
Q

Clinical presentation of hypoglycemia

A 
Often symptoms occur after missing a meal
Sweating
Palpitations
Anxiety
Blurred vision
Weakness
Light headed
Slurred speech
Loss of consciousness
112
Q

Clinical definition of hypoglycemia

A

low blood sugar below 70 mg/dl

113
Q

What blood sugar levels can cause someone to lose consciousness?

A

about 50 mg/dl

114
Q

Whipples Triad

A

1) history of hypoglycemia
2) low serum glucose at time of event
3) immediate recovery on administration of glucose

suggest a patient’s symptoms are due to hypoglycemia; or may indicate insulinoma

115
Q

How to treat hypoglycemia based on cause?

A

Exogenous insulin overdose – eat a cookie :)
Insulinoma – surgically resect if possible
Postprandial hypoglycemia – small meals every 2-3 hours
Addison’s – oral steroid

116
Q

What is ACTH? and what does it do?

A

adrenocorticotropic hormone; stimulates increased production and release of corticosteroids by adrenal glands

117
Q

What are hormones released by posterior pituitary? What are their functions?

A

ADH (antidiuretic, vasopressin) – increases water absorption in kidneys
Oxytocin – increases uterine contractions, milk release

118
Q

Pathophysiology of acromegaly

A

usually a pituitary adenoma which secretes excess GH

119
Q

Acromegaly vs Gigantism

A

excess GH during child before epiphyses closure -> Gigantism

excess GH as adult after epiphyses closure -> Acromegaly

120
Q

____ levels 5x higher than normal in Acromegaly and Gigantism.

A

IGF-1

121
Q

MRI will show _________ in about 90% of patients with Acromegaly.

A

pituitary adenoma

122
Q

Treatment of Acromegaly and Gigantism

A

Primary treatment is trans-sphenoidal resection of pituitary adenoma

Dopamine agonist (Cabergoline) to help normalize GH
Somatostatin analog (Octreotide, Lanreotide acetate)
GH receptor antagonist (Pegvisomant)
123
Q

Diabetes insipidus is a deficiency in what?

A

ADH

124
Q

Signs of Diabetes Insipidus

A

THIRSTY!!! 2-20 Liters per day

Polyuria

125
Q

What is the vasopressin challenge test and how does it help determine cause of DI?

A

Urine volume for 12 hours
Desmopressin acetate is given
Urine volume over next 12 hours

if urine volume improves with Desmopressin then pituitary or hypothalamus issue = central

if no improvement, kidney tubules = nephrogenic

126
Q

Treatment of diabetes insipidus

A

Central DI (Pituitary/Hypothalamus decreased ADH production)
Desmopressin Acetate
HCTZ

Nephrogenic DI (ADH resistance)
Indomethacin
HCTZ
127
Q

__________ is abnormal mineralization of bones AFTER closing of epiphyseal plates. __________ is abnormal mineralization BEFORE closing of plates.

A

Osteomalacia

Rickets

128
Q

Causes of Rickets

A

Vit D deficiency - sun exposure, nutrition, malabsorption, chronic renal failure

Calcium or phosphate deficiency

Phenytoin – seizure med

129
Q

Location of bone pain in Rickets and Osteomalacia mostly where?

A

pelvis

130
Q

Classic XR findings of Rickets and Osteomalacia

A

Decrease in bone density
Milkman lines
Looser zones

131
Q

Treatment of Rickets and Osteomalacia

A

Ergocalciferol (as Vit D supplement)
Phosphate supplement
Calcium supplement

132
Q

Patient comes in c/o deafness and arthralgia. XR shows bony lesions with hyper-density and bowing. Serum calcium and phosphate normal, but alk phos elevated. Likely dx?

A

Paget’s Disease

133
Q

Paget’s Disease treatment

A

1st line: Oral bisphosphonates (Alendronate, Tiludronate, Risedronate)

IV Bisphosphonates (Zoledronic acid or Pamidronate)

134
Q

Most common cause of secondary hyperthyroidism?

A

pituitary tumor

135
Q

Anti-arrhythmic drug that can cause hyper or hypothyroidism?

A

Amiodarone

“iod” = iodine, thyroid

136
Q

What are 3 zones of the adrenal cortex and what does each secrete?

A

zona glomerulosa - aldosterone
zona fasciculata - glucocorticoids (cortisol)
zona reticularis - sex hormones

137
Q

What does the adrenal medulla secrete?

A

epinephrine and norepinephrine with sympathetic stimulation

138
Q

What stimulates aldosterone secretion from adrenal gland?

A

Hypotension (renin -> angiotensin -> ADH)
Hyperkalemia
Hyponatremia

139
Q

______ prevent angiotensin-stimulated aldosterone release.

A

ACE inhibitors

140
Q

Why is there hyperpigmentation in Addison’s disease?

A

ACTH and MSH (melanocyte stimulating hormone) share common precursor POMC

When ACTH increases so does MSH

141
Q

Aldosterone production in primary and secondary adrenal insufficiency

A

Primary - aldosterone and cortisol decrease since whole adrenal gland not working

Secondary - aldosterone normal since its stimulate by RAAS; only cortisol decreases

142
Q

Over-secretion of epinephrine occurs in __________.

A

pheochromocytoma

143
Q

Location of tumors of MEN 1

A

3 P’s: parathyroid, pituitary, pancreas

144
Q

What does MEN stand for?

A

= multiple endocrine neoplasia

145
Q

Which endocrine hormone is not regulated by the pituitary?

A

PTH; secretes from parathyroid in response to low calcium

146
Q

How does PTH increase calcium?

A
  • stimulates osteoclasts to break down bone
  • increases reabsorption of calcium by kidneys
  • decreases reabsorption of phosphate by kidneys
  • increases conversion of inactive Vit D to active form (absorption of calcium in GI tract)
147
Q

PTH and Vit D effects on phosphate levels

A

Vit D increases serum phosphate

PTH decreases serum phosphate

148
Q

How does calcitonin decrease calcium levels?

A

secreted by thyroid when calcium blood levels high

increases bone absorption of calcium and decreases renal absorption of calcium

149
Q

Serum and urine findings in primary hyperparathyroidism

A

Serum: calcium and PTH high, phosphate low

Urine: calcium, phosphate, and cAMP high

150
Q

Pathologies that cause elevated Vitamin D

A

TB, sarcoidosis, lymphoma, Milk-Alkali syndrome

151
Q

How does elevated PTH affect Vit D?

A

increase conversion of 25-vit D to 1,25-vit D = increased Vit D

152
Q

How does elevated Vit D affect PTH?

A

increased Ca2+ = decreased PTH

153
Q

What is DiGeorge Syndrome?

A

congenital absence of parathyroids and thymus

154
Q

Causes of Vitamin D deficiency

A

decreased UV exposure
inadequate dietary intake
malabsorption
liver or renal disease

155
Q

What is Hungry Bone Syndrome?

A

sudden decrease in PTH after hyperparathyroid treatment causes bones to be “hungry” for calcium

156
Q

How do calcium levels affect ECG readings?

A

high calcium shortens QT

low calcium prolongs QT

157
Q

Hormone/chemical issues that cause osteoporosis

A

low estrogen
high cortiso
low calcium/Vit D

158
Q

Genetic pathology with osteoclast dysfunction and uncontrolled bone formation?

A

Osteopetrosis

159
Q

Hormones released by anterior pituitary?

A

“FLAT PEG”

FSH
LH
ACTH
TSH
Prolactin
* Endorphins
GH
160
Q

The pituitary gland sits beneath the ________ attached to the brain.

A

optic chiasm

161
Q

Why is GH level not a reliable dx test? What is measured instead?

A

GH has pulsatile release

IGF-1 used instead (stimulated by GH)

162
Q

Dx tests for suspected GH-secreting tumor?

A

IGF-1 level

Glucose challenge test (high glucose normally decreases GH)

163
Q

How is prolactin secretion controlled?

A

dopamine released from hypothalamus inhibits prolactin release from anterior pituitary until postpartum when high estrogen levels stimulate its secretion for lactation

164
Q

Sheehan’s syndrome

A

postpartum hemorrhage in mother results in hypovolemia and subsequent pituitary damage (hypopituitarism)

165
Q

Effects of insulin and glucagon on blood sugar levels

A

Insulin: glucose into cell (lowers sugar)

Glucagon: glucose to blood (raises sugar)

  • “Is your glucose gone? Get glucagon!”
  • INsulin sugar goes IN
166
Q

What other hormones, apart from glucagon, raise blood sugar levels?

A

cortisol
GH
Nor/epinephrine

167
Q

How does insulin reduce glucose levels?

A

increases glycogenesis (glycogen storage) and glycolysis (glucose breakdown)

168
Q

How does glucagon lower glucose levels?

A 
decreases glycolysis
increases gluconeogenesis (glucose formation) and glycogenolysis (glycogen breakdown into glucose)
169
Q

cosyntropin (ACTH) stimulation test =

A

Addison’s

170
Q

dexamethasone suppression test =

A

Cushing’s Syndrome

171
Q

vasopressin challenge test =

A

Diabetes Insipidus

172
Q

Side effects of Methimazole

A

rash
agranulocytosis
lupoid hepatitis
renal failure

173
Q

PTU instead of Methimazole in what patients?

A

pregnancy

PANCE review COPY (18 decks)

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