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tsomkapQ > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is Necrosis?

A

Non-programmed cell death. Nucleus destroyed first

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2
Q

What is Apoptosis?

A

Programmed cell death, no inflammation, and cell membrane dissolved first. Nucleus guides death & destroyed last

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3
Q

What is Pyknosis?

A

Nucleus turns into blobs. (shrinkage)

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4
Q

What is Karyorrhexis?

A

Nucleus fragments

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5
Q

What is Karyolysis?

A

Nucleus dissolves

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6
Q

What is a Somatotrope?

A

Growth hormone

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7
Q

What is a Gonadotrope?

A

LH and FSH

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8
Q

What is a Thyrotrope?

A

TSH

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9
Q

What is a Corticotrope?

A

ACTH

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10
Q

What is a Lactotrope?

A

PRL – Prolactin

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11
Q

What receptors do Protein Hormones use?

A

Cell membrane receptors

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12
Q

What receptors do Steroid Hormones use?

A

Nuclear membrane receptors (except cortisol cytoplasmic receptor)

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13
Q

What are the Steroid Hormones?

A

Progesterone, Estradiol (E2), Testosterone, Cortisol, and Aldosterone

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14
Q

What does Endocrine mean?

A

Secreted into bood

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15
Q

What does Exocrine mean?

A

Secreted into a duct

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16
Q

What is Autocrine?

A

Works on itself. (except T-cell activation)

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17
Q

What is Paracrine?

A

Works on its neighbor. (except sweat gland)

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18
Q

What is Merocrine?

A

Cell is maintained. (exocytosis)

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19
Q

What is Apocrine?

A

Apex of the cell is secreted

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20
Q

What is Holocrine?

A

The whole cell is secreted. (except sebaceous gland)

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21
Q

What organs do not require insulin to absorb glucose?

A

“BRICKLE”: Brain, RBC, Intestine, Cardiac / Cornea, Kidney, Liver and Exercising muscle

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22
Q

What is the function of GnRH?

A

Stimulates release of LH & FSH

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23
Q

What is the function of GRH?

A

Stimulates GH release

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24
Q

What is the function of CRH?

A

Stimulates ACTH release

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25
Q

What is the function of TRH?

A

Stimulates TSH release

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26
Q

What is the function of PRH?

A

Stimulates Prolactin (PRL) release

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27
Q

What does Dopamine (DA) do?

A

Inhibits Prolactin (PRL) release

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28
Q

What does Somatostatin (SS) do?

A

Inhibits growth hormone (GH) release

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29
Q

What does Antidiuretic hormone (ADH) do?

A

Conserves water (V2 aquaporin receptors) and vasoconstriction

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30
Q

What does Oxytocin do?

A

Milk letdown and uterine contractions

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31
Q

What does Growth Hormone (GH) do?

A

Stimulates Insulin Growth Factor-1 (IGF-1) release from the liver

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32
Q

What is the function of TSH (Thyroid stimulating hormone)?

A

Stimulates release of T3 and T4 from the thyroid.
T3= Triiodothyronine
T4= Thyroxine

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33
Q

What is the fucntion of LH (Luteinizing hormone)?

A

Stimulates Testosterone release from the testis, Androgens and Progesterone release from the ovary

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34
Q

What is the function of FSH

A

Male: sperm, MIF, inhibin B
Female: Stimulates Estradiol (E2)

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35
Q

What is the function of Prolactin (PRL)?

A

Milk production

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36
Q

What is the function of ACTH (Adrenocorticotropic hormone)?

A

Stimulates Cortisol and Androgen releases from the adrenal gland

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37
Q

What is the fucntion of MSH (melanocyte-stimulating hormones)?

A

Provides skin pigmentation

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38
Q

What are the Stress Hormones and when do they appear?

A

Immediately Epinephrine, Glucagon (20 minutes), Insulin & ADH (30 minutes), Cortisol (2-4 hours), and growth hormone (24 hours)

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39
Q

What is the Primary Diabetes Insipidus (DI)?

A

Too much water (urinates a lot)

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40
Q

What is Central (neurogenic) diabetes insipidus?

A

Brain not making or producing enough ADH

Usually result of pituitary tumor, autoimmune, trauma, or ischemic encephalopathy

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41
Q

What is Nephrogenic diabetes insipidus?

A

Brain producing lots of ADH, but

ADH (V2 aquaporin receptor) is blocked or broken. Lithium association and Demeclocycline

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42
Q

What does the Water Deprivation Test tell you?

A

If the patient fails to concentrate urine, they do not have Primary DI

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43
Q

What does giving DDAVP during the Water deprivation tests tell you?

A

> 50% increase (central complete DI),
10-50% increase (central partial DI),
<10% (psychogenic polydipsia),
no change (nephrogenic DI)

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44
Q

What is SIADH?

A

Too much ADH present causes plasma volume to expand Serum Na+ less than 120

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45
Q

What is the difference between DI and SIADH?

A

DI: diluted urine
SIADH: concentrated urine

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46
Q

What is the Psychogenic Polydipsia?

A

Pathologic water drinking will have low plasma osmolality

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47
Q

What does Aldosterone do?

A

Reabsorbs Na+ and three waters

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48
Q

What does Atrial Natriuretic Peptide do?

A

Inhibits aldosterone and dilates the afferent arteriole

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49
Q

What is a Neuroblastoma?

A

Adrenal medulla tumor in kids, dancing eyes and feet and secretes catecholamine’s

FA333 opsoclonus-myoclonus syndrome (dancing eyes/feet)

50
Q

Whatis Pheochromocytoma?

A

Adrenal medulla tumor in adults, they will have five P’s: Palpitations, Perspiration, Pallor, Pressure (HTN), and Pain (headache)

51
Q

What are the layers of the Adrenal Cortex and what do they produce?

A 
Zona Glomerulosa (Aldosterone),
Zona Fasciculate (Cortisol),
Zona Reticularis (Androgens)
52
Q

What is Conn’s Syndrome?

A

High Aldosterone (primary tumor), Cpatopril test makes it worse, and increase’s secretin hormone

53
Q

What does Calcitonin do?

A

Inhibits Osteoclasts and binds to calcium

54
Q

What is Multiple Endocrine Neoplasia I?

A

“Wermer’s” 3 P’s: Pancreas, Pituitary, Parathyroid adenoma

55
Q

What is Multiple Endocrine Neoplasia II (2A)?

A

“Sipple’s” Pheochromocytoma, Medullary Carcinoma of the Thyroid, Parathyroid Adenoma. (tumor marker RET)

56
Q

What is Multiple Endocrine Neoplasia III (2B)?

A

Pheochromocytoma, Medullary Carcinoma of the Thyroid, Mucosal Neuromas/ Marfanoid body habitus. (tumor marker RET)

57
Q

What does CCK (Cholecystokinin) do?

A

Stimulates bile release and gallbladder contraction, inhibits gastric motility (closes sphincters), and made by I-cell of duodenum

58
Q

What does cortisol do?

A

Gluconeogenesis by proteolysis and thins the skin, prevents and immune response, and decrease bone mass

59
Q

What is Addison’s disease?

A

Autoimmune destruction of adrenal cortex, causes hyperpigmentation (looks tan due to overstimulation of MSH), and increased ACTH
TB most common in developing world

FA332

60
Q

What is Waterhouse-Friderichsen syndrome (WSF) or Hemorrhagic Adrenalitis or Fulminant Meningococcemia?

A

Adrenal hemorrhage most commonly due to Meningococcus Neisseria Meningitides (septicemia)

61
Q

What can cause Cushing’s syndrome?

A

High cortisol produced from an adrenal tumor

62
Q

What is Cushing’s disease?

A

High ACTH due to pituitary tumor or Small cell carcinoma of the lungs

63
Q

When performing a low does dexamethasone test, a depression in ACTH levels occur, what does that tell you?

A

Patient is either depressed, obese, or it’s a normal variant, if the low dose Dexamethasone test does not suppress…

64
Q

When performing a high dose dex. Test, if positive…

A

Patient has a pituitary tumor

65
Q

Negative high dose Dex. and High ACTH levels?

A

Ectopic ACTH- small cell CA of the lungs

66
Q

Negative high dose Dex. and low ACTH levels?

A

Adrenal CA (high cortisol)

67
Q

What are the Survival Hormones?

A

Cortisol: permissive under stress.
TSH: permissive under normal

68
Q

What does epinephrine (Epi) do?

A

Drives gluconeogenesis and glycogenolysis

69
Q

What does erythropoietin (EPO) do?

A

Makes RBC’s (prolong RBC life)

70
Q

What does Gastrin do?

A

Stimulates parietal cells to release intrinsic factor (IF) and H+

FA69
intrinsic factor needed for Vit. B12

71
Q

What does Growth Hormone (GH) do?

A

Stimulates growth, sends Somatomedin to growth plates, Gluconeogenesis by proteolysis

72
Q

What is achondroplasia (Laron Dwarf)?

A

Patient with abnormal FGF receptors in exremities. (abnormal FGF3)

73
Q

What is the receptor problem with Midgets?

A

Patient with decreased Somatomedin receptor sensitivity

74
Q

What is Acromegaly?

A

Growth hormone tumor producing increased IGF-1 causing: bone growth in adults, coarse facial features, large furrowed tongue, deep husky voice, jaw protrusion

75
Q

What is Gigantism?

A

Childhood form of Acromegaly

76
Q

What does Gastric Inhibitory Peptide (GIP) do?

A

Increases insulin action, responsible for post-prandial hypoglycemia

77
Q

What does Glucagon do?

A

Active in Gluconeogenesis, Glucogenolysis, Lipolysis, and Ketogenesis

78
Q

What does Insulin do?

A

Pushes glucose into cells and K+ follows

79
Q

What is Type 1 Diabetes Mellitus?

A

Anti-islet cell antibody /GAD (Glutamic Acid Decarboxylase) antibody.

80
Q

What is Type 2 Diabetes Mellitus and associations?

A

Insulin receptor insensitivity, HONK coma, Acanthosis Nigricans
Hyperglycaemic Hyperosmolar Nonketotic Coma (HONK)

81
Q

How does DKA present?

A

Kussmaul respirations, fruity breath (acetone), and altered mental status

82
Q

What is the Dawn Phenomenon?

A

Morning hyperglycemia secondary to Growth Hormone

hormones that increase insulin resistance that cause blood sugar to rise (GH, glucagon, epi

83
Q

What is the Somogyi Effect?

A

Morning hyperglycemia secondary to evening hypoglycemia

happens when you take insulin before bed and wake up with high blood sugar levels

84
Q

What is factitious hypoglycemia?

A

Exogenous insulin use, labs show elevated insulin and decreased C-peptide

85
Q

What is an Insulinoma?

A

Insulin secreting tumor, labs show increased insulin and C-peptide

86
Q

What is Erythrasma?

A

Rash in the skin folds, coral-red under Wood’s Lamp

87
Q

What is Metabolic Syndrome X?

A

“Pre-DM” due to HTN, Dyslipidemia, Hyperinsulinemia, and Acanthosis Nigricans

88
Q

What are the Foot Ulcer Risk Factors?

A

Poor glycemic control (HbA1C >7), smoking, bony abnormalities, previous ulcers

89
Q

What conditions cause weight gain?

A

Obesity, Hypothyroidism, Depression, Cushing’s, Anasarca (general swelling of the whole body, usually due to abnormal fluid retention in the tissues)

90
Q

What does motilin do?

A

Stimulates segmentation, primary peristalsis, and migrating motor complexes (MMC)

91
Q

What does PTH do?

A

Stimulates osteoblast to activate osteoclasts, stimulates the reabsorption of Ca+ and the excretion of phosphate in the kidneys, and activation of vitamin D

92
Q

What does Vitamin D do?

A

Helps in calcium absorption from the GI tract

93
Q

What do the parathyroid cells secrete?

A

Parathyroid-Hormone

94
Q

What do stomach chief cells secrete?

A

Pepsin (breaks down protein)

95
Q

What is the difference between norepinephrine and epinephrine?

A

NE: Neurotransmitter
EPI: Hormone

96
Q

What diagnosis can be made with primary hyperparathyroidism?

A

Parathyroid Adenoma

97
Q

What diagnosis has secondary hyperparathyroidism?

A

Renal failure

98
Q

What is familial Hypocalciuria Hypercalcemia?

A

Patients with decreased calcium excretion

99
Q

What disease process is present when both Serum Ca2+ and Serum Phosphate (PO4-) are decreased?

A

Vitamin D deficiency

100
Q

What type (primary/secondary) of problem is there if serum Ca2+ and Serum PO4- change in same directions?

A

This is a secondary problem

101
Q

What is the most common cause of primary hypoparathyroidism?

A

Thyroidectomy

102
Q

What is pseudo-hypoparathyroidism?

A

Bad kidney, PTH receptor dysfunction, decreased urinary, cAMP

103
Q

What is pseudo-pseudo-hypoparathyroidsm?

A

G-Protein defect (PTH receptor dysfunction), and there is no calcium problem

104
Q

What is Hungry Bone Syndrome?

A

Removal of PTH and the bone sucks in calcium

105
Q

What does secretin do?

A

Secretion of bicarbonate, inhibit gastrin, tighten Pyloric Sphincter, and secreted by S-cell Duodenum

106
Q

What does somatostatin do?

A

Inhibits secretin, motilin, and CCK

107
Q

What is the function of T3 and T4?

A

Growth and differentiation

108
Q

What disease has exophthalmos?

A

Grave’s disease

109
Q

What other diseases can have exophthalmos?

A

Horner’s and Marfan’s

110
Q

What are the hyperthyroid diseases?

A
  1. Grave’s (overactive thyroid)
  2. DeQuervain’s Thyroiditis (also known as subacute granulomatous thyroiditis or giant cell thyroiditis; hyper first then hypo, following flu like illness)
  3. Silent Thyroiditis (Woman during postpartum period, symptoms are initially hyperthyroidism, then hypo, then generally recover back to normal)
  4. Plummer’s (also called toxic multinodular goitre, due to thyroid enlargement, firm thyroid nodules, and overproduction of thyroid hormone)
  5. Jod-Basedow (hyperthyroidism following administration of iodine)
111
Q

What do you see in Grave’s Disease?

A

Exophthalmos, Pretibial myxedema, anti-TSH receptor antibodies

112
Q

What do you see in DeQuervain’s disease?

A

Viral origin, painful jaw, hypothyroid

113
Q

When do you see silent thyroiditis?

A

Post-partum patients

114
Q

When will you see Plummer’s Disease?

A

Patients with benign adenoma and or patients over 50 yrs. old. In an iodine scan, it looks like a nodular patter

115
Q

What is Jod-Basedow Disease?

A

Transient hyperthyroidism due to increased iodine

patient originally comes in with iodine deficiency, given iodine causes thyrotoxicosis

116
Q

What are the hypothyroid diseases?

A

Hashimoto’s, Riedel’s, Cretinism, Euthyroid SIck syndrome, Wolff-Chaikoff

117
Q

What is Riedel’s Struma?

A

“Woody” connective tissue in neck, death due to suffocation and must rule out CA

118
Q

What is Cretinism?

A

Mom and baby are hypothyroid

119
Q

What is Euthyroid Sick Syndrome?

A

LOW T3 Syndrome and decreased conversion of T4 to T3 (increased T3r)

120
Q

What is Wolff-Chaikoff?

A

Transient hypothyroidism

121
Q

What is Plummer’s Syndrome?

A

Hyperthyroid adenoma

>40% asymmetrical uptake

122
Q

What is Plummer-Vinson Syndrome?

A

Esophageal webs, Iron-deficiency anemia, dysphagia

tsomkapQ (117 decks)

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