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ENDO 2 Exam I (2017) > Phys Review > Flashcards

Phys Review Flashcards

1
Q

Hypothalamus secretes

A 
TRH (thyrotropin-releasing hormone)
CRH (corticotropin-releasing hormone)
GnRH
GHRH
Somatostatin
Dopamine
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2
Q

Anterior Pituitary secretes

A 
TSH
FSH (follicle stimulating hormone)
LH
ACTH
MSH (melanocyte stimulating hormone)
Growth Hormone
Prolactin
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3
Q

Posterior pituitary secretes

A

Oxytocin

ADH

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4
Q

Thyroid secretes

A

T3, T4 (thyroxine)

Calcitonin

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5
Q

Parathyroid secretes

A

PTH

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6
Q

pancreas secretes

A

insulin, glucagon

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7
Q

adrenal medulla secretes

A

norepi

epi

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8
Q

Kidney secretes

A

Renin

1,25 dihydroxycholecalciferol

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9
Q

adrenal cortex secretes

A

cortisol, aldosterone, adrenal androgeens

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10
Q

testes secrete

A

testosterone

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11
Q

ovaries secrete

A

estradiol

progesterone

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12
Q

corpus luteum secretes

A

estradiol

progesterone

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13
Q

placenta secretes

A

hcg
estriol
progesterone
hpl (human placental lactogen)

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14
Q

a positive feedback hormone loop

A

action of estrogen on LH release during midcycle

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15
Q

which hormones use nuclear receptors?

A

thyroid and steroid

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16
Q

differences between lipid-soluble and water-soluble hormones

A

Lipid soluble:
intracellular receptors, stimulates synthesis of new proteins, synthesized s needed, transported attached to proteins that serve as carriers, long half-life

water-soluble:
receptors on outer surface of membrane, –> production of 2nd messengers that modify action of intracellular proteins, stored in vesicles, sometimes as prohormone, transported dissolved in plasma (free, unbound), short half-life

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17
Q

Measurement of Hormone Levels- Plasma analysis:

A

Reflective only of time of sampling
Pulsatile secretion, diurnal variation, cyclic variation, age, sleep entrainment, hormone antagonism, hormone and metabolite interaction, and protein binding can all cause variation in hormone levels

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18
Q

Measurement of Hormone Levels- Urine analysis:

A

Restricted to the measurement of catecholamines and steroid hormones
Can reflect an integrated sample

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19
Q

primary, secondary, and tertiary conditions with thyroid hormone levels

A

3o- hypothalamic failure– TRH, TSH, and T3/T4 are down

2o- pituitary failure- TRH is up, TSH and T3/ T4 are down

1o- thyroid dysfunction: thyroidities- TRH and TH are up, T3/T3 are down
Grave’s disease- TRH and TSH are down, T3/T4 are up

Tissue unresponsiveness- e.g. mutation in thyroid hormone receptor

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20
Q

ADH

A

(posterior pitutitary)
Function is to maintain normal osmolality of body fluids and normal blood volume
Released in response to increased serum osmolality
Works on principle cells of the distal tubule to increase water resorption
Induces contraction of vascular smooth muscle to protect against severe volume depletion

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21
Q

Oxytocin

A

Milk letdown

Uterine contraction

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22
Q

ADH Action on the Kidney

A

ADH increases expression of aquaporin 2 on the luminal side of principal cells
Water flow from the lumen to the renal interstitium is increased
ADH decreases urine flow and urine osmolality ↑
In the absence of ADH urine flow increases and osmolality ↓

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23
Q

Diabetes Insipidus (DI)

A

Characterized by a large volume of urine (diabetes) that is hypotonic, dilute, and tasteless (insipid)

  • Neurogenic (hypothalamic or central)- unregulated ADH
  • Nephrogenic- unresponsiveness to ADH
  • Transient
  • Primary polyuria- increased water intake due to pathologic, habitual, or psychiatric syndromes

Distinguish if polyuria is due to an increase in an osmotic agent (i.e. glucose) or due to renal disease

Diagnosis of DI confirmed by dehydration stimulus followed by the inability to concentrate urine

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24
Q

Neurogenic vs Nephrogenic diabetes insipidus

A

plasma ADH is normal to high in nephrogenic, low in neurogenic

after water deprivation, plasma ADH goes up in nephrogenic, but not in neurogenic

urine osmolality goes up in neurogenic after ADH administraion but not in nephrogenic

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25
Q

things that stimulate growth hormone

A 
decreased glucose concentration
decreased free fatty acid concentration
arginine
fasting or starvation
hormones of puberty (etrogen, testosterone)
exercise
stress
stage III and IV sleep
alpha-adrenergic agonists
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26
Q

things that inhibit growth hormone

A 
increased glucose concentration
increased free fatty acid concentration
obesity
senescence
somatostatin
somatomedins
growth hormone
beta-adrenergic agonists
pregnancy
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27
Q

Summary of GH Actions

A 
1. Diabetogenic effect- causes insulin resistance
	↓ glucose uptake
	↑ blood glucose levels
	↑ lipolysis
	↑ blood insulin levels
  1. Increased protein synthesis and organ growth (through the actions of IGF-I)
    ↑ amino acid uptake
    ↑ DNA, RNA, protein synthesis
    ↑ lean body mass and organ size
  2. Increased linear growth (through the actions of IGF-I)
    Altered cartilage metabolism
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28
Q

prolactin induces

A

dopamine synthesis

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29
Q

factors stimulating prolactin

A 
pregnancy (estrogen)
breast-feeding
sleep
stress
TRH
dopamine antagonists
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30
Q

factors inhibiting prolactin

A

dopamine
bromocriptine (dopamine agonist)
somatostatin
prolactin (negative feedbac)

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31
Q

pulsatile vs continuous infusion of GnRH

A

pulsatile secretion of GnRH prevents downregulation
of its receptors, a constant infusion will cause a decrease
in LH and FSH.

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32
Q

Steps in Thyroid Hormone Synthesis

A

Synthesis of thyroglobulin (TG) and exocytosis to the lumen
Transport of I- into cell- against chemical and electrochemical gradients
Oxidation of I-* - thyroid peroxidase
Organification of iodine into MIT and DIT; MIT = monoiodothyronine, DIT = diiodothyronine
Coupling reaction; DIT + DIT = T4, DIT + MIT = T3
Endocytosis of TG
Proteolysis of iodinated thyroglobulin; releases T3 and T4
Deiodination of residual MIT and DIT; recycling of I- and TG

  • Inhibited by propylthiouracil (PTU)
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33
Q

Transport and Deiodination of Thyroid Hormone

A

T4 and T3 circulate bound to thyroid-binding globulin (TBG) and to a lesser extent albumin and transthyretin (TTR)
TBG buffers hormone levels in the blood
99.98% of T4 is bound in circulation and 99.5% of T3 is bound
T3 is the more active thyroid hormone as it has a higher affinity for thyroid receptor (10 fold); however the ratio of T4 to T3 is 10:1
Tissues contain deiodinases to convert T4 to T3
People without thyroid function will have T3 upon treatment with T4 only

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34
Q

Normal levels of thyroid hormone

A

Total T4 5-12 μg/dL

T3 70-190 ng/dl

35
Q

Euthryoid sick syndrome

A

is characterized by hypothyroidism but the root of the problem does not lie in the thyroid or pituitary. Instead, severe illness is believed to increase the levels of diiodinase D3 which results in the formation of inactive rT3.

36
Q

things that stimulate thyroid hormone

A

TSH
thyroid-stimulating immunoglobulins
increased TBG (thyroid-binding globulin) levels (e.g. pregnancy)

37
Q

things that inhibit thyroid hormone

A

I- deficiency
deiodinase deficiency
excessive I- intake (Wolff-Chaikoff effect)
Perchlorate: thiocyanate (inhibit Na+-I- cotransport)
Propylthiouracil (inhibits peroxidase enzyme)
decreased TBG levels (e.g. liver disease)

38
Q

Summary of Thyroid Hormone Actions

A

nuclear receptor–> transcription of DNA–> translation of mRNA–> synthesis of new proteins that do the following:

growth formation, bone maturation

maturation of CNS

increases Na+-K+ ATPase, O2 consumption, heat production, BMR

increases glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, protein synthesis and degradation (net catabolic)

increases cardiac output

39
Q

Thyrotoxicosis- Associated with Hyperthyroidism

A

** TSH will be down compared to normal

  1. Grave’s disease- autoimmune thyroid disease (0.5% of population)
  2. Factitious thyrotoxicosis- exogenous thyroid hormone with gland atrophy and low thyroglobulin
  3. Toxic adenoma “hot nodule”- overproduction of thyroid hormone by the nodule with low TSH and gland atrophy surrounding the nodule
  4. Toxic nodular goiter (toxic multinodular goiter)
  5. Pituitary overproduction of TSH- rare
  6. Granulomatous thyroiditis (* subacute thyroiditis) (viral in etiology) with painful gland
    Hyperthyroidism→ euthyroidism→ hypothyroidism→ euthyroidism
  7. Subacute lymphocytic thyroiditis (silent thyroiditis) (believed to be autoimmune in etiology) with non-tender gland- transient
    Example is postpartum thyroiditis
40
Q

Hypothyroidism

A

Points of interruption

  • Thyroid gland- primary
  • Pituitary- secondary
  • Hypothalamus- tertiary
  • Tissue resistance- rare

Primary

  • Hashimoto’s (5-10% of population)- T cell-mediated but antibodies can also be present (α-TPO)
  • Radioactive ablation of the thyroid

Secondary
- Pituitary insufficiency

Tertiary
- Hypothalamic disease

41
Q

Adrenal gland zones and hormones

A

Capsule

Zona Glomerulosa- Aldosterone (controlled by Ang II, K+)
Zona fasciculata cortisol . (controlled by ACTH)
Zona reticularis- androgens (controlled by ACTH)

Medulla- epinephrine (controlled by ANS)

42
Q

aldosterone is regulated by

A

angiotensin II and potassium levels. The consequence of this control mechanism is that aldosterone and pressure-volume regulation is typically normal in individuals who have hypopituitarism.

43
Q

if 21-alpha-hydroxylase is absent

A

an excess of androgens will be present with an absence of glucocorticoids and mineralocorticosteroids.

44
Q

the absence of 17-alpha-hydroxylase will cause

A

an increase in mineralocorticosteroids but an absence of androgens.

45
Q

factors stimulating cortisol secretion

A 
decreased blood cortsol levels
sleep-wake transition
stress; hypoglycemia; surgery; trauma
psychiatric disturbances
ADH
alpha adrenergic agonists
beta-adrenergic antagonists
serotonin
46
Q

factors inhibiting cortisol secretion

A

increased blood cortisol levels
opioids
somatostatin

47
Q

actions of glucocorticoids

A

essential for survival during fasting- increase protein catabolism, decrease protein synthesis, increase lipolysis, decrease glucose utilization by tissues- net result is an increase in glucose synthesis

48
Q

actions of mineralocorticoids

A

increase Na reabsorption
increase K+ secretion
increase H+ secretion

49
Q

acute release of cortisol –>

A

metabolic responses to stress ensure sufficient energy to meet increased demand
maintain blood glucose levels necessary for consciousness
also contributes to providing energy for the incipient inflammatory and immune response
but also protects individual from potential damage of unregulated inflammation

50
Q

Response to Chronically Elevated Cortisol

A

(e.g. Cushing’s disease)
–> localized obesity (ab, neck, face)
muscle wasting and weakness, esp. at extremities
usually occurs in context of elevated insulin/ glucagon ratio
high cortisol antagonizes insulin’s effect on GLUT-4 in skeletal muscle and adipose tissue –> glucose intolerance –> hyperglycemia and hyperinsulinemia

51
Q

Addison disease

A

(primary adrenocortical insufficiency)

features: 
Hypoglycemia
Anorexia, weight loss, nausea, Vomiting
Weakness
Hypotension
Hyperkalemia
Metabolic acidosis
Decreased pubic and axillary hair in females
Hyperpigmentation

ACTH levels: increased

treatment: replace glucocorticoids and mineralocorticoids

52
Q

Cushing syndrome

A

(e.g., primary adrenal hyperplasia)

features:
Hyperglycemia
Muscle wasting
Central obesity
Round face, supraclavicular fat, buffalo hump
Osteoporosis
Striae
Virilization and menstrual disorders in females
Hypertension

ACTH levels- decreased

treatment: ketoconazole, metyrapone

53
Q

Cushing disease

A

(excess ACTH)

features- same as cushing syndrome

treatment: surgical removal of ACTH-secreting tumor

54
Q

Conn syndrome

A

(aldosterone-secreting tumor)

features: 
Hypertension
Hypokalemia
Metabolic alkalosis
Decreased renin levels

treatment: aldosterone antagonist (e.g. spironolactone), surgery

55
Q

21β-hydroxylase Deficiency

A

features:
Virilization in females
Early acceleration of linear growth
Early appearance of pubic and axillary hair
Symptoms of deficiency of glucocorticoids and mineralocorticoids

ACTH levels: increased
treatment: replace glucocorticoids and mineralocorticoids

56
Q

17α-hydroxylase Deficiency

A

features:
Lack of pubic and axillary hair in females
Symptoms of deficiency of glucocorticoids
Symptoms of excess mineralocorticoids

ACTH levels: increased

treatment: replace glucocorticoids, aldosterone antagonist (e.g. spironolactone)

57
Q

approach to dx cushing syndrome

A
  1. exclude exogenous steroid use
  2. overnight DST OR late-night salivary cortisol OR 24-hour urine free cortisol

positive?

  1. Confirm with 1-2 additional studies.

–> if positive, confirmed

58
Q

hormones of endocrine pancreas

A

insulin (most)
glucagon (some)
somatostatin (5%)

59
Q

actions of insulin

A

increases glucose uptake into cells and glycogen formation
decreases glycogenolysis and gluconeogenesis
increases protein synthesis and fat deposition
decreases lipolysis
* increases K+ uptake into cells

60
Q

factors stimulating insulin secretion

A 
increased glucose, amino acid, and fatty acid/ ketoacid concentrations
glucagon
cortisol
glucose-depending insulinotrpic peptide
potassium
vagal stimulation; Ach
sulonylurea drugs
obesity
61
Q

factors inhibiting insulin secretion

A 
decreased blood glucose
fasting, exercise
somatostatin
alpha-adrenergic agonists
diazoxide
62
Q

Actions of glucagon

A

increases glycogenolysis, gluconeogenesis, lipolysis, ketoacid formation

63
Q

factors stimulating glucagon secretion

A 
fasting
decreased glucose concentration
increased amino acid concentration (esp. arginine)
cholecystokinin (CCK)
beta-adrenergic agonists
Ach
64
Q

factors inhibiting glucagon secretion

A

insulin, somatostatin, increased fatty acid and ketoacid concentration

65
Q

Total calcium levels are maintained within a narrow range in the blood

A

Hypocalcemic < 8.5 mg/dL (2.1 mM)

Hypercalcemic > 10.5 mg/dL (2.6 mM)

66
Q

Symptoms of hypocalcemia

A

twitching, muscle cramps, tingling and numbness

67
Q

Symptoms of hyercalcemia

A

constipation, polyuria, polydipsia, lethargy, coma, death

68
Q

Changes in albumin levels can

A

change total calcium levels.

Much of the protein-bound calcium is bound by albumin.

69
Q

Effect of Acid-Base Disturbances on Plasma Protein-binding of Ca2+

A

acidemia –> increased ionized calcium in the plasma (H+ kicks it off the albumin)

alkalemia –> decreased ionized Ca in the blood (more spots for it to bind to albumin)

70
Q

Overview of Calcium Regulation

A

3 hormones

  • PTH (increases bone resorption)
  • 1,25-dihydroxyvitamin D (increases digestive absorption of Ca)
  • Calcitonin (decreases bone resoption- TONES the bone)
3 organs
- Skeleton
- Kidney
- Intestines 
Calcium sensor receptor (CaSR)
7 membrane G-protein coupled receptor
Senses extracellular calcium- ionized calcium
Receptor found on parathyroid cells, parafollicular c-cells, and renal tubular cells
71
Q

Four functions PTH

A

Triggers Ca2+, PO43- resorption from bone
Promotes Ca2+ resorption from the kidney
Promotes PO43- excretion from the kidney
Signals 1-hydroxylation of 25-hydroxycholealciferol in the kidney

72
Q

Functions of 1,25-(OH)2-vitamin D

A

Bone remodeling (promotes mineralization)
Ca2+ absorption from gut
Renal resorption of Ca2+ and PO43-

73
Q

high levels of extracellular calcium do what to PTH?

A

suppresses its secretion

74
Q

Bone Remodeling

A

Osteoprotegerin (OPG) acts as a soluble receptor for RANKL and shuts down resorption by osteoclasts

Loss RANKL ↑ bone density (osteopetrosis)
Loss OPG ↓ bone density (osteoporosis)

75
Q

1,25-dihydroxyvitmain D and bone resorption/ deposition

A

1,25-dihydroxyvitmain D is necessary for both bone resorption (acts with PTH) and for bone deposition.

76
Q

Severe vitamin D deficiencies can result in

A

osteomalacia in adults or rickets in children.

77
Q

Synthesis of 1,25-dihydroxyvitamin D

A

7-dehydrocholesterol + UV light–>
cholecalciferol (also from diet)

via liver to

25-OH cholecalciferol

via kidney to 1,25(OH)2 cholecalciferol (active form) or 24,25 inactive form

78
Q

Degree of Vitamin D Deficiency

A

0-10 ng/ml- severe
10-20- moderate
20-30- mild
over 30- normal

79
Q

PTH and Calcium Levels in Disease

A

very high PTH, low Calicum- kidney failure

high PTH and low calcium- vitamin D deficiency

very high calcium low PTH- malignancy

moderately high both- primary hyperparathyroidism

80
Q

Hypercalcemic Disorders

A 
Primary Hyperparathyroidism (increased PTH)
Hypercalcemia of Malignancy
Granulomatous Disease
Vitamin D Intoxication
Vitamin A Intoxication
Hyperthryoidism
Thiazide Diuretics
Milk-Alkali Syndrome
Immobilization
Adrenal Insufficiency
Acute Renal Failure
Familial Hypocalciuric Hypercalcemia
Heterozygous inactivating mutation in the CaSR
increased PTH and serum calcium
81
Q

Causes of Hypocalcemia

A 
Vitamin D Deficiency
Hypoparathyroidism 
Pseudohypoparathyroidism
Genetic disorder causing resistance to PTH
Hypomagnesemia
Renal Failure
Liver Failure
Acute Pancreatitis
Hypoproteinemia
82
Q

Measurement of 25- OH Vitamin D and PTH are the key tests in the differential diagnosis of hypocalcemia

A

PTH levels are low in hypoparathryoidism but normal to high in all other causes
Hypomagnesemia impairs PTH secretion and induces PTH resistance in peripheral tissues
Renal disease and liver disease interfere with vitamin D synthesis
Acute pancreatitis causes precipitation of calcium due to the release of lipid products
Hypoproteinemia will reduced total calcium levels but usually do not cause symptoms of hypocalcemia since levels of ionized calcium are typically not altered

83
Q

remembering the zones of the adrenal gland and what they produce

A

G-F-R glomerulosa, fasciculata, reticularis

Salt-Sugar- Sex
aldosterone- cortisol- androgens

ENDO 2 Exam I (2017) (13 decks)

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