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KAPLAN USMLE > KAPLAN - Physiology > Flashcards

KAPLAN - Physiology Flashcards

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USMLE® Step 1 flashcards
1
Q

Arterial blood gases (ABGs) are used in:

A

acid - base disturbances: source for the diagnostic data for determining an acedemia or alkalemia (indicative of underlying acidosis or alkalosis).

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2
Q

Three question method for acid base disturbances.

A
  1. What is the osis? (if pH <7.35, then acidosis, if pH is >7.45, then alkalosis)
  2. What is cause of osis?
  3. Was there compensation?
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3
Q

normal value of pH

A

normal pH = 7.4

normal range of pH 7.35 - 7.45

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4
Q

For respiratory disturbances, what happens?

A

Kidneys alter total bicarbonate

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5
Q

For respiratory compensation, what is compared?

A

Patient’s measure PCO2 verse a calculated (predicted) value.

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6
Q

What is altered in the 4 primary disturbances?

A

altered concentration of H+

Acidosis (excess H+), alkalosis (deficiency of H+)

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7
Q

What are the 4 primary disturbances?

A
  1. respiratory acidosis: too much CO2
  2. metabolic acidosis: addition of H+ (not of CO2 origin and/or loss of bicarbonate from the body
  3. respiratory alkalosis: not enough CO2
  4. metabolic alkalosis: loss H+ (not of CO2 origin) and/or addition of base to body
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8
Q

normal systemic value for pH, HCO3-, PCO2?

A 
pH = 7.4
HCO3- = -24 mEq/L
PCO2 = 40 mm Hg
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9
Q

Acute changes in pH/HCO3- in the 4 primary disturbances?

A
  1. respiratory acidosis: pH: DOWN, HCO3-: UP
  2. metabolic acidosis: pH: UP, HCO3-: DOWNDOWN
  3. respiratory alkalosis: pH: UP, HCO3-: DOWN
  4. metabolic alkalosis: pH: UP, HCO3-: DOWNDOWN
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10
Q

What is the CO2/HCO3- ratio in Respiratory acidosis for an acute (uncompensated) respiratory acidosis?

A

1 : 0.1 ratio of CO2 increase to HCO3- increase

Increasing CO2 drives the reaction to the right, thereby increasing HCO3-

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11
Q

It causes a marked decrease in HCO3- because the addition of H+ consumes bicarbonate (drives reaction to the left).

Alternatively, an acidosis can be caused by loss of base (bicarbonate) to the body.

A

Metabolic acidosis

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12
Q

What is the CO2/HCO3- ratio in Respiratory alkalosis for an acute (uncompensated) respiratory alkalosis?

A

1 : 0.2 ratio of CO2 decrease to HCO3- decrease

Decreasing CO2 drives the reaction to the left, thereby reducing HCO3-

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13
Q

It causes a rise in HCO3- because the loss of H+ drives the reaction to the right.

Alternatively, an alkalosis can be caused by addition of base (bicarbonate) to the body.

A

Metabolic Alkalosis

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14
Q

How do Kidneys compensate in respiratory acidosis?

A

The kidneys compensate by increasing HCO3- and eliminating H+ but the kidney take days to fully compensate.

1 : 0/35 ratio of CO2 increase to HCO3- increase in a chronic (compensated) respiratory acidosis.

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15
Q

How is metabolic acidosis characterized and compensated?

A

Low pH and HCO3-. The drop in pH stimulates ventilation via peripheral chemoreceptors thus the respiratory system provides the first, rapid compensatory response.

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16
Q

What is Winter’s equation and what is it used for?

A

Determines if the respiratory response is adequate.

Predicted PaCO2 = (1.5 x HCO3-) + 8

If predicted PaCO2 is 2 (±) then respiratory compensation has occurred.

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17
Q

How do Kidneys compensate in respiratory alkalosis?

A

The kidneys compensate by Decreasing HCO3- and conserving H+ but the kidney take days to fully compensate.

1 : 0.5 ratio of CO2 decrease to HCO3- decrease in chronic (compensated) respiratory alkalosis

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18
Q

maximum low for HCO3-

A

15 mEq/L

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19
Q

in order to retain CO2, what is done and what equation is used?

A

ventilation decreases to retain CO2

It computes the PaCO2, which denotes appropriate compensation.

Expected PaCO2 = (0.7 x rise in HCO3-) + 40

If predicted PaCO2 is 2 (±) but should not exceed 55 mm Hg. the 40 represents the normal PaCO2

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20
Q

When there is overcompensation, what caused it?

A

The body never overcompensates. There is likely a second disorder part from primary disorder.

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21
Q

What does it mean when CO2 and HCO3- go in opposite direction?

A

There is a combined disturbance – either a combined (mixed) respiratory and metabolic acidosis or a combined (mixed) respiratory and metabolic alkalosis.

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22
Q

Too much CO2

A

Respiratory acidosis

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23
Q

Too little CO2

A

Respiratory alkalosis

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24
Q

Normal value for NA+

A

140 mEq/L

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25
Q

normal value for Cl-

A

104 mEq/L

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26
Q

normal value HCO3-

A

24 mEq/L

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27
Q

how to calculate Plasma Anion Gap (PAG) and its normal value?

A

PAG: NA+ - (Cl- + HCO3-)
PAG: 12 ± 2

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28
Q

What is anion gap useful in?

A

differentiating the case of metabolic acidosis

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29
Q

common causes of elevated gap?

A 
MUDPILES:
M: methanol
U: uremia
D: diabetic ketoacidosis
P: Paraldehyde
I: Iron, Isoniazid
L: lactic acidosis
E: ethylene glycol; ethanol, ketoacidosis
S: salicylates; starvation ketoacidosis; sepsis
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30
Q

common causes of non-elevated gap?

A 
HARDUP: 
H: hyperchloremia (parental nutrition)
A: acetazolamide
R: renal tubular acidosis
D: diarrhea
U: ureteral diversion
P: pancreatic fistula
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31
Q

question 1 in diagnosis of respiratory/metabolic disturbances and how body compensates

A

Question 1 What is the osis?
As indicated above, look at pH/

If pH <7.35, then its acidosis
If pH >7.35, then its alkalosis

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32
Q

question 2 in diagnosis of respiratory/metabolic disturbances and how body compensates

A
  1. What is cause of osis?
    Follow the bicarbonate trail
    If the answer to question 1 is acidosis then HCO3- is elevated, then RESPIRATORY ACIDOSIS.
    If the answer to question 1 is acidosis then HCO3- is low, then METABOLIC ACIDOSIS.
    If the answer to question 1 is alkalosis then HCO3- is low, then RESPIRATORY ALKALOSIS.
    If the answer to question 1 is alkalosis then HCO3- is elevated, then METABOLIC ALKALOSIS.
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33
Q

How do you differentiate acute and chronic respiratory acidosis

A

acute: 1:0.1 ratio
chronic 1:0.35 ratio

rise in HCO3- for every 1 mm Hg increase in PaCO2

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34
Q

How do you differentiate the metabolic acidosis types?

A

WInter’s equation = expected PaCO2

PaCO2 is within 2, then metabolic acidosis with respiratory compensation.
PaCO2 higher than 2, metabolic and respiratory acidosis
PaCO2 is low, metabolic acidosis with a respiratory alkalosis

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35
Q

How can you differentiate in respiratory alkalosis between acute (uncompensated) and chronic (compensated)?

A

acute: 1.02 ratio
chronic: 1:0.5 ratio

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36
Q

What is the metabolic alkalosis equation and what do its results mean?

A

Expected PaCO2 = (0.7 x rise in HCO3-) + 40

Within 2; metabolic alkalosis with respiratory compensation
More than 2; metabolic alkalosis and respiratory acidosis
PaCO2 low; metabolic and respiratory alkalosis

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37
Q

What graph is used in acid-base disturbances?

A

Davenport plot

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38
Q

Results of CO2 accumulating in the body, which causes an increase in H+ (or decrease in pH) and an increase in HCO3-.

Quantitatively in the acute (uncompensated) state, for every 10 mm Hg rise in PaCO2, HCO3- rises about 1 mEq/L and pH falls by 0.08 pH units

A

respiratory acidosis

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39
Q

Respiratory Acidosis can be caused by:

A 
Respiratory center depression (anesthetic, morphine)
Pulmonary edema, cardiac arrest
airway obstruction
muscle relaxants
sleep apnea
chronic obstructive lung disease
neuromuscular defects (multiple sclerosis, muscular distrophy)
obesity hypoventilation syndrome
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40
Q

cause and result of respiratory acidosis

A

Cause: increase in PaCO2
Cause: decrease in pH, slight increase in HCO3-

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41
Q

metabolic Acidosis can be caused by:

A

caused by a gain in fixed (not of CO2 origin) acid and/or a loss of base. The increased H+ drives the reaction to the left, decreasing HCO3- forcing the reaction to the left produces some CO2, but the hyperventilation evoked by the acidosis eliminates CO2.

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42
Q

how is metabolic acidosis determined?

A

Can be determined anion gap
MUDPILES for elevated anion gap
HARDUP if gap is normal

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43
Q

Cause and result of metabolic acidosis?

A

Cause: gain in H+ as fixed acid and/or a loss of HCO3= (via GI tract or kidney)
Result: decrease in pH and HCO3-; compensatory fall in PaCO2

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44
Q

Cause of respiratory alkalosis and examples of causes?

A 
Caused by an increase in alveolar ventilation relative to body production of CO2 (hyperventilation).
Respiratory alkalosis can be caused by:
anxiety
fever
hypoxemia
pneumothorax (in some cases)
ventilation-perfusion inequality
hypotension
high altitude
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45
Q

Cause and result of respiratory alkalosis

A

Cause: decrease in PaCO2
Result: decrease in H+ (increased pH) and slight decrease in HCO3-

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46
Q

What causes metabolic alkalosis and examples

A

loss of fixed acid and/or gain of base. the decreased H+ forces the reaction to the right, increasing HCO3-

Causes:
vomiting or gastric suctioning
loop and thiazide diuretic use
Bartter’s, GItelman’s, and Liddle’s syndrome
intracellular shift of hydrogen ions as in hypokalemia
primary hyperaldosteronism
loss of bicarbonate free fluid (contraction alkalosis)

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47
Q

Cause and result of metabolic alkalosis

A

Cause: loss of H+ and/or gain in HCO-3
Result: increase in pH and HCO3-; compensatory rise in PaCO2

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48
Q

equation to compute anion gap

A

Na+ - (Cl- + HCO3-)

MUDPILES vs HARDUP

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49
Q

Graphical depiction of the interplay of pH, HCO3- and PaCO2 as it relates to acid base disorders

A

Davenport plot

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50
Q

ENDOCRINOLOGY

A

ENDOCRINOLOGY

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51
Q

IP3 =

A

inositol triphosphate

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52
Q

DAG =

A

diacylglycerol

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53
Q

Lipid-Soluble Hormones examples

A

(steroids, thyroid hormones)

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54
Q

Water-Soluble Hormones examples

A

(peptides, proteins)

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55
Q

Intracellular actions of Lipid-Soluble Hormones

A

Stimulates synthesis

of specific new proteins

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56
Q

Intracellular actions of Water-Soluble Hormones

A

Production of second messengers, e.g., cAMP

Insulin does not utilize cAMP, instead activates membrane-bound tyrosine kinase

Second messengers modify action of intracellular proteins (enzymes)

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57
Q

receptors of Lipid-Soluble Hormones

A

Inside the cell, usually in nucleus

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58
Q

receptors of Water-Soluble Hormones

A

Outer surface of the cell membrane

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59
Q

Storage of Lipid-Soluble Hormones

A

Synthesized as needed

Exception: thyroid hormones

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60
Q

Storage of Water-Soluble Hormones

A

Stored in vesicles

In some cases, prohor- mone stored in vesicle along with an enzyme that splits off the active hormone

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61
Q

Plasma transport of Lipid-Soluble Hormones

A

Attached to proteins that serve as carriers

Exception: adrenal androgens

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62
Q

Plasma transport of water-Soluble Hormones

A

Dissolved in plasma (free, unbound)

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63
Q

Half-life of Lipid-Soluble Hormones

A

Long (hours, days)

 to affinity for protein carrier

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64
Q

Half-life of water-Soluble Hormones

A

Short (minutes)

 to molecular weight

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65
Q

The liver produces proteins that bind lipid-soluble hormones, e.g.:

A

cortisol-binding globulin
thyroid-binding globulin
sex hormone-binding globulin (SHBG)

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66
Q

Liver dysfunction and androgens can decrease and ________ can increase the circulating level of binding proteins.

A

estrogens

For example, a rise in circulating estrogen causes the release of more binding protein by the liver, which binds more free hormone.

This explains why during pregnancy and other states with a rise in estrogen levels:
Total plasma lipid-soluble hormone increases.
Free plasma hormone remains constant at a normal level; thus, the individual does not show signs of hyperfunction.

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67
Q

A phenomenon in which one type of hormone must be present before another hormone can act; for example, cortisol must be present for glucagon to carry out gluconeogenesis and prevent hypoglycemia.

A

Permissive action

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68
Q

Thyroid is a fairly constant system and T4 has a half-life of about __________. Thus, a random measurement of total T4 is usually a good estimate of daily plasma levels.

A

6–7 days

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69
Q

Peaks vs nadirs

A

peaks (erroneous hyperfunction)

nadirs (erroneous hypofunction)

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70
Q

Growth hormone is secreted in pulses and mainly at night. This is not reflected in a fasting morning sample. However, growth hormone stimulates the secretion of __________ which circulates attached to protein and has a long half-life (20 hours).

A

IGF-I

Plasma IGF-I measured at any time during the day is usually a good index of overall growth hormone secretion.

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71
Q

what does a urinalysis measure?

A

Restricted to the measurement of catecholamines, steroid hormones, and water-soluble hormones such as hCG and LH.

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72
Q

A distinct advantage of urine analysis is that it provides an integrated sample.

Example:

A

A “24-hour urine free cortisol” is often necessary to pick up a low-level Cushing’s syndrome and to eliminate the highs and lows of the normal circadian rhythm.

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73
Q

A primary disorder of endocrine system?

A

A primary disorder means dysfunction originating in the endocrine gland itself, either hyper- or hypo-function.

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74
Q

Examples of a primary disorder include:

A

– excess cortisol from an adrenal adenoma (Conn’s disease)
– decreased thyroid secretion (Hashimoto’s thyroiditis)
– reduced ADH secretion (central diabetes insipidus)

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75
Q

A secondary disorder of endocrine system?

A

A secondary disorder indicates that a disturbance has occurred causing the gland secrete more or less of the hormone.

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76
Q

Examples of a secondary disorder include:

A

– Cushing disease (pituitary adenoma secreting ACTH) resulting in hypercortisolism
– a dehydrated patient with elevated plasma osmolality causing high ADH levels

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77
Q

causes of hypofunction of endocrine system

A

Can be caused by autoimmune disease (e.g., type I diabetes, hypothyroidism, primary adrenal insufficiency, gonadal failure), tumors, hemorrhage, infection, damage by neoplasms

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78
Q

hypofunction stimulation test:

Hypothalamic hormones test ________

A

anterior pituitary reserve

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79
Q

hypofunction stimulation test:

Injection of the pituitary trophic hormone (e.g., ACTH) tests ____________

A

target gland reserve

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80
Q

hypofunction stimulation test:

Injection of arginine tests ________________

A

growth hormone release

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81
Q

causes of hyperfunction of endocrine system

A

Caused by hormone-secreting tumors, hyperplasia, autoimmune stimulation, ectopically produced peptide hormones (e.g., ACTH, ADH)

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82
Q

hyperfuntion stimulation tests:

Failure of glucose to suppress growth hormone diagnostic for ______

A

acromegaly

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83
Q

hyperfuntion stimulation tests:

Failure of dexamethasone (low dose) to suppress cortisol diagnostic for _________

A

hypercortisolism

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84
Q

what is Multiple endocrine neoplasia (MEN) and how does it classify?

A

Multiple endocrine neoplasia (MEN) represents a group of inheritable syndromes characterized by multiple benign or malignant tumors.

o MEN 1: hyperparathyroidism, endocrine pancreas, and pituitary edenomas
o MEN 2A: medullary carcinoma of the thyroid, pheochromocytoma, hyperparathyroidism
o MEN 2B: medullary carcinoma of the thyroid, pheochromocytoma, hyperparathyroidism typically absent.

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85
Q

What is synthesized in neuronal cell bodies in the arcuate and paraventricular nuclei?

A 
hypothalamic hormones
thyrotropin-releasing hormone (TRH)
corticotropin-releasing hormone (CRH)
growth hormone–releasing hormone (GHRH)
somatostatin (SST)
dopamine
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86
Q

What is synthesized in the preoptic nucleus?

A

gonadotropin-releasing hormone (GnRH)

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87
Q

TRH

A

thyrotropin-releasing hormone

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88
Q

TSH

A

thyroid-stimulating hormone or thyrotropin

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89
Q

CRH

A

corticotropin-releasing hormone

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90
Q

ACTH

A

adrenocorticotropic hormone or corticotropin

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91
Q

GnRH

A

gonadotropin-releasing hormone

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92
Q

LH

A

luteinizing hormone

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93
Q

FSH

A

follicle-stimulating hormone

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94
Q

GHRH

A

growth hormone–releasing hormone

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95
Q

GH

A

growth hormone

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96
Q

SST

A

somatostatin

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97
Q

Characteristic sequential loss of function of hypothyroidism

A

growth hormone and gonadotropin, followed by TSH then ACTH and finally prolactin.

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98
Q

Kallman syndrome – (tertiary) defective:

A

GnRH synthesis; ↓ LH ↓ FSH ↓ sex steroids

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99
Q

_________ is the most common tumor affecting the hypothalamic–pituitary system in children (pituitary adenomas rare).

A

Craniopharyngioma

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100
Q

The pituitary in pregnancy is enlarged and therefore more vulnerable to infarction. Sometimes when delivery is associated with severe blood loss, the ensuing shock causes arteriolar spasm in the pituitary with subsequent ischemic necrosis. Some degree of hypopituitarism has been reported in 32% of women with severe postpartum hemorrhage.

Symptoms vary, depending on the extent and location of pituitary damage, but failure to lactate for days following birth is a strong sign of pituitary damage.

A

Sheehan syndrome

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101
Q

Pulsatile system and the pulsatile release of GnRH prevents downregulation of ________ receptors.

A

gonadotroph receptors

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102
Q

What is mass effect?

A

The mass effect causes sequential loss of GH and gonadotropin followed by TSH, ACTH, and finally prolactin.

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103
Q

What is the most common tumor and the most common manifestation?

A

Prolactinomas are the most common tumor, and hypogonadism is the most common manifestation.

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104
Q

what are the Secreted hormones of the posterior pituitary gland?

A

arginine vasopressin (ADH), oxytocin — both are peptide hormones.

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105
Q

ADH function

A

ADH is a major controller of water excretion and regulator of extracellular osmolarity.

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106
Q

what can stimulate ADH secretion?

A

Angiotensin II and CRH can stimulate the release of ADH.

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107
Q

Neural control mechanisms that regulate secretion of ADH by the posterior pituitary. The principal inputs are inhibition by:

A

Baroreceptor and cardiopulmonary mechanoreceptors and stimulation by osmoreceptors.

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108
Q

Synthesis of ADH?

A

the supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus

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109
Q

Storage and releases ADH?

A

Posterior pituitary

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110
Q

What are Osmoreceptors?

A

Osmoreceptors are neurons that respond to increased plasma osmolarity, principally plasma sodium concentration. They synapse with neurons of the SO and PVN and stimulate them to secrete ADH from the posterior pituitary.

They also stimulate consumption of water through hypothalamic centers that regulate thirst.

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111
Q

SO and PVN also receive inputs from where?

A

The SO and PVN also receive input from cardiopulmonary mechano- receptors, as well as arterial baroreceptors. High blood volume or blood pressure tends to inhibit secretion of ADH.

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112
Q

main target tissue of ADH

A

The main target tissue is the renal collecting duct (V2 receptors).

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113
Q

Actions of ADH?

A

ADH increases the permeability of the duct to water by placing water
channels (aquaporins) in the luminal membrane.

ADH, acting via the V1 receptor, contracts vascular smooth muscle.

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114
Q

What is Atrial Natriuretic Peptide (ANP)?

A

ANP is the hormone secreted by the heart. ANP is found throughout the heart but mainly in the right atrium. The stimuli that release ANP (two peptides are released) are:

Stretch, an action independent of nervous involvement

CHF and all fluid overload states

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115
Q

ANP function in kidneys

A

ANP also increases sodium loss (natriuresis) and water loss (diuresis) by the kidney because it inhibits aldosterone release as well as the reabsorption of sodium and water in the collecting duct.

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116
Q

The consequences of Diabetes Insipidus can be explained on the basis of the lack of an effect of ________

A

ADH on the renal collecting ducts.

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117
Q

Sufficient ADH is not available to affect the renal collecting ducts.
Causes include familial, tumors (craniopharyngioma), autoimmune, trauma
Pituitary trauma – transient diabetes insipidus
Sectioning of pituitary stalk – triphasic response: diabetes insipidus, fol- lowed by SIADH, followed by a return of diabetes insipidus
Destruction of the hypothalamus from any cause can lead to diabetes insipidus. Forms of hypothalamic destruction are stroke, hypoxia, head trauma, infection, cancer or mass lesions.
CDI = ADH deficiency. CDI is treated with replacing ADH as vasopressin or DDAVP (desmopressin).

A

Central diabetes insipidus (CDI)

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118
Q

Due to inability of the kidneys to respond to ADH l Causes include familial, acquired, drugs (lithium) l Hypokalemia
Hypercalcemia

A

Nephrogenic diabetes insipidus

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119
Q

What is able to diminish ADH’s effectiveness on principal cells?

A

Lithium, low potassium, and high calcium

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120
Q

Excessive secretion of ADH causes an inappropriate increased reabsorption of water in the renal collecting duct.

A

Syndrome of Inappropriate ADH Secretion (SIADH)

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121
Q

causes of SIADH

A

Ectopic production of ADH (any CNS or small cell lung pathology)

Drug induced: SSRI, carbamazepine

Lesions in the pathway of the baroreceptor system

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122
Q

Pathophysiology of SIADH

A

Increased water retention, hyponatremia, but clinically euvolumic

Inappropriate concentration of urine, often greater than plasma osmolarity

With hyponatremia, a normal person should have urine sodium and osmolarity that are low. In SIADH, it is a disease because urine sodium and osmolarity are inappropriately high.

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123
Q

Treatment of SIADH

A

Fluid restriction but not salt restriction

Sodium disorders cause neurological symptoms.

Only mild hyponatremia from SIADH can be managed with fluid restriction.

Severe disease needs 3% hypertonic saline or V2 receptor antagonists.

Conivaptan and tolvaptan are V2 receptor antagonists; they stop ADH effect on kidney tubule.

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124
Q

One of the most common disorders of fluid and electrolyte balance in hospitalized patients

Is usually equivalent to a hypo-osmolar state (exception hyperglycemia) l Involves both solute depletion and water retention but water retention is usually the more important factor

Solute depletion can occur from any significant loss of ECF fluid. The hyponatremia is the result of replacement by more hypotonic fluids.

When it develops rapidly (< 48 hours) and is severe (Na < 120 mEq/L), patient is at risk for seizures and respiratory arrest. Often treated aggres- sively with hypertonic saline (3%) and diuretics or ADH antagonists.

When it develops more slowly, it appears to be well-tolerated and patient is asymptomatic. Aggressive treatment may result in “central pontine myelinolysis.” General recommendation is to slowly raise Na concentration over a period of days.

A

HYPONATREMIA

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125
Q

Caused by marked reduction in water excretion and/or increased rate of water ingestion. Would include congestive heart failure and cirrhosis

A

Hypervolemia

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126
Q

Indicates solute depletion. Would include mineralocorticoid de ciency, diuretic abuse, renal disease, diarrhea, and hemorrhage

A

Hypovolemia

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127
Q

Would include SIADH and primary (psychogenic) polydipsia. A clinically equiv- alent presentation may occur in glucocorticoid de ciency or hypothyroidism.

A

Clinical euvolemia

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128
Q

The major action of ADH is the reabsorption of _____ and _____, but not electrolytes, in the renal collecting duct.

A

water

urea

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129
Q

ANP, found mainly in the tissue of the right atrium, is released in response to stretch. The major action of ANP is ______ and ______.

A

diuresis

natriuresis

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130
Q

what is SIADH?

A

Inappropriately elevated secretion of ADH. Characterized by euvolemia but hyponatremia.

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131
Q

ADRENAL CORTEX

A

ADRENAL CORTEX

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132
Q

________ controls the release of both cortisol and adrenal androgens.

A

ACTH

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133
Q

_______ is stimulated by a rise in angiotensin II and/or K+.

A

Aldosterone

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134
Q

Zona Aldosterone of adrenal gland.
Hormone:
Controlled by:

A

Angiotensin II

[K+]

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135
Q

Zona fasciculata of adrenal gland.
Hormone:
Controlled by:

A

Cortisol

ACTH

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136
Q

Zona reticularis of adrenal gland
Hormone:
Controlled by:

A

Androgens

ACTH

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137
Q

Medulla of adrenal gland
Hormone:
Controlled by:

A

Epinephrine

Autonomic nervous system

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138
Q

T/F:

LH has no effect on the production of adrenal androgens

A

TRUE

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139
Q

HSD =

A

hydroxysteroid dehydrogenase

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140
Q

OH =

A

Hydroxylase

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141
Q

In females and prepubertal males, urinary 17-ketosteroids are an index of ____________.
l In adult males (postpuberty), urinary 17-ketosteroids are 2/3 adrenal and 1/3 testicular, and thus mainly an index of ____________.

A

adrenal androgen secretion.

adrenal secretion

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142
Q

_______ converts androgen into estrogen.

A

Aromatase

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143
Q

e starting point in the synthesis of all steroid hormones is the transport of cholesterol into the mitochondria by __________. This is is the rate-limiting step.

A

steroidogenic acute regulatory protein (StAR)

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144
Q

The enzyme catalyzing the conversion of cholesterol to pregnenolone is ___________

A

side-chain cleavage enzyme (SCC, also called desmolase.).

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145
Q

Angiotensin II is the main stimulus to the zona glomerulosa, which produces ______, the major mineralocorticoid.

A

aldosterone

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146
Q

_________: Main glucocorticoid secreted by the adrenal cortex, responsible for most of the hypothalamic and anterior pituitary negative feedback control of ACTH secretion.

A

Cortisol

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147
Q

Normal hormonal output of the zona reticularis consists of the following:

_______: These weak water-soluble androgens represent a sig- nificant secretion; however, they produce masculinizing characteristics only in women and prepubertal males when secretion is excessive.

A

Adrenal androgens

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148
Q

Stress hormones usually act to mobilize energy stores. The stress hormones are:

_______ : mobilizes fatty acids by increasing lipolysis in adipose tissue

_______ : mobilizes glucose by increasing liver glycogenolysis

_____ : mobilizes fat, protein, carbohydrate

______, in some forms of stress such as exercise: mobilizes glucose via glycogenolysis and fat via lipolysis

A

Growth hormone

Glucagon

Cortisol

Epinephrine

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149
Q

Metabolic Actions of _______:

It promotes the mobilization of energy stores, speci cally:

Protein: It promotes degradation and increased delivery of hepatic gluconeogenic precursors.

Lipids: It promotes lipolysis and increased delivery of free fatty acids and glycerol.

Carbohydrate: Cortisol raises blood glucose, making more glucose available for nervous tissue. Two mechanisms are involved:
– It counteracts insulin’s action in most tissues (muscle, lymphoid, and fat).
– It increases hepatic output of glucose by regulating the enzymes involved in gluconeogenesis, particularly phosphoenolpyruvate carboxykinase (PEPCK) (not from liver glycogenolysis).

A

Cortisol

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150
Q

what does cortisol do with glucagon?

A

Promotes glycogenolysis in the liver (some lipolysis from adipocytes as well). Without cortisol, fasting hypoglycemia rapidly develops. Cortisol permits gluca- gon to raise blood glucose.

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151
Q

What does cortisol do with Catecholamines?

A

Promotes both alpha and beta receptor expression.

Beta receptor function involves glucose regulation, lipolysis, and bronchodilation.

Alpha receptor function is pivotal for blood pressure regulation.

Without cortisol, blood pressure decreases.

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152
Q

Secretion of CRH increases in response to stress and in the early morning. What are the hours?

A

Peak cortisol secretion occurs early in the morning between the 6th and 8th hours of sleep.

Secretion then declines slowly during the day and reaches a low point late in the evening.

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153
Q

CRN + cortisol relationship

A

Increased AM CRH = increased AM cortisol

Increased AM cortisol = increased AM blood sugar and lipid levels

Increased AM sugar and lipid levels help get you out of bed

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154
Q

what stimulates the release of the secretion of cortisol (and adrenal androgens) of adrenal cortex?

A

ACTH

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155
Q

__________ suppresses the release of ACTH by acting on the hypothalamus and anterior pituitary.

A

Cortisol

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156
Q

What causes darkening of the skin in relation to hormones?

A

Excessive secretion of ACTH (e.g., primary adrenal insuciency) causes darkening of the skin.

Its is due to the melanocyte-stimulating hormone (α-MSH) sequence within the ACTH molecule, and the β-MSH activity of β-lipotropin.

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157
Q

role of β-Lipotropin?

A

Role not well understood

Precursor to β-MSH and endorphins. Endorphins modulate the percep- tion of pain.

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158
Q

primary target tissue for aldosterone and its function?

A

The primary target tissue for aldosterone is the kidney, where it increases Na+ reabsorption by the principal cells of the kidney’s collecting ducts.

Because water is reabsorbed along with the Na+, aldosterone can be considered to control the amount of Na+ rather than the concentration of Na+ in the ECF.

Aldosterone also promotes the secretion of H+ by the intercalated cells of the col- lecting duct, and K+ secretion by the principal cells.

The Na+-conserving action of aldosterone is also seen in salivary ducts, sweat glands, and the distal colon.

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159
Q

_________ promotes the activity of Na/K-ATPase–dependent pump that moves Na+ into the renal ECF in exchange for K+.

In addition, it also enhances epithelial Na+ channels (ENaC) in the luminal membrane of principal cells. The net effect is to increase Na+ reabsorption, which in turn increases water reabsorption.

It regulates Na+ to regulate extracellular volume.

A

Aldosterone

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160
Q

Acutely, ACTH increases aldosterone secretion. However, the primary regulators of aldosterone secretion are circulating levels of _____ and _____.

A

Ang II and K+

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161
Q

What are the main sensory cells of the afferent arteriole?

A

The main sensory cells are the granular cells (also called juxtamedullary cells) of the afferent arteriole. They are modified smooth-muscle cells that surround and directly monitor the pressure in the afferent arteriole. This signal in many cases is in response to a reduction in circulating fluid volume.

These cells are also innervated and stimulated by sympathetic neurons via norepinephrine and beta receptors. Thus the release of renin induced by hypovolemia is enhanced by increased sympathetic neural activity.

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162
Q

Long-term regulation of blood pressure and cardiac output is accomplished by the ____________.

A

renin-angiotensin-aldosterone system

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163
Q

what does renin do?

A

Renin is an enzyme that converts a circulating protein produced in the liver, angiotensinogen into angiotensin I

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164
Q

What does ACE do?

A

Angiotensin converting enzyme (ACE), found mainly in endothelial cells of pulmonary vessels, converts angiotensin I into angiotensin II.

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165
Q

what does Angiotensin II do?

A

Angiotensin II has potent ef- fects to stimulate secretion of aldosterone and to cause arteriolar vasoconstric- tion. It also directly stimulates reabsorption of sodium in the proximal tubule

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166
Q

How does Angiotensin II raises blood pressure?

A

Angiotensin II raises blood pressure by 2 independent actions:

The direct vasoconstrictive effects of angiotensin II increase total peripheral resistance.

It stimulates the adrenal cortex to secrete aldosterone, resulting in increased reabsorption of Na+.

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167
Q

In addition to its effects to serve as a direct vasoconstrictor and increase aldosterone secretion, angiotensin II also:

A
  • Increases ADH release from posterior pituitary
  • Increases thirst
  • Increases sodium reabsorption in proximal tubule
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168
Q

There is hypercortisolism regardless of origin, including chronic glucocorticoid therapy

A

Cushing syndrome

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169
Q

It is hypercortisolism due to an adenoma of the anterior pituitary (microadenoma)

A

Cushing disease

170
Q

what is 1-mg overnight dexamethasone suppression test used for?

A

For the presence of Cushing syndrome regardless of the cause
Normal; cortisol decreases
Hypercortisolism; cortisol not suppressed
False-positives from depression or alcoholism

171
Q

what is High-dose dexamethasone used for?

A

To differentiate pituitary adenoma from ectopic ACTH secretion and adrenal tumors
Pituitary source; cortisol decreases
Ectopic ACTH, adrenal tumor; cortisol not suppressed

172
Q

ACTH level tests used for?

what do its results mean?

A

Used after 24 hour urine cortisol establishes presence of hypercortisolism

ACTH levels establish etiology of hypercortsolism

Low ACTH = Adrenal source of cortisol overproduction

Normal or high ACTH = Pituitary or Ectopic source

High dose dexamethasone distinguishes Pituitary vs Ectopic source

173
Q

ACTH stimulation test diagnoses _______.

To diagnose atrophied adrenal nonresponsive

Normal; cortisol increases after ACTH

Adrenal insufficiency: no change in cortisol level

A

adrenal insufficiency.

174
Q

T/F: Metyrapone testing is no longer performed.

A

TRUE

175
Q

What is this:

ACTH independent

Cortisol elevated, ACTH depressed

Most are benign adrenocorticol adenomas

Adrenal adenoma usually unilateral and secretes only cortisol; decreased adrenal androgen and deoxycorticosterone (hirsutism absent)

Presence of androgen or mineralocorticoid excess suggests a carcinoma

A

Primary hypercortisolism (adrenal source)

176
Q

What is this:

ACTH dependent

Hypersecretion of ACTH results in bilateral hyperplasia of the adrenal zona fasciculata and reticularis

Elevated ACTH, cortisol, adrenal androgen, deoxycorticosterone

A

Secondary hypercortisolism (pituitary vs. ectopic source)

177
Q

What are the Two main subcategories of Secondary hypercortisolism?

A

Pituitary adenoma

Ectopic ACTH syndrome

178
Q
  • Usually a microadenoma (< 1 cm dia.)
  • This is Cushing disease
  • Increased ACTH not sufficient to cause hyperpigmentation
  • Dexamethasone suppressible
A

Pituitary adenoma

179
Q
  • Most frequently in patients with small cell carcinoma of the lung
  • Greater secretion of ACTH than in Cushing disease and hyperpigmentation often present
  • Ectopic site nonsupressible with dexamethasone
A

Ectopic ACTH syndrome

180
Q

High-dose dexamethasone
– ACTH suppressed =
– ACTH not suppressed =

A

– ACTH suppressed = Cushing disease (pituitary source)

– ACTH not suppressed = ectopic ACTH syndrome

181
Q

What is this:

  • Obesity because of hyperphagia, classically central affecting mainly the face, neck, trunk, and abdomen: “moon facies” and “buffalo hump”
  • Protein depletion as a result of excessive protein catabolism
  • Inhibition of inflammatory response and poor wound healing
  • Hyperglycemia leads to hyperinsulinemia and insulin resistance. l Hyperlipidemia
  • Bone breakdown and osteoporosis
  • Thinning of the skin with wide purple striae located around abdomen and hips
  • Increased adrenal androgens, when present in women, can result in acne, mild hirsutism, and amenorrhea.
  • In men, decreased libido and impotence
  • Mineralocorticoid effects of the high level of glucocorticoid and deoxycorticosteroid lead to salt and water retention (hypertension), potassium depletion, and a hypokalemic alkalosis.
  • Increased thirst and polyuria
  • Anxiety, depression, and other emotional disorders may be present.
A

Characteristics of Cushing Syndrome

182
Q

What is this:

  • Autoimmune origin with slow onset in about 80% of cases
  • Loss of 90% of both adrenals required before obvious clinical manifestations
  • With gradual adrenal destruction, basal secretion is normal but secretion does not respond to stress, which may initiate an adrenal crisis.
  • Bilateral hemorrhage as the origin results in an adrenal crisis. Hyperpigmentation, hyponatremia, and hyperkalemia usually absent
  • Orthostatic intolerance due to diminished alpha-receptor function and low blood volume.
  • Abnormalities in GI function
  • Loss of axillary and pubic hair in women due to loss of androgens, amenorrhea
  • Insufficient glucocorticoids leads to hypoglycemia and an inability of the kidney to excrete a water load
  • Severe hypoglycemia in children but rare in adults
A

Primary Hypocortisolism (in primary adrenal insufficiency, Addison’s disease)

183
Q

What is this:

  • Most commonly due to sudden withdrawal of exogenous glucocorticoid therapy
  • Trauma, infection, and infarction most common natural origin of ACTH deficiency
  • In the early stages baseline hormone values are normal but ACTH reserve compromised and stress response subnormal (glucocorticoids adminis- tered presurgery)
  • May be associated with the loss of other anterior pituitary hormones (pan- hypopituitarism) or adenomas secreting prolactin or growth hormone
  • Atrophy of the zona fasciculata and zona reticularis
  • Zona glomerulosa and aldosterone normal; no manifestations of mineralocorticoid deficiency
  • Consequences as stated for cortisol deficiency
  • Severe hypoglycemia and severe hypotension unusual (RAAS is still intact)
  • Hyponatremia due to water retention
A

Secondary hypocortisolism (secondary adrenal insufficiency)

184
Q

What is this:

  • Most common cause is a small unilateral adenoma, on either side
  • Remainder mostly bilateral adrenal hyperplasia (idiopathic hyperaldosteronism)
  • Rarely due to adrenal carcinoma
  • Increased whole body sodium, fluid, and circulating blood volume
  • Hypernatremia is infrequent.
  • Increased peripheral vasoconstriction and TPR
  • Blood pressure from borderline to severe hypertension
  • Edema rare (sodium escape*)
  • Modest left ventricular hypertrophy
  • Potassium depletion and hypokalemia create symptoms of weakness and fatigue.
  • Detection of hypertension with hypokalemia is often the initial clue for this disease
  • Increased hydrogen ion excretion and new bicarbonate create metabolic alkalosis.
  • A positive Chvostek or Trousseau’s sign is suggestive of alkalosis leading to low calcium levels.
  • Cortisol is normal.
  • Suppression of renin a major feature
A

Primary hyperaldosteronism (Conn’s syndrome)

185
Q

What is this:

  • In most cases a primary over-secretion of renin secondary to a decrease in renal blood flow and/or pressure
  • Renal arterial stenosis, narrowing via atherosclerosis, fibromuscular hyperplasia.
  • Renin-secreting tumor rare
  • Modest to highly elevated renin
  • Modest to highly elevated aldosterone
  • Hypokalemia and metabolic alkalosis
A

Secondary hyperaldosteronism with hypertension

186
Q

What is this:

Sequestration of blood on the venous side of the systemic circulation is a common cause of ______. This results in decreased cardiac output and thus decreased blood flow and pressure in the renal artery. The following conditions produce this disease through this mechanism:

  • Congestive heart failure
  • Constriction of the vena cava
  • Hepatic cirrhosis
A

Secondary hyperaldosteronism with hypotension

187
Q

This type of deficiency is the most common of the congenital enzyme deficiencies.

Tissues affected: zona glomerulosa, zona fasciculata, zona reticularis

A

21 β-hydroxylase deficiency

188
Q

what does this mean?

21 β-OH

A

21 β-Hydroxylase blockade

189
Q

Consequence of 21 β-OH?

A

Consequence: Result is a decreased production of aldosterone, the main miner-
alocorticoid.

190
Q

What does a 17 α-Hydroxylase blockade point do in the testes?

A

Decreased production of all androgens including testosterone

191
Q

What does a 17 α-Hydroxylase blockade point do in the testes?

A

Decreased production of estrogens and androgens

192
Q

What is this?

  • Accounts for about 90% of the cases
  • 75% of the cases have mineralocorticoid deficiency
  • Neonates may present with a salt-wasting crisis.
  • Salt wasters tend to have hyponatremia, hyperkalemia, and raised plasma renin.
  • 17-hydroxyprogesterone is elevated.
  • Increased androgens lead to virilization of the female fetus and sexual ambiguity at birth
  • Males are phenotypically normal at birth but develop precocious pseudopuberty, growth acceleration, premature epiphyseal plate closure, and diminished final height.
  • Goal in treatment is to bring glucocorticoid and mineralocorticoid back to the normal range which would also suppress adrenal androgen secretion.
  • Give hydrocortisone to act as feedback inhibition on pituitary.
A

21 β-Hydroxylase deficiency

193
Q

What is this?

  • Extremely rare
  • Usually diagnosed at the time of puberty when the patient presents with hypertension, hypokalemia, and hypogonadism
  • Individuals have eunuchoid characteristics.
A

17 α-Hydroxytlase deficiency

194
Q

In ________ β-hydroxylase deficiency, there is mineralocorticoid de ciency, salt wasting and hypotension, androgen excess and female virilization.

A

21 β-hydroxylase deficiency

195
Q

In _______ β-hydroxylase deficiency, there is mineralocorticoid excess, salt retention and hypertension, androgen excess as in the preceding.

A

11 β-hydroxylase deficiency

196
Q

In 17 α-hydroxylase deficiency, there is mineralocorticoid excess, adrenal androgen de ciency, and hypertension with gonadal steroid de ciency and hypogonadism.

A

17 β-hydroxylase deficiency

197
Q

ADRENAL MEDULLA

A

ADRENAL MEDULLA

198
Q

what does the adrenal medulla secrete?

A

Secretion of the adrenal medulla is 20% norepinephrine and 80% epinephrine.

199
Q

what converts norepinephrine into epinephrine?

A

Phenylethanolamine-N-methyltransferase (PMNT) converts norepinephrine into epinephrine.

200
Q

Most circulating norepinephrine arises from _____.

A

postganglionic sympathetic neurons

201
Q

T/F: Because many of the actions of epinephrine are also mediated by norepinephrine, the adrenal medulla is not essential for life.

A

TRUE

202
Q

what kind of people suffer from orthostatic hypotension?

A

The vasoconstrictive action of norepinephrine is essential for the maintenance of normal blood pressure, especially when an individual is standing. Plasma norepinephrine levels double when one goes from a lying to a standing position. People with inadequate production of norepinephrine suffer from orthostatic hypotension.

203
Q

when does Epinephrine increase?

A

Epinephrine is a stress hormone and rapidly increases in response to exercise, exposure to cold, emergencies, and hypoglycemia.

204
Q

metabolic function of Epinephrine in liver.

A

Liver: Epinephrine increases the activity of liver and muscle phosphorylase, promoting glycogenolysis. This increases glucose output by the liver.

205
Q

metabolic function of Epinephrine in Skeletal muscle.

A

Skeletal muscle: Epinephrine promotes glycogenolysis but because muscle lacks glucose-6-phosphatase, glucose cannot be released by skeletal muscle; instead, it must be metabolized at least to lactate before being released into the circulation.

206
Q

metabolic function of Epinephrine in Adipose tissue.

A

Adipose tissue: Epinephrine increases lipolysis in adipose tissue by increasing the activity of hormone-sensitive lipase. Glycerol from TG breakdown is a minor substrate for gluconeogenesis.

207
Q

metabolic function of Epinephrine in metabolic rate

A

Epinephrine increases the metabolic rate. This will not occur without thyroid hormones or the adrenal cortex.

208
Q

what is this:

  • Adrenal tumors that secrete epinephrine and norepinephrine in various ratios
  • Usually unilateral benign tumors
  • Characteristic of MEN 2A and MEN 2B
  • Paragangliomas are extra-adrenal pheochromocytomas of sympathetic ganglia located primarily within the abdomen and that secrete norepinephrine.
  • Most consistent feature is hypertension. Symptoms include headache, diaphoresis, palpitations, and anxiety. -Increased metabolic rate and hyperglycemia also occur.
  • Pheochromocytomas are highly vascular and encapsulated.
  • Episodic release of hormone, particularly when it is mainly norepinephrine, can abruptly cause a hypertensive crisis. Can be induced by physical stimuli that displaces abdominal contents.
  • Most reliable initial test is plasma metanephrines or 24-hour urine cat- echolamines or metanephines.
  • Usually curable but can be fatal if undiagnosed
  • Treat with alpha blocker followed by surgical removal.
A

pheochromocytoma

209
Q

The most reliable test of Epinephrine?

A

urine metanephrines.

210
Q

ENDOCRINE PANCREAS

A

ENDOCRINE PANCREAS

211
Q

Delta cells, which constitute about 5% of the islet cells, are interspersed between the alpha and beta cells and secrete ________.

A

somatostatin

212
Q

Alpha cells, which constitute about 20% of the islet cells, secrete ______ and tend to be located near the periphery of the islet.

A

glucagon

213
Q

Beta cells constitute 60–75% of the islet cells. Beta cells synthesize preproinsulin, which is cleaved to form proinsulin, which, in turn, splits into _______ and _____ both of which are secreted in equimolar quantities.

A

insulin and C peptide

214
Q

what is the long-term marker of endogenous insulin secretion

A

C-peptide

For many years, C-peptide was considered to have no biological function, but more recently this has been called into question. Studies suggest that C-peptide receptors exist on cells. In addition, C-peptide may serve a protective role, helping to prevent the renal, neural, and microvascular pathologies seen when it is absent, i.e., type I diabetes mellitus.

215
Q

-insulin receptor-

  • The portion of the insulin receptor that faces externally has the ___________.
  • The portion of the insulin receptor that faces the cytosol has _________ activity.

When occupied by insulin, the receptor phosphorylates itself and other proteins.

A

hormone-binding domain

tyrosine kinase activity

216
Q

The most important controller of insulin secretion is _____. Above a threshold of 100 mg%, insulin secretion is directly proportional to it.

A

plasma glucose

217
Q

Glucagon is a peptide hormone. It is secreted by the _______ of the pancreatic islets.

A

α-cells of the pancreatic islet

218
Q

The primary target for glucagon action is the _______, where its action is mediated by an increase in the concentration of cAMP. The cAMP activates protein kinase A, which, by catalyzing phosphorylation, alters the activity of enzymes mediating the actions given below.

A

liver hepatocyte

219
Q

T/F: Skeletal muscle is a target tissue for glucagon.

A

FALSE

220
Q

What is this:

Increases liver glycogenolysis.
Increases liver gluconeogenesis.
Increases liver ketogenesis and decreases lipogenesis.
Increases ureagenesis.
Increases insulin secretion.
Increases lipolysis in the liver.
A

Specific Actions of Glucagon on the Liver

221
Q

Stimuli that inhibit glucagon secretion

A

Hyperglycemia
Insulin
Somatostatin

222
Q

Stimuli that promote glucagon secretion

A

Hypoglycemia

Amino acids arginine

223
Q

most important physiologic promoter for glucagon secretion and the most important inhibitor?

A

Low plasma glucose (hypoglycemia) is the most important physiologic promoter for glucagon secretion, and elevated plasma glucose (hyperglycemia) the most important inhibitor.

224
Q

Amino acids, especially _________, also promote the secretion of glucagon. us, glucagon is secreted in response to the ingestion of a meal rich in proteins.

A

dibasic amino acids (arginine, lysine)

225
Q
  • Accounts for about 90% of all the cases of diabetes
  • Strong genetic component
  • Body build is usually obese (particularly central or visceral).
  • Usually, but not always, middle-aged or older
  • The number of younger individuals in this category is increasing.
  • Characterized by variable degrees of insulin resistance, impaired insulin secretion, and increased hepatic output of glucose. Insulin resistance precedes secretory defects and in the early stages hyperinsulinemia is able to overcome tissue resistance. Ultimately beta cell failure can occur.
  • Insulin levels may be high, normal, or low.
  • Resistance to insulin is not well understood. It is thought to be due to postreceptor defects in signaling, which ultimately lead to a decrease in the number of glucose transporters. Reducing plasma glucose and thus plasma insulin can increase receptor sensitivity toward normal.
  • Plasma glucose good screening for type 2. Elevated glucose due to elevated hepatic output.
  • With a controlled diet and exercise, the symptoms of type 2 diabetes often disappear without the necessity for pharmacologic therapy.
  • Individuals tend to be ketosis resistant. The presence of some endogenous insulin secretion appears to protect from development of a ketoacidosis. If it does develop, it is usually the result of severe stress or infection (increased counterregulatory homones, suppressed insulin).
  • In nonobese patients, a deficient insulin release by the pancreas is often the problem, but varying degrees of insulin resistance can also occur.
A

type 2 diabetics

226
Q

A group of metabolic derangements that includes atherogenic dyslipidemia (low HDL) and high triglycerides, elevated blood glucose, hypertension, central obesity, prothrombotic state, and a proinflammatory state. The clustering of these risk factors increases the probability of developing cardiovascular disease and type 2 diabetes.

A

Metabolic Syndrome (Syndrome X)

227
Q
  • Genetic association less marked than the other type
  • Genetically predisposed individuals whose immune system destroys pancreatic beta cells
  • Symptoms do not become evident until 80% of the beta cells are destroyed. l Body build usually lean
  • Usually, but not always, early age of onset
  • Due to an absence of insulin production
  • Increased glucagon secretion also generally occurs
  • Three target tissues for insulin—liver, skeletal muscle, and adipose tissue—fail to take up absorbed nutrients (glucose, amino acids, and fatty acids), thus increasing their levels in the blood.
A

diabetes mellitus type 1

228
Q

What is this:

  • Without any insulin, excessive lipolysis provides fatty acids to the liver, where they preferentially converted to ketone bodies because of the unopposed action of glucagon.
  • Blood pH and bicarbonate decrease due to the metabolic acidosis.
  • Increased alveolar ventilation is the respiratory compensation for the metabolic acidosis. When the arterial pH decreases to about 7.20, ventilation becomes deep and rapid (Kussmaul breathing).
  • An acidic urine results as the kidneys attempt to compensate for the acidosis.
  • The severe acidosis is in addition to the dehydration and net decrease in total body sodium and potassium.
  • Treatment is replacement of fluid and electrolytes and administration of insulin
  • DKA treatment is first 2-3 liters of normal saline and IV insulin. Subcutaneous insulin may not be fully absorbed because of decreased skin perfusion. Hyponatremia is common because of hyperglycemia. For each 100 point increase in glucose above normal, there is a 1.6 decrease in sodium.
  • When hyponatremia is present with hyperglycemia, management is cor- rection of the elevated glucose level. When glucose comes to normal, the sodium corrects.
A

Diabetic Ketoacidosis (DKA)

229
Q

What is the ratio in Diabetic Ketoacidosis (DKA)?

A

100 mg ELEVATION glucose = 1.6 meq DECREASE sodium

230
Q

What is this:

  • Most common islet cell tumor
  • Found almost exclusively within the pancreas and hypersecrete insulin
  • Most common symptoms due to the hypoglycemia (confusion, disorienta- tion, headache)
  • Association with MEN 1
  • Insulin measured to determine insulin-mediated versus noninsulin-mediated hypoglycemia
  • Insulin-secreting tumor: insulin and C-peptide both elevated l Factitious hypoglycemia: C-peptide below normal
  • Treat with removal
A

Insulinomas

231
Q

Which hormone is this:

  • It is produced in adipose tissue and is thought to be a “long-term” regulator of appetite and energy balance.
  • Secretion is circadian, with the highest levels occurring at night and the nadir in the morning. Individual meals do not stimulate the release of it.
  • Its receptor is a member of the cytokine family of receptors, which activate gene transcription factors.
  • It decreases hypothalamic neuropeptide Y (NPY), which is a potent activator of feeding (orexigenic). By inhibiting NPY synthesis, it promotes satiety (anorexigenic).
  • It increases energy expenditure, in part by increasing fatty acid oxidation, and it decreases fat stores.
  • Lack of and/or resistance to it causes obesity.
A

Leptin

232
Q

Which hormone is this:

  • It is produced in adipose tissue, and it increases insulin sensitivity and tissue fat oxidation.
  • Dysregulation of adiponectin, along with production of cytokines by adipocytes, may play a role in obesity, insulin resistance, and cachexia. —–Plasma levels of it are low in Type II diabetics, and infusion of this hormone decreases plasma glucose in experimental animal models of diabetes mellitus.
  • The mechanism of action and regulation of secretion are not well understood, but it does appear to inhibit liver output of glucose.
A

adiponectin

233
Q

Which hormone is this:

  • It is produced by cells of the stomach.
  • Circulating levels of ghrelin are reduced in response to a meal and highest in the fasting state.
  • It activates hypothalamic NYP neurons and is thus a potent orexigenic hormone.
  • It also stimulates the release of growth hormone (GH), although its physiologic significance/ role is not well understood. Because of ghrelin’s effects on GH and appetite, however, it may prove beneficial for restoring GH levels in the elderly and anorexic conditions, such as cancer.
  • It levels are decreased in obese individuals and elevated by low calorie diets, strenuous exercise, and patients with Prader-Willi syndrome.
  • Ghrelin is a peptide hormone that works via Gq and Gs. Its mechanism of action and regulation of secretion are not well understood.
A

Ghrelin

234
Q 
Administration of the \_\_\_\_\_\_\_\_ class of compounds to diabetics increases the circulating levels of adiponectin, which may be part of
the mechanism by which these drugs reduce plasma glucose.
A

thiazolidinedione (TZD)

235
Q

_______ is a genetic condition affecting many parts of the body. In infancy, this condition is characterized by hypotonia, feeding dif culties, poor growth, and delayed development. Beginning in childhood, affected individuals develop an insatiable appetite, which leads to chronic hyperphagia and obesity.

A

Prader-Willi syndrome

236
Q

HORMONAL CONTROL OF CALCIUM AND PHOSPHATE

A

HORMONAL CONTROL OF CALCIUM AND PHOSPHATE

237
Q

Both calcium and phosphate absorption in the GI tract are stimulated by the active form of __________.

A

vitamin D (calcitriol)

238
Q

where is 99% of total calcium?

A

bone

239
Q

How is the calcium stored as?

A

Mostly as complex calcium phosphate salts (hydroxyapatites).

240
Q

Bone remodeling involves the interplay between bone-building cells (_______) and cells that break down bone (________).

A

osteoblasts

osteoclasts

241
Q

Osteoblasts cause bone deposition and they secrete two proteins

A

RANK-L (Receptor Activator of Nuclear KappaB Ligand)

OPG (osteoprotegerin)

242
Q

function of RANK-L (Receptor Activator of Nuclear KappaB Ligand)?

A

This protein binds to the RANK receptor, which is expressed on precursor cells resulting in their differentiation into active osteoclasts. Active osteoclasts also express the RANK receptor, which, when stimulated, activates osteoclastic activity.

243
Q

function of OPG (osteoprotegerin)?

A

This protein binds RANK-L, there by preventing it from binding onto precursor or osteoclast cells. This reduces differentiation and overall osteoclastic activity. Thus, OPG acts as a “decoy” for RANK-L.

244
Q

which hormone influences bone remodeling?

A

parathyroid hormone (PTH)

245
Q

________ is well known for conserving bone integrity and it does so by at least two mechanisms.
First, it induces the synthesis of OPG.
Second, it reduces the secretion of cytokines by T-Lymphocytes. These cytokines stimulate differentiation of precursor cells into active osteoclasts and they stimulate activity of mature osteocytes. By inhibiting these cytokines and increasing OPG, this hormone reduces the activity of osteoclasts.

A

Estrogen

246
Q

Glucocorticoids function in bones

A

Glucocorticoids increase bone breakdown by inducing the synthesis and release of RANK-L and by inhibiting the synthesis of OPG.

247
Q

what Weight-bearing mechanical stress do to bones?

A

Weight-bearing mechanical stress increases the mineralization of bone.

248
Q

Actions of PTH in bone?

A

Increases Ca2+ reabsorption in distal tubule of the kidney

Inhibits phosphate (Pi) reabsorption in proximal tubule of the kidney.

Stimulates the 1-alpha-hydroxylase enzyme in kidney, converting inactive vitamin D to its active form.

Causes bone resorption, releasing Ca2+ and Pi into the blood.

249
Q

role of Parathyroid Hormone-Related Peptide?

A
  • PTHrP is a paracrine factor secreted by many tissues; e.g., lung, mammary tissue, placenta.
  • It may have a role in fetal development. In postnatal life, its role is unclear.
  • The majority of humoral hypercalcemias of malignancy are due to overexpression of PTHrP.
  • PTHrP has a strong structural homology to PTH and binds with equal affinity to the PTH receptor.
250
Q

Half of calcium in plasma is ______.

A

free calcium

251
Q

What displaces Ca2+ from protein?

A

Free H+

252
Q

What promotes resorption (BONE BREAKDOWN)?

A

RANK-L

253
Q

What reduces resorption?

A

OPG

254
Q

What regulates bone remodeling endogenously?

A

PTH endogenously promote RANK-L (bone resorption)

255
Q

What happens if you give a single OPG bolus and why?

A

reduce osteoclastic activity

DR. BRITT WILSON DOESNT KNOW

256
Q

Which t-lymphocytes activates osteoclasts?

A

IL-1, IL-6, TNF

257
Q

What do high glucocorticoids do?

A

Increase RANK-L

Decrease OPG

258
Q

What are things that breakdown weight bearing stress?

A

being sedentary
bedridden
weightlessness (astronauts)

259
Q

What happens in absence of weight bearing stress?

A

Plasma Ca2+ tends to be in the upper region or normal/

Plasma PTH decreases.

Urinary calcium increases.

260
Q

Phosphate Trashy Hormone

A

PTH since it gets rid of phosphate

261
Q

another names for vitamin D3?

A

calcitriol

cholecalciferol

262
Q

What is the vitamin D3 synthesized in the skin and catalyzed by ultraviolet light?

A

7-Dehydrocholesterol

263
Q

What is the best indicator of total body stores of Vitamin D3?

A

25 OH Vitamin D (main circulating form but very low activity)

264
Q

Organs where PTH works?

A

Kidneys and bones

265
Q

Causes of hypercalcemia?

A

Lithium: Decrease responsiveness of PT gland to calcium
Sarcoidosis & other granulomatous disorders: 1-alpha-OH
-elevated thyroid hormone (osteoclasts?)
-Milk-alkali syndrome (got milk and Tums?)
Thiazide diuretics

266
Q

Drugs used to slow bone breakdown?

A

Bisphosphonates: calcitonin works quickly

Etidronate
Pamidroante
Alendronate

267
Q

Function of Calcitonin

A

“Calcitonin Tones-down Calcium”

268
Q

clinical signs of hypoparathyroidism?

A

Trousseau’s sign

Chvostek’s Sign

269
Q

What can happen with a surgical removal of thyroid?

A

Hupomagnesemia; DiGeorge’s syndrome since there no more PARAthyroid glands

270
Q

What can cause hypocalcemia?

A 
alkalosis via hyperventilation
transfusion of citrated blood
rhabdomyolysis or tumor lysis
subsequent hyperphosphatemia
DiGeorge's syndrome
271
Q

Drugs used for osteoporosis

Denosumab

A

Blocks RANK-L

272
Q

Drugs used for osteoporosis

Teruparatide

A

Synthetic PTH

273
Q

Drugs used for osteoporosis

Calcitonin

A

“Calcitonin Tones-down Calcium”

274
Q

Drugs used for osteoporosis

Raloxifene

A

SERM

275
Q

Patient has:
skull increase in size
Skin overlying things, lower back, and skill warm to touch
increased plasma ALP but normal CA2+ and Pi
Increased urine hydrixyproline

A

Paget’s disease: disorder of bone remodeling

276
Q

Treatment for Paget’s disease?

A

Bisphosphonates:
Etidronate
Pamidroante
Alendronate

277
Q

To sense the free calcium, the parathyroid cell depends upon high levels of expression of the ______.

A

calcium-sensing receptor (CaSR)

278
Q

Calcitonin (CT) is a peptide hormone secreted by the __________ of the thyroid gland. It is released in response to elevated free calcium.

A

parafollicular cells (C cells)

279
Q

function of calcitonin?

A
  • Calcitonin lowers plasma calcium by decreasing the activity of osteoclasts, thus decreasing bone resorption. Calcitonin is useful in the treatment of Paget’s disease, severe hypercalcemia, and osteoporosis.
  • Calcitonin is not a major controller of Ca2+ in humans. Removing the thyroid (with the C cells) or excess of calcitonin via a C cell tumor (med- ullary carcinoma of the thyroid) has little impact on plasma calcium.
  • No deficiency or excess disease has been described.
280
Q

Differences in vitamin D2 and D3?

A

Vitamin D2 (ergocalciferol) is a vitamin but can functionally be considered a prohormone. It is a normal dietary component.

A slightly different form, vitamin D3 (cholecalciferol), is synthesized in the skin. Its active form (1,25 di-OH D3) is a hormone secreted by cells of the kidney’s proximal tubule.

281
Q

How many days do biphosphonates need to be fully active?

A

Bisphosphonates need 2-3 days to be fully effective

282
Q

What is Chvostek’s sign?

A

Chvostek’s sign is induced by tapping the facial nerve just anterior to the ear lobe.

283
Q

What is Trousseau’s sign?

A

Trousseau’s sign is elicited by inflating a pressure cuff on the upper arm.

A positive response is carpal spasm.

284
Q
  • This is a rare familial disorder characterized by target tissue resistance to parathyroid hormone.
  • Exhibits same signs and symptoms as primary hypoparathyroidism except PTH elevated
  • It is usually accompanied by developmental defects: mental retardation, short and stocky stature, one or more metacarpal or metatarsal bones missing (short 4th or 5th finger).
A

Pseudohypoparathyroidism

285
Q

Predictive indices for a secondary disorder:

When the plasma calcium and phosphate are changing in the same direction, the origin is usually a secondary disorder.

  • Secondary hyperparathyroidism: ___________
  • Secondary hypoparathyroidism: ____________
A

both decrease

both increase

286
Q

What is this:

  • It is a loss of bone mass (both mineralization and matrix) with fractures, due to normal age-related changes in bone remodeling as well as additional factors that exaggerate this process.
  • Bone mass reaches a peak subsequent to puberty. Heredity accounts for most of the variation but physical activity, nutrition, and reproductive hormones play a significant role, especially estrogens even in men.
  • Secondary ________ can occur in thyrotoxicosis and particularly with elevations in glucocorticoids.
  • A mainstay of treatment involves the use of bisphosphonates that are rapidly incorporated into bone and reduce the activity of osteoclasts.
  • Calcitonin inhibits bone resorption
A

Osteoporosis

287
Q

Diagnosing lab results:

  • If bone mineral density is 2.5 standard deviations below the average, then this equals to _____.
  • If bone mineral density is 1 to 2.5 standard deviations below the average, then this equals _____.
A

Osteoporosis

osteopenia

288
Q

Osteoporosis treatment:

A

Osteoporosis can also be treated with:

  • Denosumab: inhibitor of RANKL. RANKL is a TNF family of cytokine that activates osteoclasts; denosumab therefore, inhibits osteoclasts.
  • Teriparatide: synthetic PTH. When used intermittently, teriparatide has a stimulatory effect on osteoblastic bone formation.
  • Calcitonin
  • Raloxifene: selective estrogen receptor modifier
289
Q

What is this:

-Origin is the abnormal mineralization of bone and cartilage.
-before plate closure
-expansion of the epiphyseal plates and the most striking abnormalities are the bowing of the legs and protuberant abdomen
-Most common cause in adults is a malabsorption disorder, e.g., celiac
disease; a vitamin D deficiency can also cause
-Rarely caused by enzyme deficiencies when substrate availability is normal.

A

Rickets

290
Q

What is this:

-Origin is the abnormal mineralization of bone and cartilage.
-after plate closure
-symptoms are more subtle.
-Most common cause in adults is a malabsorption disorder, e.g., celiac
disease; a vitamin D deficiency can also cause
-Rarely caused by enzyme deficiencies when substrate availability is normal.

A

osteomalacia

291
Q

Difference between rickets and osteomalacia?

A

Rickets is before plate closure, osteomalacia is after plate closure.

292
Q

Function of PTH at kidneys?

A

At the kidney, PTH:

(1) increases distal tubule calcium reabsorption
(2) inhibits proximal tubule phosphate reabsorption
(3) stimulates the 1-alphahydroxylase enzyme.

293
Q

The most common cause of hypercalcemia is:

A

primary hyperparathyroidism (↑ calcium, ↓ phosphate).

294
Q

The most common cause of primary hypoparathyroidism is:

A

surgery (↓ calcium, ↑ phosphate).

295
Q

Vitamin D de ciency induces a secondary hyperparathyroidism (___ calcium, ___ phosphate) and a decrease in bone mass (rickets, osteomalacia).

A

(↓ calcium, ↓ phosphate)

296
Q

Vitamin D excess induces a ________ and the increased activity of vitamin D directly decreases bone mass.

A

secondary hypoparathyroidism (↑ calcium, ↑ phosphate)

297
Q

Chronic renal failure often induces a hyperphosphatemia and a _________.

A

secondary hyperparathyroidism (↓ calcium, ↑ phosphate).

298
Q

THYROID HORMONES

A

THYROID HORMONES

299
Q

How much iodine or iodide do we need to take every day?

A

Dietary intake of about 500 μg per day is typical, mainly in the form of iodide (I–) or iodine (I). To maintain normal thyroid hormone secretion, 150 μg is the minimal intake necessary. I– is the form absorbed from the small intestine.

300
Q

The functional unit of the thyroid gland is the _____.

A

follicle

301
Q

The lumen is filled with thyroglobulin, which contain large numbers of ______.

A

thyroid hormone molecules

302
Q

Surrounding the lumen are the follicle cells, which function to:

A

both synthesize and release thyroid hormones.

303
Q

Iodine uptake is via a sodium/potassium pump powered sodium/iodide symporter on the basal membrane (NIS). is pump can raise the concentration of I ̄ within the cell to as much as 250 times that of plasma. The pump can be blocked by anions like perchlorate and thiocyanate, which compete with I.

Along the apical membrane, the I ̄ is transported into the lumen by an anion- exchanger called _____.

A

pendrin

304
Q

Enough hormone is stored as iodinated thyroglobulin in the follicular colloid to last the body for ______.

A

2–3 months

305
Q

T3 and T4 Half life:

A

T4 half-life = 6 days

T3 half-life = 1 day

306
Q

Thyroid hormone and cholesterol:

A

Thyroid hormone accelerates cholesterol clearance from the plasma.

307
Q

Thyroid hormone and the Eyes?

A

Thyroid hormones are required for conversion of carotene to vitamin A, and, as a consequence, hypothyroid individuals can suffer from night blindness and yellowing of the skin.

308
Q

Where does the thyroid hormone act on the heart?

A
  • Acting on the SA node, they directly increase heart rate.
  • Cardiac output is increased, and both heart rate and stroke volume are elevated.
  • Systolic pressure increases are due to increased stroke volume, and diastolic pressure decreases are due to decreased peripheral resistance.
  • Thyroid hormones in the normal range are required for optimum cardiac performance.
309
Q

main cause of Primary Hypothyroidism?

A

Most common cause is Hashimoto’s thyroiditis, an autoimmune destruction of the thyroid with lymphocytic infiltration; ↑ TPO antibodies; early stages have a diffusely enlarged thyroid progressing in the later stages to a smaller atrophic and fibrotic gland.

310
Q

end stage of untreated hypothyroidism?

A

Myxedema coma is the end stage of untreated hypothyroidism. The major features are hypoventilation, fluid and electrolyte imbalances, and hypothermia and ultimately shock and death.

311
Q

results of Untreated postnatal hypothyroidism?

A

Untreated postnatal hypothyroidism results in cretinism, a form of dwarfism with mental retardation.

312
Q

What is this:

  • untreated hypothyroidism
  • Individuals often appear normal following delivery but may display some respiratory difficulty, jaundice, feeding problems, and hypotonia.
  • Abnormalities rapidly develop in nervous system maturation, which are irreversible and result in mental retardation.
  • Prepubertal growth, including bone ossification, is retarded in the absence of thyroid hormones.
  • stippled epiphysis
  • There is no evidence that thyroid hormones act directly on growth or bone formation. Rather, thyroid hormone appears to be permissive or act synergistically with growth hormone or growth factors acting directly on bone.
  • Acquired hypothyroidism during childhood results in dwarfism but there is no mental retardation.
  • At puberty, increased androgen secretion drives an increased growth hormone secretion. This will not occur with depressed levels of thyroid hormones.
A

Cretinism

313
Q

another name for Primary Hyperthyroidism

A

Graves’ Disease

314
Q

_________ by definition is the clinical syndrome whereby tissues are exposed to high levels of thyroid hormone (= hyperthyroidism)

A

Thyrotoxicosis

315
Q

The most common cause of thyrotoxicosis is ____________, a primary hyperthyroidism.

A

Graves’ disease

316
Q

What is Graves’ disease?

A

Graves’ disease is an autoimmune problem in which one antibody is directed against the thyroid receptor. It is referred to as the thyroid stimu- lating antibody (TSI or TSH-R).

In addition TPO antibodies and those against thyroglobulin are also found in Graves’ disease.

317
Q

What do you look for in a patient with Grave’s disease by just looking at them?

A

The wide-eyed stare (exophthalmos) in patients with Graves’ is caused by an infiltration of orbital soft tissues and extraocular muscles and the resulting edema, and this process is caused by the antibodies.

318
Q

Untreated hyperthyroidism may decompensate into a condition called

A

Untreated hyperthyroidism may decompensate into a condition called “thyroid storm.”

319
Q

Acute treatment of Grave’s disease

A

l Beta blockers are the most rapid in effect
l Methimazole or propylthiouracil stops the production of hormone
l Iodine in high dose stops incorporation of iodine into the gland
l Steroids such as dexamethasone stop conversion of T4 to T3
l Long-term permanent cure is ablation of the gland with radioactive iodine

320
Q

What is goiter?

A

A goiter is simply an enlarged thyroid and does not designate functional status. A goiter can be present in hypo-, hyper-, and euthyroid states. There is no correlation between thyroid size and function.

321
Q

What catalizyes oxidation, iodination and coupling?

A

Peroxidase

322
Q

What blocks oxidation, iodination and coupling?

A

Thiomides (propulthiouiracil and methimazole)

323
Q

Why are T4 made more than T3?

A

More DIT than MIT

324
Q

Whats the Wolff-Chaikoff effect?

A

the increase in iodine causes temporary decrease in thyroid hormone secretion

325
Q

Thyroxine (T4) + activation via 5’ monodeiodianse =

A

T3

326
Q

Thyroxine (T4) + degradation via 5’ monodeiodianse =

A

Reverse T3

327
Q

Low done makes _____ T3 and _____ T4

A

more T3 and Less T4

328
Q

GROWTH HORMONE

A

GROWTH HORMONE

329
Q

name all anabolic hormones

A

anabolic hormones (i.e., growth hormone, insulin, thyroid hormones, and androgens)

330
Q

First noted sign in puberty in females and males and why?

A

First noted sign in a female is breast development; first by estrogen (promotes duct growth) then progesterone (promotes development of milk-producing alveolar cells).

First noted sign in a male is enlargement of the testes (mainly FSH stimulating seminiferous tubules).

331
Q

Pubic hair development in males and females is dependent on _________.

A

androgen

332
Q

When does growth spur occur in females and in males?

A

In females, the growth spurt begins early in puberty and is near completion by menarche.

In males, the growth spurt develops near the end of puberty.

333
Q

What is this:

  • It is caused by a post pubertal excessive secretion of growth hormone.
  • It is almost always due to macroadenoma (> 1 cm dia) of the anterior pituitary and second in frequency to prolactinomas.
  • There is a slow onset of symptoms, and the disease is usually present for 5 to 10 years before diagnosis.
  • There is characteristic proliferation of cartilage, bone and soft tissue, visceral, and cardiomegaly.
  • Observable changes include enlargement of the hands and feet (acral parts) and coarsening of the facial features, including downward and forward growth of the mandible. Also, increased hat size.
  • Measurement of IGF-I is a useful screening measure and confirms diagnosis with the lack of growth hormone suppression by oral glucose.
A

acromegaly

334
Q

How do you diagnose acromegaly?

A
  • Elevated IGF level
  • Failure of suppression of GH/IGF after giving glucose
  • MRI shows lesion in brain in pituitary
335
Q

Treatment for acromegaly?

A

Surgical removal by trans-sphenoidal approach is first. Removal of an over-producing adenoma is the first treatment in most of endocrinology with the exception of prolactinoma.

336
Q

What is used for treatment if surgery fails?

A

If surgical removal fails, use the growth hormone receptor antagonist, pegvisomant, or octreotide. Octreotide is synthetic somatostatin. Cabergoline is a dopamine agonist used when other medications have failed.

337
Q

if surgery and other methods fail, what is the last resort treatment?

A

Radiation is used last, only after surgery, pegvisomant, octreotide and cabergoline have failed.

338
Q

Where is GnRH made and what does it release?

A

GnRH—synthesized in preoptic region of hypothalamus and secreted in pulses into hypophyseal portal vessels
• produces pulsatile release of LH and FSH
• pulsatile release of GnRH prevents downregulation of its receptors in anterior pituitary

339
Q

Where is LH and FSH made and what does it secrete?

A

LH and FSH—produced and secreted by gonadotrophs of anterior pituitary
• LH stimulates Leydig cells to produce testosterone.
• FSH stimulates Sertoli cells

340
Q

What produces produces negative feedback for LH?

A

Leydig cell testosterone—some diffuses directly to Sertoli cells, where it is required for Sertoli cell function.
• produces negative feedback for LH

341
Q

What produces negative feedback for FSH?

A

Sertoli cell inhibin B—produces negative feedback for FSH

342
Q

What is the substance responsible for this?

  • Some target tissue express this enzyme, which converts testosterone into the more potent dihydrotestosterone.
  • Sexual differentiation: differentiation to form male external genitalia l Growth of the prostate
  • Male-pattern baldness
  • Increased activity of sebaceous glands
  • Synthesis of NO synthase in penile tissue
A

5a-reductase

343
Q

What provides the nourishment that is required for normal spermatogenesis?

A

Sertoli cells

344
Q

DEFINE: any steroid that controls the development and maintenance of masculine characteristics

A

Androgen

345
Q

DEFINE: a natural male androgen of testicular origin, controlled by the luteinizing hormone (LH)

A

Testosterone

346
Q

DEFINE: a more active form of testosterone made by 5-alpha-reductase. It makes the penis, prostate, and scrotum on an embryo.

A

Dihydrotestosterone

347
Q

DEFINE: a synthetic androgen, which is an anabolic steroid sometimes used by athletes

A

Methyl testosterone

348
Q

DEFINE: natural weak androgens (male and female) of adrenal origin, controlled by ACTH. These are DHEA and androstenedione.

A

Adrenal androgens

349
Q

DEFINE: peptide hormones secreted into the blood. They inhibit the secretion of FSH by pituitary gonadotrophs.

A

Inhibins

350
Q

DEFINE: an enzyme that stimulates the aromatization of the A-ring of testosterone, converting it into estradiol. e physiologic importance of this conversion is not understood; however, approximately a third of the estradiol in the blood of men arises from Sertoli cells, and the remainder arises from peripheral conversion of tes- tosterone to estradiol by an aromatase present in adipose tissue.

One sign of a Sertoli cell tumor is excessive estradiol in the blood of the a ected man.

A

Aromatase

351
Q

Normal male development requires the presence of 3 hormones:

A

testosterone, dihydrotestosterone, and the Müllerian inhibiting factor (MIF).

352
Q

Why are men built bigger than women?

A

The capacity of androgens to stimulate protein synthesis and decrease protein breakdown, especially in muscle, is responsible for the larger muscle mass in men as compared with women.

Exogenous androgens (anabolic steroids) are sometimes taken by men and women in an attempt to increase muscle mass.

353
Q

Normally, the scrotum provides an environment that is _______ °C cooler than the abdominal cavity. e cooling is accomplished by a countercurrent heat exchanger located in the spermatic cord. Also, the temperature of the scrotum and the tes- tes is regulated by relative degree of contraction or relaxation of the cremasteric muscles and scrotal skin rugae that surround and suspend the testes.

A

4 °C cooler

354
Q

Erection: Symphathetic or parasympathetic?

A

(a parasympathetic response)

Erection is caused by dilation of the blood vessels in the erectile tissue of the penis (the corpora- and ischiocav- ernous sinuses).

355
Q

This dilation increases the inflow of blood so much that the penile veins get compressed between the engorged cavernous spaces and the Buck’s and dartos fasciae.

_______, working through cGMP, mediates the vasodilation.

A

Nitric oxide (NO)

356
Q

What is Emission?

A

Emission is the movement of semen from the epididymis, vas deferens, seminal vesicles, and prostate to the ejaculatory ducts.

357
Q

Emission: Symphathetic or parasympathetic?

A

The movement is mediated by sympathetic (thoracolumbar) adrenergic transmitters.

358
Q

how is ejaculation caused?

A
  • Ejaculation is caused by the rhythmic contraction of the bulbospongiosus and the ischiocavernous muscles, which surround the base of the penis.
  • Contraction of these striated muscles that are innervated by somatic motor nerves causes the semen to exit rapidly in the direction of least resistance, i.e., outwardly through the urethra.
359
Q

Causes of Hypogonadism:

A
  • Noonan syndrome
  • Klinefelter’s syndrome
  • Hypothalamic-pituitary disorders (Kallman’s syndrome, panhypopituitarism)
  • Gonadal failure/sex steroid synthesis failure
360
Q

DEFINE: an individual with the genetic constitution and gonads of one sex and the genitalia of the other.

A

Pseudohermaphrodite

361
Q

DEFINE: female fetus exposed to androgens during the 8th to 13th week of development, e.g., congenital virilizing adrenal hyperplasia.

A

Female pseudohermaphroditism

362
Q

DEFINE: lack of androgen activity in male fetus, e.g., defective testes, androgen resistance

A

Male pseudohermaphroditism

363
Q

Eyaculation: Symphathetic or parasympathetic?

A

ejaculation requires sympathetic involvement.

364
Q

Days in the menstrual cycle?

A

menstrual cycle (approximately 28 days)

365
Q

What is the first day of bleeding of the menstrual cycle called?

A

By convention, the first day of bleeding (menses) is called day 1 of the menstrual cycle.

366
Q

Name the Phases of the menstrual cycle.

A
  1. Follicular phase
  2. Ovulation phase
  3. Luteal phase
  4. Menses
367
Q

Phase of the menstrual cycle that (first 2 weeks) is also called the proliferative or preovulatory phase. This phase is dominated by the peripheral effects of estrogen, which include the replacement of the endometrial cells lost during menses.

A

Follicular phase

368
Q

Phase of the menstrual cycle that (approximately day 14) is preceded by the LH surge, which induces ovulation.

A

Ovulation phase

369
Q

Phase of the menstrual cycle that (approximately 2 weeks) is dominated by the elevated plasma levels of progesterone, and along with lower levels of secreted estrogen, creates a secretory quiescent endometrium that prepares the uterus for implantation.

A

Luteal phase

370
Q

Phase of the menstrual cycle that Withdrawal of the hormonal support of the endometrium at this time causes necrosis and menstruation.

A

Menses

371
Q

Menstrual cycle phase 1 - 14 is called

A

follicular phase

372
Q

DEFINE: atretic

A

to die

373
Q

________ promotes growth and increased sensitivity to FSH; thus the follicle continues to develop. The remaining follicles, lacking sufficient FSH, synthesize only androgen and become atretic (die).

A

Estradiol

374
Q

What Possess the follicle’s only FSH and what is its function?

A

Granulosa Cells: Possess the follicle’s only FSH receptors. When coupled to FSH, these act via cAMP to increase the activity of aromatase; aromatase converts the androgens to estrogens (mainly estradiol).

375
Q

How do you calculate ovulation day?

A

Cycle length – 14 = ovulation day

376
Q

Menstruation is due to a lack of _______

A

a lack of gonadal sex steroids.

377
Q

What is the main circulating estrogen following menopause?

A

Estrone: Some is secreted from the ovary but much is formed in peripheral tissues such as adipose tissue from androgens. These androgens originate from both the ovary and the adrenal glands.
This is the main circulating estrogen following menopause. Fat cells have aromatase. Adipose tissue creates modest levels of estrogen.

378
Q

Define: Amenorrhea

A

amenorrhea means the lack of menstral bleeding.

379
Q

What causes amenorrhea?

A
  • In the absence of anatomic abnormalities (and pregnancy), it usually indicates a disruption of the hypothalamic–pituitary axis or an ovarian problem.
  • A hypothalamic–pituitary origin would include Kallman’s syndrome, functional hypothalamic amenorrhea, amenorrhea in female athletes, eating disorders, hypothyroidism (possibly because high TRH stimulates prolactin), and pituitary tumors such as prolactinomas.
  • Ovarian causes could be premature ovarian failure (premature meno- pause), repetitive ovulation failure, or anovulation (intermittent bleeding), or a polycystic ovary.
380
Q

What is this:

  • Characterized by elevated LH/FSH ratio.
  • Clinical signs include: infertility, hirsutism, obesity, insulin resistance, and amenorrhea or oligomenorrhea
  • The enlarged polycystic ovaries are known to be associated with increased androgen levels (DHEA).
  • It originates in obese girls. The high extraglandular estrogens (mainly estrone) selectively suppress FSH. Ovarian follicles do have a suppressed aromatase activity and thus a diminished capacity to convert androgen into estrogen, but the adrenals may also contribute to the excess androgens as well.
  • High androgens promote atresia in developing follicles and disrupt feedback relationships. Look for high LH and DHEA levels.
  • The overall result is anovulation-induced amenorrhea with an estrogen- induced endometrial hyperplasia and breakthrough bleeding.
  • Although poorly understood the hyperinsulinemia is believed to be a key etiologic factor.
A

Polycystic Ovarian Syndrome

381
Q

Treatment for amenorrhea in PCOS

A

metformin

382
Q

Treat androgenization with:

A

spironolactone

383
Q

What is this:

  • Defined as an excessive generally male pattern of hair growth.
  • Virilization refers to accompanying additional alterations, such as deepening of the voice, clitoromegaly, increased muscle bulk, and breast atrophy.
  • It is often associated with conditions of androgen excess such as congenital adrenal hyperplasia and polycystic ovarian syndrome.
  • Axillary and pubic hair are sensitive to low levels of androgen.
  • Hair on the upper chest, face (scalp region not involved), and back requires more androgen and represents the pattern seen in males.
  • Circulating androgens involved are testosterone, DHEA, DHEAS, and androstenedione in response to LH and ACTH.
  • Measurements of DHEAS as well as a dexamethasone suppression test helps in separating an adrenal from an ovarian source.
  • Polycystic ovarian syndrome is the most common cause of ovarian androgen excess.
A

Hirsutism

384
Q

what constitutes Low sperm count?

A

Low sperm counts (<20 million/mL of ejaculate)

385
Q

Within a week or two of fertilization, trophoblastic cells of the placenta begin secreting hCG.

What is the function go hCG?

A

In short, hCG prevents regression of the corpus luteum, thus allowing it to continue producing estrogens and proges- terone.

386
Q

Why do we check hCG?

A

hCG doubles in the early weeks of pregnancy. Because it maintains secretion of progesterone from the corpus luteum, progesterone is a sensitive marker of early fetal well-being.

387
Q

What are some markers for fetal well-being?

A

hPL (hCS) is secreted in proportion to the size of the placenta and is an index of placental well-being.

hCG doubles in the early weeks of pregnancy. Because it maintains secretion of progesterone from the corpus luteum, progesterone is a sensitive marker of early fetal well-being.

Estriol: The placenta expresses aromatase. This enzyme converts the A and tes- tosterone from the fetus into estrogens, estriol being the primary one. Thus, estriol becomes a good marker for fetal well-being.

388
Q

Why is there no hypertension in a pregnancy?

A

Cardiac output increases but peripheral resistance decreases and as a result there is no hypertension associated with a normal pregnancy (parallel circuit of placenta)

389
Q

obstetric hemorrhage =

A

Sheehan syndrome

390
Q

The pubic symphysis, cervix, and vagina become more distensible. ese changes make passage of the fetus through the birth canal easier. The peptide hormone __________, which is secreted by the placenta, also promotes these changes. Its action is not essential.

A

relaxin

391
Q

_______ cause contraction of the uterus and are thought to initiate the labor process.

A

Prostaglandins

When a fetus dies, toxic products originating from the fetus increase prostaglandin release in the uterus, thus initiating contractions and a spontaneous abortion (miscarriage). Similarly, administration of prostaglandins induces abortion.

392
Q

Breast feeding is a form of contraceptive???

A

Yes, For the suckling stimulus to inhibit GnRH secretion completely, the stimulus must be prolonged and frequent. Supplementation of the mother’s milk with other fluids or sources of energy reduces the baby’s suckling and allows gonadotropin secretion, follicular growth, and ovulation to occur.

Breastfeeding is a form of contraceptive because it should stop ovulation.

393
Q

GASTROINTESTINAL

A

GASTROINTESTINAL

394
Q

What are the layers of the gastrointestinal tract?

A

Mucosa
Submucosa
Muscularis externa
Serosa

395
Q

What does norepinephrine (NE) do in the gastrointestinal (GI) system?

A

↓ motility
↓ secretions
↑ constriction of sphincters

An increase in sympathetic activity slows processes.

396
Q

What does ACh do in the gastrointestinal (GI) system?

A

↑ motility

↑ secretions

397
Q

What does VIP do in the gastrointestinal (GI) system?

A

↓ constriction of sphincters

398
Q

What does GRP do in the gastrointestinal (GI) system?

A

↑ gastrin

399
Q

What is VIP?

A

VIP = vasoactive intestinal peptide, an inhibitory parasympathetic transmitter

400
Q

What is GRP?

A

GRP = gastrin-releasing peptide; stimulates the release of gastrin from G cells

401
Q

Oscillation of membrane potential is generated by interstitial cells (inter-stitial cells of ________) that act as pacemakers. This is referred to as slow waves or basic electrical rhythm, and if threshold is reached it generates action potentials.

A

Cajal

402
Q

What is this:

  • Failure of the LES to relax, resulting in swallowed food being retained in the esophagus
  • Caused by abnormalities in the enteric nerves
  • Peristaltic waves are weak
A

Achalasia

403
Q

What is this:

  • LES doesn’t maintain tone
  • Acid reflux damages esophageal epithelium
A

Gastroesophageal reflux disease (GERD)

404
Q

What is this:

  • Spasms of esophageal muscle
  • Presents with characteristics of a heart attack (e.g., chest pain)
  • Barium swallow shows repeated, spontaneous waves of contraction
A

Diffuse esophageal spasm

405
Q

What is Dysphagia?

A

difficulty in swallowing.

406
Q

Migrating Motor Complex (MMC)

A
  • A propulsive movement initiated during fasting that begins in the stomach and moves undigested material from the stomach and small intestine into the colon.
  • Repeats every 90–120 minutes during fasting.
  • When one movement reaches the distal ileum, a new one starts in the stomach.
  • Correlated with high circulating levels of motilin, a hormone of the small intestine
  • This movement prevents the backflow of bacteria from the colon into the ileum and its subsequent overgrowth in the distal ileum.
407
Q

What do Parietal cells secrete?

A

HCl

Intrinsic factor combines with vitamin B12 and is reabsorbed in the distal ileum. This is the only substance secreted by the stomach that is required for survival. It is released by the same stimuli that release HCl.

408
Q

What do Chief Cells secrete?

A

Pepsinogen

409
Q

What do Mucous Neck Cells secrete?

A

protective mucus, HCO3 combination

410
Q

There are 3 natural substances that stimulate parietal cells:

A
  • Acetylcholine (ACh), acting as a transmitter; release is stimulated by sight/smell of food and reflexly in response to stomach distension (vagovagal reflex).
  • Locally released histamine; stimulated by Ach and gastrin
  • The hormone gastrin; stimulated by release of GRP
411
Q

As stomach pH falls, ________ is released, which inhibits gastrin and reduces acid secretion (feedback regulation of acid secretion).

A

somatostatin (SST)

412
Q

Most of the control of pancreatic secretion is via:

A

secretin and CCK

413
Q

What makes poop yellow?

A

A major bile pigment, bilirubin is a lipid-soluble metabolite of hemoglobin. Transported to the liver attached to protein, it is then conjugated and excreted as water-soluble glucuronides. ese give a golden yellow color to bile.

414
Q

What makes poop brown?

A

Stercobilin is produced from metabolism of bilirubin by intestinal bacteria. It gives a brown color to the stool.

415
Q

Increased levels of plasma bilirubin produce _______. If severe, bilirubin can accumulate in the brain, producing profound neurological disturbances (_________).

A

jaundice

kernicterus

416
Q

What is celiac disease?

A 
Celiac disease is an immune reaction
to gluten (protein found in wheat) that damages intestinal cells; the end result is diminished absorptive capacity of the small intestine.
417
Q

Hartnup’s disease

A

Many of the amino acid transporters are selective for speci c amino acids. Hartnup’s disease is a genetic deficiency in the transporter for tryptophan.

418
Q

REGION OF THE GASTRO INTESTINAL TRACT?

  • Hypertonic fluid enters this region, and following the movement of some water into the lumen, the fluid becomes and remains isotonic.
  • The absorption of most divalent ions and water-soluble vitamins begins here and continues through the small intestine.
  • Injested iron and calcium tend to form insoluble salts. The acid environment of the stomach redissolves these salts, which facilitates their absorption in the small intestine. Iron and calcium absorption is diminished in individuals with a deficient stomach acid secretion.
  • Calcium absorption is enhanced by the presence of calbindin in intestinal cells, and calcitriol (active vitamin D) induces the synthesis of this protein.
  • Intestinal cells express the protein ferritin, which facilitates iron absorption.
A

Duodenum

419
Q

REGION OF THE GASTRO INTESTINAL TRACT?

  • Overall, there is a net reabsorption of water and electrolytes.
  • The cellular processes involved are almost identical to those described in the renal physiology section for the cells lining the nephron proximal tubule.
A

Jejunum

420
Q

REGION OF THE GASTRO INTESTINAL TRACT?

  • Net reabsorption of water, sodium, chloride, and potassium continues, but there begins a net secretion of bicarbonate.
  • It is in the distal ileum, and only in the distal ileum, where the reabsorp- tion of bile salts and intrinsic factor with vitamin B12 takes place.
A

Ileum

421
Q

REGION OF THE GASTRO INTESTINAL TRACT?

  • This part does not have digestive enzymes or the protein transporters to absorb the products of carbohydrate and protein digestion.
  • Also, because bile salts are reabsorbed in the distal ileum, very few lipid- soluble substances are absorbed in the colon.
  • There is a net reabsorption of water and sodium chloride, but there are limitations.
  • Most of the water and electrolytes must be reabsorbed in the small intestine, or the it becomes overwhelmed.
  • Most of the water and electrolytes are absorbed in the ascending and transverse colon; thereafter, it has mainly a storage function.
  • The colon is a target for aldosterone, where it increases sodium and water reabsorption and potassium secretion.
  • Because there is a net secretion of bicarbonate and potassium, diarrhea usually produces a metabolic acidosis and hypokalemia. It commonly presents as hyperchloremic, nonanion gap metabolic acidosis, as described in the acid-base section.
A

Colon

422
Q

what is diarrhea?

A

Except for the infant where it can be hypotonic, diarrhea is a loss of isotonic fluid that is high in bicarbonate and potassium.

KAPLAN USMLE (1 decks)

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