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Endo/Repro > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What are the two parts of the adrenal (suprarenal) glands

A

Cortex

Medulla

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2
Q

Function of cortex in the adrenal glands

A

Secretes corticosteroids derived from cholesterol

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3
Q

Function of medulla in the adrenal glands

A

Secretes catecholamines derived from tyrosine

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4
Q

Corticosteroids released from the adrenal cortex (3)

A 
Glucocorticoids (eg- Cortisol)
Mineralcorticoids (ex- Aldosterone)
Sex steroids (testosterone)
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5
Q

Catecholamines secreted from the adrenal medulla (2)

A

Epinephrine and norepinephrine

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6
Q

Layers of the adrenal cortex (superficial to deep)

A

Zona glomerulosa
Zona fasciculata
Zona Reticularis

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7
Q

Layers of the adrenal glands

A

Capsule
Adrenal cortex
Adrenal medulla

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8
Q

Zona glomerulosa is ____% of the adrenal cortex thickness

A

15%

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9
Q

What does the Zona glomerulosa secrete? What is the primary hormone?

A

Mineralocorticoids

Primary hormone = aldosterone

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10
Q

What stimulates aldosterone release?

A

Angiotensin II and Potassium

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11
Q

Function of Aldosterone

A

Controls blood pressure and blood volume
Controls electrolyte balance through the kidney
Causes reabsorption of Na, Cl, H20
And excretion of K and H

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12
Q

______% of adrenal cortex thickness is the Zona fasciculata

A

75%

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13
Q

Zona fasciculata secretes:

Its primary hormone is:

A

Glucocorticoids

Primary hormone is cortisol (stress hormone)

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14
Q

The zona fasciculata is under what control?

A

Hypothalamic-pituitary axis control (CRH and ACTH)

Cortisol provides negative feedback to the hypothalamus and the anterior pituitary

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15
Q

______% of thickness in the adrenal cortex that is the zona reticularis

A

10%

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16
Q

What does the zona reticularis secrete?

Primary hormones?

A

Adrogens

DHEA (dehydroepiandosterone) and androstenedione

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17
Q

Zona Reticularis control mechanism is influenced by:

A

ACTH

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18
Q

Dihydrotesterone and estradiol synthesis occur where?

A

In peripheral tissues and gonads

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19
Q

How is pregnenolone made?

A

Cholesterol enters mitochondria of cells and is cleaved by cholesterol desmolase (P-450scc)

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20
Q

Rate limiting step in adrenal steroid production .

Why?

A

Synthesis of pregnolone

It can be converted into any of the other steroid hormones

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21
Q

Adrenal cholesterol is most provided by:

A

Blood LDL

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22
Q

Adrenal cholesterol is obtained by:

A

Receptor mediated endocytosis (rate influenced by ACTH)

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23
Q

______ release cholesterol from the endosomes

A

Lysosomes

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24
Q

Synthesis of hormones occurs where?

A

In mitochondria and ER

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25
Q

Aldosterone- ____% of all mineralcorticoid activity. Very ___

A

90%

Potent

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26
Q

Mineralocorticoids (5)

A 
Aldosterone
Cortisol
Corticosterone
Cortisone
Deoxycorticosterone
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27
Q

Aldosterone synthesis steps

A 
Cholesterol 
To pregnenolone 
Progesterone
11-Deoxycortocosterone DOC
Corticosterone
18 (OH) Corticosterone 
Aldosterone
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28
Q

Cortisol- ____% of ______ activity, very potent

A

95%

glucocorticoid

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29
Q

Glucocorticoid minor in humans

A

Corticosterone

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30
Q

Glucocorticoids that are almost as potent as cortisol

A

Cortisone

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31
Q

Synthetic glucocorticoids

A

Prednisone (cortisol X 4)
Methylprednisone (Cortisol X 5)
Dexamethason (Cortisol X 30)

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32
Q

90-95% of cortisol is bound to:
Some to:
The rest:

A

Transcortin (cortisol-binding globulin)
Some to albumin
The rest (tiny amount) as free cortisol

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33
Q

Half life of cortisol

A

60-90 min

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34
Q

60% of aldosterone is bound to _____
40 % :

Half life is:

A

Albumin

Free aldosterone

20 min

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35
Q

Transcortin is produced where?

A

In the liver

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36
Q

________ proteins slow hormone inactivation. They help maintain:

A

Trasport proteins

Helps maintain hormones in circulation

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37
Q

All adrenal cortical hormones are metabolized to :

A

Inactive conjugated forms in the liver (mostly conjugated with glucuronic acid)

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38
Q

25% of inactive conjugated forms are excreted where?

The remaining are excreted:

A

Into bile

In the urine

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39
Q

Cortisol also binds to _________ receptors

A

Mineralocorticoids receptors

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40
Q

What has greater activity than cortisol?

A

Aldosterone (3000x greater)

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41
Q

Kidney has a receptor to metabolize ______ to _____

A

Cortisol to cortisone (11beta-hydroxysteroid) which nullifies most of cortisol’s mineralocorticoid effects there.

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42
Q

Aldosterone has effects on:

A

Sweat glands, salivary glands, intestinal epithelial cells

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43
Q

What are aldosterone’s effects on the kidney?

A

Increases renal tubular reabsorption of sodium and potassium secretion - especially in the principal cells of the distal tubules and collecting tubules

Also stimulates secretion of H+ via H+/ATPase in the intercalated cells of collecting tubules

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44
Q

Aldosterone antagonists

A

Spironalctone

Eplerenone

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45
Q

Sodium channel blockers

A

Amiloride

Triamterene

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46
Q

ECT sodium concentration only ____ slightly with:

A

Rises

Increased aldosterone secretion

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47
Q

What are physiologic mechanisms that keep sodium concentration for getting too high?

What are these called?

A

Osmotic absorption of water
Increased thirst and water intake
Resulting volume/pressure increase stimulates pressure disrespect and natriuresis

Called the “aldosterone escape”

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48
Q

Diseases of excess aldosterone

A

Hypokalemia

Alkalosis

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49
Q

Hypokalemia is due to:

It causes:

A

Increased loss of K+ in the urine and uptake into cells

Causes severe muscle weakness

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50
Q

Alkalosis is due to:

A

Stimulation of H+ pump in intercalated cells

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51
Q

Diseases of deficient aldosterone

A

Hyperkalemia

NaCl depletion and blood volume depletion progressing to shock

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52
Q

Hyperkalemia is due to:

A

Retention of K+ in the ECF

Cardiac toxicity

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53
Q

How does aldosterone increase reabsorption of NaCl and secretion of K+?

A

By the ducts of the salivary glands and sweat glands (helps to conserve Na+ in times if increased secretion of sweat or saliva)

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54
Q

Where does aldosterone enhance Na+ absorption? What does this lead to?

A

By the intestines

Leads to the absorption water and Cl- (and other anions)

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55
Q

What would happen to the intestines without aldosterone

A

NaCl and water are unabsorbed which will lead to diarrhea

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56
Q

How does aldosterone enter the cell?

A

Diffusion

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57
Q

Receptor that binds with aldosterone

A

Mineralocorticoid receptor (MR)

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58
Q

After MR/aldosterone complex diffuses into the nucleus, what is induced?

A

DNA transcription into mRNA

Which is then translated into proteins such as: Na+/K+ ATPase and epithelial sodium channels

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59
Q

What increases aldosterone secretion?

A

Increased K+ concentration in the ECF

And

Angiotensin II concentration in the ECF

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60
Q

What slightly decreases aldosterone secretion?

A

Increased Na+ ion concentration in the ECF

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61
Q

What is necessary for aldosterone secretion?

A

ACTH from the anterior pituitary gland

But it has little effect in controlling the RATE of secretion

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62
Q

At least 90% of glucocorticoid activity is due to:

A

Cortisol (aka hydrocortisone)

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63
Q

_____ provides a smaller amount of glucocorticoid activity?

A

Corticosterone

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64
Q

Cortisol effects what 4 things?

A

Carbohydrate metabolism

Protein metabolism

Fat metabolism

Stress and inflammation resistance

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65
Q

Cortisol and carbohydrate metabolism stimulates:

A

Gluconeogenesis

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66
Q

Gluconeogenesis induces

A

Production of enzymes in the liver to convert amino acids into glucose

Mobilization of amino acids from tissues outside liver (mainly muscle)

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67
Q

Newly made glucose is stored largely as:

A

Glycogen in the liver; access by epinephrine and glucagon as needed

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68
Q

Decreased glucose utilization by cells is likely due to

A

inhibition of NADH oxidation

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69
Q

Elevated blood glucose is due to:

A

The combined effects of gluconeogenesis and decreases glucose utilization of cells

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70
Q

Elevated blood glucose causes

A

Insulin secretion (Cortisol also decreases insulin sensitivity)

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71
Q

Excess in cortisol secretion causes:

A

Adrenal diabetes

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72
Q

Reduction of cellular protein (DOES/DOES NOT) occur in the liver.

What does this do the protein?

A

Does not

Decreases protein synthesis

Increases protein catabolism

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73
Q

Excess of cellular protein can cause

A

Severe weakness

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74
Q

The liver (INCREASES/DECREASES) plasma protein production

A

Increases

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75
Q

Since plasma proteins are largely produced by the _______, they increase in the _______.

A

Liver

Blood

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76
Q

Increased blood amino acids decrease:

They increase:

A

Decrease transport of amino acids into extrahepatic cells

Increase release of amino acids into blood from protein catabolism

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77
Q

Amino acids in the liver are used for what?

A

To make plasma proteins, increase protein synthesis and for gluconeogenesis

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78
Q

Cortisol causes

  • Release of free fatty acids from:
  • increased _____ of fatty acids in cells
A

Adipocytes

Oxidation

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79
Q

Excess cortisol leads to fat:

A

Accumulation in the face and torso

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80
Q

In regards to fat, glucose causes:

A

Decreased glucose utilization
Decreased sensitivity to insulin
Increased lypolysis

Release of:
Glycerol

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81
Q

In regards to muscle, increase of glucose causes:

A

Increase in:
Protein degradation

Decrease in:
Protein synthesis
Glucose utilization
Sensitivity to insulin

Release of:
Amino acids

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82
Q

In the liver, increased amino acids and glycerol causes:

A 
Increase in:
Glycogen storage
Gluconeogenesis
Activity of enzymes
Amounts of enzymes

Release of:
Glucose

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83
Q

Types of stress (physical or neurogenic)

A

Trauma or surgery

Infection of any debilitating disease

Intense heat or cold

Psychological distress

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84
Q

Stress causes increase in:

A

ACTH secretion which then increases cortisol secretion

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85
Q

Stages of inflammation (5)

A

Inflammatory cells release histamine, bradykinin, prostaglandins, etc. (pain)

Increase in blood flow (erythema, heat)

Increased permeability, leakage of plasma into ISF including protein (edema)

Infiltration by leukocytes

Ingrowth of fibrous tissue and healing

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86
Q

2 basic anti inflammatory effects of cortisol

A

1- block early stages of inflammation (prevention of inflammation)

2- Causes rapid resolution of inflammation to allow healing

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87
Q

Inflammation prevention…

  • stabilizes _________
  • decreases ______
  • decreases________
  • suppresses___________
  • Lowers ______
A 
Stabilizes lysosomal membranes 
Decreases capillary permeability 
Decreases migration of leukocytes 
Suppresses the immune system 
Lowers fever
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88
Q

What are the two ways of resolving inflammation?

A

Blocks inflammatory mediators

Speeds healing by mobilization of aa for tissue repair and increasing glucose and FA

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89
Q

_______ are given therapeutically to reduce inflammation

A

Glucocorticoids

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90
Q

T or F: glucocorticoids fixes the underlying problem of inflammation

A

False; glucocorticoids DOESNT fix the underlying problem of inflammation just reduces it therapeutically

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91
Q

Most metabolic effects of steroid hormones require ______ minutes for proteins to be synthesized and ________ for full effect

A

45-60 min

Hours-days

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92
Q

________ from the AP (anteiror pituitary) stimulates cortisol secretion

A

ACTH (corticotropin)

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93
Q

What mechanism is used to stimulate cortisol release via ACTH?

A

Adenylyl cyclase/ cAMP

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94
Q

_________ leads to the activation of ________ which converts cholesterol to pregnenolone

A

PKA; desmolase

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95
Q

______ is inturn controlled by corticotropin releasing factor (CRH) from the hypothalamus

A

ACTH

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96
Q

Cortisol excess exerts negative feedback on what glands?

A

Pituitary gland and hypothalamus

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97
Q

_______ inhibits the hypothalamus and anterior pituitary

A

Cortisol

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98
Q

Pain from physical damage is transmitted to the ________

***stress source

A

Median eminence

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99
Q

Mental stress from the __________ is transmitted to the _________

A

Limbic system; posterior medial hypothalamus

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100
Q

_________ is the precursor to ACTH

A

Pro-opiomelanocortin (POMC)

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101
Q

POMC also produces what hormones other than ACTH?

A

Melanocytes stimulating hormone (MSH)
Lipotropin
Endorphin

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102
Q

Cortisol stabilizes:

This decreases:

A

Lysosomal membranes

Decreases release of pro-inflammatory enzymes

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103
Q

Cortisol decreases:

A

Capillary permeability

Migration of leukocytes

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104
Q

How does cortisol decrease migration of leukocytes?

A

By blocking inflammatory mediators

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105
Q

Cortisol suppresses what system

A

The immune system (especially T cells)

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106
Q

How does cortisol lower fever?

A

By decreasing IL-1 production

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107
Q

Cortisol inactivates or removes:

A

Inflammatory products

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108
Q

Cortisol speeds healing by:

A

Mobilization of amino acids for tissue repair

Increasing glucose and fatty acid availability for critical systems

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109
Q

Glucocorticoids are given therapeutically to:

A

Reduce inflammation

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110
Q

DHEA and androstenedione are continually secreted by ________, especially during:

A

Zona Reticularis

Fetal development

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111
Q

Much of pubic and axillary hair in remains is due to

A

Adrenal adrogens

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112
Q

Small amounts of ____ and _____ are secreted from the adrenals

A

Estrogens

Progesterone

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113
Q

Most abundant steroid hormone

A

DHEA

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114
Q

DHEA causes cells to make

A

Testosterone and estradiol

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115
Q

DHEA levels decline with:

A

Age, stress and disease

Lower levels associate with increased disease and increased mortality

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116
Q

DHEA’s association with cortisol

A

It balances and counteracts cortisol’s effects

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117
Q

DHEA reduces

A

Pain and inflammation

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118
Q

DHEA improves:

A

Immune system function,

And, in women, fertility and sexual function

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119
Q

Addison’s disease, AKA:

A

Hypoadrenalism

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120
Q

Primary hypoadrenalism

A

Autoimmunity causes atrophy of the adrenal glands

Destruction of tumor or tuberculosis

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121
Q

Secondary hypoadrenalism

A

Impaired pituitary and decreased release of ACTH

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122
Q

Symptoms of Addison’s disease

A

Bronze pigmentation of skin

Hypoglycemia

Changes in distribution of body hair

Postural hypotension

GI disturbances

Weight loss

Weakness

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123
Q

Adrenal crisis in Addison’s disease

A

Profund fatigue

Dehydration

Vascular collapse (decreased BP)

Renal shut down

Decreased serum NA

Increased serum K

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124
Q

Mineralocorticoid deficiency :

Decreased:

A

ECF volume, hypotension

Cardiac output- shock and death

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125
Q

______ and ______ are continually secreted by the zona reticularis especially during fetal development

A

DHEA and androstenedione

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126
Q

Testosterone and estradiol are synthesized from _____

A

DHEA

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127
Q

Levels of DHEA _____ with age, stress, and disease

A

Decline

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128
Q

______ balances and counteracts cortisol effects

A

DHEA

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129
Q

_______ reduces pain and inflammation, improves immune system functions and improves fertility and sexual function

A

DHEA

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130
Q

What is the disease associated with hypoadrenalism?

A

Addison’s disease

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131
Q

What is the disease associated with hyperadrenalism?

A

Cushing syndrome

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132
Q

What is primary Addison’s disease? (Hypoadrenalism)

A

Autoimmunity causes atrophy of the adrenal glands

Destruction by tumor or tuberculosis

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133
Q

Symptoms of Mineralocorticoid deficiency

A

Hyponatremia

Hyperkalemia

Acidosis

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134
Q

Review slide 49 for glucocorticoid deficiency

A

Review slide 49

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135
Q

In primary hypoadrenalism, _______ levels are high, causing MSH to be hyper-secreted

A

ACTH

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136
Q

Hyperadrenalism, AKA

A

Cushing’s syndrome

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137
Q

Causes of Cushing’s syndrome

A

Adenoma of the ant. Pituitary- secretes too much ACTH (most common)

Hypothalamus produces too much CRH (Rare)

Tumor elsewhere in the body secretes ACTH

Adenoma of the adrenal cortex- secretes too much cortisol

Prolonged glucocorticoid therapy

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138
Q

Symptoms of Cushing’s syndrome

A

“Buffalo torso” and “moon face”

Acne and excess facial hair

Hyperglycemia (adrenal diabetes)

Severe weakness from protein depletion in the muscles

Osteoporosis (lack of collagen)

Purple stria (tearing of subcutaneous tissue)

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139
Q

What causes buffalo torso and moon face in cushing’s syndrome?

A

Mobilization of fat from the extremities to the trunk and edema

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140
Q

Primary aldosteronism, AKA

A

Conn’s syndrome

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141
Q

Causes of conn’s syndrome

A

Tumor of zona glomerulosa

Hypersecretion of aldosterone

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142
Q

Features of Conn’s syndrome (6)

A

Hypokalemia

Metabolic Alkalosis

Slight increase in ECF and blood volume

Hypertension

Periodic muscle paralysis from hypokalemia

Decreased renin production

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143
Q

Conn’s syndrome should be considered in any hypertensive pt with:

A

Muscle weakness, polydipsia, and/or hypokalemia

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144
Q

Causes of Conn’s syndrome

A

75%- Adrenal adenoma

25%- Adrenal hyperplasia

Rarely- Adrenocortical cancer

145
Q

Adrenal medulla is usually studied along with the:

A

Autonomic nervous system

146
Q

Catecholamines synthesis occurs where?

From what?

A

In the cytoplasm of chromatin cells

From tyrosine

147
Q

Stimulation of release of catecholamines

A

Direct sympathetic innervation

148
Q

Alpha 1,2 receptors are used for: (6)

A 
Vasoconstriction
Iris dilation
Intestinal relaxation
Bronchoconstriction 
Increased heart contractility 
Hepatic glucose production
149
Q

Beta 1,2 receptors stimulate (7)

A 
Vasodilation 
Increased heart rate
Increased heart contractility
Intestinal relaxation
Bronchodilator
Glycogenolysis
Lipolysis
150
Q

Steps of short term stress response

A

1- hypothalamus sends nerve signals via spinal cord

2- nerve signals are sent to adrenal medulla

3- epinephrine and norepinephrine are secreted

151
Q

Long term stress response steps

A

1- Hypothalamus stimulates anterior pituitary with releasing hormone

2- anterior pituitary releases ACTH into blood

3- ACTH sent to the adrenal cortex

4- Corticosteroids are released into bloodstream

152
Q

Review slide 57

A

Review slide 57

153
Q

Pheochromocytoma, AKA:

A

Catecholamine- secreting adrenal tumor

154
Q

Epidemiology of Pheochromocytoma

A

Adults- both sexes, all ages (especially 30-50 years)

155
Q

Biological behavior of Pheochromocytoma

A

90% benign, 10% malignant

156
Q

Pheochromocytoma secretes high levels of ________, most secrete ________

A

High levels of catecholamines, most secrete norepinephrine.

157
Q

Clinical presentation of Pheochromocytoma

A

Episodic or sustained hypertension, sweating, palpitations, hyperglycemia, glycosuria

158
Q

Macroscopic features of Pheochromocytoma

A

Mass, often hemorrhagic; 10% bilateral; 10% extra-adrenal

159
Q

Microscopic features of Pheochromocytoma

A

Nests of large cells, vascular stroma

160
Q

Excess inflammation can cause

A

Can prevent or slow healing

161
Q

Most metabolic effects of cortisol require ______ (time) for proteins to be synthesized, and (time) for full effect

A

45-60 min

Hours-days

162
Q

For steroid hormone metabolism:
The hormone enters the ______, and attaches to the _____ _____.

This creates a _____ _____ ____.

A

Cytoplasm
Steroid receptor
Hormone-receptor complex

163
Q

For steroid hormone synthesis:

After binding to the steroid receptor in the cytoplasm, what happens to the hormone-receptor complex?

A

It enters the nucleus

Here it binds to receptor sites on chromatid, activating mRNA transcription

164
Q

ACTH aka:

A

Corticotropin

165
Q

ACTH comes from the:

It stimulates :

A

Anterior pituitary

Cortisol secretion

166
Q

How does ACTH stimulate cortisol secretion

A

Adenylyl Cyclase/cAMP mechanism

Protein kinase A leads to activation of desmolase, which converts cholesterol to prefnenolone

167
Q

ACTH is controlled by ______ which is secreted by the ______

A

Corticotropin releasing factor

Hypothalamus

168
Q

Review slide 44

A

Review slide 44

169
Q

Cortisol inhibits the:

A

Hypothalamus and anterior pituitary

170
Q

Cortisol stimulates (4)

A

Gluconeogenesis
Protein mobilization
Fat mobilization
Stabilizes lysosomes

171
Q

Stress sources for pain:

Mental stress:

A

Pain- from physical damage - transmitted to the median eminence

Mental stress- From the lambic system
- transmitted to the posterior medial hypothalamus

172
Q

Precursor to ACTH

A

Pro-opiomelanocortin (POMC)

173
Q

Breakdown of POMC also produces

A

Melanocyte stimulating hormone
Lipotropin
Endorphin
And a few others

174
Q

When ACTH rate is high, this means that:

A

Other POMC products may also be overproduced

175
Q

What type of gland is the pancreas

A

Both endocrine and exocrine

176
Q

Pancreatic acini is (ENDOCRINE/EXOCRINE)

Secretes:

A

Exocrine

Digestive juices

177
Q

Islets of Langerhans is (ENDOCRINE/EXOCRINE)

Cells inside them

A

Endocrine

Alpha cells
Beta Cells
Delta Cells

178
Q

Alpha cells in the pancreas (islets) release

A

Glucagon

179
Q

Beta cells in the pancreas (islets) release:

A

Insulin, amylin

180
Q

Delta cells in the pancreas (Islets) releases

A

Somatostatin

181
Q

Insulin is associated with:

A

Energy abundance

182
Q

Insulin is secreted when?

A

When energy rich foods are eaten (especially carbohydrates)

Stimulated by high blood glucose

183
Q

Insulin promotes:

A

Storage of excess energy

184
Q

Insulin effects in the liver

A

Glucose -> Glycogen

185
Q

Insulin effects in adipocytes

A

Fatty acids -> TAGs

186
Q

Insulin effects of other cells

A

Amino acids -> protein

187
Q

After translation, insulin is initially

A

Preproinsulin

188
Q

Preproinsulling is cleaved in the ______, to form:

A

ER

Proinsulin

189
Q

Proinsulin is cleaved in the _______ into:

A

Golgi

Insulin and “C pepetide”

190
Q

What happens to insulin once cleaved?

A

It is packaged into secretory vesicles

When released, it circulates unbound

191
Q

Half life of insulin

A

Approx 6 min

192
Q

C peptide binds to a ____ _____ and activates

A

Membrane receptor

Some enzymes

193
Q

How is c-peptide used clinically?

A

Used as a measurement in insulin-treated patients

Can be assessed for any endogenous insulin production

194
Q

C peptide is useful for

A

Monitoring beta cell function in people with diabetes who are on insulin therapy

195
Q

Insulin receptor has ___ subunits

A

4

196
Q

What type of receptor is an insulin receptor

A

Enzyme-linked

197
Q

Autophosphorylation of the insulin receptor activates:

A

Tyrosine kinase

198
Q

Tyrosine kinase activates

A

Tissue specific IRS (insulin receptor substrate) enzymes

199
Q

Insulin receptor substrates:

A 
Growth and gene expression
Glycogen synthesis
Fat synthesis
Protein synthesis
Glucose transport
200
Q

____% of body cells increase glucose uptake

A

80

201
Q

Glucose uptake- most profound effect is in:

A

Muscle and fat

202
Q

Most brain cells are _____ independent

A

Insulin

203
Q

Mechanism of glucose uptake

A

Fusion of vesicles containing glucose (GLUT4)

Transport proteins to the cell membrane

204
Q

GLUT1 is responsible for:

A

Baseline uptake

***Ubiquitous and present in many cells

205
Q

GLUT2 is found where?

A

Liver
Kidney
Pancreatic Beta cells
Intestine

THIS IS BI-DIRECTIONAL

206
Q

GLUT3 found in:

A

Neuron
Placenta

Has high affinity

207
Q

GLUT 4 found in

It is ______ dependant

A

All muscles
Adipocytes
Heart

Insulin dependant

208
Q

Muscle mostly depends on _____ ______ between meals

A

Fatty acids

209
Q

Circumstances when muscle uses more glucose

A

Exercise- Increases permeability to glucose

After a meal- Insulin increases glucose uptake, then stored as glycogen if not needed

210
Q

Mechanism of storing glucose as glycogen in the liver

A

Insulin inactivates glycogen phosphorylase

Stimulates glucokinase

Stimulates glycogen synthase

211
Q

What happens to excess glucose after glycogen is maximized

A

It is converted to fatty acids (VLDL)

212
Q

What happens in the liver when there is lack of insulin

A

Reverse effects on phosphorylase, glucokinase and glycogen synthase

Glycogen is broken down

213
Q

What is activated to release glucose into the blood? Why?

A

Glucose phosphates

Insulin is low.

214
Q

Most brain cells are permeable to _____ and do not need ____

A

Glucose

Insulin

215
Q

Brain normally only uses glucose for _______, therefore depends on:

A

Energy

Blood glucose

216
Q

When blood glucose falls to low in the brain, what happens?

A

Hypoglycemic shock occurs (fainting, seizures and coma)

217
Q

Insulin in adipose promotes:

A

Fatty acid synthesis by liver that is then transported to fat cells (VLDL)

Also glucose transport into fat cells, mostly to form glycerol

218
Q

Insulin in adipose inhibits

A

Hormone-sensitive lipase (HSL), thereby inhibiting release of fat from adipocytes

219
Q

For protein metabolism, insulin promotes:

It prevents:

A

Promotes protein formation

Prevents protein degradation

220
Q

For protein metabolism, insulin stimulates:

It inhibits:

A

Amino acid uptake by cells

Protein catabolism

221
Q

For protein metabolism, insulin increases:

It decreases:

A

mRNA translation into new protein
And
Gene expression for enzymes needed for carb, fat, and protein storage

Decreases: Liver gluconeogenesis (amino acids are NOT converted to sugar)

222
Q

What causes weight gain the most?

A

Growth hormone AND insulin together

223
Q

When insulin is deficient, what happens to hormone sensitive lipase

A

It becomes active, releases large amounts of fatty acids and glycerol into the blood

224
Q

When insulin is deficient, what happens to glucose concentrations?

A

They rise

225
Q

When insulin is deficient, what happens to plasma cholesterol and phospholipids?

A

They rise- accelerating atherosclerosis

226
Q

Excessive beta oxidation of fats in the liver creates:

A

Excess acetyl-CoA, which is then converted to Acetoacetic acid

227
Q

What happens to excess acetoacetic acid that cannot be metabolized back to acetyl-CoA in other tissues

A

It forms ketone bodies (Beta-hydroxybutyric acid and acetone)

228
Q

Ketoacidosis may lead to:

A

Coma and death

229
Q

Acetoacetate is created from:

It is converted into:

A

Breakdown of fatty acids

Into BHB or turned into acetone

230
Q

Beta-hydroxybutyric acid formed from:

Why is this not technically a ketone?

A

Acetoacetate

Because of its structure- we consider it as one within the keto diet

231
Q

Acetone is created as:

It breaks down:

How is it removed?

A

As a side product of acetoacetate

Quickly

From the body through the waste or the breath

232
Q

Norepinephrine ->normetanephrine via what enzyme?

Epinephrine-> metanerphine via what enzyme

A

COMT (catechol-O-methyltransferse)

COMT

232
Q

Epinephrine and norepinephrine are converted to dihydroxymanfdelic acid via what enzyme?

A

MAO ( monoamine oxidase)

233
Q

What happens when there is a protein depletion and increased plasma amino acids?

A

Catabolism of proteins increase
Large amounts of amino acids are released into the plasma
Some amino acids are used for gluconeogenesis (also glycerol and lactic acid)

234
Q

Glucose enters/leaves the pancreatic beta cell via the

A

GLUT 2 channel

235
Q

What happens with pancreatic beta cell when blood glucose is high

A

More glucose enters the cell, stimulating ATP synthesis

236
Q

ATP closes the ____ channel, causing

A

K+

Depolarization

237
Q

What happens when K+ channel closes in pancreatic beta cell

A

V-gated Ca+2 channel opens and Ca+2 triggers exocytosis of insulin

238
Q

What inhibits exocytosis of insulin in the pancreatic beta cell

A

Somatostatin and NE

239
Q

normal fasting blood glucose level:

A

80-90 mg/100 ml

240
Q

What happens immediately after acute elevation of blood glucose? (After meal)

A

10x increase in insulin

241
Q

What happens w insulin about 15 min after meal?

A

Increase due to new insulin synthesis (there is a dip between the 1st and second phase)

242
Q

Most potent amino acids

A

Arginine and lysine

243
Q

There is a higher response with arginine and lysine than _____ alone, when they are all combined together

A

Glucose

244
Q

Gastrointestinal hormones that control insulin secretion

A

Gastric, secretin, cholecytokinin, glucose-dependent insulinotrophic peptide (AKA gastric inhibitory peptide)

245
Q

Gastrointestinal hormones cause:

A

An “anticipatory” increase in blood insulin

246
Q

Other hormones that control insulin secretion

A

Glucagon
Growth hormone
Cortisol

247
Q

Factors that increase insulin secretion:

A 
Increased blood glucose
Increased blood FFA
Increased blood amino acids
Gastrointestinal hormones (gastric, CCK, secretin, GIP) 
Glucagon, growth hormone, cortisol
Parasympathetic stimulation (Ach)
Insulin resistance, obesity
248
Q

Factors that decrease insulin secretion

A 
Deceased blood glucose
Fasting 
Somatostatin
Alpha-adrenergic activity (NE)
Leptin
249
Q

Type 1 diabetes mellitus

A

Insulin dependent (IDDM)
Lack of insulin secretion by pancreas
Autoimmune disease against beta cells, viral infections, genetics— there are factors

250
Q

Type II diabetes mellitus

A

Non-insulin dependent (NIDDM)

Decreased sensitivity to insulin (insulin resistance)

251
Q

Signs and symptoms of type 1 diabetes

A 
Increased blood glucose
Glucose readings
Polyurea
Dehydration
Polydipsia
Polyphagia with weight loss
Blood vessel damage
Peripheral neuropathy
Hypertension/kidney disease
Atherosclerosis
Ketoacidosis (metabolic acidosis)
252
Q

Which type of diabetes is more common

A

Type II- 90-95% more common

253
Q

Type II diabetes usually occurs:

It is often associated with:

A

After age 30, gradual onset

Obesity

254
Q

Type II insulin levels:

Also comes with:

A

Increased

Mild hyperglycemia

Beta cell exhaustion

Less problems with ketoacidosis than type 1

255
Q

Diabetes complications:

Macrovascular:

A 
Stroke
Heart disease and hypertension
Peripheral vascular disease
Foot problems
Unstable plaque ruptures
256
Q

Microvascular diabetes complications

A 
Diabetic eye disease (retinopathy and cataracts)
Renal disease
Neuropathy
Foot problems
Blood clot blocks blood flow
257
Q

Hyperinsulin

A

Too much insulin

258
Q

Causes of too much insulin

A

Adenoma of islets of langerhans (rare)

Insulin “shock”

259
Q

Insulin shock-
Insulin causes:
Nervous system ____

A

Excessive drop in plasma glucose

Starves

260
Q

Insulin shock initially leads to:

Then hypoglycemia progresses to:

A

Hallucinations, tremors, nervousness

Seizures, coma

261
Q

What causes insulin shock?

A

Too much insulin in the blood due to overdose during an insulin shock

262
Q

Too much insulin results in:

A

Too little blood glucose

263
Q

What will counteract insulin shock

A

Immediate intake of sugar

264
Q

Structure of glucagon

A

Large polypeptide

265
Q

Glucagon is secreted by

A

Alpha cells of the islets

266
Q

Effects of glucagon:

A 
Increase glycogenolysis (liver)
Increased gluconeogenesis (liver)

Activated adipose cell lipase

267
Q

How does glucagon stimulate glycogenolysis

A

Uses adenyl cyclase/cAMP/Protein Kinase A mechanism

PKA activates phosphorylase b kinase into phosphorylase a kinase

Degradation of glycogen into glucose-1-phosphate is promoted

This is then dephosphorylated and glucose is released from liver cells

These steps exhibit “amplification”

268
Q

Gluconeogenesis increases:

A

Rate of amino acid uptake by liver cells

269
Q

Gluconeogenesis includes conversion of:

A

Some amino acids into glucose by activating enzymes repsponsible

270
Q

at high levels, glucagon activates:

A

Adipose cell lipase making fatty acids available to the body

271
Q

What stimulates glucagon secretion

A

Hypoglycemia
Autonomic activation
Increased plasma amino acids (aa would increase insulin production, however in the case of glucagon, the amino acids are used for gluconeogenesis)

272
Q

Inhibition of glucagon secretion

A

Hyperglycemia
Insulin
Somatostatin

273
Q

Structure of somatostatin

A

Polypeptide

274
Q

Somatostatin is secreted by

A

Delta cells

275
Q

Effects of somatostatin

A

Depresses insulin and glucagon secretion

Decreases stomach motility, GI absorption

Extends time over which food is assimilated into tissues

276
Q

Somatostatin is AKA as

A

The growth hormone inhibitory hormone from the hypothalamus

277
Q

Stimulation of somatostatin increases:

A 
Plasma glucose, amino acid, and FA levels
GI hormones (gastric, secretin, cholecytokinin, GIP)
278
Q

Inhibition of somatostatin

A

Decreased plasma glucose, amino acid, FA levels

279
Q

What are the two enzymes involved in catecholamines degradation?

A

MAO

COMT

280
Q

Insulin and glucagon levels for glycogen synthesis

A

Insulin increases

Glucagon decreases

281
Q

Insulin and glucagon levels for glycolysis (energy release)

A

Insulin increases

Glucagon decreases

282
Q

Insulin and glucagon levels for lipogenesis

A

Insulin increases

Glucagon decreases

283
Q

Insulin and glucagon levels for protein synthesis

A

Insulin increases

Glucagon decreases

284
Q

Insulin and glucagon levels for glycogenolysis

A

Insulin decreases

Glucagon increases

285
Q

Insulin and glucagon levels for gluconeogenesis

A

Insulin decreases

Glucagon increases

286
Q

Insulin and glucagon levels for lypolysis

A

Insulin decreases

Glucagon increases

287
Q

Insulin and glucagon levels for ketogenesis

A

Insulin decreases

Glucagon increases

288
Q

Insulin’s effect on:

Blood sugar:

Cell sugar utilization:

Cell fatty acid utilization:

Protein synthesis:

Speed of response:

A

Bs- decreases

CSU- Increases

CFU- decreases

PS- increases

SOR- Fast

289
Q

GH effects on:

Blood sugar:

Cell sugar utilization:

Cell fatty acid utilization:

Protein synthesis:

Speed of response:

A

BS- increase

CSU- decrease

CFU- increase

PS- Increase

SOR- slow

290
Q

Glucagon effect on:

Blood sugar:

Cell sugar utilization:

Cell fatty acid utilization:

Protein synthesis:

Speed of response:

A

BS- increase - with gluconeogenesis

CSU- decrease

CFU- increase

PS- decrease

SOR- fast

291
Q

Epinephrine effect on:

Blood sugar:

Cell sugar utilization:

Cell fatty acid utilization:

Protein synthesis:

Speed of response:

A

Bs- increase

CSU- increase

CFU- increase

PS- N/A

SOR- fast

292
Q

Cortisol effects on

Blood sugar:

Cell sugar utilization:

Cell fatty acid utilization:

Protein synthesis:

Speed of response:

A

BS- Increase

CSU- decrease

CFU- increase

PS- decrease (except liver)

SOR- slow

293
Q

Blood Ca+2 and PO4 concentrations depend on: (3)

A

Intestinal absorption rate
Renal excretion rate
Bone mineral uptake/release

294
Q

Major regulatory factors of Ca+2 and PO4

A

Parathyroid hormone

Calcitonin

Vitamin D

295
Q

Ca+2 secreting organs

A

Bone

Kidney

Intestine

296
Q

Important Ca+2 functions

A

Muscle contraction

Nerve impulse transmission
Blood clotting factor
Bone matrix component
Neurotransmitter release

297
Q

ECF concentration must be:

A

Tightly controlled

298
Q

Signs of hypocalcemia

A

Nervous system hyper-excitability

Poor blood clotting

Numbness and tingling

Tetany, spasms

Cardiac arrhythmia

299
Q

Signs of hypercalcemia

A

Nervous system compression (depression, conduction, lethargy)

Cardiac arrhythmia

Constipation, nausea, vomiting

300
Q

Percentage for normal body calcium distribution for
ECF/plasma

Cells

In bones

A

ECF- 0.1%

Cells- 1%

Bones- 99%

301
Q

Calcium distribution in plasma

A

50% ionized calcium
41% protein-bound calcium
9% Ca+2 complexed to anions

302
Q

Phosphate distribution in body

A

85% in bones

14-15% in cells

< 1% in ECF

303
Q

Depending on _____, phosphate forms:

A

PH

HPO4^-2

H2PO4^-1

304
Q

Functions of phosphates

A

Bone matrix
Intracellular buffer
Renal tubular buffer
Phosphorylation (ATP, Enzymes, Etc)

305
Q

Hyper/Hypo phosphatemia

A

Not generally significant except phosphate depletion may lead to bone demineralization

306
Q

Review picture in slide 102

A

Slide 102

307
Q

Osteoid in bones give:

Includes:

A

Tensile strength

Collagen fibers
Ground substance

308
Q

Bone salts give:

Includes:

A

Compressive strength

Hydroxyapatite crystals Ca10(PO4)6(OH)2
Non crystalline amorphous substances - CaHPO4.2H2O
- Ca3(PO4)2.3H2O

309
Q

What inhibits HAP deposition in tissues other than bone?

A

Pyrophasphate

310
Q

Calcification of osteoblasts process

A

Osteoid is laid down

Osteoblasts become encased and become osteocytes

Precipitation of bone salts in osteoid

Woven bone (new bone) becomes low HAP, high amorphous salts

Replaced by stronger bones (higher HAP)

Some amorphous salts are always there and easily exchanged

311
Q

Formation of osteocyte

A

Osteogenic cells

To osteoblasts

To osteocytes

312
Q

Osteoclasts secrete

A

Proteolytic enzymes and acid, which tunnels into bone

  • osteoblasts fill in the new bone
313
Q

Calcification and absorption =

A

Remodeling

314
Q

Review slide 106 for Vitamin D

A

Slide 106

315
Q

Active form of vitamin D

A

1/25 dihydroxycholecalciferol

316
Q

Vitamin D promotes

A

Intestinal calcium absorption (Calcium binding protein)

Phosphate absorption by intestines

317
Q

Vitamin D decreases

A

Renal calcium and phosphate excretion (minor)

318
Q

Excessive vitamin D leads to

A

Bone absorption

319
Q

Small amounts of vitamin D leads to

A

Bone calcification

320
Q

Parathyroid hormone (PTH) without vitamin D leads to

A

No absorption

321
Q

Anatomy of parathyroid gland

A

4 small glands located post to the thyroid gland

2 on the left
2 on the right

322
Q

Parathyroid gland-
Chief cells secrete:
Oxyphil cells:

A

PTH

Function of oxyphil cells is unknown

323
Q

PTH target tissues

A

Bone- cAMP dependant

Kidneys- cAMP dependant

Intestines- indirectly due to PTH effects on vitamin D

324
Q

PTH increases:

How?

A

Blood CA+2 levels

Mainly by bone absorption

325
Q

PTH decreases:

How?

A

Blood phosphate levels

Mainly by increase excretion by kidneys

326
Q

What inhibits PTH release

A

Rising Ca+2 in blood

Calcitonin, Vitamin D

327
Q

PTH activates:

A

Osteoclasts- calcium and phosphate ions release in the blood as a result.

328
Q

Specific effect PTH has on intestines

A

Increases the calcium and phosphate absorption from food (bc of increased vitamin D)

329
Q

How does PTH affect the kidneys

A

Promotes activation of vitamin D
Decreases calcium excretion
Increases phosphate excretion (which overrides increased phosphate absorption from bone)
Occurs mainly in the distal tubules collect tubules

330
Q

2 phases of bone absorption by PTH:

A

Rapid phase (osteolysis)

Slow phase

331
Q

Rapid phase of bone absorption is mediated by:

It causes:

A

Osteocytes and osteoblasts (have PTH receptors)

Causes release of calcium and phosphorus salts

332
Q

Slow phase of absorption is mediated by:

It breaks down:

A

Osteoclasts activated indirectly by osteocytes and osteoblasts. This stimulate osteoclasts and increase development of new osteoclasts

Breaks down osteoid as well as minerals

333
Q

PTH is stimulated by:

A

Decreased ECF Ca+2, histamine, epinephrine

334
Q

PTH is released in a ______ pattern

A

Diurnal

335
Q

What happens with hypoparathyroidism

A

Calcium reabsorption from bones is depressed

336
Q

What happens to ECF Ca+2 levels with hypoparathyroidism

A

It decreases (hypocalcemia)

337
Q

Hypoparathyroidism results in

A

Tentany

338
Q

Signs of hypoparathyroid

A

Muscle spasm of hands and feet

339
Q

Potential causes of hypoparathyroidism

A

Autoimmune disorder

Thyroid surgery complication

Genetic

340
Q

Peptide released by parafollicular cells of the thyroid gland

A

Calcitonin

341
Q

Calcitonin target tissue

A

Bone

342
Q

Effects of calcitonin

A

Decrease in:

Osteoclasts activity
Osteocytic osteolysis
Formation of new osteoclasts

343
Q

Prolonged decrease in osteoclasts activity leads to:

Therefore:

A

Decreased osteoblast activity

No appreciable changes in calcium ion concentration

—there is a very weak effect on kidney to increase calcium excretion

344
Q

Hyperparathyroidism causes extreme:

A

Osteoclastic activity

345
Q

Hyperparathyroidism increases:

A

ECF Ca+2 levels (hypercalcemia)

346
Q

Hyperparathyroidism causes decreased:

A

Phosphate levels

347
Q

Hyperparathyroidism and its effect on bones

A

It weakens bones with frequent fractures

Cystic bone “osteitis fibrosa cystica”

348
Q

Hyperparathyroidism causes high:

A

Plasma alkaline phosphate seems

349
Q

Hyperparathyroidism causes depression of:

A

Nervous system, muscle weakness and constipation

350
Q

Hyperparathyroidism causes metastic:

A

Calcification

And kidney stones

351
Q

Primary causes of Hyperparathyroidism

A

Tumor

Autoimmune disease

352
Q

Secondary causes of Hyperparathyroidism

A

Vitamin D deficiency\

353
Q

Vitamin D deficiency leads to

A

Hypocalcemia and hypersecretion of PTH
(Rickets- child)
(Osteomalacia- adult)

354
Q

Types of physiological alkaline phosphatase (ALP)

A

Infancy
Puberty
Pregnancy
Intestinal isoenzymes

355
Q

Bone diseases that cause increase serum alkaline phosphatase enzyme activity

A

Hyperparathyroidism
Osteomalacia, rickets
Paget’s disease of bone
Osteomyelitis

356
Q

Hepatobiliary diseases that cause increase serum alkaline phosphatase enzyme activity

A

Hepatitis
Cholestasis
Cirrhosis

357
Q

Another cause of alkaline phosphatase

A

Carcinoma of the bronchus

358
Q

Effects of rickets

A

Short stature (stunted growth)

Odd-shaped skull

Spine deformities

Pigeon chest

Odd-shaped ribs

Pelvic Deformities

Wide wrist joints

Wide knee joints

Bowlegs

Wide ankle joints

Endo/Repro (4 decks)

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