BIOM 4090 > Unit 1 > Flashcards

Unit 1 Flashcards

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1
Q

analog

A

chemical compound with similar structure and properties to another compound, but differs by a single element or group

eg. amoxicillin is an analog of penicillin

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2
Q

ligand

A

and ion, molecule or group that binds to another chemical entity to form a larger complex

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3
Q

recombinant technology

A

produced by combining genetic material from more than one origin or source in genetic engineering
lab technique used to join rna from different sources to produce novel rna

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4
Q

circadian rhythm

A

daily cycle of biological activity based on a 24 period and it is influenced by regular variations in the environment

eg. alternation of night and day with sleep and wake patterns

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5
Q

agonist

A

any substance that brings about a change in biologic function through its chemical action by activating a molecule/receptor that plays a regulatory role

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6
Q

antagonist

A

any substance that brings about a change in biologic function through its chemical action by inhibiting a molecule/receptor that plays a regulatory role

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7
Q

drug permeation

A

penetration and spread of drugs through a cellular substance

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8
Q

down regulation

A

process by which a cell decreases the number of a cellular component such as rna or protein in response to external variables

eg. cell decreases the number of receptors to a hormone or NT to reduce sensitivity

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9
Q

JAK/STat family

A

janus kinase and signal transducers and activators of transcription proteins are a family of transcription factors that bind as homo or hetero dimers to recognition sites in gene promoters
mediates signalling from a variety of membrane receptors
eg. IF, IN, hematopoietic and growth factors

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10
Q

g proteins and second messengers

A

guanine nucleotide-binding proteins that transmit chemical signals for hormones or neurotransmitters outside the cell
causes changes in activity of an enzyme or ion channel and the concentration of an intracellular second messenger like cAMP

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11
Q

half life

A

the time it takes for a substance to lose half of its pharmacological, physiologic or radiological activity or the time it takes for the blood plasma concentration of a substance to halve its steady state

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12
Q

first pass effect

A

the metabolism of orally admin drugs by GI and hepatic enzymes, resulting in a reduction of the amount of unmetabolized drug reaching systemic circulation

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13
Q

hormones

A

chemical messengers involved in the regulation and coordination of bodily functions through cell-cell communication

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14
Q

how can hormones act?

A

autocrine (on themselves locally) or paracine (on nearby cells) or endocrine (enter the bloodstream to bind to receptors and affect distant targets)

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15
Q

neurotransmitters

A

hormones secreted by neurons
travel short distances to synapses

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16
Q

neurohormones

A

hormone secreted by neurones
secreted into the bloodstream

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17
Q

what endocrine hormones are synthesized by the body

A

amines, proteins, peptides and steroids

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18
Q

what type of hormone are catecholamines

A

an example of amine hormones that are stored for release

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19
Q

what type of hormone are insulin and growth hormone

A

peptide hormones
stored for release

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20
Q

what are examples of lipophillic hormones

A

non polar hormones
sex steroids and corticosteroids

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21
Q

which hormones are not stored but released released immediately and have delayed biologic effects

A

lipophillic, non polar hormones such as steroids

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22
Q

how do endocrine hormones travel

A

in the blood stream bound to carrier proteins

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23
Q

what are 2 types of carrier proteins for endocrine hormones

A

corticosteroid binding globulin CBG and thyroxine-binding globulin TBG

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24
Q

is the hormone active or inactive when bound to globulins

A

inactive, allowing transport and protection from metabolism

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25
t or f: all hormones in the blood are inactive
false a small fraction of unbound free, biologically active hormone is found in the blood
26
what is different about free hormone found in the blood
it usually has a short plasma half life, ranging from seconds to minutes despite this, it can still have effects that persist after it has been metabolized usually metabolized by the liver and excreted as bile or urine
27
what is required for receptor and hormone binding
ligand must have affinity for the receptor dictating specificity and control
28
how are receptors used for drug intervention
agonists and antagonists
29
what are the receptor types used by hormones to target cells
1. cell surface receptors 2. nuclear and cytosolic receptors
30
explain cell surface receptors
g protein receptors such as channels or second messengers which bind growth factors, insulin and IGFs involve ligand binding and signal transduction for a response (immediate to rapid)
31
explain nuclear and cytosolic receptors
steroids, thyroid hormones, vit D and retinoic acid which are lipophillic ligands receptors will generate a response following binding and transcription usually a delay in response
32
what makes up the endocrine system
hypothalamus-anterior pituitary-target gland axes including: gonads, thyroid and adrenal cortex independent glands such as pancreas, posterior pituitary gland and parathyroid
33
what is another word for the anterior pituitary
adenohypophysis
34
what does the hypothalamus control
the posterior and anterior lobes of the pituitary
35
How does the anterior pituitary differ structurally from the posterior pituitary?
The anterior pituitary is glandular, while the posterior pituitary is a neural structure.
36
How is hormone secretion in the anterior pituitary controlled?
the hypothalamus: via releasing/inhibiting hormones peripheral target organs: via negative feedback
37
What type of cells are found in the anterior pituitary?
A heterogeneous collection of cells that respond to specific stimuli and secrete hormones into the systemic circulation.
38
How do neurosecretory cells in the hypothalamus regulate the anterior pituitary?
They secrete releasing or inhibiting hormones into a capillary network and portal vein, which stimulate or inhibit anterior pituitary hormone secretion.
39
What is the role of anterior pituitary hormones?
To control other endocrine glands.
40
Where are posterior pituitary hormones synthesized?
In the cell bodies of supraoptic and paraventricular neurons in the hypothalamus.
41
How are posterior pituitary hormones transported and released?
Transported down axons to the posterior pituitary, stored, and then released into systemic circulation.
42
How do the vascular supplies differ between anterior and posterior pituitary lobes?
They have separate vascular supplies; the anterior pituitary uses the hypothalamic–pituitary portal system, while the posterior pituitary is supplied by blood vessels that carry hormones directly from hypothalamic neurons.
43
What types of molecules are hypothalamic releasing and inhibiting hormones?
Peptides, proteins, or amines that usually bind to G-protein coupled receptors to produce effects.
44
hormone disorders occur when
1. too much hormone is made (hypersecretion) 2. too little hormone is made (hyposecretion) 3. hormone levels are normal but receptors dont work properly
45
endocrine drug main uses
fix hormone imbalances act a different levels of the axis be used for non-endocrine conditions (eg. inflammation, cancer)
46
what type of feedback regulates the anterior pituitary
negative feedback
47
where can therapeutic intervention occur in the AP axis
at the hypothalamus pituitary or target organ level
48
what is hormone hypersecretion
excessive production or secretion of a hormone
49
what causes primary hormone hypersecretion
a tumour in the hormone secreting gland
50
what causes secondary hormone hypersecretion
a tumour in a gland that regulates another gland eg. pituitary
51
example of primary vs. secondary cortisol hypersecretion
primary: adrenal adenoma secondary: pituitary adenoma
52
what is hormone hyposecretion
decreased hormone production or secretion
53
name causes of primary gland hyposecretion
autoimmune destruction, congenital disorders, surgery, aging, toxins, nutritional deficiencies
54
which endocrine glands are commonly affects by autoimmune destruction
pancreas and thyroid
55
can hyposecretion be secondary or tertiary
yes, due to pituitary or hypothalamic dysfunction
56
can symptoms of hypo or hyper secretion occur even if hormone levels are normal
yes, if hormone receptors are defective, overexpressed or altered
57
how can hormone receptors be abnormal
overexpression, genetic mutation or drug induced changes
58
example of receptor overexpression in cancer
ovarian tumours expressing GnRH receptors
59
drugs that can alter receptor expression
insulin and glucocorticoids
60
non endocrine uses of glucocorticoids
inflammation, allergies, septic shock, immunosuppression
61
how do glucocorticoids help in cancer therapy
supress lymphocytic effects in hematologic (lymphocyte/WBC cancer) malignancies trigger apoptosis in lymphocytes, reduce proliferation and decrease survival used with combo chemotherapy to reduce tumour burden and help with symptoms
62
which cancers respond to glucocorticoids
lymphoma and multiple myeloma
63
how are anti-estrogens used clinically
to treat breast cancer by blocking estrogen receptors
64
how are anti-androgens used clinically
to treat prostate cancer by blocking androgen receptors
65
list additional uses of endocrine drugs
contraception, labour induction, osteoporosis prevention, assisted reproduction, behaviour modification
66
What are the two main components of the adrenal gland?
Adrenal medulla (inner) and adrenal cortex (outer).
67
What type of hormones does the adrenal cortex secrete?
Steroid hormones (adrenocorticosteroids).
68
Name the three classes of adrenocorticosteroids.
Mineralocorticoids, glucocorticoids, and androgens.
69
Name the three zones of the adrenal cortex (outer → inner).
Zona glomerulosa → zona fasciculata → zona reticularis.
70
Which zone produces mineralocorticoids?
A: Zona glomerulosa.
71
Which hormones regulate the zona glomerulosa?
Angiotensin II, potassium, and (minor) ACTH.
72
Which zones are ACTH-dependent?
Zona fasciculata and zona reticularis.
73
What hormone does the hypothalamus release to regulate cortisol?
Corticotropin-releasing hormone (CRH).
74
How does CRH reach the anterior pituitary?
Through the hypothalamic-pituitary portal system.
75
What pituitary hormone stimulates cortisol release?
Adrenocorticotropic hormone (ACTH)
76
Which adrenal zones produce cortisol?
Zona fasciculata (primarily) and zona reticularis.
77
How does cortisol regulate its own production?
By negative feedback on CRH and ACTH.
78
What additional feedback does ACTH provide?
ACTH also inhibits CRH for fine control.
79
What are the three regulators of aldosterone synthesis?
Renin-angiotensin system, blood potassium, ACTH.
80
What triggers renin release?
Decreased extracellular fluid volume or renal perfusion.
81
Where is renin released from?
Juxtaglomerular cells of the kidney.
82
What converts angiotensin I to angiotensin II?
Angiotensin-converting enzyme (ACE).
83
Where is ACE highly expressed?
Lung capillary endothelium.
84
Where does angiotensin II act to stimulate aldosterone?
Zona glomerulosa of the adrenal cortex.
85
What is the precursor for all adrenal steroid hormones
Cholesterol.
86
What is the rate-limiting step in steroid synthesis?
Conversion of cholesterol to pregnenolone.
87
What enzyme performs this conversion?
Cytochrome P450 side-chain cleavage enzyme.
88
How is cortisol transported in blood?
5% free, 20% albumin-bound, mostly bound to CBG (transcortin).
89
When is cortisol biologically active?
When it is free (not bound to CBG).
90
Where are glucocorticoid receptors located?
In the cytoplasm.
91
What happens after cortisol binds the GR? A: The complex moves to the nucleus and alters gene transcription.
The complex moves to the nucleus and alters gene transcription.
92
How does aldosterone differ in transport?
It circulates mostly free and binds mineralocorticoid receptors (MR).
93
What metabolic effect does cortisol have overall?
Increases blood glucose.
94
How does cortisol act in the liver?
A: Increases gluconeogenesis and glycogen storage.
95
What is cortisol’s effect on inflammation?
A: Suppresses inflammatory mediator production.
96
What renal effect does aldosterone have?
Increases sodium reabsorption and potassium/hydrogen excretion.
97
What is aldosterone’s main physiological role?
Blood pressure regulation.
98
Which glucocorticoids are long-acting and high potency?
Dexamethasone and betamethasone.
99
Which drug has strong mineralocorticoid activity?
Fludrocortisone.
100
Most common cause of Cushing’s syndrome?
Exogenous (iatrogenic) corticosteroid use.
100
What is hyperadrenocorticism also called?
Cushing’s syndrome.
101
Key features of Cushing’s syndrome?
Moon face, buffalo hump, muscle wasting, thin skin, osteopenia.
102
What is hypoadrenocorticism called? A: Addison’s disease.
103
Most common cause of Addison’s disease?
Autoimmune adrenal destruction.
104
What is acute adrenal crisis?
Life-threatening adrenal insufficiency requiring IV steroids/fluids.
105
Name cortisol synthesis inhibitors.
Ketoconazole, aminoglutethimide, trilostane.
106
Why must glucocorticoids be tapered?
To allow recovery of the hypothalamic-pituitary-adrenal axis.
107
what does the thyroid regulate
metabolism, growth, energy use, cardiovascular function
108
what is thyroid tissue mostly made of, which produces thyroid hormones
mostly follicular cells c cells produce calcitonin
109
what are the main hormones of the thyroid
T4 thyroxine- major T3 active rT3 inactive
110
Where is the thyroid gland located?
In the neck, inferior to the larynx, on the ventral surface of the trachea.
111
What is the basic structural unit of thyroid hormones?
Two iodinated tyrosine molecules linked by an ether bond.
112
What enzymes convert T4 to T3 or rT3?
Deiodinases (D1, D2, D3).
113
Which deiodination produces active hormone?
Removal of iodine from the outer ring → T3.
114
Which deiodination produces inactive hormone?
Removal of iodine from the inner ring → rT3.
115
Role of D1?
Produces most circulating serum T3.
116
Role of D2?
Local conversion of T4 to T3 (brain, pituitary).
117
Role of D3?
Converts T4 to inactive rT3.
118
What hypothalamic hormone regulates the thyroid?
Thyrotropin-releasing hormone (TRH).
119
How does TRH reach the anterior pituitary?
Via the hypothalamic-pituitary portal system.
120
What pituitary hormone stimulates the thyroid gland?
Thyroid-stimulating hormone (TSH).
121
What does TSH stimulate?
Synthesis and release of T4 and T3.
122
What inhibits TSH secretion?
High thyroid hormone levels, somatostatin, glucocorticoids, sex hormones, and excess iodide.
123
How does iodide enter thyroid follicular cells?
Via the Na⁺/I⁻ symporter on the basolateral membrane.
124
What enzyme oxidizes iodide and catalyzes coupling?
Thyroid peroxidase (TPO).
125
What is organification?
Iodination of tyrosine residues on thyroglobulin.
126
What are MIT and DIT?
Mono- and di-iodinated tyrosines.
127
What combinations form T3 and T4?
MIT + DIT → T3; DIT + DIT → T4.
128
How are T3 and T4 released?
Colloid is endocytosed, digested in lysosomes, and hormones enter blood.
129
How much circulating thyroid hormone is protein-bound?
~99% (mainly to thyroid-binding globulin).
130
Half-life of T4 vs T3?
T4 ≈ 7 days; T3 ≈ 1 day.
131
is T3 or T4 more biologically potent
T3 (≈4× stronger than T4).
132
How do thyroid hormones act at the cellular level?
Nuclear receptors → altered gene transcription.
133
Major physiologic effects of thyroid hormones?
Increased metabolism, oxygen consumption, growth, and cardiac activity.
134
hypothyroidism
slowed metabolism low T4, high TSH
135
hyperthyroidism
accelerated metabolism high T3/T4, low TSH
136
Most common cause of hypothyroidism worldwide?
Iodine deficiency.
137
Most common cause in developed countries?
Hashimoto’s thyroiditis.
138
Lab findings in hypothyroidism?
Low free T4, high TSH.
139
Drug of choice for hypothyroidism?
Levothyroxine (T4).
140
Why is levothyroxine preferred?
Long half-life and stable blood levels.
141
Most common cause of hyperthyroidism?
Graves’ disease.
142
Pathophysiology of Graves’ disease?
IgG antibodies activate the TSH receptor. antibody stimulation, not excess TSH
143
Lab findings in hyperthyroidism?
High T3/T4, low TSH.
144
First-line antithyroid drugs?
Methimazole and propylthiouracil.
145
Mechanism of thioamides?
Inhibit thyroid peroxidase (organification & coupling).
146
Definitive therapy for many patients?
Radioiodine (I-131).
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