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Physiology 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q
  1. what is homeostasis
  2. how does the internal environment stay stable
  3. set points
A
  1. The process of maintaining a constant internal environment despite changing conditions. Regulation/ Constancy of internal environment
    Homeostasis isn’t equilibrium! Dynamic steady state ( ions move between ECF and ICF
  2. through external/ internal change
  3. there exists a normal range of function that is acceptable for homeostais (homeostatic temp= 30 but feedback doesnt work until tem reaches 31/28
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2
Q

Feedback

  1. Positive vs Negative
  2. cortisol regulation (7 steps)
A
  1. Negative stimulus is stabalizing while positive is reinforcing and invovles an outside factor (further and further more and more)
  2. Hypothalmus prodcues CRH horome which stimulates anterior pituitary which produces ACTH horomone that stimulates aderenal cortex that produces cortisol
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3
Q
  1. Maintaining homeostasis and other body
    functions requires
  2. Three types of local control
  3. long distance communication (3)
A
  1. Maintaining homeostasis and other body functions requires intercellular communication
  2. (A) Gap junctions: form direct cytoplasmic connections betwen adjacent cells. Small ions and molecules
    move through gap junctions connecting cells
    (B) Contact dependant signals: require interaction between membrane molecules on two cells. Membrane protein binds to membrane protein
    (C)Autocrine: a0 Autocrine signals: act on the same cell that secreted them. Paracrine signals are secreted vy one cell and diffuse to adjacent cell. Molecules move through interstitial fluid over short distance
  3. i) Endocrine system: **hormones ** are secreted by endorine galnds into blood where cells with the right receptors respond
    ii) Nervous system: Neurotransmitters are chemicals secreted by neurons that diffuse across a small gap to target cells
    **(neuroendocrine)Neurohormones ** chemicals released by neurons into blood for action at target cell
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4
Q

Long distance communication

  1. Simple and Complex Reflexes
  2. In local control vs in relfex control
A
  1. – Simple are mediated either by the nervous or the endocrine system
    – Complex reflexes are mediated by both systems and go through several integrating systems
  2. In local control, cells in the vicinity of the change initiate the response. In reflex control cells at a distant sute control the reponse
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5
Q

Neural vs Endocrine Reflex
Specificty, nature of signal, speed, duration of action, coding for stimulus intensity

A

Specificity:
N: Each neuron terminates on a single target cell or on a limited number of adjacent target cells.
E: Most cells of the body are exposed to a hormone. The response depends on which cells have receptors for the hormone.
**Nature of Signal: **
N: Electrical signal that passes through neuron, then chemical neurotransmitters that carry the signal
from cell to cell. In a few cases, signals pass from cell to cell through gap junctions.
E: Chemical signals secreted in the blood for distribution throughout the body.
**Speed: **
N: Very rapid
E: Distribution of the signal and onset of action are much slower than in neural responses.
**Duration of Action: **
N: Usually very short. Responses of longer duration are mediated by neuromodulators.
E: Responses usually last longer than neural responses.
**Coding for Stimulus Intensity: **
N: Each signal is identical in strength. Stimulus intensity is correlated with increased frequency of signaling.
E: Stimulus intensity is correlated with amount of hormone secreted.

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6
Q

What are hormones
Exocrine vs Endocrine
Primary Endocrine Organs (9)
Secondary Endocrine Organs (8)

A

Hormones; dervied from tissues that can release chemicals. Endorine system comminucated via hormones
Exocrine: substances secreted to enivronment external to self (through duct?)
Endocrine: secreted into bloodstream
Primary: main function is to release hormone): Hypothalmus, Pituotary Gland, Adrenal Gland, Testes, Placenta, Ovaries, Thyroid gland, parathyroid gland, Pineal gland
Secondary: release hormones and do something else: Heart, liver, pancrease, kidneys, stomach and small intestine, adipose tissue, skin

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7
Q

8 features of hormones

A
  • can be made in different places in the body
  • chemicals made by cells in specific endocrine glands or other tissues
  • transported in the blood to distant targets
  • bind to specific receptors
  • may act on multiple tissues
  • alter activity of target cells
  • action must be terminated
  • maintain homeostasis or precipitate change in many physiological processes
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8
Q

Two types of hormones and their properties (3 properties per classification as well as membrane solubility, ynthesis, release and transport in blood )

A
  1. Hydrophilic/Lipophillic hormones
    – Water soluble, can dissolve in plasma
    – Not lipid soluble (lipophobic), cannot cross plasma membranes
    – Examples: peptide hormones, protein hormones and catecholamines
    Membrane solubility:not lipid
    soluble
    Synthesis: In advance, stored
    Release: Exocytosis
    Transport in Blood: Dissolved
  2. Hydrophobic/Lipophobic hormones
    – Not water soluble, do not dissolve in plasma
    – Lipid soluble (lipophilic), readily cross plasma membrane
    – Examples: steroid and thyroid hormones
    Membrane solubility: lipid soluble
    Synthesis: On demand because their not easy to store, will leak out cause they are diffusable
    Release: Diffusion
    Transport in Blood: Bound to
    carrier proteins
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9
Q
  1. What are the three main types of hormones? They’re chemistry, examples and transport
A
  1. Peptide/Protein (3 or more amino acids)
    Chemistry: Made from chains of amino
    acids
    Ex:Insulin
    transport: Hydrophilic, so mix easily with blood plasma
  2. Steroid (derived from cholesterol)
    Chemistry: Derived from cholesterol
    Ex: Sex steroids (estrogen), cortisol
    transport: Hydrophobic, so bind
    to transport proteins in the blood
  3. Amine (derived from single amino
    acids)
    Monoamine
    Chemistry: Made from amino acids
    Ex: Catecholamines (epinephrine), thyroxine
    transport:Hydrophilic, so mix easily
    with blood plasma
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10
Q

Peptide/Protein Hormones (9)

A

Linked amino acids
Most hormones
Made in advance
Synthesized like secreted proteins
Stored in vesicles
Release by exocytosis upon a signal
Water soluble (dissolved in plasma)
Short half life in plasma
Bind to membrane receptors

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11
Q

single preprohormone can contain
Active peptides released depends on

A

Several copies of the same hormone or more than one type of hormone
- Active peptides released depends on specific proteolytic processing enzymes in cell at the time

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12
Q

Steroid Hormones

  1. Synthesized only from
  2. how is it made
  3. where is it not stored
  4. how is it released
  5. solubility
  6. lifetime
  7. how does it get to target cells
  8. one more point
A
  1. Synthesized only from cholesterol
  2. Made on demand
  3. Not stored in vesicles
  4. Released from cell by simple diffusion
  5. Water insoluble (bound to carriers in blood)
  6. Long half life
  7. Diffuse into target cells or taken up by
    endocytosis of steroid hormone carrier
    proteins
  8. Cytoplasm or nucleus receptors (but can also act on plasma membrane receptors)
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13
Q

Type of hormone made depends on
1. cholesterol in adrenal gland makes
2. cholesterol in ovary makes

A

Type of hormone made depends on the which
enzymes are present in the cell and which organ the cholesterol is in. Each organ has different enzymes
1. Adrenal cortex: aldoesterone and cortisol
2. ovary: estradiol

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14
Q

Amine Hormones

  1. Synthesized only from
  2. Types of derivatives and how they behave
A
  1. Synthesized only from tryptophan or tyrosine
  2. Tryptophan derivative: Melatonin (behaves like peptides or steroids)
    Tyrosine derivatives:
    Catecholamines (behave like peptides)
    Thyroid hormones (behave like steroids)
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15
Q

Melatonin
when is it secreted
where is it made
three diverse effects

A
  • Darkness hormone
  • Secreted at night (Sleep)
  • Made in pineal gland (also gi tract, leukocytes, other brain regions)
    Diverse effects:
  • Transmits information (light-dark
    cycles to govern the biological clock)
  • Immune modulation
  • Anti-oxidant
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16
Q

Synthesis of catecholamines

starting point, where is it synthesized, where is it stored, how is it relased, solubility, binding

A
  1. start from tyrosine
  2. Synthesized in adrenal medulla (mainly in cytosol)
  3. Stored in vesicles prior to release
  4. Released via exocytosis
  5. Lipophobic, water soluble
  6. Bind to membrane receptors
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17
Q

Control of Hormone Release
1. Endocrine cells directly sense what, then
2. Goes from a=>b=>.c
3. Hormones released from the x and
y regulate z

A
  1. Endocrine cells directly sense stimuli, then
    secrete the hormone
  2. stimuli => endocrine cells (has the capapcity to create hormone) => hormone released
  3. Hormones released from the hypothalamus and anterior pituitary regulate the release of several
    hormones
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18
Q

How do the stimuli trigger hormone release?
6 points

A

Act through intracellular pathways to:
* change the membrane potential
* increase free cytosolic Ca2+
* change enzymatic activity
* increase the transport of hormone substrates
into the cell
* alter transcription of genes coding for
hormones or for enzymes needed for
hormone synthesis
* promote survival and in some cases growth
of the endocrine cell

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19
Q

Hormone Interactions

Most cells sensitive to more than one hormone and exhibit interactive effects
Three types of effects

A
  • Synergistic effects:
    Multiple hormones act together for greater effect
    Synergism between FSH and testosterone on sperm production
  • Permissive effects
    One hormone enhances the target organ’s response to a second later hormone
    Estrogen prepares uterus for action of progesterone
  • Antagonistic effects
    One hormone opposes the action of another
    Insulin lowers blood glucose and glucagon raises it
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20
Q

How do hormones signal?
4 steps

A
  1. Hormone binds to receptor
  2. Changes the conformation and activity of the receptor
  3. Alters the activity of intracellular signaling pathways
  4. Leads to change in synthesis of target proteins and/or modification of existing target proteins
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21
Q

What characteristics do receptors share?
7

A
  • Large proteins
  • Families
  • Can be multiple receptors for one ligand or more than one ligand for a receptor
  • Variable number in target cell (~500-100,000)
  • Can be activated and inhibited
  • Located in cell membrane, cytoplasm,
    nucleus
  • saturable
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22
Q

4 Properties of
receptors

A
  • High affinity
  • Saturable
  • Specific
  • Reversible
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23
Q

What are the two main types
of receptors?
4 and 5 points

A

1)Intracellular receptors (bind lipid soluble
hormones)
- lipophillic signal molecules diffuse through CM
- binding to Cytosolic and nuclear receptor
- Directly alter gene transcription = genomic
- slower responses related to change in gene activity
effects
2)Plasma/Cell membrane receptors
- G protein-coupled receptors
- Receptor-enzyme receptors
- Receptor-Channel
- Integrin Receptor
- Rapid cellular response

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24
Q

Hormone Receptors and

Mode of Action

Peptide hormones
- Cannot do what
- bind to
- Steroid hormones
- - penetrate what
- influence what
- duration

A
  • Peptide hormones
    – Cannot penetrate target cell
    – Bind to surface receptors and
    activate intracellular processes through second messengers
    * Steroid hormones
    – Penetrate plasma membrane and bind to internal receptors (usually in nucleus)
    – Influence expression of genes of target cell
    – Take several hours to days to show effect due to lag for protein synthesis
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25
Q

Hormone response elements

A
  • specific DNA sequences
  • Sometimes receptors recruit co repressors to inhibit transcription
  • Only genes with the response elements will be activated/repressed
26
Q

Four categories of membrane receptors

A
  1. Receptor Channel: Ligand binding opnes or closes the channel
  2. G protein coupled receptor: Ligand binding to g- protein coupled receptor opens ion channel or alters enzyme activity
  3. Receptor-enzyme: Ligand binding to a recepttor enzyme activates intracellular enzyme
  4. intergrin receptor: lingand binding to intergrin receptors alters anzymes or the cytoskeleton
27
Q

G Protein–Coupled Receptors (GPCR)
5 points

A
  • Membrane-spanning proteins
  • Cytoplasmic tail linked to G protein, a three-part transducer molecule
  • G protein-coupled adenylyl cyclase-cAMP system is the signal transduction system for many protein hormones
  • G protein-coupled receptors use some lipid second messengers: e.g., diacylglycerol (DAG) and inositol
    trisphosphate (IP3)
  • When G proteins are activated, they
    – Open ion channels in the membrane
    – Alter enzyme activity on the cytoplasmic side of the
    membrane
28
Q

GPCR-Adenylyl Cyclase Signal Transduction and Amplification
5 steps

A
  1. Signal molecule binds to G protein–
    coupled receptor (GPCR), which
    activates the G protein.
  2. G protein turns on adenylyl cyclase,
    an amplifier enzyme.
  3. Adenylyl cyclase converts ATP to
    cyclic AMP.
  4. cAMP activates protein kinase A.
  5. Protein kinase A phosphorylates
    other proteins, leading ultimately
    to a cellular response
29
Q

what does Gq activate and what are the steps

A

Gq activates phospholipase C
1. Signal activates receptor and associated g protein. Alpha subunit is the q version
2. G-protein activates phospholipase C (PL-C) an amplifier enzyme
3. PL-C converts membrane phospholipids into diacyglycerol which remains in the membrane and IP3 which diffuses into cytoplasm
4. DAG activates prtoein kinase C which phosphorylates proteins
5. IP3 causes relase of Calcium from organelles creating a calcium signal

30
Q

What does G-alpha 1 do and how

A

Gai inactivates/ inhibits adenylyl
cyclase
Hormone => Ri
|
inhibitory regulative G protein (Gi)
| Inhibit
Adenylyl cyclase
ATP ——X———-PPi and cAMP

31
Q

3 main types of G proteins: target and activity

A

Target Activity
Gs Adenylyl cyclase stimulatory
Gq Phospholipase C stimulatory
Gi Adenylyl cyclase inhibitory

32
Q

Fight or flight responses in liver, fat, heart, skeletal muscle, blood vessel, intestine, skin, kidney
- hormone responsible

A

Liver: glucose release
Fat: fatty acid release
Heart: muscle contraction
Skeletal muscle, blood vessels: less vasoconstriction
Intestine, skin, kidney: vasoconstriction
- **epinephrine and nonrepinephrine **

33
Q

Epinephrine + a-Receptor vs Epinephrine + b2
-Receptor

A

alpha recetptor: vessel constricts
beta” dialation

34
Q

How is signalling modulated?

6 points

A
  1. Hormone degraded
  2. Receptor down-regulation or up-regulation
  3. Receptor desensitization
  4. Breakdown of second messengers
  5. Modification of any component in the pathway
  6. Biological effect provides feedback to reduce hormone secretion
35
Q

Why is calcium critical for normal
physiology?

A
  • Intracellular signaling
  • Hormone secretion
  • Blood clotting
  • Neural excitability
  • Muscle contraction
  • Building & maintaining bone
36
Q

Locations of Calcium

A

1) extracellular matrix
2) extracellular fluid
3) intracellular Ca 2+

37
Q
  1. total body Calcium=
  2. Percentage of where Ca is found
  3. Calcium exchange
A
  1. intracellular + extracellular (ECF/plasma + bone)
  2. 99% bone, 0.9% cell (free Ca), ECF (0.1%)
  3. a) Calcium from diet goes to small intenstine, too much Ca sent to kidney which ;eaves through urine.
    b) Small intestine can send Ca to ECF.
    c) Bone, kidney and cells can exchange Ca with ECF
38
Q
  1. three cells in bone that are responsible for the formation and maintenance of bone:
  2. Making bone =
A
  1. Osteoblasts: Bone forming cells
  2. Osteoclasts: Break down bone/ bone resorption
  3. Osteocytes: Maintain bone/matrix. (These are previously osteoblasts that are completely surrounded by bone matrix => Therefore just maintain bone in its mmediate vicinity
  4. Making bone = creating calcium phosphate complexes (calcium crystallization)
39
Q

Osteoblasts promote osteoclast formation
via

A
  • RANKL/RANK interaction
  • RANK = receptor activator of nuclear factor kappa B
  • RANKL = RANK ligand
  • Osteoprotegerin (OPG) secreted by osteoblasts blocks RANKL/RANK interaction= no osteoclst
  • ## Inactive osteoclasts precursours have RANK receptors that need to bind to RANKL on osteoblasts to promote differentiation and fusion (osteoblast fuses with osteoclast precursor) in order to create a osteoclast
40
Q
  1. Which three hormones control plasma Ca2+ levels?
  2. which target sites do they act on
A
  1. Parathyroid hormone (PTH)
    Calcitriol (aka 1,25 dihydroxycholecalciferol)
    Calcitonin
    2.
    Act on three target sites:
    – Bones
    – Kidneys
    – Digestive tract
41
Q

Parathyroid hormone (PTH)
1. Released from
2. Function
3. Stimulus
4. “Parathyroid cells are exquisitely sensitive to
5. PTH increases plasma [Ca2+] by
6. PTH effects on bone

A
  1. Released from the parathyroid glands (chief cells) (4 glands attached to thyroid glands
  2. Function: Increases plasma Ca2+ concentration
  3. Stimulus: Low plasma Ca2+
  4. “Parathyroid cells are exquisitely sensitive to changes in extracellular calcium concentration. Before Ca reaches 1.20mM in blood, PTH rapidly increases
  5. PTH increases plasma [Ca2+] by acting
    directly on bone and kidney
  6. PTH acts on osteoblasts by increasing cAMP to increase RANKL and decrease OPG expression. More osteoclasts are formed leading to bone resorption and more Ca is rleased in blood
42
Q

calcitriol/ vit D3

  1. 3 organs are crucial in the development of calcitriol
  2. Calcitriol targets
  3. Formation of calcitriol (5 steps)
  4. How does calcitriol act?
A

1. 3 organs are crucial in the development of calcitriol
1) Skin
2) Liver
3) Kidney
2. Calcitriol targets intestine, bone and kidney to increase serum
calcium
3. 7-dehydrocholesterol exposed to sunglight through skin => cholecalciferol (vitamin D3) goes to liver => 25-hydroxycholecalciferol goes to kidney and with PTH becomes calcitirol (active form)
4. Increase Ca2+ uptake from small intestine because calcitirol helps absorb calcium. Renal Ca2+ reabsorption
and mobilization from bone

43
Q

How is blood phosphate controlled?

A

PTH: increases phosphate release from bone and decreases phosphate reabsorption in kidney so that it will leave in urine
Calcitriol: increases phosphate absorption by intestine and reabsorption by kidney so that calcitirol can make more bone

44
Q

PTH raises plasma Ca2+ in
three ways:

A

1)PTH mobilizes calcium from bone:
osteoclasts via RANKL and OPG
mechanism (indirectly through
Osteoblasts)
2)PTH enhances renal reabsorption of
Ca2+ (and kicks out phosphate!)
3)Calcitriol – PTH enhances the
production of Calcitriol
4) Both work at Bone/Kidney/Intestines to
increase absorption!

45
Q

Calcitonin
where is it secreted from
what kind of hormone
release is triggered by
what also have Ca2+-sensing receptors

A
  • Opposite of PTH and calcitrol
  • Secreted from C cells of the thyroid gland
  • Calcitonin is a peptide hormone
  • Release triggered by high plasma [Ca2+]
  • C cells also have Ca2+-sensing receptors
46
Q
  • Calcitonin “Tones down”
  • ## Role in humans? 4
A

Calcitonin “Tones down” calcium levels
– Protect the skeleton from Ca2+ loss during pregnancy and lactation
– Reduces activity of osteoclasts (inhibits
bone resorption)
– Stimulates osteoblasts – deposit calcium away from blood into bone
– Inhibits calcium reabsorption by kidneys

47
Q

What happens when calcium
homeostasis is not maintained?

A
  • Hypercalcemia (TOO MUCH):
    GROANS (constipation)
    MOANS (psychic moans = fatigue, lethargy, depression)
    BONES (bone pain)
    STONES (kidney stones)
    Psychiatric OVERTONES (including depression and
    confusion) ++Weakness
  • Hypocalcemia (TOO LITTLE)
    C = Convulsions
    A = Arrhythmias
    T = Tetany
    S = Spasms, Seizures, & Stridor
48
Q

Ca2+ homeostasis is affected by:
Decreased Ca2+ stimulates

A
  • Ca2+ homeostasis is affected by:
    – Dietary intake
    – Urinary output
    – Distribution in bone, cells, and ECF
  • Decreased Ca2+ stimulates PTH
    – Promotes Ca2+ resorption from bone, enhances renal Ca2+ reabsorption, and increases Ca2+ through its effect on calcitriol
49
Q
  1. How is water distributed in the body?
  2. What are the average daily water gains
    and losses?
  3. Excessive water loss disrupts what and how
A
  1. 2/3 ICF, 1/3 ECF (75% Interstitial Fluid and 25% Plasma)
  2. Water gain (2.2 L intake, 0.3L metabolic production) - Output (2.5L through urine (1.5) sweat and lungs (0.9L) and feces (0.1L) = 0
  3. Excessive water loss disrupts homeostasis = hypotension/shock
    -Excessive water loss →less extracellular
    fluid → decreased blood pressure
    -confused, chest pain, very low blood
    pressure, make no urine!
    -TOO much water – backs up in the lungs,
    legs, abdomen
    – Difficulties in breathing, walking
50
Q

How and where is urine formed?
What is the nephron
What is the nephron/kidney responsible for

A
  1. Urine is formed in the nephron by filtration, reabsorption, secretion
  2. The nephron is the functional unit of the kidney
  3. The nephron/kidney is Responsible for:
    - Excreting waste
    - Regulates blood volume
    - Controls electrolytes
    - Blood pH
    - Vitamin D!!!!! (via PTH)
51
Q

How do hormones regulate water, Na+
and K+ balance?

A

Vasopressin:
Increase H2O reabsorption
Aldosterone
Increase Na+ reabsorption
Increase K+ secretion
Atrial natriuretic peptide
Decrease Na+ and H2O reabsorption
Increase K+ reabsorption

52
Q
  1. Vasopressin (antidiuretic hormone, ADH): synthesized in the
  2. secreted from the
  3. Primary function:
  4. What is the most potent stimulus for
    vasopressin release
  5. Vasopressin and water
A
  1. Vasopressin (antidiuretic hormone, ADH): synthesized in the hypothalamus,
  2. secreted from the posterior pituitary
  3. Primary function:
    * Increase water reabsorption in the kidneys
    – Conserve body water
    – Water balance and fluid homeostasis
    – Increases blood volume and blood pressure
    → Regulating permeability of cells in the kidney
    Increased permeability = increased reabsorption and low urine output
  4. Osmolarity is the most potent stimulus for vasopressin release
  5. Vasopressin inserts water pores into distal convoluted tubule/collecting duct cell membranes
53
Q
  1. WHat is aldosterone
  2. Functions
  3. Aldosterone synthesis is controlled by
  4. Stimulators/ Inhibitor
  5. Aldosterone acts on the
A

1. Aldosterone, a steroid synthesized
in the adrenal cortex that regulates
sodium and therefore water homeostasis
2. Functions: Impt!
1) Na+ Reabsorption (retain water)
2) K+ Secretion
3)Acts on distal tubule and collecting
duct
3. Aldosterone synthesis is controlled by
negative feedback: simple (K+ osmolarity)
& complex (renin-angiotensin II)
4. Stimulators
1. High [K+]plasma
2. Angiotensin II (via Blood pressure)
→ RAAS – Renin-angiotensinogen pathway
Inhibitor
3. High osmolarity (extracellular fluid)
5. Aldosterone acts on the distal tubule and collecting duct.
Prevents degradation of apical Na+ channe and Increases expression of
Na+ and K+ channels and
Na+/K+ATPase

54
Q
  1. Renal juxtaglomerular cells secrete what when
  2. what does angiotesin 2 do
A
  1. Renal juxtaglomerular cells secrete the enzyme renin when blood pressure falls
  2. Angiotensin 2
    - Increases vasopressin
    - Stimulates thirst
    - Potent vasoconstrictor
    - Increases proximal tube Na+
    retention
55
Q

Family of natriuretic peptides
3 types, what do they do
Effects of ANP and BNP, where is it released from

A
  • stimulate water release and act as hormones
    CNP: brain, pituitary, vessels, kidneys
    ANP: atria (myocardial cells), neurons
    Released from Atrial myocardial
    cells and neurons
    BNP: ventricles (myocardial cells), neurons. Realsed from Ventricular myocardial
    cells and neurons
    Effects of ANP and BNP: decreased Na+ and H2O reabsorption (lowers blood pressure)
    Increase K+ reabsorption
    Suppresses renin, aldosterone, vasopressin
56
Q

Adrenal medulla =
Adrenal cortex =
main hormone of adrenal medulla, why and stimulus of its release

A

Adrenal medulla = modified sympathetic ganglia. secretes catecholamines. Neuroendorcine tissue
Adrenal cortex = steroid factory/ Secretes steroid hormones
Main hormone is epinephrine because it is secreted in sufficient quantity to exert effects
Stimulus for release = activation of the sympathetic nervous system (“fight or flight” response)

57
Q

What is the role of epinephrine?
Clinical use of epinephrine

A
  1. Mediate the rapid stress response
  2. Epipen:
    Epi-Pen counter-acts the symptoms of anaphylactic shock by promoting:
    Bronchodilation (let air in )
    Vasoconstriction (intestine, skin, kidneys)
    Vasodilation (skeletal and cardiac muscles): lets BP go back to normal
58
Q

Strcture of Adrenals (zones and what they secrete)
Main hormones produced by Adrenal cortex

A

From top to bottom:
Capsule: thin connective tissue that keeps the organ whole, no endocrine function
Zona glomerulosa: secretes aldosterone
Zone fasciulata: Gluccocoticoids
Zona reticularis: sex hormones
Adrenal medulla: catecholamines
Main hormones produced by the
adrenal cortex
DHEA: dehydroepiandosterone, Androstendione, Corticosterone, Cortisol, Aldosterone

59
Q
  • Adrenal cortex secretes
  • Cortisol is
  • Control pathway of secretion is the
  • role
  • how is it secreted
  • Protective effect against x through y
  • Metabolic effects
A
  • Adrenal cortex secretes steroid hormones, aldosterone (sodium-potassium balance), glucorticoids, sex hormones
  • Cortisol is the main glucocorticoid
  • Control pathway of secretion is the hypothalamicpituitary-adrenal pathway
  • Continuous secretion, diurnal rhythm
  • Role in the mediation of long-term stress
  • Protective effect against hypoglycemia through
    permissive effect
  • Metabolic effects – primarily catabolic
    1. Promotes gluconeogenesis
    2. Causes breakdown of skeletal muscle proteins
    3. Enhances lipolysis
    4. Suppresses the immune system
60
Q
  1. Cortisol actions on Bone formation, immune system, liver, muscle, adipose tissue, pancreatic insulin
  2. Analogs of cortisol are used as drugs to
A
  1. Bone formation: supressed, Immune system: supressed
    Liver: gluconeogensis
    Muscle: protein catabolicm
    Adipose tissue: Lipolysis
    Pancreatic Insulin release: supressed
  2. Analogs of cortisol are used as drugs to
    suppress the immune system by Inhibit inflammatory responses. Long-term use can result in inhibition of ACTH
    secretion and atrophy of cortisol-secreting cells
61
Q

ADRENAL HORMONE DISORDERS

Addison’s Disease:
also known as, what does it do, causes, symptoms
Cushing’s syndrome: causes and what is it

A

Addison’s Disease
* Also known as: adrenal insufficiency
* Hyposecretion of adrenal steroid hormones
* Causes: destruction of the adrenal cortex by
autoimmunity, sometimes infection
* Symptoms: hypotension, hypoglycemia
Cushing’s syndrome: Cortisol excess
Causes:
* tumours
* cortisol therapy
Symptoms: hyperglycemia, muscle protein breakdown, lipolysis but build up of fat on trunk and face, increased appetite, mood elevation followed by depression, difficulty with learning and memory

Physiology 1 (12 decks)

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