Endocrine System- Endocrine Review By Komar And Biochemistry By Girl Bridges

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Endocrine System- Endocrine Review by Komar and Biochemistry by Girl Bridges

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Endocrine System- Endocrine Review by Komar and Biochemistry by Girl Bridges

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Hemocrine

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hormone released from cell and enters blood vessels.

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Paracrine

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hormone released from cell and interacts with receptor(s) on nearby cells.

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Intercrine

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direct transfer of messenger molecule into adjacent cells via gap jcts.

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Juxtacrine

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messenger molecule remains associated with cell membrane of signaling cell and interacts with receptor on adjacent cell.

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Autocrine

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hormone secreted and interacts with receptor on the same cell

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Neurocrine

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messenger molecules produced by neurons
Synaptic: messenger molecule traverses synaptic space
Non-synaptic (neurosecretion): messenger molecule is carried to site of action by ECF or blood.

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Solinocrine

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messenger molecule secreted into lumen of ductal system (i.e. GI, respiratory, urogenital).

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Intracrine

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uptake of hormonal precursor and intracellular conversion to effective hormone and subsequent binding to intracellular receptor.

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are hormonal effects all or nothing?

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Not ‘all or nothing’ but ratio in regards to other factors (relationship of one hormone to other hormones in its environment in the body that will allow it to have a characteristic effect)

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for every kinase there is a _____ that can de-________ the residue that was just phosphorylated. and give and example.

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phosphatase that can dephosphorylate

type 2 diabetes. for some, it's not that they don't have insulin, it's that you're insulin resistant, and have increased levels of phosphatases that dephosphorylate the insulin receptor substrates, so this dampens the signal and leads to insulin resistance.

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Desensitization may occur

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Uncoupling: Many GPCRs are uncoupled from associated G-proteins after ligand binding ; Triggered by receptor phosphorylation

Endocytosis: Insulin receptor is endocytosed after ligand binding; GPCRs are often internalized after uncoupling; Recycling or degradation can occur

Modification by other proteins resulting in decreased signaling activity (without changing receptor #)

Altered expression

One hormone may regulate expression, internalization, etc of the receptor for a different hormone

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examples of primary/secondary endocrine organ failures

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Primary endocrine organ failure –
genetic; acquired -> Congenital Adrenal Hypoplasia
agenesis ->
genetic defect in hormone biosynthetic pathway (CAH)
destruction (autoimmune; infection) -> Hashimoto's
deficiency in precursor (iodine) -> thyroid hormone production

Secondary organ failure (hypogonadal due to hypopituitarism)

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Endocrine organ hyperfunction

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Primary (tumor – parathyroid adenoma; autoimmune – Grave’s)
Secondary (ACTH pituitary adenoma; ectopic production - cancer)

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function first,

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structure second. during assessment of endocrine disease

Biochemical dysfunction

Measure hormone levels

Basal
caveats: half-life; physiologic rhythm; relationship to other factors

Dynamic: stimulation: to confirm hypofunction
inhibition: to confirm hyperfunction

Structure
Imaging (CT; MRI; ultrasound); confirmatory of diagnosis; identify
location of tumor to target treatment
Aspiration