Week 1 Physiology

Front 1

Explain how each of the following contributes to K+ homeostasis: GFR, NA/K pump, Aldosterone, Renal Tubular FLow

Back 1

GFR: If GFR is reduced, hyperkalemia will result due to decreased K+ excretion
NA/K Pump: Maintains intracellular K+ concentration
Aldosterone: Increases K+ secretion by the principle cells and also increases Na+ reabsorption by stimulating the NA/K pump
Renal Tubular Flow: when flow rate increases, luminal K+ is diluted, which increases secretion of K+

Front 2

Describe the components of the Thirst center in the 3rd ventricle

Back 2

Hypothalamic osmoreceptors and circumventricular volume receptors. hypovolemia triggers the hypothalamic osmoreceptors to release ADH and thirst.

Front 3

Describe how poplypeptide hormones interact with their membrane receptors

Back 3

Peptide hormones bind to the receptor, cause a G protein mediated change. Can be agonists or antagonists

Front 4

Describe the intracellular signaling mechanisms of peptide hormones

Back 4

G proteins have 3 subunits. The alpha subunit binds GTP, activating it. it can be stimulatory or inhibitory. Alpha subunit binds to adenylyl cyclase, and converts AMP to CAMP. this activates Protein Kinase A.
It can also go by the phospholipase C mechanism: PLC cleaves PIP2 to DAG and IP3. IP3 causes CA2+ release and this causes actions

Front 5

Describe 2 mechanisms where a hormone can have different effects in different types of cells:

Back 5

1. By having different types of receptors
2. By having different types of G proteins
3. By having different available subsets of effector molecules

Front 6

Explain the concept of a target cell and how target cells respond to hormones:

Back 6

Its a target cell for a hormone if it has functional receptors for that hormone and appropriate cofactors including Intracellular signaling molecules and transcription factors.

Front 7

Describe the 2 major types of hormone release and how the type of release impacts the way a hromone is regulated:

Back 7

The first class is those that are stored in membrane vesicles.

The second class are those secreted immediately upon synthesis in a manner not mediated by membrane vesicle fusion. the stimulus for its release is the same as its synthesis

Front 8

Describe how the effects of ligand receptor interactions are mediated for membrane associated and intracellular hormone receptors

Back 8

1. 7 transmembrane domain receptors G proteins
2. Intrinsic tyrosine kinase activity
3. soluble transducer molecules
4. Nuclear receptors

Front 9

Describe how CGRP and POMC are made and processed

Back 9

POMC is made by the hormone CRF. POMC is packaged into vesicles and are matured via proteolysis and concentration.
CGRP comes from the Calcitonin gene of CNS neurons. it is made from a 128AA precursor. CGRP is a vasodilator

Front 10

Describe the paraventricular and supraoptic nuclei in terms of their location, axons, and axon terminals, what hormones do they synthesize and what are their functions and target organs?

Back 10

1. Paraventricular nucleus: release ADH and Oxytocin. regulates water balance. Gives rise to the supraopticohypophyseal tract, which goes to the neurohypophysis.
2. Supraoptic Nucleus: makes ADH and oxytocin. projects to the neurohypophysis via supraopticohypophyseal tract

Front 11

List the 3 main classes of adrenal steroids, fxns, and common precursors, and the sources for cholesterol synthesis

Back 11

1. mineralocorticoids: fluid and electrolyte balance
2. Glucocorticoids: maintain energy
3. Sex steroids: skeletol, muscle, and long bone growth.
All come from pregnenolone which is made from cholesterol

Cholesterol comes from: LDL,HDL, storage, and de novo synthesis

Front 12

Describe the role of receptors in steroid hormone action, the organization of a typical receptor, the interactions of receptors with their specific ligands, and with the target gene sequences and the resultant effects on target gene expression:

Back 12

steroid ligand binding induces conformational changes and causes HSP to dissociate and receptors to form hetero or homo dimers. This exposes a nuclear translocation signal and initiates transport of the hormone receptro complex to the nucleus. the complex interacts with transcription regulatory factors associated with specific target genes. this causes the response.

Front 13

Describe the following for aldosterone and cortisol: Cell source, effects, MOA, and target cell type

Back 13

Aldosterone:
Cell Source: Zona Glomerulosa
Effects: Increases Na reabsorption and K excretion, increases H excretion
MOA: Regulated by Blood Volume
Target CElls: Principle cells and intercalated cells
Cortisol: Zona fasiculata
Effects: promotes lipolysis, degrades aa's, raises blood glucose, blocks ACTH release
MOA: ACTH and CRH
Target Cells: Liver and skeletol muscle mostly.

Front 14

Describe 2 major mineralocorticoids in humans and explain how availability of free hormone and affinity of the hormone for its receptor affect mineralocorticoid activity

Back 14

Aldosterone and 11 deoxycorticosterone (DOC). they have rougly the same affinity for the receptor and circulate at approximately equal concentrations. aldosterone is the more important one becuase more of it exists as free state.

Front 15

explain the regulation of aldosterone by :
RAA system, K, NA, ACTH, Dopamine, ANP, vasopressin, Somatostatin

Back 15

RAA: increases aldosterone by stimulating cholesterol desmolase and aldosterone synthesis
K: increases the release of aldosterone as K goes up
NA: decreases in ECF b/c of decreases in NA cause increaed aldosterone
ACTH: initiates the first step of aldosterone synthesis
DOpamine: blocks aldosterone
ADH: modest stimulatory effect on aldosterone
Somatostatin: blocks aldosterone