Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

6-11 ENDOCRINE RENAL > Physiology > Flashcards

Physiology Flashcards

1
Q

Mechanisms of hormone release

A
  1. humoral - respond to changing levels of ions or nutrients in the blood
  2. Neural - stimulation by nerves
  3. Hormonal - stimulation received from other hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Components of an endocrine axis

A
  1. Detection of homeostatic imbalance
  2. Ligand-Receptor activates secretory apparatus
  3. Release of hormone from cell
  4. Hormone in extracellular fluid – blood transport
  5. Target organ recognition of hormone - receptor
  6. End organ response to hormone
  7. Detector sense return to homeostasis – negative feedback
  8. Hormone cleared
  9. Synthesis of hormone reserves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 types of hormones

A
  1. Hydrophilic = protein/peptide hormones
  2. Really small/variable = tyrosine derived hormones
  3. Hydrophobic = steroid hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Storage, release and inactivation of protein/peptide hormones

A

Storage: secretory granules or vesicles
Release/action: Hydrophilic bind cell surface receptors and activate intracellular signalling pathways
Rapid acting and short lived
Inactivation: internalised by receptor mediated endocytosis, sequestered by kidney –> excreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Steroid hormones and inactivation

A

Lipids: derived from cholesterol. Include: cortisol, aldosterone, testosterone and progesterone.
Lipophilic:
- Require transport proteins - Bind intracellular receptors
Inactivation (Liver)
1. Cytochrome P450 oxidase 2. Conjugated
3. Excretion in bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Examples of tyrosine-derived hormones and which bind extracellular and nuclear receptors

A

Catecholamines - adrenaline, and NA (extracellular)
Thyroid hormones - thyroxine (nuclear)
Dopamine (extracellular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What determines how sensitive a receptor is to a hormone?

A
  • number of receptors
  • affinity of the receptor
  • downstream signalling molecules

Capacity for maximal response is determined mainly by the number of functional cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Overload desensitisation

A

Prolonged exposure to stimulus decreases cells response to the level of exposure.
Allows receptors to respond to changes in concentration of a signal rather than absolute concentration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Biggest endocrine organ?

Most important endocrine organ?

A

Biggest - gut

Important - H-P-x axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hormones produced in the anterior pituitary

A 
GH
ACTH
TSH
LH
PRL
FSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hormones stored in the posterior pituitary

A

Oxytocin and vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Regulation of ACTH release

A

• Stimulation of release • CRH and ADH (hypothal.)
• Stress
• Hypoglycemia
• Circadian pattern of
release
• Highest levels early AM • Sleep-wake cycle (jet-
lag)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is produced from pre-pro-opiomelanocortin?

A
  • ACTH
  • Endorphin
  • Lipotrophin
  • Melanocyte-stimulating hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Action of ACTH

A

• ACTH stimulates secretion of adrenal glucocorticoids
• Binds cell-surface melanocortin type II receptors (MC2R) • GPCR  adenylyl cyclase  cAMP  protein kinase A
• Most dense in the zona fasciculata
• Regulates steroid hormone secretion (2 ways)
1. RAPID = stimulate lipoprotein uptake into cortical cells, cholesterol delivery
2. LONG TERM = stimulate transcription of steroidogenic enzyme genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adrenal gland hormones produced

A

Adrenal medulla - catecholamines
Zona reticularis - sex hormones
Zona fasciculata - glucocorticoids (cortisol)
Zona glomerulosa - mineralocorticoids (aldosterone)

**corticosteroids = glucocorticoids and mineralocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What mediates secretion of mineralocorticoids (aldosterone)?

A
  • produced in zone glomerulosa

- mediated by mostly angiotensin II, and local increase in [K+]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Action of aldosterone in the kidney

A
  • ↑ active K+, H+ secretion
  • ↑ Na+/K+-ATPase
  • active Na+ reabsorption (water follows) • ↑ increases of BP and blood volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Action of glucocorticoids

A
  • CHO metabolism – elevates blood [glucose]
  • Stimulate gluconeogenesis (mobilises AAs, ↑ conversion anzymes) • ↓ cellular glucose use (oxidation of NADH)
  • Lipid metabolism – elevates blood [fat] • Mobilises FAs from adipose tissue
  • Also stimulates b-oxidation  energy
  • Protein metabolism – elevates blood [Protein, AA]
  • Mobilises AAs from non-hepatic tissues (enhances liver protein synthesis)
  • Anti-inflammatory
  • Blocks early stage inflammatory inception
  • Increases healing of inflammation
  • Suppresses cellular immune response, stabilises lysosomes, reduces vessel permeability.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Production of cortical sex hormones

A
  • Synthesised in the zona reticularis
  • DHEA (dehydroepiandrosterone)
  • Androstenedione
  • Converted in peripheral tissues to testosterone, oestrogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Secretions of the pancreatic islet of Langerhan cells

A

α-cells: secrete glucagon

β-cells: secrete insulin (+ amylin) ∆-cells: secrete somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Precursor thyroid hormone

A

Thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Thyroid hormones and what they are derived from

A

Derived from tyrosine

  1. thyroxine T4 (usually transformed into T3 within target cells, because T4 has low biological activity) - main one secreted and circulated in bloodstream
  2. Triiodothyronine T3 - binds to receptors, and has more biological potency than T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

2 major components of thyroid hormone synthesis

A
  1. Iodine

2. Thyroglobulin precursor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Function of iodine in thyroid hormone synthesis

A

 Thyroidhormonesneedlargeamountsofiodine(I2).  Scarce, low levels absorbed. (DRI 1mg/week)
 Iodine is absorbed as iodide (I-) and converted to iodine.
 Thyroidglandshavepowerfuliodidepumpstoconcentrateiodine
within the thyroid gland. ([I-] in follicular cells 20-50x > plasma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Steps in thyroid hormone biosynthesis and secretion

A
  1. Iodine trapping
  2. Oxidation of iodide
  3. Synthesis of thyroglobulin
  4. Iodination of tyrosine residues
  5. Coupling of tyrosine residues
  6. DIT+DIT=T4
  7. MIT+DIT=T3
  8. Endocytosis and digestion of colloid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the consequence of a faulty iodide pump in the thyroid follicular cell?

A

Severe hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Importance of high concentration iodine storage

A

Allows storage of large amounts of TH precursor, so the body becomes somewhat independent of day to day Iodine availability.

Iodination of precursor to form mature thyroglobulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Function of thyroid binding globulin

A

Binds T3 and T4 and provides water solubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Thyroid hormone binds intracellular nuclear receptors and regulate the activity of genes including:

A
  • Na-K pump
  • gluconeogenic enzymes
  • respiratory enzymes
  • Myosin heavy chain
  • beta-adrenergic receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can TSH increase thyroid activity?

A
  1. Increases hormone synthesis: Increases activity of NIS iodide pump Increases thyroglobulin production

2.Increases thyroid hormone secretion
• Vesicular reuptake
• Exocytosis

  1. Increases blood flow to the thyroid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is accelerated by TH?

A
  1. Oxidative metabolism
  2. CHO metabolism
  3. Lipid metabolism
  4. Nitrogen metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is hypothyroidism characterised by and what are some symptoms?

A

Low T3 + T4
High TRH + TSH

Signs: lack of energy, weight gain, poor tolerance of cold, enlarged thyroid gland (Hashimoto’s disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is hyperthyroidism characterised by and what are some symptoms?

Causes?

A

High T3 + T4
Low TRH + TSH

Signs: poor heat tolerance, goiter, exophthalmos, muscle wasting and weakness, sweating, weight loss, fatigue

Cause: AI hyperthyroidism, thyroid tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Effects of hypercalcemia and hypocalcemia

A

Hypercalcemia – depresses neuromuscular activity (blocks Na+ channels raises AP threshold - bathmotropy), kidney stones

Hypocalcemia – Potentiates neuromuscular activity (positive
bathmotropy – lowers AP threshold), impairs clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

SI enterocyte Ca2+ absorption

A
  • TRPV6 is a Ca2+-specific channel (Ca2+-dependent fbk inhibition)
  • Calbindin binds cytosolic Ca2+ - prevents free Ca2+ blocking TRPV6
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which part of the nephron is most important in retaining Calcium?

A

Proximal tubule - 70% of calcium retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

90% of calcium is ________ reabsorbed in the nephron

A

Passively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Function of osteoblasts and osteoclasts in calcium serum levels

A

Osteoblasts
– bone-forming cells: responsible for bone deposition – ↓serum [Ca2+]

Osteoclasts
– bone-eating cells: resorb the previously formed bone – ↑serum [Ca2+]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Actions of PTH on bone

A

Increases bone degradation (releases Ca2+).
Rapid action (minutes)
• ↑ osteocyte membrane permeability for Ca2+ →liquid Ca2+ of bone enters the cells→ Ca2+ pump transports Ca2+ to the extracellular fluid →↑ serum [Ca2+]
Delayed action (12~14h)
• ↑ osteoclast activity→↑ serum [Ca2+]
• ↑ production of osteoclast →↑ serum [Ca2+]
NET RESULT: increased release of Ca2+ from bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Actions of PTH on kidney

A

• decreased renal Ca2+ excretion
Action
• Increases reabsorption of Ca2+ from thick ascending limb and distal tubule
• ↑ Ca2+ -ATPase and Na+-Ca2+ antiporter
• ALSO, Stimulates transcription of 1-alpha hydroxylase
Vitamin D activation in kidney
NET RESULT: increased plasma calcium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Function of calcitonin

A
  • Major target cell – osteoclast
  • Acts through calcitonin receptor (cAMP mechanism)
  • Inhibits activity of osteoclasts→↓bone turn over
  • Inhibits osteoclast formation
  • Minor effect – decreases kidney Ca2+ reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Effects of growth hormone

A

GH directly activates growth of bone, soft tissue and viscera
• Metabolic switch (burn fat, store protein/CHO)
• Increased protein synthesis (↑ translation, transcription - new
muscle etc.)
• Increased amino acid transport (↑ tissue protein storage)
• Increased lipolysis (burn fat for fuel)
• Reduced glucose transport and metabolism
• Increased IGF production in liver (and other organs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the starvation paradox?

A

• If nutrients are required for growth, why would starvation trigger GH release?
• GH helps us survive prolonged starvation by switching metabolism away from proteins as a fuel source (“protein-sparing”).
- allows body to switch from using proteins/glucose to sustain life, to storing glucose/proteins in tissues
- burn through fats first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Function of IFs

A

Regulate proliferation, differentiation and metabolism

  • Resemble insulin in structure and function (i.e. regulates CHO metabolism)
  • IGFs stimulate amino acid uptake and activate protein & DNA synthesis
  • Strongly mitogenic and hypertrophic
  • 2 Isoforms:
  • IGF-1 = adult form, IGF-II = foetal form • autocrine and paracrine effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Synergistic effects of signalling from insulin and IGF

A
  • protein translation
  • autophagy
  • apoptosis
  • oxidative stress
  • gene transcription
  • proliferation
46
Q

Consequence of over secretion of GH before and after puberty

A

Before puberty - XS growth that continues throughout childhood and puberty, leading to extremely tall stature/gigantism

After puberty - thickening of bones in hands, feet and jaw causing a disease called acromegaly

47
Q

Action of parathyroid hormone, vit D and calcitonin in calcium regulation?

A

¥ Parathyroid hormone – increases plasma [Ca2+]
¥ Vitamin Ds (1, 25, D) – increases plasma [Ca2+]
¥ Calcitonin – reduces plasma [Ca2+]

48
Q

Action of PTH on bone

A 
Rapid action (minutes) 
¥	↑ osteocyte membrane permeability for Ca2+ →liquid Ca2+ of bone enters the cells→ Ca2+ pump transports Ca2+ to the extracellular fluid →↑ serum [Ca2+] 
Delayed action (12~14h)

¥ ↑ osteoclast activity→↑ serum [Ca2+]
• ↑ production of osteoclast →↑ serum [Ca2+]
NET RESULT: increased release of Ca2+ from bone

49
Q

Action of PTH on kidney

A

decreased renal Ca2+ excretion
Action
¥ Increases reabsorption of Ca2+ from thick ascending limb and distal tubule

¥ ↑ Ca2+ -ATPase and Na+-Ca2+ antiporter

¥ ALSO, Stimulates transcription of 1-alpha hydroxylase
Vitamin D activation in kidney

NET RESULT: increased plasma calcium levels

50
Q

Consequences of vitamin D deficiency

A

Deficiency - “rickets” - low Ca2+ levels , which results in:
o soft and pliable bones (bending/distortion)

o impaired ossification of the newly created osteiod

Type I - Mainly due to Vit D deficiency (lack of sunlight, diet)
Type II - Vit D receptor (VDR) mutation

51
Q

Normal ECF [H+] and normal variation/ pH

A

40nEq/L +-3-5

pH = 7.4

52
Q

Acidosis and alkalosis pH levels

A

Acidosis: < 7.35
Alkalosis: >7.45

53
Q

Venous blood has a lower pH to arterial blood due to:

A

Carbon dioxide levels being higher

54
Q

How does pH effect metabolism and the neuromuscular system?

A

Metabolism: every step is pH dependent so altered pH reduces reaction efficiency due to enzymes

NM system: acidosis results in hypo excitability, alkalosis results in hyperexcitability
Due to acidosis increasing serum [K+] and alkalosis reducing it

55
Q

Defense mechanisms to acid-base changes in the body

A

Chemical buffering (immediate but exhaustible)
• Solutions that resist change in pH
• Intracellular and extracellular buffers provide an immediate response to acid-base disturbances – bone also buffers
Pulmonary regulation (minutes/hours and limited capacity)
• PCO2 is regulated by changes in tidal volume and resp rate
• A decrease in pH increases in tidal volume or respiratory rate
• CO2 is exhaled blood pH increases
Renal regulation (hours-days and v powerful with infinite capacity)
• The kidneys control pH by adjusting the amount of HCO3- that is excreted or reabsorbed
•

Reabsorption of HCO3- is equivalent to removing free H+

56
Q

Chemical buffer systems

A

Bicarbonate
Phosphate
Proteins - and Hb in RBCs
Ammonia

57
Q

What speeds up the conversion of carbon dioxide and water into bicarbonate?

A

Carbonic anhydrase

58
Q

Processes involved in renal control of pH

A
  1. Secretion of H+
  2. Reabsorption of filtered HCO3-
  3. Generation of new HCO3-
59
Q

Mechanisms of hypokalaemia when plasma pH increases

A
  1. Na+/K+ ATPase: alkalosis causes a shift of K+ form the plasma ICF
  2. Electroneutrality is king: increase in plasma [HCO3-] will exceed renal PCT reabsorption capacity, and K+ will be excreted as an obligate cation partner to HCO3-
60
Q

Difference between respiration and metabolic acidosis

A

Resp: ppCO2 increases massively

Metabolic: massive decrease in HCO3-

61
Q

Types of nephrons

A

Cortical nephrons – 80% of nephrons

• Renal corpuscle in outer portion of cortex and short loops of Henle extend only into outer region of medulla –

Juxtamedullary nephrons – other 20% (important in water balance)
• Renal corpuscle deep in cortex and long loops of Henle extend deep into medulla
• Peritubular capillaries and vasa recta

  • Ascending limb has defined thick and thin regions
  • Enable kidney to secrete very dilute or very concentrated urine
62
Q

Which part of the nephron contacts the glomerulus again and what is the purpose?

A

Purpose: feedback
Part: thick ascending loop of henle

63
Q

What does glomerular filtration rate depend on?

A
  • permeability of membrane
  • surface area of membrane
  • filtration pressure
64
Q

Myogenic auto regulation of Glomerular filtration rate

A

¥ Automatic regulation of RBF + GFR

¥ In response to slight changes in BP

¥ Control at the local level (e.g. smooth
muscle cells)

(a) ↑ MAP automatically induces vasoconstriction of afferent arteriole↓ flow↓ GFR and bringing it back to normal
(b) ↓ MAP induces afferent arteriole vasodilation↑ flow and GFR, and bringing GFR back to normal levels.

65
Q

Tubuloglomerular feedback regulation of glomerular filtration rate

A

Juxtaglomerular apparatus: macula densa
- alter glomerular resistance in response to changes in the flow rate through the distal nephrons

MD - monitors tubular fluid composition by the amount of sodium and chloride present

66
Q

Hormones regulating GFR

A

Atrial natriuretic peptide (ANP):
- dilate Aff/ constrict Eff. = ↑↑ GFR (noΔRBF)

Angiotensin II: complex
- Constrict Aff / super constrict Eff = ↓RBF but ↓/noΔ GFR (GFR maintained due to greater efferent constriction)

67
Q

What is taken out of blood to turn it into filtrate?

A

Cells, platelets or big proteins

68
Q

What does filtrate contain?

A

Na Ca Mg K HCO3 PO4 glucose, AA, small proteins, urea

69
Q

What proportion of glucose and salts are normally reabsorbed?

A

Glucose 100%

Salt 99.5%

70
Q

The importance of sodium movement and active transport in the neprhon

A

Sodium is important for setting up concentration gradients to drag other ions - it drive a lot of secondary transport (very important in glucose and amino acid uptake)

Co or counter transport

71
Q

Pinocytosis in the nephron

A

The cell forms a vesicle around the filtrate that touches the cell and reabsorbs it - passive and non specific but often collects proteins - hence we don’t have protein in urine normally

72
Q

Is active transport saturable in the nephron?

A

Yes - in diabetes the glucose transport is saturated and hence there is glucose in the urine

73
Q

What is passive transport rate in the nephron dictated by?

A
  • electrochemical gradient
  • permeability
  • time
74
Q

Water transport in the renal tubule

A

Through tight junctions and aquaporins
PCT: very leaky so water follows ions quickly
Ascending LOH: impermeable
DCT/CT/CD: varied permeability

75
Q

Where is obligatory sodium reabsorption in the renal tubule?

A

67% in the proximal tubule and 25% in the loop of henle

Remainder is under hormonal control on the DCT

76
Q

Where is the obligatory and hormonal control of water reabsorption in the renal tubule?

A

PCT - 65% obligatory
LOH - 15% oblig (but there is more sodium reabsorption hence it is semi impermeable to water)
DCT/CD - 20% under hormonal control

77
Q

Reabsorption and secretion in PCT

A

Na+, Cl-, K+ (65%), glucose + AA (100%), water (65%)

ALSO most secretion: wastes and H+

78
Q

Heterogeneity in the PCT

A

1ST HALF: majority of glucose and AA reabsorbed

2ND HALF: sodium reabsorbed with chloride

79
Q

Difference between descending and ascending LOH in relation to water movement

A

Descending - thin and highly water permeable
Ascending - thick and impermeable to water (active reabsorption of sodium, chloride and potassium

–> osmolarity reduces as it goes through the ascending limb

80
Q

Cells in the collecting tubule

A

Principle cells - reabsorb Na+ and secrete K+

Intercalated cells - secrete H+, reabsorb HCO3- K+

81
Q

How is urine made more dilute through the renal tubule?

A

In the thick ascending LOH, salts are reabsorbed but water is not because it is impermeable and osmotic flood gates are not opened in the CD

82
Q

Producing concentrated urine

A

Open up all the aquaporins so that water can follow salt movement

Leaky DCT/CT/CD - so h2o can be resorbed from the normally impermeable segments

83
Q

Where do aldosterone and angiotensin II act?

A

Aldosterone - Collecting tubule and duct

Angiotensin II - PCT, thick ascending LOH, collecting tubule

84
Q

How does ADH regulate osmolarity?

A
  1. An ↑ ECF osmolarity (ie - ↑ [Na+]) causes osmoreceptor cells to shrink.
  2. Osmoreceptor shrinkage AP relay post. Pit. release ADH
  3. ADH kidneys ↑ water permeability of DCT/CT/CDs ↑ resorption/Bvol
  4. H2O is conserved while Na+/solutes continue to be excreted dilution of ECF solutes
85
Q

Where are the osmoreceptors found? and ADH production

A

Brain, ADH synthesis in supraoptic (most) and paraventricular (some) nuclei

86
Q

Where does ADH act?

A

Increases water permeability of DCT/CT/CD
Usually aquaporin 2 channels are held in vesicles inside the cell, so ADH causes exocytosis of aquaporin vesicles to allow water transport

87
Q

When is renin secreted?

A

From the granular cells of JGA - when there is low salt concentration in DCT(low BP)

88
Q

What triggers renin secretion by the granular cells?

A

o ↑renin secretion due to
– ↓ [NaCl] in DCT macula densa cells (low GFR - JG fbk)
o ↓ stretch on afferent arterioles (low BP)

o ↑ sympathetic stimulation (baroreceptor reflex)

89
Q

What regulates aldosterone secretion?

A

Angiotensin 2 and local potassium concentration

90
Q

How does aldosterone activate signal transduction?

A
  • gene transcription in hours

- non genomic activation in minutes

91
Q

What is the action of aldosterone on the principle cells in the cortical CT?

A

o Stimulates basolateral Na/K+-ATPase (cortical CT)
o Also increase the Na+ permeability of the luminal membrane
o And Na+/K_ and Na+/H+ counter transporters

92
Q

What is the potassium secretion rate from the renal tubule regulated by?

A
  1. Na+K+-ATPase activity
  2. K+ electrochemical gradient
  3. K+ permeability
93
Q

Stimuli for thirst (4)

A

¥ Hypertonicity – hypothalamic osmoreceptors – NaCl accounts for 92% of ECF tonicity

¥ Hypovolaemia: low P baroreceptrs (great veins and right atrium)

¥ Hypotension: high P baroreceptors (carotid and aorta)

¥ Angiotensin II: V potent dipsogen (renal hypotension)

94
Q

Two primary stimuli for hunger for salt

A
  1. Reduced ECF [Na+]

2. Reduced BP/Bvol

95
Q

What receptors do glucocorticoids and mineralocorticoids bind?

A

GC - NR3C1

MC - NR3C2

96
Q

What is glucagon secretion mediated by?

A

Stimulated: low plasma glucose, cortisol, adrenaline, CCK, gastrin

Inhibited: Glucose, insulin, SS

97
Q

Action of somatostatin

A

Acts locally to inhibit BOTH insulin and glucagon secretion

98
Q

How does thyroid hormone increase CHO metabolism

A

T3

  • increases glucose absorption by intestine
  • increase glucose oxidation in liver, fat, muscle
99
Q

Thyroid hormone in lipid metabolism

A

TH determines rate of lipolysis and lipogenesis in liver

Stimulates mobilisation from fat cells - increasing free fatty acids and reducing plasma TG cholesterol

100
Q

TH deficiency in children

A

Short stature, bony retardation, malformed facial structure, severe and irreversible mental and physical retardation

101
Q

Action of PTH on kidney

A

Increases resorption of calcium from TAL and Distal tubule
Increases activity of Ca ATPase and Na+Ca2+ antiporter
Also stimulates transcription of 1 alpha hydroxyls to activate vitamin D which increases intestinal absorption

102
Q

Calcitonin

A

Synthesised by parafollicular cells of the thyroid in response to increased plasma calcium concentration. Antagonises PTH in calcium regulation

103
Q

Function of calcitonin

A
  • acts through calcitonin receptor cAMP
  • inhibits osteoclast activity
  • inhibits osteoclast formation
  • slightly decreases kidney Ca reabsorption
104
Q

Excretory function of kidneys

A
  • urea, uric acid, creatinine, bilirubin, foreign substances and XS substances
105
Q

Pressure involved in net filtration in the glomerulus

A
  1. glomerular blood hydrostatic pressure
  2. capsular hydrostatic pressyre
  3. blood colloid osmotic pressure
106
Q

What is the myogenic mechanism in regulating GFR?

A

Occurs when stretching triggers contraction of smooth muscle cells in the afferent arterioles and REDUCES GFR

107
Q

What is the tubuloglomerular mechanism involved in regulating GFR?

A

Macula dense provides feedback to glomerulus, inhibiting release of NO and causing afferent arterioles to constrict = REDUCED GFR

108
Q

How does the macula densa monitor and alter GFR?

A

Monitors tubular fluid.

If there is a high concentration of NaCl in DCT, then it inhibits the release of adenosine/NO = afferent arteriole constriction and reduced GFR

If there is a low concentration of NaCl in the DCT, then adenosine and NO result in afferent arteriole dilatation and increased GFR

109
Q

Action of ANP on GFR and RBF

A

Dilate Aff, constrict Eff = increased GFR and no change to RBF

110
Q

Action of angiotensin 2 on GFR and RBF

A

Constrict Aff, super constrict Off = reduced RBF, no change to GFR

111
Q

What stimulates renin secretion from the granular cells of the JGA in the endothelial wall?

A
  • low NaCl conc. detected by macula densa cells in DCT (low GFR)
  • low stretch on afferent arterioles (low BP)
  • sympathetic stimulation

6-11 ENDOCRINE RENAL (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions