Brainscape's Knowledge GenomeTM

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


See full index

A2 ME3031 ENDO DM > 02: Physiology II > Flashcards

02: Physiology II Flashcards

1
Q

Define the term and give examples of obligatory and non-obligatory glucose utilising tissues

A

OBLIGATORY: can only metabolise glucose

e.g. brain

Vs
non-obligatory: most other tissues

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

State the range of plasma glucose that may be expected in normal resting subjects who have fasted overnight

A
  • Normal range: 4.2-6.3mM / 5mM *

Hypoglycaemia = BG <3mM

*

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

Describe the process by which insulin is released

A

(Pancreas Islets - Beta Cells)

Insulin (anabolic peptide hormone) stimulates Lipogenesis & glycogenesis
= fat store formation and stimulates uptake of glucose from blood to tissues

  • Katp channels (Beta cells)
  • plasma glucose enter beta cells via GLUT resulting in ⇧ATP = Katp to close.
  • ⇧[K+] within cell = depolarising = Voltage Ca2+ channels open
    => insulin vesicle exocytosis triggered
  • low [BG] = Katp open = hyperpolarised Beta cells = insulin secretion prevented
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the process by which glucagon is released

A

(Pancreas Islets - Alpha Cells)

Glucagon (catabolic) controls Glycogenolysis and Gluconeogenesis (Liver) = create and maintain glucose pool

*stimulated by [A.A] increase as well

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

Describe how the release of insulin impacts on the release of glucagon and vice versa

A

Glucagon stimulates insulin release via the initiation of gluconeogenesis.

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

Describe the sites of action, and mechanism of action, of insulin on blood glucose levels

A

Triggered by glucose and A.A (absorptive state) but primarily by ⇧[blood glucose].

MUSCLE AND FAT INSULIN-DEPENDENT ONLY
Insulin binds tyrosine kinase R. on insulin-dependent tissues = ⇧glucose uptake
* muscle & adipose = insulin stimulates GLUT4 transporters = glucose uptake for primary energy use

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

Describe the sites of action, and mechanism of action, of glucagon on blood glucose levels

A

Within the liver, GLUCAGON stimulates the breakdown of the glycogen to release free glucose in order to maintain [blood glucose] pool.

Significantly active during post-abs state

Glucagon receptors Gprotein coupled R linked to adenylate cyclase/cAMP
= ⇧glycogenolysis
⇧glucogeno
Formation of ketones from FA via lipolysis

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

Describe how the release of glucagon impacts on the metabolism of fat and protein

A

Catabolic = Breaks down Fatty Acids and Amino Acids

@ muscles

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

Describe the interaction between insulin and the counter-regulatory hormones (glucagon, adrenaline, cortisol, GH)

A

Insulin-Glucagon =

Insulin-Adrenaline = (counterregulatory hormone to insulin)

glucagon and epinephrine (adrenaline) levels rise and more glucose is released from the liver.

growth hormone and cortisol levels rise, which causes body tissues (muscle and fat) to be less sensitive to insulin = inhibiting glucose uptake.

As a result, more glucose is available in the blood stream.

Insulin-Cortisol = Glucose releasing/formation + PROTEIN CATABOLISM (uniquely)
*inhibits glucose uptake

Insulin-Growth Hormone = Permissive effect: . GH meanwhile counteracts effects of insulin = glucose-releasing

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

Describe how glucose metabolism can change in times of stress (exercise, starvation, diabetes)

A

STARVATION = Fuel source shifts from glucose to A.A = new proteins and converted to fat; as well as formation of KETONES in prolonged hypoglycaemia

EXERCISE = d/t stress and sympathetic innervation, glucagon release is promoted = glucose-releasing processes in order to maintain the pool

  • insulin-independent up-regulation of GLUT4
  • ⇧insulin-sensitivty

DIABETES =

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Compare and contrast Type 1 and Type 2 Diabetes Mellitus

A

T1DM: AuIm B Cell; no insulin, absolute dependence for insulin
*HYPOGLYCAEMIA:

T2DM: non-insulin dependent DM; peripheral insensitivity to insulin = insulin resistance.
* tissue and muscles no longer respond to normal levels of insulin
* hyperinsulinaemia
= hyperglycaemia d/t inadequate tissue response and glucose uptake

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

Appreciate the aetiology and risk of diabetic ketoacidosis

A

Poorly controlled insulin-dependent diabetes:

lack of insulin depresses ketone body uptake = building up = acidosis pH <7.1

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

Stimuli inhibiting Insulin release

A

low [bg]
somatostatin
sympathetic a2 effects
stress (hypoxia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stimuli inhibiting Insulin release

A

low [bg]
somatostatin
sympathetic a2 effects
stress (hypoxia)

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

Significancee of GI hormones

A

GI hormones released via Vagal activity during an oral intake of glucose stimulate include insulin via vagal stimulation ALONGSIDE direct effects of B cells PLUS incretin hormone stimulation
=> ⇧insulin

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

Stimuli inducing insulin release

A 
⇧[BG]
⇧ [plasma A.A]
Glucagon
Incretin hormones controlling GI secreton
Vagal Nerve activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Significance of A.A and stimulating insulin and glucagon

A

A.A stimiulate BOTH in order to maintain a balance by inducing glucagons glucose mobilising effects in order to counteract the effects of insulin. Such an adaptation was borne from carnivorous diets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Stimuli inducing glucagon release

A 
[BG] <5mM
⇧[AA]
Sympathetic innervation + epinephrine, B2 effect
Cortisol
Stress: exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Stimuli inhibiting glucagon release

A

glucose
FFA + ketones
insulin
somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Somatostatin

A
  • inhibit activity of GIT, ensure steady plasma concentrations
  • suppresses both insulin and glucagon as a paracrine
  • inhibits secretion of GH from anterior pit.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GLUCOSE TOLERANCE TEST

A

Fasting [BG] measured
Oral glucose load
[BG] measured again

= [BG] should returning to fasting levels. Elevation after 2 hours is indicative of DM, cannot distinguish.

(MW of glucose = 180)
[BG]/180 = concentration of glucose (mM)

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

Summarise the factors that control secretion of GH

A

GH secreted from pit.; released during deep delta sleep

STIMULATION:
GHRH (hypothalamus)
*⇩energy supply (exercise, cold, fasting) = ⇧demand for energy = ⇧GHRH = ⇧GH
* ⇧AA in plasma (proteinous meal)
* physical stress & illness
* delta sleep: ⇧FH = growth spurts/tissue repair
* oestrogen and testosterone

INHIBITION:
negative fedback of IGH-I
autocrine negative feedback of GH in ant pit.
* GHIH
* ⇧Glucose, FFA
* Ageing
* Cortisol (catabolic effect not GHIH release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Outline the direct and indirect action of GH

A

Mediated through IGF-1 (indirect actions),

  • HYPERTROPHY in target tissues
  • HYPERPLASIA in target tissues

via tyrosine kinase R =

1) LONG BONE GROWTH (indirect via IGF-1)
* IGF-1 (liver) in response to GH release as a negative feedback loop (switch off GH and GHRH)
* IGF-I and GH are peptides but are peculiarly transported bound to carrier proteins
* thereby resevoir of bound + protection + ⇧1/2Life

2) METAB. REG. (direct)
* enhancing blood glucose and FFAs to promote growth
*NET ⇧blood glucose of GH dominate IGF-I
* ⇧GLUCONEOGENESIS (liver)
* ⇧ lipolytic sens in adipocytes
* ⇩ INSULIN SENS. IN MUSCLE AND ADIPOSE
= release of energy stores / anti-insulin / diabetogenic in xcess
* ⇧ AA & prot. synth in all cells = anabolic

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

Describe how different endocrine hormones interact to regulate growth

A

thyroid hormones and insulin critical for GH function for growth = PERMISSIVE ACTION before it will stimulate growth.

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

Describe the endocrine factors that regulate growth at different stages of life

A

GH (GHReleasingHormone & GHInhibHormone): balance between these 2 hormones dictate GH released from hypothalamus.
*10mos post-birth

IGF-1: INTERMEDIATE OF GH critical for GH hormone, binds much more tightly to carriers than GH

THYROID HORMONES:

  • infancy 8-10mos
  • thyroid deficiency greatly affects developing infants = obvious post feeding.

INSULIN:
*infancy 8-10mos

SEX STEROIDS: puberty; enhance release of growth hormones

  • excess GH secretion due permissive effects of sex steroids
  • ⇧IGF-1 = ⇧growth
  • also terminate growth @ end of puberty; epiphyseal fusion

CORTISOL: antagonistic role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the endocrine factors that regulate growth at different stages of life

A

GH (GHReleasingHormone & GHInhibHormone): balance between these 2 hormones dictate GH released from hypothalamus.

  • 10mos post-birth; therefore irrelevant during intra-uterine and infant development
  • exerts role on bone growth and elongation

IGF-1: INTERMEDIATE OF GH critical for GH hormone

THYROID HORMONES:

  • infancy 8-10mos
  • thyroid deficiency greatly affects developing infants = obvious post feeding.

INSULIN:
*infancy 8-10mos

SEX STEROIDS: puberty; enhance release of growth hormones

  • excess GH secretion due permissive effects of sex steroids
  • ⇧IGF-1 = ⇧growth
  • also terminate growth @ end of puberty; epiphyseal fusion

CORTISOL: antagonistic role

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

Define the terms: somatotrophin; somatostatin; somatomedin

A

SOMATOTROPHIN: hormone released from the ANT. PIT. (SOMATOTROPH = cells relating to growth)

SOMATOSTATIN: hormones such as GHIH, which stops growth

SOMATOMEDIN: hormone intermediate in the stimulation of tissue growth by growth hormone. (e.g. IGF-1 as it mediates action of GH)

28
Q

Describe and explain the effects on GH secretion in response to a fall in plasma glucose following administration of insulin

A

⇧GHRH = GH d/t hypoglycaemia

29
Q

Describe and explain the effects on GH secretion in response to a rise in plasma amino acids after the digestion and absorption of a large protein meal.

A

proteinous meal = rise in AA = ⇧GHRH = GH+
* fat breakdown
aa conv to protein
bone and cartilage growth

30
Q

Describe how uncontrolled excessive secretion of GH in adulthood (as in the disease acromegaly) could be diabetogenic (i.e. cause symptoms of diabetes mellitus).

A

Excess action of GH which is anti-insulin in nature would release energy stores and thus increase [plasma glucose] and FA.

31
Q

Insulin Vs GH

A

BOTH

  • ⇧AA uptake
  • ⇧ prot synth

only insulin
* ⇧GLUCOSE UPTAKE
* only muscle and adipose tissue are insulin sens
meanwhile
GH mobilises glucose stores; and bone and brain dev. hugely supported by GH actions and indirectly muscle d/t A.A uptake

32
Q

Causes of abn GH secretion

A

HYPERSECTRION:
-endocrine tumours: gigantism (before bone fusing), acromegaly (after bone fusing)

HYPOSECR. / HYPORESP.:

  • GHRH def. (hypothalm. origin)
  • GH def. (pit. origin)
  • GH underexpr./mutation = depressed IGF-1 release + loss of IGF-1 inhib = ⇧⇧[GH] = d/t lack of negative feedback
  • precocious puberty: XS GnRH
  • hypothyroid dwarfism: loss of permissive TH on GH
33
Q

Outline the types of cell in the thyroid gland and their arrangement

A

C CELLS: calcitonin (Ca2+ reg. hormone)

FOLLICULAR CELLS: surround hollow thyroid follicle filled with COLLOID (TH store)

  • produce enzymes to make TH + THYROGLOBULIN
  • secreted into colloid
  • concentrate iodide (plasma) into colloid + combines with tyrosine kinase residues in colloid = TH
34
Q

Describe the main actions of TSH and other stimuli on thyroid cells.

A

TSH (pit.) stimulates uptake of colloid by follicular cells via ENDOCYTOSIS
*proteolytic enzymes

(hypothalamus)
*COLD, EXERCISE, PREGNANCY stimulate TRH
> TSH release
* somatostatins inhibit TSH
* glucocorticosteroids inhibit TSH and T4>T3 conversion
35
Q

Outline the steps by which thyroxine (T4) and tri-iodothyronine (T3) are formed and are secreted into the extracellular fluid.

A

(colloid)
Iodine + Tyrosine > MIT (monoiodotyrosine)
MIT + Iodine > DIT (diiodotyrosine)

conjugation catalysed by THYROID PEROXIDASE in COLLOID:
MIT + DIT > T3 (triiodothyronine
DIT + DIT > T4 (tetraiodothyronine/Thyroxine)

endocytosed and exocytosed follicle cell and through MCT to BLOOD

  • T3 and T4 lipid soluble
  • bind to THYROXINE-BINDING GLOBULIN within PLASM
36
Q

Describe the T3 / T4 ratio in thyroid secretion, protein binding of T4 and T3 in plasma,conversion of T4 into T3 in target tissues, and the significance attributed to these.

A

T4 higher binding affinity to TBG (binding globulin) = longer 1/2L, T4 commonest circulating form

VS T3 commonest TH binding to TH receptors d/t higher affinity

  • free hormone exerts inhibitory effect on TSH and TRH
  • Half of T4 in plasma is deiodinated by DEOIDINASE ENZYMES, remaining fraction inside target cells
37
Q

Describe the locations of T3 receptors

A

Nuclear receptors therefore having an effect on cell function and overall metabolism (development, growth, metabolism, and cardiac function.)

38
Q

Explain the catabolism of T4 and T3

A

T3 catabolised upon reaching target cell nuclear receptors. Additionally, around half of plasma T4 is deiodinised = T3 ready for physiological activity plus the remaining fraction of T4 is converted at the target cell.

39
Q

TH Dysfunction

A

HYPERTHYROIDISM:
*Graves Disease: antiAb mimic TSH and continually stimulate thyroid, ⇧TH inhibits TSH release from ant pit thus [TSH]plasma very low.

*Thyroid adenoma: hormone secreting tum.

= Wt. loss and heat intolerance, muscle weakness, hyperexcitable reflexes, ⇧cardio funct. (TH permissive to epinephrine and B receptors)

HYPOTHYROIDISM:

  • Hashimoto’s Disease: AuIm attack
  • Iodine deficiency
  • Idiopathic

= Wt. gain, cold intolerance, brittle nails/thin skin, slow reflexes, fatigue, ⇩cardio funct.

40
Q

TH Dysfunction

A

HYPERTHYROIDISM:
*Graves Disease: antiAb mimic TSH and continually stimulate thyroid, ⇧TH inhibits TSH release from ant pit thus [TSH]plasma very low.

*Thyroid adenoma: hormone secreting tum.

= Wt. loss and heat intolerance, muscle weakness, hyperexcitable reflexes, ⇧cardio funct. (TH permissive to epinephrine and B receptors)

HYPOTHYROIDISM:

  • Hashimoto’s Disease: AuIm attack
  • Iodine deficiency
  • Idiopathic

= Wt. gain, cold intolerance, brittle nails/thin skin, slow reflexes, fatigue, ⇩cardio funct.

41
Q

Explain the dietary intake of foods containing materials metabolised to thiocynanates or isothiocynanates.

A

Thiocyanate is a potent competitive inhibitor of the thyroid sodium-iodide symporter.

Iodine is an essential component of thyroxine. Since thiocyanates will decrease iodide transport into the thyroid follicular cell, they will decrease the amount of thyroxine produced by the thyroid gland. As such, foodstuffs containing thiocyanate are best avoided by iodide deficient hypothyroid patients

42
Q

Significance of Goitre

A

INCREASED TROPHIC ACTION OF TSH ON FOLLICULAR CELLS (hypo) or OVERACTIVITY = HYPERTROPHIC

43
Q

Significance of Goitre

A

INCREASED TROPHIC ACTION OF TSH ON FOLLICULAR CELLS (hypo) or OVERACTIVITY = HYPERTROPHIC

44
Q

Classify the adrenal hormones according to their main physiological effects and the endocrine gland cell types that secrete them.

A

ADRENAL MEDULLA: neuroendocrine, secretes catecholamines from postganglionic cell
*EPINEPHRINE, NE, and DOPAMINE: response to stress maintain BP

ADRENAL CORTEX: true endocrine

  • MINERALOCORTICOIDS - aldosterone (Na and K regulation)
  • GLUCOCORTICOIDS - cortisol (plasma glucose regulation)
  • SEX STEROIDS

=> stress response and survival

45
Q

Outline diagrammatically the structure of the adrenal gland, indicating its zonation.

A

ADRENAL MEDULLA => catecholamine

ADRENAL CORTEX:
ZONA RETICULARIS => SEX HORMONES

ZONA FASCICULATA => GLUCOCORTICOIDS

ZONA GLOMERULOSA => ALDOSTERONE

46
Q

Outline the main pathways involved in the synthesis of steroid hormones; and indicate the main agents and points of control.

A 
CHOLESTEROL
=> PROGESTERONE
* > CORTICOSTERONE > ALDOSTERONE
* > CORTISOL
(21-hydroxylase)

CHOLESTEROL
=> PROGESTERONE + DHEA => ANDROSTENEDIONE
> ESTRONE
> ANDROSTENEDIONE > TESTOSTERONE > estradiol
> DHT

  • different enzymes found in different adrenal zones in order to make different enzymes
    e. g. aldosterone enzymes found in zona glomerulosa
47
Q

Outline inborn errors of the adrenal glands (congenital adrenal hyperplasia).

A

21-hydroxylase defect = aldosterone and crotisol def.

  • salt and glucose balance disruptuon
  • excessive adrenal androgen production
  • hyperplasia d/t nil cortisol to negative feedback ACTH and CRH = continous adrenal cortex stimulation
48
Q

Describe the normal circadian basal rhythm

A

Cortisol and ACTH releasing rythm; cortisol LONGER HALF-LIFE THAN ACTH
peak at 6-9AM, nadir at midnight

peaks throughout the day d/t stress stimuli

49
Q

Describe the physiological actions of glucocorticoid hormones such as cortisol

A

Influences glucose metabolism, 95% of plasma cortisol bound to CORTISOL BINDING GLOBULIN
bind to receptors found in all nucleated cells

  • gluconeo
  • PROTEOLYSIS
  • LIPOLYSIS
  • ⇩INSULIN SENSITIVTY
    = maintain glucose pool by providing substrates and protects pool by providing alternative fuel via FFA

=> maintain blood glucose levels during stress, permissive on glucagon

(additional actions)

  • negative effect on Ca2+ = ⇩abs from gut, ⇧excretion at kidney = net ca2+ loss
  • depressive impairment on mood and cognition (hypercortisolaemia)
  • permissive effects on NE: a-receptor effect = vasoconstrictive ∴ low cortisol = hypoT
  • suppression of immune system: cortisol ⇩circulating lymphocyte count and Ab formation, inhibits inflamm response
50
Q

Outline the physiological effects of mineralocorticoids such as aldosterone.

A

Acts on kidney and regulates mineral resorption and excretion e.g. Na+ resorption and K+ excretion

  • ⇧aldosterone: Na+ retention = H20 retention + K+ depletion = ⇧BLOOD VOL. AND BP
  • ⇩aldosterone: Na loss = H20 loss and ⇧[K+]plasma = ⇩BV + BP
51
Q

Outline the risks associated with rapid withdrawal of glucocorticoid therapy.

A

Side effects of glucocorticoid Rx

  • severe suppression of immune system = infection risk
  • protein cat. = muscle wasting
  • lipolysis = thin skin

*rapid withdrawal of therapy = cause symptoms of adrenal insufficiency d/t enhanced effects on negative feedback w/ rx and establishes atrophy and decline in ACTH action d/t exogenous cortisol

52
Q

Outline the possible consequences on plasma hormone levels of disorders affecting hypo/hypersecretion from the primary, secondary or tertiary glands associated with the hypothalamic-pituitary-adrenal (HPA) axis

A

1º secretions of CRH
*promoted by stress

2º secretions of ACTH
*promoted by stress

3º secretions of cortisol

  • alcohol, caffeine, lack of sleep DISINHIBIT the HPA = depression of negative feedback neurones = amplifying stress effects = ⇧CRH + ACTH
  • subsequent elevation cortisol = immune system depression
53
Q

Discuss the clinical features and biochemical diagnosis of hypersecretion syndromes of the adrenal gland (Cushing’s syndrome, pheocromocytoma) (more in clinical lectures)

A

CUSHINGS SYNDROME: Cushings Disease (hypercortisolaemia) is strongly associated with hypertension d/t permissive norephinephrine relationship

  • 1º d/t adrenal cortex tumour (Cushings Syndrome)
  • 2º d/t pit gland tumour with ACTH (Cushins Disease)
  • Iatrogenic: too much cortisol
  • catabolic wasting of the extremities; fat redistributed to face and trunk

PHEOCROMOCYTOMA: neuroendocrine tumour in adrenal medulla = XS catecholmaines
= ⇧HR = ⇧CO = ⇧BP
= Diabetogenic d/t adrenergic effect on glucose metabolism

54
Q

Describe the clinical features, diagnosis and management of adrenal hyposecretion (Addison’s disease) (more in clinical lectures)

A

Hyposecretion of all adrenal steroid hormones d/t AuImm destruction of adrenal cortex

  • hyperpigmentation due to XS melanocyte-stimulating hormone (MSH) (1º disorder)
  • ACTH = MSH levels d/t same precursors
  • hypoT d/t loss of permissive effect of cortisol on adrenoceptors and loss of Na+ = hypovol.
  • Crisis = extreme hypoT and hypoglycaemia
55
Q

Discuss the importance of glucocorticoids in acute psychological stress (guidelines for the management of patients on replacement steroids) (more in clinical lectures)

A

Glucocorticoids act via mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) in the hippocampus
=> stress related psychiatric disorders

  • consolidation of new memories
  • impair retrieval of LT memory info.
56
Q

Summarise diverse roles of calcium, demonstrating the importance of the regulation of calcium concentration.

A

free calcium rare; BONES, INTRACELLULAR: mitochondria, EXTRACELLULAR FLUId: bound

  • Signalling: exocytosis, contraction, altering enzyme function
  • blood clotting
  • apoptosis
  • skeletal strenth
  • membrane excitability: Ca2+ decreases Na+ permeability => MOST CRITICAL in short term homeostasis

HYPOCALCAEMIA: ⇧neuronal Na+ perm. = hyperexcitation. => tetany

HYPERCALCAEMIA: ⇩Na+ perm. = reduce excitability and depress activity, e.g. cardiac arrhythmias

• calcium stored in the form of hydroxyapatite (Ca10(PO4)6(OH)2) so phosphate homeostasis

57
Q

Explain the overall effect of PTH on plasma Ca2+ and phosphate concentrations

A

PTH: polypeptide hormone (parathyroid glands)
= ⇧[Ca2+]plasma
• Released in response to ⇩free [Ca2+ ]plasma
1) stimulate Ca2+ and Phosphate RESORPTION = release

2) inhibit osteoblast = ⇩Ca2+ deposition
3) ⇧REABS of Ca2+ from KIDNEY TUBULES = ⇩urine excretion
4) ⇧renal excretion of phosphate = ⇧free[Ca2+] via preventing deposition (requiring phosphate)
5) CALCITRIOL SYNTH (kidney) promoting CALCIUM ABS. @ gut and kidney

CALCITRIOL (Vitamin D): steroid prod. liver and kidneys
= ⇧[Ca2+]plasma
* ⇧Ca2+ gut abs
* Facilitates renal abs of Ca2+
* mobilises Ca stores in bone by stimulating osteoclast activity
= complement PTH action to increase Ca2+plasma

58
Q

Describe effects of PTH on renal formation of 1, 25 – dihydroxycholecalciferol

A

PTH stimulates CALCITRIOL @ KIDNEYS in order to ⇧[Ca2+]plasma

  • Inactive vitamin d (cholecalciferol) diet/skin becomes activated.
  • Formation of calcitriol is enhanced by the hormone prolactin in lactating women @ kidney
59
Q

Describe the effect of 1, 25 - dihydroxycholecalciferol on Calcium absorption from the gut

A

1, 25 - dihydroxycholecalciferol ⇧intestinal absorption of Ca2+

⇩plasma [Ca2+]
=> ⇧PTH = ⇧Calcitriol = ⇧intestinal abs of Ca2+

60
Q

Outline the effect of 1, 25 - dihydroxycholecalciferol on parathyroid gland function.

A

⇧plasma Ca2+ INHIBITS PTH = ⇧Osteoblast deposition and ⇩osteoclast resorption

61
Q

Describe the nature and function of calcitonin.

A

peptide hormone released from PARAFOLLICULAR CLEAR CELLS of the thyroid gland

= ⇩[Ca2+]plasma
via
*bind to osteoclast and inhibit bone resorption
* ⇧renal excretion

62
Q

Describe the investigations used to detect abnormalities of calcium control especially hypercalcaemia.

A
  • Blood test: calcium test

- Calcium in urine

63
Q

List and explain the most common causes, symptoms and signs of hyper and hypocalcaemia

A 
Vit D deficiencies
Overactive osteoclasts (Pagets)

*CORTISOL inhibits osteoblasts = ⇩[Ca2+]plasma = reactive ⇧PTH => ⇧bone resorption
osteoporosis

  • INSULIN ⇧bone formation and antagonises cortisol
  • OESTROGEN ⇧bone formation via osterogen R on osteoblast
  • GH - constant stimuli for bone prod.
  • PROLACTIN: ⇧calcium absorption from the guy by synth of CALCITRIOL
64
Q

State the principles of management for cases of hyper and hypocalcaemia

A
  • Diet and vitamin D (hypo)
  • Calcitonin in Paget’s Disease (overactive osteoclasts)
  • calcitonin action: osteoclast binding inhibiting resorption and promotion of excretion
65
Q

Calcium distribution in the blood

A

50% FREE = physiologically active

40% PROTEIN BOUND = albumin and globulin

10% COMPLEXED as anions

  • Binding capacity is increased under alkalotic conditions.
    = hypocalcaemic tetan y as plasma proteins bind more Ca2+

opposite occurs with ACIDOSIS = ⇩binding capacity and ⇧⇧free Ca2+

66
Q

Significance of Vitamin D Deficiency

A

In Vit D deficiency PTH works hard to maintain plasma [Ca2+] and in doing so continually removes Ca2+ from bone resulting in bones which are soft and, if still growing, become bent. In adults, easily fractured.

=> RICKETS, OSTEOMALACIA

*reactive ⇧PTH d/t Vit D def. and ⇩Ca abs and [plasma] results in PHOSPHATE DEFICIENCY = aggravating Ca2+ loss from bone

A2 ME3031 ENDO DM (11 decks)

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