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substances/control Flashcards

1
Q

Baroreceptors

  1. trigger
  2. response to increase in BP
A
  1. located in carotid sinus and aortic arch. Activated by stretch receptors which respond to pressure.
    Atrial baroreceptors are involved in short term regulation of BP. They detect changes in BP and relay impulses to the vasomotor center in the medulla.
  2. If there is an increase in BP:
    (1) increased parasympathetic outflow to the heart means contractility and HR are reduced, so cardiac output is reduced. CO=HR x SV
    (2) decreased sympathetic outflow to the arterioles results in vasodilation, so TPR is reduced
    (3) BP= COXTPR, so blood pressure is lowered
  3. If there is decrease in BP:
    (1) Increased sympathetic outflow to the heart means contractility and heart rate are increased and so cardiac output is increased: CO=HRxSV.
    (2) Increased sympathetic outflow to the arterioles results in vasoconstriction and so TPR is increased.
    (3) BP=COxTPR and so blood pressure is increased.
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2
Q

Chemoreceptors

A
  • Central chemoreceptors, located in the medulla oblongata, respond to increase in H+ conc in ECF.
  • Peripheral chemoreceptors are located in the aortic and carotid bodies, They respond to decreased PaCO2.
  • Metabolic acidosis compensation: chemreceptors are stimulated and the respiratory centre (in the medulla), sends nervous impulses to the external intercostal muscles and the diaphragm, via the intercostal nerve and the phrenic nerve, respectively, to increase breathing rate and the volume of the lungs during inhalation. PaCo2 decreases.
  • Metabolic Alkalosis compensation5: Chemoreceptors are inhibited, reduced respiration, PaCO2 increases.
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3
Q

aldosterone

A

Aldosterone is synthesised in the adrenal cortex by glomerulosa cells.

Acts on the principal cells in the nephron collecting duct and increases transcription of ENaC channels and H+/K+ ATPase pumps. More Na+ is reabsorbed and more K+ is secreted, H2O is retained -> blood pressure raised.

Aldosterone also causes the release of ADH from the posterior pituitary.

Aldosterone release is induced by Angiotensin II and it closes ENaC channels.

Aldosterone release is inhibited by ANP.

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4
Q

ADH(vasopressin)

A

ADH is produced by the posterior pituitary, when it is stimulated by the supraoptic nucleus in the hypothalamus. ADH release is stimulated by Angiotensin II.

If osmolarity increases, ADH secretion will increase.

ADH is a vasoconstrictor.

  1. Osmoreceptors in the hypothalamus detect an increase in plasma osmolality.
  2. The posterior pituitary is signalled to release ADH.
  3. ADH acts on the collecting ducts and increases insertion of aquaporin 2 channels, permeability to H2O increases, more H2O is retained.
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5
Q

Acetylcholine

A

Acetylcholine is a neurotransmitter which is used at the neuromuscular junction (it is a chemical that motor neurons of the nervous system release to activate muscles).

Acetylcholine is the parasympathetic neurotransmitter in the lungs, receptors are muscarinic (g protein coupled) and nicotinic (ligand gated ion channels).

Functions:
- Bronchoconstriction and vasodilation of pulmonary vessels
-

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6
Q

ANP

A

ANP is a renal vasodilator. It inhibits aldosterone release induced by Angiotensin II and it closes ENaC channels. ANP decreases blood pressure.

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7
Q

stretch receptors

(1) Bladder

A

(1) stretch receptors are stimulated when the bladder fills. Afferent impulses stimulate parasympathetic action of the detrusor muscle- it contracts. urethral sphincters relax; this is mediated by inhibition of neurones to them. The PAG is stimulated.

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8
Q

CCK

A

CCK is a peptide hormone which is responsible for stimulating the digestion of fat and protein. It is synthesised and secreted from enteroendocrine cells in the duodenum.

  • CCK release is stimulated by presence of fatty acids and amino acids in the chyme entering the duodenum and presence of acetylcholine.
  • CCK stimulates the acinar cells of the pancreas to release pancreatic digestive enzymes to catalyse the digestion of fats, proteins and carbs.
  • CCK mediates satiety by acting on CCK receptors in the CNS. CCK also has stimulatory effects on the vagus nerve.
  • Increased CCK levels causes increased anxiety
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9
Q

adrenaline/noradrenaline

A

Adrenaline and noradrenaline are catecholamines produced by the adrenal medulla of the kidneys. Secretion is regulated by autonomic innervation, mainly sympathetic.

-Noradrenaline is the sympathetic neurotransmitter in the lungs. It leads to bronchodilation and vasoconstriction on pulmonary vessels.

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10
Q

oestrogen

A

During ovulation, Oestrogen is produced and released by granulosa cells in the ovary using aromatase enzyme. Following ovulation, the ruptured follicle transforms into a corpus luteum which releases large amounts of progesterone and oestrogen.

Functions:

(1) stimulates the development of the female external genitalia and the differentiation of the mullerian duct.
(2) at low levels, Oestrogen inhibits gonadotropin release. at high levels, oestrogen exerts a positive feedback on gonadotropin secretion, which stimulates the LH surge.
(3) High oestrogen levels following ovulation inhibit LH and FSH levels.
(4) causes hyperplasia and hypertrophy of endometrial cells. Also stimulates myometrial growth.

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11
Q

growth hormone

A

growth hormone secretion from anterior pituitary. Increased secretion occurs at puberty. It is affected by starvation, exercise, trauma, hypoglaecemia, deep sleep.

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12
Q

insulin- what is it and what does it do; mechanism and function.

A

Insulin is a peptide hormone made in the beta cells of the islet of langerhans (cells of the pancreas).

Insulin binds to membrane receptors -> intracellular signalling cascade stimulated -> GLUT-4 mobilisation to plasma membrane -> GLUT-4 integrates into plasma membrane -> glucose enters cell via GLUT-4.

Insulin functions;

  1. Suppresses hepatic glucose output: decreases glycogenolysis and gluconeogensis.
  2. Increases glucose uptake into fat and muscle cells.
  3. Suppresses lipolysis and muscle breakdow
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13
Q

insulin release

A

Phase 1- stored insulin is released rapidly
Phase 2- slower release of newly synthesised insulin

Glucose binds to beta cells -> glucose is converted into glucose-6-phosphate -> ADP is converted to ATP -> K+ channels close -> membrane depolarisation -> Ca2+ channels open -> Ca2+ influx -> insulin release.

After a meal, insulin levels increase; glucose goes to the liver and muscles to replenish muscle stores. Excess glucose is converted into fats.

Cortisol inhibits insulin, acts to increase blood glucose.

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14
Q

progesterone levels in the body

A

Menstruation:
Progesterone is the predominant hormone responsible for the secretory phase, released from the corpus luteum in the ovary. Progesterone production is stimulated by human chorionic gonadotropin (the level of this hormone decreases when the placenta develops and takes over).
High progesterone and oestrogen conc inhibit LH and FSH levels after ovulation. oestrogen and progesterone concentrations fall towards the end of the luteal phase because the corpus luteum degenerates into the corpus albicans if fertilisation does not occur. Therefore progesterone and oestrogen are no longer released.

Pregnancy: Progesterone inhibits uterine contractility so the foetus is not delivered prematurely. Oestrogen prepares the uterus and regulates progesterone levels. It also inhibits LH and FSH and so prevents further mensrual cycles during pregnancy.

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15
Q

lutenising hormone

A

GnRH is released by the hypothalamus and acts on the anterior pituitary to release FSH and LH.

In men, LH stimulates Leydig cells to produce testosterone.

In women, LH acts on theca cells, stimulating androgen release. Androgen diffuses from theca to granulosa cells to stimulate ovulation.

LH levels increase during menopause as they are not inhibited by negative feedback by oestrogen.

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16
Q

follicle stimulating hormone

A

GnRH from hypothalamus stimulates release of LH and FSH.

FSH acts on granulosa cells to stimulate the conversion of androgen into oestrogen (aromatase enzyme).

Menstruation: FSH levels decrease in the follicular phase, causing the non-dominant immature follicles to degenerate. FSH levels decrease after ovulation because they are inhibited by the high progesterone and oestrogen concentrations. FSH levels increase at the end of the cycle because the fall in progesterone and oestrogen concentrations mean FSH is no longer inhibited and so its plasma concentration begin to rise.

In men, FSH causes the production of sperm,

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17
Q

testosterone

A

Testosterone is released by the interstitial cells of Leydig in the seminiferous tubules in the testicle. Leydig cells start producing testosterone around week 8. Testosterone stimulates differentiation of the Wolffian duct.

Testosterone production is stimulated by the effect of LH on testes.

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18
Q

Briefly describe the mechanism of LH and FSH.

A

Hypothalamus -> GnRH -> anterior pituitary -> FSH/LH -> sertoli cells, leydig cells/granulosa cells, theca cells -> oestrogen, testosterone, inhibin -> negative feedback on hypothalamus and pituitary.

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19
Q

Describe the hypothalamo-pituitary-testicular-axis.

A

GnRh from hypothalamus acts on the anterior pituitary to release LH and FSH. LH acts on Leydig cells stimulating testosterone release. FSH acts on sertoli cells stimulating inhibin release. Inhibin and testosterone have a negative feedback affect on the hypothalamus and anterior pituitary.

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20
Q

What is dihydrotestosterone?

A

An active metabolite of testosterone. It modulates external genitalia differentiation -> penis, scrotum and prostate.

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21
Q

Name 7 molecules that are reabsorbed in the proximal convoluted tubule.

A

Na+, K+, Cl-, HCO3-, H2O, amino acids, glucose.

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22
Q

What is tubuloglomerular feedback?

A

Macula densa cells of the DCT detect NaCl levels and use this as an indicator of GFR.
NaCl levels increase as GFR increases.

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23
Q

Name the 3 things to make up the Glomerular Filtration barrier.

A
  1. Fenestrated capillary endothelium.
  2. Double layer basement membrane.
  3. Foot processes of podocytes.
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24
Q

What ion is pumped out of the ascending limb into the medullary interstitium?

A

Na+. This increases the medullary osmolarity.

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25
Q

What hormonal pathway is likely to be responsible for a decrease in urine production?

A

Renin angiotensin aldosterone system.

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26
Q

Name 6 hormones produced by the anterior pituitary gland.

A
  1. FSH.
  2. LH.
  3. GH.
  4. ACTH (Adrenocorticotropic hormone)
  5. TSH.
  6. Prolaction.
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27
Q

Name 2 hormones produced by the posterior pituitary gland.

A
  1. ADH.

2. Oxytocin.

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28
Q

Oxytocin function

A

Uterine contractions

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29
Q

What are the two types of hormone and where are their receptors located?

A
  1. Steroid hormones- made at response. Steroid hormone receptors are intracellular; steroids pass through the plasma membrane bound to proteins.

2- Peptide hormones are stored and released at response- e.g. pituitary hormones (peptides). Peptide hormone receptors are located on cell membranes.

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30
Q

What does thyroid hormone affect?

A

Increased metabolism, increased sympathetic action, heat production, essential for growth and development too.

31
Q

Briefly describe the mechanism of prolactin.

A

Hypothalamus -> dopamine -> anterior pituitary -> prolactin -> mammary glands -> milk production -> positive feedback on dopamine.

32
Q

Briefly describe the mechanism of ACTH (Adrenocorticotropic hormone)

A

Hypothalamus -> CRH (Corticotropin-releasing hormone) -> anterior pituitary -> ACTH -> adrenal glands -> cortisol release -> negative feedback on hypothalamus and pituitary.

33
Q

Briefly describe the mechanism of LH and FSH.

A

Hypothalamus -> GnRH -> anterior pituitary -> FSH/LH -> sertoli cells, leydig cells/granulosa cells, theca cells -> oestrogen, testosterone, inhibin -> negative feedback on hypothalamus and pituitary.

34
Q

What does the parathyroid control?

A

Serum Ca2+. (Hyperparathyroidism -> hypercalcemia). PTH increases the absorption of Ca2+ and is secreted when Ca2+ levels fall.

35
Q

TSH

A

TSH from anterior pituitary stimulates thyroid gland to produce thyroxine. TSH would be high as there would be little negative feedback as less T4 and T3 are being produced.

Low TSH = overactive thyroid.
Lots of T4 and T3 being produced and so there is more negative feedback on the pituitary and less TSH.

36
Q

What are the 4 cells to make up the islets of langerhans?

A
  1. Beta cells: insulin. (70%)
  2. Alpha cells: glucagon. (20%)
  3. Delta cells: somatostatin. (8%)
  4. Pancreatic polypeptide secreting cells. (2%)
37
Q

Somatostatin

A

Somatostatin is a peptide hormone that is present in cells throughout body. It inhibits hormones- including growth hormone, gastrin, secretin and CCK

38
Q

Secretin

A

Regulates water homeostasis. Produced by S cells of duodenum.
- Inhibits gastric acid secretion from parietal cells of stomach
- Stimulates the production of bicarbonate from ductal cells of pancreas
- Stimulates bile production by liver
-

39
Q

Functions of Insulin

A
  1. Suppresses hepatic glucose output: decreases glycogenolysis and gluconeogensis.
  2. Increases glucose uptake into fat and muscle cells.
  3. Suppresses lipolysis and muscle breakdown.
40
Q

Functions of Glucagon

A
  1. Stimulates hepatic glucose output: increases glycogenolysis and gluconeogenesis.
  2. Reduces peripheral glucose uptake.
  3. Stimulates release of gluconeogenic precursors.
  4. Stimulates lipolysis and muscle breakdown.
41
Q

What glucose transporter allows glucose uptake into muscle and fat cells? & Mechanism

A

GLUT-4.

Insulin binds to membrane receptors -> intracellular signalling cascade stimulated -> GLUT-4 mobilisation to plasma membrane -> GLUT-4 integrates into plasma membrane -> glucose enters cell via GLUT-4.

42
Q

3 places where glucose sensors are located.

A
  1. Pancreatic islets.
  2. Medulla.
  3. Hypothalamus.
43
Q

What hormones from the hypothalamus stimulate the anterior pituitary to release GH?

A

GHRH (+ve affect) and SMS (-ve affect).

44
Q

What hormone from the hypothalamus stimulates the anterior pituitary to release prolactin?

A

Dopamine.

45
Q

What hormones are involved in pregnancy?

A
  1. Human chorionic gonadotropin- It stimulates oestrogen and progesterone production. The levels of this hormone decrease when the placenta develops and takes over.
  2. Oestrogen
  3. Progesterone
  4. Prolactin- It stimulates the mammary glands to produce milk (lactation).
  5. Prostaglandins- They have an important role in labor initiation.
  6. Oxytocin- Stimulates uterine contraction and milk production stimulated by suckling. It is also thought to help express caring behaviours.
  7. Relaxin- It is involved in cervical ripening.
46
Q

Cortisol functions

A
  1. Permissive action on smooth muscle cells that surround blood vessels; this helps to maintain BP.
  2. Maintains concentrations of enzymes involved in metabolic homeostasis.
  3. Anti-inflammatory and anti-immune functions: dampens the immune response.

4- Stress response:

  1. Mobilises energy sources: increases protein catabolism, lipolysis and gluconeogenesis. This help to maintain blood glucose levels.
  2. Enhanced vascular reactivity; maintains vasoconstriction with noradrenaline.
  3. Suppresses inflammatory and immune responses.
  4. Inhibition of non-essential functions e.g. growth and reproduction.
47
Q

Why is there increased cortisol released in response to stress?

A

Stress poses a threat to homeostasis. Cortisol acts to maintain BP, provide extra energy sources and to shut down non-immune functions so homeostasis can be maintained.

48
Q

Why is infertility a consequence of stress?

A

When someone is stressed, their cortisol levels increase, the extra cortisol acts to shut down non-essential functions such as reproduction and so can result in infertility.

49
Q

5 functions of Angiotensin II

A
  1. Vasoconstriction.
  2. Increases Na+ reabsorption.
  3. Stimulates the adrenal cortex to release aldosterone.
  4. Stimulates ADH release.
  5. Increase sympathetic activity.
50
Q

What enzyme catalyses the formation of bicarbonate and hydrogen ions from CO2 and H2O?

A

Carbonic anhydrase.

51
Q

Slow acting stretch receptors

A

Located in smooth muscle around airways. Activated by lung distension. They inhibit inspiration and so promote expiration.

52
Q

Rapidly acting stretch receptors

A

Located between airway epithelial cells. Activated by lung distension and irritants. Activation of RASRs creates bronchoconstriction.

53
Q

C fibers J receptors

A

J (juxtacapillary) receptors (or pulmonary C-fiber receptors)= sensory nerve endings located within the alveolar walls in juxtaposition to the pulmonary capillaries of the lung, and are innervated by fibers of the vagus nerve.

They are activated by increased interstitial fluid volume. They cause rapid, shallowing breathing

54
Q

Difference in hpoxia response of systemic vessels and pulmonary vessels.

A

Hypoxia leads to vasodilation of systemic vessels and vasconstriction of pulmonary vessels (so as to redirect blood to O2-rich alveoli).

55
Q

The two types of white blood cells (leukocytes)

A

Phagocytes- surround and asorb pathogens & break them down, effectively eating them.

Lymphocytes- help the body to remember previous invaders and recognise them if they come back to attack again

56
Q

Phagocytes

A

(1) Neutrophils- the most common type of phagocyte, tend to attack bacteria. Main cell involved in acute inflammation. 6 stages of action:
1. Identify threat.
2. Activation.
3. Adhesion.
4. Migration.
5. Phagocytosis.
6. Bacterial killing

(2) Monocytes- the largest type. Resident phagocyte in the lungs and they coordinate the inflammatory response.
(3) Macrophages- these patrol for pathogens and also remove dead and dying cells. Alveolar macrophages are derived from monocytes. They release interleukins.
(4) Mast Cells- filled with basophil granules, found in numbers in connective tissue and releasing histamine and other substances during inflammatory and allergic reactions.

57
Q

Lymphocytes

A

(1) B Lymphocytes: produce antibodies and help alert the T lymphocytes. Antibodies:
- IgG; mark microbes so other cells can recognise and deal with them
- IgM: is expert at killing bacteria
- IgA: congregates in fluids such as tears and saliva, where it protects gateways into the body.
- IgE: protects against parasites and is also to blame for allergies.
- IgD: stays bound to B lymphocytes, helping them to start the immune response.

(2) T Lymphocytes: they destroy compromised cells in the body and alert other leukocytes.
- Helper T Cells; coordinate immune response; some communicate with other cells, some stimulate B cells to produce more antibodies, others attract more T cells and cell-eating phagocytes.
- cytotoxic T cells; these attack other cells. Particularly useful for fighting viruses.

58
Q

Inflammation mechanism

A

The causative agents of acute inflammation are pathogens and damaged tissues. Causative agents of chronic inflammation are persistent acute inflammation, persistent foreign bodies and autoimmune reactions. Inflammation is also the result of necrosis.

Vasodilation results in the exudation of plasma. Neutrophils and monocytes migrate into tissues. Neutrophils are the main cells involved in acute inflammation, main cells of chronic inflammation are mononuclear cells- e.g. monocytes, macrophages, lymphocytes, plasma cells.

Primary mediators of acute inflammation= vasoactive amines, primary mediators of chronic inflammation= cytokines, growth factors, ROS etc.

59
Q

Granulocytes

A

WBCs which have secretory granules in their cytoplasm- i.e. neutrophils, basophils and eosinophils.

(1) Neutrophils
(2) Eosinophils: crucial part of killing parasites.
(3) Basophils
(4) Mast cells

60
Q

mechanism of different types of hypersensitivity reactions

A

Type 1 reaction:

  • Mechanism: immunological memory to something causing an allergic response. IgE antibodies bind to mast cells -> histamine release.
  • Anaphylaxis, hayfever etc. Can be caused by pollen, allergens.

Type 2:

  • Mechanism: immunoglobulins bound to surface antigens.
  • Transfusion mismatch or transplant rejection.

Type 3:

  • Mechanism: immune complexes, activation of complement.
  • Fungi and pigeon droppings etc. (pigeon fancier’s lung).

Type 4:

  • Mechanism: T cell mediated.
  • Reactions to TB.
61
Q

Name 2 local factors that result in vasoconstriction.

A

Endothelin, internal BP.

62
Q

Name 5 local factors that result in vasodilation.

A

Hypoxia, NO, K+ (accumulate from AP), CO2, H+, adenosine.

63
Q

What neural factors result in vasoconstriction?

A

Sympathetic nerves that release noradrenaline.

64
Q

What neural factors result in vasodilation?

A

Parasympathetic innervation.

65
Q

Name 3 hormonal factors that result in vasoconstriction.

A

Angiotenisn 2, ADH, Adrenaline (binds to alpha-adrenergic receptors in smooth muscle).

66
Q

Name 2 hormonal factors that result in vasodilation.

A

Atrial natriuretic peptide, Adrenaline (binds to beta2 receptors).

67
Q

What do parietal cells secrete?

A

HCl and intrinsic factor.

68
Q

What do chief cells secrete?

A

Pepsinogen and gastric lipase.

69
Q

What cells secrete Gastrin?

A

Enteroendocrine cells / G cells.

70
Q

What cells secrete somatostatin?

A

D cells.

71
Q

What cells secrete histamine?

A

Enterochromaffin like cells.

72
Q

What are the 4 phases important in regulating gastric acid secretion? Do these phases turn secretion on or off?

A 
1. Cephalic phase - turning ON. Stimulised by sight, smell, taste of food, chewing. The parasympathetic nervous system is triggered by stimuli. This releases Ach. Ach acts on parietal cells and on gastrin and histamine. HCl secretion increases.
Functions of HCl in stomach; 
(1) Solubilisation of food particles. 
(2) Kills microbes. 
(3) Activates pepsinogen forming pepsin.
  1. Gastric phase - turning ON. Stimulated by gastric distension, presence of peptides and amino acids in the stomach.Gastrin is released in response to the stimuli. This acts on parietal cells and triggers release of histamine (histamine then acts on parietal cells too). HCl secretion increases.
  2. Gastric phase - turning OFF. Stimulated by low pH in gastric lumen.Gastrin is inhibited in response to stimuli and histamine is therefore indirectly inhibited. Somatostatin is also released and this inhibits parietal cells. HCl secretion decreases.
  3. Intestinal phase - turning OFF. Stimulated by low pH in duodenal lumen, duodenal distension, presence of amino acids and fatty acids in the duodenum. The enterogastrones secretin and CCK are released in response to stimuli. Secretin inhibits gastrin and stimulates further somatostatin release. HCl secretion decreases.
73
Q

Histamine

A

Histamine is found in nearly all tissues of the body where it is stored in granules of tissue mast cells (and also basophils).

Functions include:

  • contraction of smooth muscle tissues of the lungs, uterus and stomach
  • dilation of blood vessels which increases permeability and lowers blood pressure
  • stimulation of gastric acid secretion in the stomach
  • acceleration of heart rate
  • neurotransmitter carrying chemical messages between nerve cells.
74
Q

What enzyme digests starch in the small intestine?

A

Pancreatic amylase. (it breaks alpha 1-4 linkages)

Phase 1 cards (27 decks)

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