Q1

Outline the physiological effects of thyroid hormones.

  • Heart: chronotropic; inotropic (increased number of B-adrenergic receptors; increased response to catecholamines; increased proportion of a-myosin heavy chain);
  • Adipose tissue: catabolic (stimulated lipolysis);
  • Muscle: catabolic (increased protein breakdown);
  • Bone: developmental (promote normal growth(Cretin) and skeletal development);
  • Nervous system: promote normal brain development;
  • Gut: metabolic (increased CHO absorption);
  • Lipoprotein: metabolic (formation of LDL receptors);
  • other – calorigenic (increased metabolic rate, increased stimulation O2 consumption)

Pass criteria:

  • 3 to pass including heart

Describe the mechanism regulating thyroid hormone.

  • Negative feedback effect of T4 and T3 on hypothalamus and pituitary to inhibit TRH and TSH secretion respectively.
  • Cold stimulates thyroid hormone secretion, stress and glucocorticoids inhibit

 


Q2

What metabolic effects does insulin have on the liver?

  • decreased ketogenesis;
  • increased protein synthesis;
  • increased lipid synthesis;
  • decreased glucose output due to decreased gluconeogenesis, increased glycogen synthesis, increased glycolysis

 

What are the effects of insulin deficiency on the body over?

  • Decreased cellular glucose uptake
  • Total body dehydration and acidosis.

 


Q3

What is the physiological role of aldosterone?

  • Aldosterone causes Na+ and water retention, expanded ECF volume and shutting off the stimulus to increased renin secretion

What conditions increase aldosterone secretion?

  • Primary: – Stress hormone, low pressure/volume states
  • Secondary: Hyperaldosteronism: (eg. CCF, cirrhosis & nephrosis).
  • Drugs

 


Q4

What factors affect Antidiuretic Hormone (ADH) secretion?
Prompt: ADH is also known as vasopressin. What stimulates vasopressin secretion?

  • Plasma osmotic pressure – increase POP leads to increase ADH secretion. Sensitive to changes around 285mosm/kn\g
  • Extracellular fluid volume – inverse relationship between ADH secretion and ECF volume. Primary mediators are the low pressure receptors in great veins, atria and pulmonary vessels
  • Pain, emotion, stress, nausea vomiting– all increase ADH
  • Standing
  • Drugs – eg, carbamazepine, clofibrate increase, alcohol decreases
  • Angiotensin II – increases

 


Q5

What physiological factors affect renin secretion?

  • Afferent arteriolar pressure – increased pressure at the level of JG cells in kidney causes decrease in renin secretion & vice versa
  • Na & K transport across macula densa – increased  reabsorption leads to decreased renin secretion & vice versa
  • Angiotensin II – inhibitory feedback to JG cells
  • Circulating catecholamines – increased SNS activity increases renin
  • Other – Prostaglandins – increases renin; vasopressin – decreases renin

Pass Criteria:

  • 3 out of 5 bold to pass

 


Q6

What are the main regulatory factors for aldosterone secretion?

  • Renin-angiotensin system
  • ACTH
  • Rise in plasma K concentration (via the adrenal cortex)

Pass Criteria:

  • Bold to pass

 


Q7

What happens to the insulin secretion when a person is injected with 50ml of 50% Dextrose?

  • It would go up

Describe the mechanism of insulin secretion.

  • The insulin is dumped from the beta cells of the Islets of Langerhans within 3-5 minutes followed by a plateau at 2-3 hrs by activation of the enzyme system
  • Glucose is metabolised by the glucokinase and this involve ATP, decrease potassium efflux and increase calcium entry into cells that cause release of insulin by exocytosis

 


Q8

What are the physiologic actions of glucagon?

  • Glycogenolysis in liver – not muscle
  • Gluconeogenesis from amino acids

Only at very high levels.

  • Lipolysis –
  • Ketogenesis
  • +ve inotropic effect on heart
  • Inc blood flow to kidneys
  • Stimulates secretion of GH, insulin and somatostatin

What factors affect glucagon secretion?

  • Stimulators
    • Beta adrenergic stimulants Cortisol, protein meal,vagal stimulation
    • Starvation,stress, exercise, CCK, gastrin, theophylline
  • Inhibitors
    • Glucose —-most important insulin
    • Somatostatin
    • FFA
    • Ketones
    • alpha Adrenergic stimulators.
    • GABA
    • Phenytoin

 


Q9

Describe the biosynthesis and storage of norepinephrine at the synaptic junction?

  • Dietary tyrosine mostly (some formed from phenylalanine)
  • Tyrosine transported into catecholamine-secreting neurones by concentrating mechanism tyrosine -> dopa by tyrosine hydroxylase -> dopamine by dopa decarboxylase in cytoplasm
  • Rate-limiting step [tyrosine -> dopa] is subject to feedback inhibition by dopamine and norepinephrine]
  • Dopamine enters granulated vesicles à norepinephrine by dopamine beta-hydroxylase (DBH)
  • Norepinephrine stored bound to ATP, with  protein  chromogranin A

Pass Criteria:

  • At least 4 in correct order

How is Norepinephrine removed from the synaptic junction?

  • Norepinephrine is removed from the synaptic junction by:
    • binding to postsynaptic receptors
    • binding to presynaptic receptors
    • reuptake into presynaptic neurons
    • catabolism (MAO)
  • Catabolism at noradrenergic nerve endings is catalysed by MAO (monoamine oxidase) and COMT
    • (COMT mainly in liver, also at postsynaptic noradrenergic nerve endings
  • Norepinephrine -> DOMA (3,4-dihydroxymandelic acid) & DHPG (3,4-dihydroxymandelic aldehyde)
  • -> VMA (vanillylmandelic acid) & MHPG (3-methoxy-4- hydroxyphenylglycol) by systemic COMT
  • These deaminated derivatives are physiologically inactive

 


Q10

What are the effects of thyroid hormones?

  • Widespread actions
  • Metabolically active tissues
  • Heart  – increased rate
  • Brain  – development
  • Brain – reticular Act. System
  • Gut  – increased carbohydrate absorbtion
  • Muskuloskeletal growth
  • Adipose – lipolysis

Pass Criteria:

  • 4 out of 7

What is the mechanism of action?

Intracellular

  • At the nuclear level
  • O2 consumption regulator.
  • T3 binds better than T4 to receptor
  • Hormone/receptor binds to DNA
  • Affects gene expression
  • Two genesites
  • Alpha Chromosome 17
  • Beta Chromosome 3

Pass Criteria:

  • 4 out of 8

 


Q11

What are the physiological effects of glucocorticoids?

  • Metabolic; increased protein catabolism, increased hepatic glycogenesis and gluconeogenesis (raised plasma glucose). Raise peripheral tissue insulin resistance
  • Permissive effects on other reactions
  • Are required for catecholamines to produce calorigenic and lipolytic effects,pressor responses (vascular reactivity) and vasodilatation
  • Inhibit ACTH secretion (feedback)
  • Impair water excretion (mechanism unclear)
  • Reduce circulating basophils and eosinophils and increase other elements
  • Required for stress response
  • Affect EEG waveforms (mild personality changes in insufficiency)

How is glucocorticoid secretion regulated?

  • Basal secretion and stress response both dependent on ACTH
  • (Other substances may stimulate adrenal directly but no evidence of role in physiologic regulation)
  • Free glucocorticoids produce negative feedback on ACTH secretion at both hypothalamic and pituitary levels. Effect mediated by action on DNA
  • Stress response ACTH secretion mediated almost exclusively via hypothalamic release of  corticotrophin releasing hormone
  • Circadian rhythm. ACTH released in irregular bursts throughout day but much more common in early morning. 75% of cortisol secreted at this time

 


Q12

Describe the effects of insulin on various tissues.

  • Adipose: glucose in, fatty acid + glycerol synthesis, TG deposition, K in
  • Muscle: glucose in, glycogen synthesis, Aas in, protein synthesis, ketones in, K in
  • Liver: glycogen, protein + lipid synthesis,
  • General: cell growth

What is the time frame for these effects?

  • Rapid: glucose, AAs, K into sensitive cells
  • Intermediate: protein synthesis, glycolysis and synthesis, inhibition gluconeogenesis
  • Delayed: lipogenesis

 


Q13

What are the effects of thyroid hormones on different body tissues?
Prompt: What are the effects of thyroid hormone on the heart?

  • Heart: chronotropic, inotropic (increased beta receptors, enhanced response to catecholamines)
  • Adipose tissue: catabolic (lipolysis)
  • Musculoskeletal: catabolic (increased protein breakdown), developmental (promote growth and development)
  • Most (except adult brain, uterus, testes, spleen): calorigenic (increased O2 consumption of metabolically active tissues)
  • CNS: developmental (promotes brain development)
  • GIT: metabolic (increased carbohydrate absorption)
  • Lipoprotein: metabolic (increased LDL receptors)

Pass criteria:

  • Need 2 of first 4 to pass PLUS 2 others

 


Q14

How do the effects of noradrenaline and adrenaline differ on the cardiovascular system?

  • BP: norad; ad
  • HR: norad; ad
  • CO: norad; ad
  • TPR: norad; ad

How do the effects of adrenaline differ with serum concentration?

  • Low concentrations – some beta effects, high concentrations alpha predominates

 


Q15

Describe the typical serum / urine effects in hyperaldosteronism?

  • Na/ Cl mild increased, fluid retention (follows Na),
  • decreased K, alkalosis (alkalaemia only if K+ depletes)
  • Urine K+/ H increased

How does aldosterone exert its effects in the kidney?

  • Mineralocorticoid- Via Principal cells- collecting ducts

2 effects:

  • Genomic- Intracellular to nuc signalling > mRNA
    • a) Inc ENAC insertion/ activity (quick)
    • b) > production (slow)
  • Membrane bind IP3 mediated Na/K exchange >

All = > Na reabsorb K/H loss to urine

 


Q16

What are the actions of the parathyroid hormone on Calcium?

  • PTH increased plasma Ca++ by:
    • increased Ca++ mobilization increased bone reabsorption,
    • increased Ca++ reabsorption in distal tubule and (3) Ca reabsorption

Pass Criteria:

  • Ca ++ increased  PO4 decreased + some idea of how these achieved OR additional other mechs

What are the other effects of PTH?

  1. decreased plasma phosphate: decreased POreabsorption in proximal tubules
  2. increased 1,25 dihydrocholecalciferol: renal  ( > Ca absorption)
  3. Over a longer time: increased osteoblastic and osteoclastic stimulation- prob anabolic

Pass Criteria:

  • Parathyroid related hormone- (prob fetal/ cartilage growth + teeth/ breast- skin) ?
  • PO4 < +1 other in either section

 


Q17

What are the effects of thyroid hormones on nervous and vascular systems?

  • CNS
    • Development CNS -cerebral cortex, basal ganglia cochlea
    • increased activity, mentation speed/ agitation (catechol / dop+ direct brain effects)
    • increased refexes
  • CVS
    • 1)vasodil (2ary heat)
    • circ vol/ HR/ CO
    • Ht- > myosin heavy chain (+ isoforms)/ faster twitch genes (+ Ca ++, Na K ATPase etc?) + down reg others, > contraction/ HR/ speed of contraction
    • > sens to Catechols (synergistic effects + up regulated ß receptors and effector systems) HR, contract more

Pass Criteria:

  • 3-4 overall at least 1 in each

What other physiological effects does thyroid hormone have on the body?

  • Lipolysis – adipose tissue
  • Formation of LDL receptors on lipoprotein
  • Protein breakdown in muscle
  • Skeletal development promoted
  • Increased carbohydrate absorption from the gut
  • Stimulates O2 consumption by metabolically active tissues
  • Increased BSL/ insulin resistance

Pass Criteria:

  • At least 2

 


Q18

Describe the effects of Vasopressin.

  • Retention of water (antidiuretic hormone) (V2 receptors)
  • Vasoconstrictor effect (V1A receptors)
  • Central effect brain (area postrema) to decrease CO
  • Glycogenolysis in liver (V1A receptors)
  • Mediate increased ACTH secretion (V1B receptors)
  • Neurotransmitter in brain and spinal cord

How does vasopressin cause retention of water?

  • Increases permeability of CD, acting on V2 receptors
  • Insertion of protein water channels (aquaporin 2) in uminal membranes.
  • Water enters hypertonic interstitium
  • Urine becomes concentrated and volume decreases
  • Retention of water in excess of solute

What stimuli affect vasopressin secretion?

  • Factors increasing vasopressin secretion
    • increased effective osmotic pressure of plasma
    • decreased ECF volume
    • Pain, emotion, “stress”, exercise, standing
    • Nausea and vomiting
    • Clofibrate, carbamezepine, angiotensin 2
  • Factors decreasing vasopressin secretion
    • decreased effective osmotic pressure of plasma
    • increased ECF volume

 


Q19

What happens when insulin binds to an insulin receptor?

  • Insulin receptor: tetramer – 2 alpha and 2 beta glycosolated subunits
    alpha subunits extracellular + bind insulin; beta subunits span membrane, intracellular parts have tyrosine kinase activity
  • Insulin binding triggers tyrosine kinase activity of beta subunits -> autophosphorylation of  beta subunits on tyrosine residues
  • -> phosphorylation and  de-phosphorylation of  proteins
  • -> Effectors and secondary mediators – Insulin receptor substrate (IRS-1);phosphoinositol 3-kinase (PI3K)
  • Once bound, insulin receptors aggregate in patches and are  endocytosed -> enter lysosomes -> broken down or recycled
  • Peak effect 30 minutes IV / 1 hour oral

What are the principal actions of insulin?

  • Net effect: storage of CHO, protein and fat
    • Rapid (seconds): ­ increased transport of glucose, amino acids and K into insulin-sensitive cells
    • Intermediate (minutes): stimulation of protein synthesis and inhibition of protein degradation; activation of glycolytic enzymes and glycogen synthase;inhibition of phosphorylase and gluconeogenic enzymes
    • Delayed (hours): ­ mRNAs for lipogenic\other enzymes

 


Q20

Describe the actions of Aldosterone?

  • Increase reabsorption of Na+ from urine
    • Acts on principal cells (P cells) of collecting ducts, leading to increased amounts of Na+ exchanged for K+ and H+ in renal tubules, producing a K+diuresis and fall in urine pH
  • Increase reabsorption of Na+ from sweat, saliva and colon

Pass Criteria:

  • Aldosterone cause retention of Na+ in ECF leading to ECF volume expansion

List the stimuli that increase aldosterone secretion?

  • ACTH from pituitary
  • Renin from kidney via angiotensin II
  • Direct stimulatory effect of rise in plasma K+ concentration on adrenal cortex
  • Clinical causes:
    • Surgery
    • Anxiety
    • Physical trauma
    • Haemorrhage
    • High K intake and Low Na intake
    • Standing
    • Constriction of IVC in thorax
    • 2hyperaldosteronism  (eg CCF, cirrhosis, nephrosis)

Pass Criteria:

  • Bolded PLUS 2 others

Describe the feedback regulation of aldosterone secretion?

  • Fall in ECF / blood volume -> reflex increase in renal nerve discharge &decrease in renal artery pressure
  • -> increase in renin secretion -> increase in angiotensin II -> increase in aldosterone secretion
  •  -> Na+ & water retention  -> expanded ECF volume  -> decrease in stimulus that initiated renin secretion

Pass Criteria:

  • Bolded

 


Q21

Describe the effects of increased aldosterone.

  • Increased reabsorption of Na+ from urine, sweat, saliva and colonic contents
  • Na+ retention in ECF
  • K+ diuresis and depletion
  • Hypertension
  • ECF volume expansion

Pass criteria:

  • 3 out of 5 to pass

List factors that increase aldosterone secretion.

  • Haemorrhage / physical trauma / ECV contraction / surgery
  • Anxiety
  • Low Na+ intake
  • High Kintake
  • Constriction of IVC in thorax
  • Secondary hyperaldosteronism (CCF, cirrhosis, nephrosis)

Pass criteria:

  • 3 out of 6 to pass

How is aldosterone secretion regulated?

  • ACTH from the pituitary
  • Renin from kidney, via angiotensin II
  • Direct stimulatory effect of K+ on adrenal cortex

 


Q22

Describe the changes in ACTH secretion that occur in response to stress.

  • Increased ACTH secretion
  • Mediated through hypothalamus by CRH
  • CRH produced in paraventricular nuclei, secreted in medial eminence and transported in portal hyperphysical vessels to anterior pituitary
  • Multiple nerve endings converge on paraventricular nucleii
  • Destruction of median eminence means stress response is blocked

Pass criteria:

  • Bold PLUS 1 other

What are the physiological consequences of sudden cessation of steroid therapy after prolonged treatment?

  • Low glucorticoid levels with inability to increase
  • Prolonged exogenous glucocorticoid inhibits ACTH secretion. Normally a drop in resting corticoid levels stimulate ACTH secretion (feedback loop)
    • Inhibitory effect pituitary and hypothalamus due action on DNA
    • Degree of pituitary inhibition proportional to level glucocorticoid
    • ACTH inhibiting activity of steroids parallels glucocorticoid potency
  • Adrenal atrophic and unresponsive
  • Pituitary unable to secrete normal amounts of ACTH for one month, probably secondary to decreased ACTH synthesis
  • After one month a slow rise in ACTH levels to supranormal levels, stimulates adrenal with increased glucocorticoid output. Feedback inhibition causes a gradual decrease in ACTH levels to normal
  • Avoid by tapering dose over long period

 


Q23

What are the effects of thyroid hormones?

  • At least two organ systems and one effect on each

How are thyroid hormones synthesised?

  • Active iodide transport;
  • binding to thyroglobulin;
  • MIT and D IT join to form T3 and T 4.

What is the mechanism of action of thyroid hormones?

  • Enter cells;
  • binds to specific receptors;
  • hormone-receptor complex binds DNA & effects gene expression.

 


Q24

What hormones are produced by the pituitary?

  • Knowledge of anterior and posterior pituitary with 4 of6 of the anterior pituitary (TSH, ACTH, GH, FSH, LH, prolactin) and one of vasopressin or oxytocin

What are the physiologic effects of vasopressin.

  • Renal retention of water in excess of solute reducing body fluid osmolality or concept

 


Q25

What are the principal actions of insulin?

Storage of carbohydrate, prot and fat, varies with tissues Rapid- seconds. Glc, amino acids and K± into insulin sens cells

Intermediate- minutes. Stimulates prot synthesis, inhibits prot degradation, activates glycolytic enzymes & glycogen synthase, inhibits phosphorylase and gluconeogenic enzymes.

Delayed- Hrs. increase in mRNA for lipogenic & other enzymes

Pass:
Ole and K from rapid.
2 others
Answer must reflect understanding of effects on carbohydrate, protein and fat

What happens when insulin binds to its receptor?

  • Binds to a cell membrane-based stereospecific insulin receptor on insulin-sensitive cells
  • Insulin binding triggers tyrosine kinase activity of f3 subunits —> autophosphorylation of J3

subunits on tyrosine residues

  • The above reaction –>. phosphorylation and de-phosphorylation of proteins that are

effectors and secondary mediators.

Pass: Binding results in activation of secondary protein effectors (tyrosine kinase activity) and mediators. (phosphorylation)

 


Q26

Outline the steps in the synthesis of catecholamines.

Ty0Hylase

Tyrosine? DOPA

? DOPA
Decarboxylase
Dopamine

?Dopamine
ßhydraviase
Adrenaline ? Nor Adrenaline
PNMT (adrenal medulla, some central)

Adrenaline/Noradrenaline

Pass: Tyrosine to dopamine to noradrenaline, plus one of the synthesis enzymes

What happens to noradrenaline after it is released into the synaptic cleft?

Removed by post-synaptic and pre-synaptic binding, reuptake and catabolism

IC) MAO decreased COMT (EC)

VMA

Pass: 3 out of 4 processes

 


Q27

What is the normal range of osmolality of ECF?

285-295mosm/L

Pass: Accept 280-300

How is this maintained?

Maintained by Vasopressin-secreting and thirst mechanisms
If osm decreased, thirst is decreased,  Vp secretion is decreased, resulting in urinary loss of free water
If osm increased, thirst is increased, Vp secretion is increased, leading to renal reabsorption of free water in renal collecting ducts/pyramids

Pass: 3 of 4 Bold

What other stimuli affect Vp secretion increased
Prompt: Anti-diuretic Hormone.

VP secretion increased by:

(increased effective plasma osm pressure)
decreased ECF volume (via low pressure receptors)
Pain, emotion, exercise, stress (eg surgery)
Nausea & vomiting
Angiotensin II
Standing
Clofibrate, carbamazepine

Pass: 2 of 4 Bold


VP secretion increased by:

(increased effective plasma osm pressure)
decreased ECF volume
Alcohol

Pass: 1 of 2 Bold

 


Q28

What are the physiologic effects of the glucocorticoids?

  1. Intermediary metabolism of carbohydrate, protein, fat
  2. Inhibit ACTH secretion
  3. Maintain reactivity of vascular (and bronchial) smooth muscle to catecholamines
  4. Allow excretion of a water load (mechanism unclear)
  5. Blood – Increased RCC, increased WCC (mainly PMNs), but , decreased Lymphocites and Lymph node size
  6. CNS — irritability, apprehension, inability to concentrate (eg in exams)
  7. “stress response”

(Up to 3 specific prompts, eg “what are the vascular effects of glucocorticoids?”)

Pass: 3 bold

 


Q29

Describe the steps in synthesis of thyroid hormones.
Prompt: What are thyroid hormones made from?

Thyroid epithelial cells secrete thyroglobulin (comprising 134 tyrosines) and iodine into colloid. Iodide transport is via a symport with sodium (NIS). Thyroid peroxidise makes iodotyrosines (MIT and DIT) then combines them to make T3 and T4. Some reverse T3 (inactive) also made. Endocytosis and lysis of colloid releases free hormone. All steps TSH controlled. T3 also made peripherally by deiodination of T4.

What are the physiological effects of T4?
Prompt: How do thyroid hormones alter metabolism?

Binds to intracellular thyroid receptors in the nuclei. Complex binds to DNA and alters gene expression. T3 more rapid and potent. Incr metabolism and catabolism of most cells (brain and others excluded). Lipid and carb mobilisation and usage. Inc CVS and CNS activity. Normal reproductive cycle and growth. Effects incr by catecholamines.
Pass: Core knowledge in bold. Subunits combine together

 


Q30

Which catecholamines act as neurotransmitters?

Noradrenaline, Adrenaline and Dopamine

Pass: Bold

Describe the sequence of events at a noradrenergic synapse, following stimulation of a sympathetic nerve.
Prompts: How is noradrenaline released? How is noradrenaline removed from the synaptic cleft? What enzymes are involved in the breakdown of noradrenaline?

Noradrenaline, which has been stored in granulated vesicles, is released into the synaptic cleft by

exocytosis.

Noradrenaline acts on postsynaptic and to a lesser extent presynaptic and glial receptors.

In addition to binding to receptors, Noradrenaline is also removed from the synaptic cleft by:

Reuptake into presynaptic neuron (via a Neuro Transmitter Transporter (NTT)) and then is broken down to inactive product by Monoamine Oxidase (MAO) located on mitochondria.

• Broken down to inactive product by Catechol-O-methyl transferase (COMT) located on the postsynaptic membrane.

Pass: Bold

 


Q31

What are the main effects of insulin?

1.            Increased glucose into cells (adipose, liver, muscle)
2.            Protein synthesis
3.            Glyogenolysis
4.            K into cells

Pass: 3 of 4

What is the mechanism of action of insulin?

Insulin binds to insulin receptors on insulin sensitive cells, triggers autophosphorylation of the insulin receptor which is necessary for the insulin effects. There is receptor mediated endocytosis into the cell and the insulin-receptor complexes trigger cytoplasmic proteins to produce various other proteins. There are at least 4 insulin related substrate (IRS) proteins in cells.

Pass: Must describe that insulin binds to receptor and is taken into cell where secondary mediators are formed.

 


Q32

What hormones are secreted by the adrenal medulla?

Adrenalin, noradrenalin and dopamine.

Pass: Must have all 3

What are the major effects of these hormones?

  1. alpha and ß effects.
  2. increase HR and force contraction, vasoconstriction, hypertension, alertness, metabolic rate, glycogenolysis

Pass: Must describe at least 5 effects

 


Q33

What are the effects of glucocorticoids?

Action on intermediary metabolism of carbo, proteins, fats. Permissive action for glucagon, catecholamines — calorigenic, lipolytic, pressor, bronchodilator, vascular reactivity. CNS vs irritability, apprehension, inability to concentrate. Renal — excretion of water by increased GFR. Anti-inflammatory vs cytokines. Resistance to ‘stress’ —noxious stimuli increasing ACTH.

How are they metabolised? How are they controlled?

Cortisol liver, conjugated to glucuronic acid; inactivation depressed by liver disease

 


Q34

Name the endogenous catecholamines. Where are they produced?

PROMPT – Match catecholamines with source.

  • Adrenal medulla
    • Adrenaline
    • Noradrenaline
    • Dopamine
  • Intrinsic Cardiac Adrenergic Cells
    • Adrenaline
  • Sympathetic Nervous System Cells
    • Dopamine

Pass Criteria:

  • Bold to pass

What are the physiological effects of adrenaline and noradrenaline?

  • Metabolic
    • Glycogenolysis
    • Increased metabolic rate
    • Mobilisation of free fatty acids
    • Increased lactic acid
  • Cardiovascular
    • Vasoconstriction and dilation
    • Increase heart rate and strength
  • Receptor-specific
    • Alpha 1: Constriction of blood vessels, smooth muscles (especially noradrenaline)
    • Alpha 2: Mixed smooth muscle effects (especially adrenaline)
    • Beta 1: Cardiac ionotropy and chronotropy, irritability (both)
    • Beta 2: Dilation blood vessels liver & muscle, other smooth muscle relaxation (adrenaline)
    • Beta 3: Lipolysis, detrusor relaxation (especially adrenaline)

Pass Criteria:

  • 1 metabolic
  • 1 bold cardiovascular

 


Q35

List the physiological effects of glucocorticoids.

  1. Increased protein catabolism
  2. Increased hepatic glycogenolysis and gluconeogenesis, increased glucose-6-phosphatase –> increased plasma glucose
  3. Anti-insulin effects on peripheral tissues
  4. Inhibit ACTH secretion
  5. Controls vascular reactivity to noradrenaline and adrenaline
  6. Control ability to excrete water load
  7. Increased neutrophils/platelets/red blood cells and decreased eosinophils/lymphocytes/basophils

Pass Criteria:

  • 2 bold and 2 others

What are the vascular effects of abruptly stopping long term glucocorticoids?

  • Vascular smooth muscle becomes unresponsive to noradrenaline and adrenaline
  • Capillaries dilate and increased permeability
  • Failure to respond to noradrenaline impairs vascular compensation for hypovolaemia and promotes vascular collapse

Pass Criteria:

  • Must have general concept

What is the benefit of elevated glucocorticoid levels in stress?

  • Effect on vascular activity to catecholamines plus necessary for catecholamines to mobilise free fatty acids for emergency energy source

 


Q36

What are the physiological effects of glucocorticoids?

  • Permissive action
    • Catecholamine effects – pressor/vascular reactivity
    • Bronchodilation
  • Metabolic
    • Increase protein catabolism
    • Increase hepatic glycogenolysis and gluconeogenesis -> increase in plasma glucose
    • Anti-insulin effects on peripheral tissues
    • Increase lipolysis
  • Free water excretion (decreased vasopressin)
  • Immunological
    • Decreased inflammation/allergic response/ lymphocyte activity
  • Haematological – increase neutrophils/platelets/red blood cells
  • CNS
    • EEG slowing
    • Personality changes

Pass Criteria:

  • Bold
  • 2 metabolic
  • 1 other

How is glucocorticoid secretion regulated?

  • Glucocorticoids (cortisol) – secreted from the adrenal cortex; secretion dependent on ACTH secretion from the anterior pituitary
  • ACTH secretion is regulated by CRH released from the hypothalamus in response to low cortisol levels or stress)
  • Glucocorticoids provide a negative feedback loop on the hypothalamus and the anterior pituitary to reduce ACTH secretion

Pass Criteria:

  • Bold

Q37

How is plasma calcium regulated?

  • 1,25-dihydroxycholecalciferol (from vit D) increases Ca absorption from gut & kidneys
  • PTH mobilises Ca from bone, increased Ca reabsorption in kidney, increased 1,25 DHCC formation in kidneys
  • Calcitonin (from thyroid) inhibits bone resorption, increases Ca excretion in urine

Pass Criteria:

  • 2 of 3 bold to pass

How is the synthesis of 1,25-dihyroxycholecalciferol (vit D) regulated?

  • 1,25-DHCC formed in kidney by 1a-hydroxylase
  • High Ca/high PO4 in 1,25-DHCC (increases inactive 24,25-DHCC instead)
  • Low ca increases PTH which stimulates 1a-hydroxylase (low PO4 directly stimulates 1a-hydroxylase)

Pass Criteria:

  • Bold