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Semester 2 > Physiology and Metabolism > Flashcards

Physiology and Metabolism Flashcards

1
Q

Why is there a need for 2 pathways in carbohydrate metabolism

A

glyco is a catabolic reaction and breaks down sugars to be able to use them for energy. Gluco is anabolic and allows simple sugars to bond for storage

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2
Q

What are the steps of glycolysis enzymes that catalyse each step

A
  • whiteboard it *
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3
Q

what is catabolism

A

Process where complex substance are degraded to simpler molecules
Generally there is a net release of chemical energy

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4
Q

What is Anabolism

A

Process of synthesis of complex organic molecules
net input of energy required

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5
Q

What is fermentation

A

energy yeiling metabolic pathway with no net change in the oxidation state of products compared to substrates

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6
Q

What is lactate

A

formed by active skeletal msucle, limited release of energy, pyruvate reduced by nadh to form lactate (catalysed by lactate dehydrogenase)

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7
Q

Why do we need to make glucose

A

Long periods in absence of carbohydrate, intense exercise

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8
Q

What are the main organs that make glucose

A

liver and kidney cortex

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9
Q

What are the bypasses of the 3 irreversible reactions for glycolysis

A

” white board”

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10
Q

The cori cycle

A

whiteboard

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11
Q

Whats the regulation of glycolysis and glucogeopnesis

A

pyruvate kinase - activated by fructose -1,6-bisphosphate
pyruvate carboxylase - activited ny high levels of acetyl-CoA
Phosphoenolpyruvate carboxykinase- inhibited by high levels of ADP

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12
Q

What are the divisions of the nervous system

A

CNS = brain + spinal cord
PNS= autonomic nerovus sysem- para, sym
Somatic nervous system - sensory, motor

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13
Q

what does pomc activation result in

A

satiety

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14
Q

what does agrp/npy neuron activation result in ?

A

hunger

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15
Q

Are nerves from the cns efferent of afferent

A

efferent and motor

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15
Q

What is the importance of energy homeostasis for the brain

A

Glucose providing most essential source for neurons
Glucose needs to be regulated and maintained within a narrow physiological range

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16
Q

Describe the role of leptin in obesity and include evidence from a rodent model

A

On POMC neurons it acitvate on agrp they inhibit
Leptin signals satiety, without proper signalling you dont feel full so you keep eating. Leptin released from adipocytes upton eating. Mice have a Ob/ob mutation in gene respoible from production of leptin meaning they excessively eat

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17
Q

What is the hypothalamus responsible for

A

It has neurones of AgRP + POMC.

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18
Q

What is the arcuate nucleus

A

contains 2 major neuronal populations involved in metabolic control: AgRP nad POMC
Astrocyetes in the arcuate nucleus hold high capacity transporters that function as nutrient sensors
for appetite controlling neurons

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19
Q

What is POMC

A

Signals satiety
* POMC neurons secrete melanocytestimulating hormone (MSH) -
suppresses appetite
* Mutations in POMC gene associated
with increased body weight in
Labradors

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20
Q

What is AgRP/NPY

A

Agouti-related peptide and neuropeptide Y are coexpressed in neurons of ARC
* Signals increased appetite; decreases metabolism and
energy expenditure
* Levels increase during periods of fasting
* AgRP/NPY neurons express ghrelin receptors
* AgRP is inverse agonist at melanocortin-Rs (MC3/4-R)

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21
Q

describe the signalling between arc and pvn

A

POMC and AgRP/NPY neurons
project from the ARC to the PVN to
control food intake and energy
balance
* Influenced by glucocorticoids
(cortisol), leptin, and insulin

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22
Q

describe the ventromedial hypothalamus

A

Saiety centre, signals feeling of fullness, expresses high levels of leptin receptor and MC4R, involved in thermogenesis

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23
Q

describe the paraventricular nucleus

A

autonomic control area- metabolism control, growth, reproduction, stress
source of oxytocin, corticotropin ,RH thyrotropin-RH, vasopressin

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24
Q

Describe the lateral hypothalamus

A

stimulation of feeding behaviour, wakefulness, regulation of body temp, digestive function, pain, perception
Contains primary orexigenic nucleus ( appertite-stimulating)

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25
Q

What are meanocortins
what are the receptors

A

Anorexigenic peptides, cleaved from pomc precurosr polypeptide
expressed in hyptohalamus and brain stem, mc4r - mutations are cause of autosomal dominant obesity, accounting for 6% of all cases of early-onset obesity

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26
Q

What is the dvc

A

part of brain stem composed of , area postrema , nucleus of solitary tract, dorsal motor nucleus of vagus nerve
Intergrates peripheral satiety signlas, regulates energy balance

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27
Q

Hoe do nutrients cross the blood brain barrier

A

transport mechanism that can be active or passive
leaky regions- median eminence in hypothalamus
area postreme in brain stem

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28
Q

What nutrients cross the bbb and how

A

Drugs medicnes
Efflux transporters, solute carriers, passive diffusion, paracellular tranporters, receptor-mediated transcytosis, adsorptive transcytosis

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29
Q

describe insulin

A

produced by beta cells of pancreas, released upon eating due to increased blood glucocse, signals satiety in the brAIN

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30
Q

Describe insulin transport and signalling in the brain

A
  1. receptor-mediated transcytosis
  2. passive diffusion
    3.ins in csf transported by tanycytes
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31
Q

Regulation of hepatic glucose

A

insulin signals in ARC to supress activation of vagal cholinergic efferent neurons that innervate the liver, kupffer cells to secrete IL-6 which acivates its receptor on liver cells, thsi phosphorylates STAT3 to repress transcription of gluconeogenic enzymes, hepatic glucose production inhibited

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32
Q

what is the area postrems

A

area with leaky bbb, detect messengers in blood and transduce into neural signal, detects circulating hormones, involved in vomitting thirst and BP

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33
Q

What are the neuroendocrine signals

A

Leptin, insulin, orexin, gherlin, cck, glp-1

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34
Q

describe intranasal insulin

A

enables the delivery of insulin to the CNS in absence of systematic uptake and realted peripheral side effects, via olfactory pathway, accumulates in CSF

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35
Q

what is orexin

A

stimulates wakefulness and increases appetite, produced in neurons of LH, these cells are inhibited by leptin and are activated by ghrelin and hypoglycemia, glucose inhibits orexin production, links sleep regulation metabolism, lack of orexin causes narcolepsy

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36
Q

Ghrelin

A

hunger hormone, produced by GI tract, primarily stomach
Activates AGRP cells in ARC, anterior pituaitry, also cells in raphe nuclei.
leptin and insulin sensitive
Levels reduced in obese patients

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37
Q

CCK

A

signals satiety and aids digestion, cells produced from small intestine, causes release of bile and digestive enzymes, in absence larger meals are consumed, activates vagal fibers innervating stomach and intestine resulting in altered NTS activity, activates GLP-1 neurons

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38
Q

GLP-1 what is it

A

Signals atiety, inhibts gastric emptying, produce in intestine and NTS, projections to hypothalamus, dmv
decreases blood glucose by enhancing insulin secretion

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39
Q

insulin resistance

A

blood glucose remains elevated, eating HFD causes IR but mechansim unknown
reduced insulin sensitivity in hypothalamus of hfd-fed mouse

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40
Q

What is leptin resistance

A

obesity patients have a reduction in leptin sensitivity - inability to detect satiety despite high energy stores and high levels of leptin, leads to increased hunger and reduced energy expenditure

41
Q

What are leptin mutations

A

8 found so far, cause extreme obesity from infancy with hperphagia, treatment with recombinant leptin leads to weight loss and normalised plasma lipid and insulin levels

42
Q

What is the function of the thyroid gland

A

development in the brain, pituitary- tsh product + growth hormone, Heart - cardiac output+heart rate+, muscle - protein metabolism, liver - mitosis, adipose tissue- lipolysis, skeletal system- growth and maturation

43
Q

What is the thyroid made up of and what does it produce

A

throid follicles
tetraiodothyronine
trio
stores hormones for 100 day supply

44
Q

What is hypothyroidism and what are the symptoms

A

long term cardiovascular diseases, split into primary secondary and tertiary variants
Fatigue, lethargy, weight gain, constipation

45
Q

How do you test for hypothyriodism

A

blood test= check serum TSH and FT4
Both normal= normal function
TSH slightly elevated= sub clinical hypo
TSH high, FT4 low = primary hypothyroidism
TSH normal or low, FT4 low = central hypothyroidism or euthyroid sick syndrome
OR radiotherapy, MRI, anti thyroid auto antibodies test

46
Q

what are the causes of hypothyroidism

A

primary= failure of thyroid gland
-autoimmune, antibodies against TPO, large number of wbc in thyroid gland, gene or environment
Secondary= pituitary disease, reduced TSH
Tertiary = hypothalamic disease

47
Q

What are the cardiovascular consequences of hypothyroidism

A

heart failure, dyslipidemia (imbalance of cholesterol), high blood pressure, intima thickeness, myxedema

48
Q

How do you treat hypothyroidism

A

daily synthetic hormone

49
Q

what does primary hypothyroidsm look like ?

A

gland is diffused symmetrically and enlarged

50
Q

What does central hypothyroidsm look like and hwo to diagnose

A

its rare and the causes are due to adenomas, also due to tumours, vascular disease, trauma, inflammation
CT or MRI , measure anti-thyroid autoantibodies

51
Q

What is hyperthyroidism

A

excess thyroid hormones (graves disease) most common.

52
Q

WHat are the causes of hyperthyroidism

A

graves disease, nodular struma, solitary toxic adenoma, thyroiditis,
rare= TSH secreting adenoma, thyroid cancer, metastatic tumors

53
Q

Describe graves histology

A

Scattered lumpohcytes, scant colloid, packed follicles with tall columnar epithelium

54
Q

What re the symptoms of hyperthyroidims

A

fatigue, sweating, hair loss, hand tremors, rapid irregular heart beat, enhanced catecholamine signalling through increased beta- adrenergenic receptor density on the cell surface

55
Q

What is a thyroid storm?

A

mortality rate of 8-25%, rapid increase in thyroid hormone levels after not using antithyroid drug or radioactive iodine treatment

56
Q

How to inestigate hyperthyroidism

A

medical history + physical exam, radioactive iodine uptake and thyroid scan, blood test measuring T4 and TSH, take rai after 6 -24 hours u test radioactivity

57
Q

Testing for hyperthyroidism

A

Low TSH, high/normal FT4 + T3 = radio + scan of thyroid - if low uptake = thryoiditis, ectopic thy hormone, exogenous Th - if high uptake = homogenous rai distrubution = graves OR Nodular rai - single areas = toxic adenoma or - multiple area of accumulation = toxic multinodular

58
Q

how do you treat hyperthyroidism

A

radioactive iodine - causes the gland to shrink and ecess disappears from body within weeks to months
Anti-thyroid medications- include tapazole and propylithiouracil
Beta blockers- ease tremors, rapid heart and palpations
surgery- vary rare and risky as it can damage vocal cords and parathryoid glands , you would need life long levothyroxine to still supply w th also calcium levels

59
Q

what are the adrenocortical hormones

A

secretion of adrenocortical steroids and aldosterone are controlled, respectively by adrenocorticotrphic hormone (acth) and angiotensin

60
Q

What are the effects of corticosteroids

A

alterations in carbohydrate, protein andlipid metabolism, maintenance of fluid and electrolyte balance ; and preservation of normal function of the cardiovascular, immune, renal, endocrine, nervous, and musculoskeletal systems.

61
Q

What is addisons disease

A

primary adrenal insufficiency, rare, cause- bilateral adrenal cortex destruction reducing hormones
any disease that causes damage to adrenal cortex can result in addisons
decreased cortisol production followed by loss of aldosterone both resulting in ACTH increase

62
Q

What is secondary adrenal insufficiency

A

starts in pituitary - when is doesnt make enough ACTH the adrenal glands wont make cortisol and over time the glands will shrink and stop working

63
Q

What is tertiary adrenal insufficiency

A

starts in hypothalamus, it makes CRH, this tells the pituaitary to make ACTH , it is then a dominoe effect like the secondary

64
Q

explain symptoms of addisons disease

A

-Glucocorticoids promote gluconeogenesis in liver, whereas in skeletal muscle and white adipose tissue they decrease glucose uptake and utilisation by antagonizing insulin response, also regulate glycogen metabolism
-hyper pigmentation of the skin occurs because (MSH) and ACTH share the same precursor molecule, (POMC).
-lack of aldosterone can cause hyponatremia. (low sodium in the blood). Hyponatremia can cause confusion, fatigue, and muscle twitches and seizures, also cause hyperkalemia (high potassium). Severe hyperkalemia can cause life-threatening changes in your heart rhythm.
Digestive manifestations are thought to be a direct consequence of glucocorticoid and mineralocorticoid deficiency, however their mechanisms are not well known

65
Q

What are the symptoms of addisons

A

hair loss, blurry vision, abdominal pain, decreased appetite, hyperpigmentation, shaking or tremors depression

66
Q

How do u diagnose addisons

A

SYNACTHEN TEST
9Am cortisol taken, inhectic synthetic acth, take further plain clotte tube blood smaple at 30 and 60 mins after inhection,
rise in cortisol and low aldestorone means addisons( whiteboard signs)

67
Q

Adrenal insufficiency treatment

A

Primary adrenal insufficiency — Treatment of adrenal insufficiency requires a daily dose of a glucocorticoid (hydrocortisone) and mineralocorticoid (Fludrocortisone) usually for life.
Androgen replacement may be recommended for women.
The goal of treatment is to stabilize hormone levels and relieve symptoms

68
Q

IS T4 the most biological active thryoid hormone

A

no false

69
Q

arae fatigue and weight gain key symptoms of hypothyroidism

A

yes true

70
Q

primary hypothyroidism is characterised by high TSH and low T4 , true or false

A

yes true

71
Q

Anti-thyroid auto antibodies are present in central hypothyroidism

A

no false

72
Q

Hyperthyroidism increases adrenergic signalling

A

yes true

73
Q

Radioactive iodine uptake will shows graves disease by a single intense zone

A

no false

74
Q

Cortisol primarily regulates mineral balance

A

no false

75
Q

Addisons is not characterised by hypothalamus or pituitary problems

A

yes true

76
Q

21 hydroxylase is typically a target in autoimmine adrenal insufficiency

A

yes true

77
Q

Secondary adrenal insufficiency can be determined by measuring TSH and T4 levels

A

false

78
Q

what is cushings syndrome and what are the symptoms

A

Cushings syndrome- extremely high levels of cortisol
Symptoms
- Weight gaim, thin arms and legs, round face, increased fat around the base of the neck
- Fatty hump between the soldiers, easy bruising, wide purple stretch marks

79
Q

what are complications of cushings syndrome

A

Complications
- Heart attack and stroke
- Blood clots in legs and lungs
- Infections
- Bone loss and fractures
- High blood pressure
- Unhealthy cholestrol levels
- Mood changes ie depression
- Memory or conentration troubles
- Insulin resistance and prediabetes
- Type 2 diabetes

80
Q

what is the cause of cushings syndrome (exogenous)

A

common cause of Cushing’s syndrome is the long-term, high-dose use of the cortisol-like glucocorticoids (exogenous cushings). These medicines are used to treat other medical conditions, such as asthma, rheumatoid arthritis, and lupus.

81
Q

what is the endogenous cause of cushings syndrome?

A

70% is pituitary tumour
15% adrenal tumour
15% of unknown causes

82
Q

what is the treatment for cushings syndrome

A

pituitary- directed drugs
adrenal directed drugs
glucocorticoid receptor directed drugs
pituitary surgery
pituitary radiotherapy
bilateral adrenalectomy

83
Q

Define drug metabolism

A

biotransformation of pharmaceutical substances in the body

84
Q

What are xenobiotics

A

chem substances not naturally produced or likely presnt inside an organism

85
Q

what is detoxification

A

toxic subtances removed from the body

86
Q

what is drug metabolism responsible for

A

converting lipophilic drugs to more hydrophillic compounds to facilitate their excretion
the reactions increase = water solubility, reactivity, size

87
Q

what is first pass metabolism

A

drug gets metabolized at a specific location in the body that results in a reduced concentration of the active drug upon reaching its site of action or the systemic circulation
This is normally in the liver
it can reduce bioavailability and therfore be a problem fro oral drugs

88
Q

describe phase 1 metabolism in aspirin

A

cytochrome p450 enzymes, oxidation reduction and hydrolysis:
e.g aspirin to salicylic acid,
removal of the OCOCH3 group from the benzene and an addition of hydroxyl group

89
Q

what are prodrugs

A

a biologically inactive compound which can be metabolised in the body to produce a drug

90
Q

metabolism of paracetamol on whiteboard

A

x

91
Q

what is the role of Cytochrome P450

A

responsible for 75% of phase I metabolism. catalysts in the transformation of both exogenous and endogenous through oxidation Cytochrome P450 (CYP) enzymes in eukaryotes can be divided into two main
groups with regards to their location in the cell:
* Mitochondrial and Microsomal (i.e. ER-bound) P450s
monooxygenation reactions: both groups of CYPs make use of
NADPH as an electron donor

92
Q

what is the role of cytochrome p450 in metabolism (isoforms)

A

multiple isoforms can can recognise and the same molecule
some expression can be increased by drugs or food (induction)
some drugs can inhibit CYP isoforms

93
Q

what are the factors that influence drug response

A

ethnicity, age, pregnancy, genetics, disease, drug interactions

94
Q

activation of cyp

A
  • whiteboard
    water.
95
Q

what is the evolutionary goal of biotransformation ?

A

increase the rate of excretion or xenobiotics or drugs
it can detoxify or bioactivate xe to more toxic forms that cause tumorigenicity

96
Q

describe phase 2 metabolism

A

glucuronidation, sulfation, acetylation, methylation,
conjugation with glutathione, and conjugation with amino acids (glycine, taurine
and glutamic acid) that strongly increase hydrophilicity

97
Q

describe phase 2 conjugation in metabolsim

A

conjugation of functional groups with hydrophilic endogenous
substrates Addition of small, polar groups: glutathione, glucuronic acid, sulphate,
methyl, amines/amino acids, OH (glucuronyl, methyl, sulphate) NH2
(glucuronyl, acetyl) COOH (glucuronyl, glycine)
 Makes drugs less reactive and therefore more readily excreted by the kidney Increases hydrophilicity - more soluble so they can be extracted easier catalyzed by UDP-glucuronosyltransferase
mainly occurs in the liver

98
Q

describe haem metabolism

A

synthesis of haem bone marrow it is incorporated into haemoglobin, * also used for the synthesis of cytochromes and related compounds. * The former are components of the electron transport chain, which is involved in
oxidative phosphorylation.

99
Q

is toxicity more likely at a lower rate or higher

A

Toxicity is likely at lower plasma concentrations in ‘slow acetylators’ than in ‘fast acetylators’.

100
Q

what is TPMT

A

nvolved in the metabolism of
azathioprine, which is used as a cytotoxic and also as an
immunosuppressant agent. The enzyme TPMT shows pharmocogenetic
variation and about 90 per cent of the UK population have high enzyme
levels. 10 per cent are heterozygotic for TPMT deficiency and about 0.3 per cent are homozygotic for no functional activity. The latter two groups are more susceptible to azathioprine toxicity. Determination of red cell TPMT activity prior to azathioprine administration may give a
guide as to in whom the drug should be avoided or given at a lower dose.

101
Q
A

Semester 2 (5 decks)

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