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REVISION BDS > endocrine physiology p138 > Flashcards

endocrine physiology p138 Flashcards

1
Q

3 modes of communication in the body

A

cell -> cell (neural synapse)

cell -> several cells (paracrine)

several cells -> many cells (endocrine)

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2
Q

process of synapse

A

impulse arrievs at terminal presynaptic cell

transmitter released from storage vesicles

transmitter diffuses in synaptic cleft

transmitter binds to receptor on posynaptic cell

alters postsynaptic cell:

  • excitatory e..g impulse generated, muscle contracts, glnf secretes
  • inhibitory e.g. postsynaptic cell is switched off

transmitter action is terminated

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3
Q

drug actions on synapses

A

enhance or block

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4
Q

paracrine communication

A

one cell to several

immune cells often

often part of cascade reactions

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5
Q

autocrine commuication

A

chemcial acts on a cell releasing it (self-feedback)

can also be regulated by drugs

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6
Q

endocrine transmission

A

secreted by a gland

hormone sent to all parts of the body via blood stream

acts only on cells with correct membrane protein corresponding to it

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7
Q

nerves

A

actions very specific and often localised

rapid transmission

sutiable for rapid responses e.g.:

  • vol. muslce contractions
  • thinking
  • salivary secretions
  • oral/pharyngeal and oesphageal functions
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8
Q

hormones

A

can affect many cells (different body parts)

co-ordinated body wide actions

slow to act but effect persists

suitable for prolonged controls e.g.

  • small intestine gland response
  • control of metabolism/growth
  • regulation of blood calcium and glucose
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9
Q

can nerves and hormones work together

A

some body functions involve both types of communication

  • regulation of blood pressure
  • stress reactions
  • thermal regulation
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10
Q

2nd messengers

A

peptide transmitters (1st messengers) can’t cross cell membrane so instead act on a receptor protein on the cell membrane

intracellular effects are therefore regulated by second messengers

  • G proteins and cAMP
  • calcium ions (G proteins/ Ca2+)
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11
Q

steroid hormones

properties

A

can pass through target cell membrane and act on receptors inside the target cell

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12
Q

anterior pituitary hormones

A
  • adrenocorticotropic hormone (ACTH)
  • follicle stimulating hormone (FSH)
  • luteinsing hormone (LH)
  • thyroid stimulating hormone (TSH)
  • growth hormone (GH)
  • prolactin (PL)
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13
Q

hypothalmic anterior pituitary hormones

A

hypothalamus secretes ‘releasing’ hormones

passed to the anterior pituitary via blood vessels - hypothalamic pituitary portal vessels

trigger hormone secretion from ant pituitary

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14
Q

hypothalmic AP hormones

A
  • corticotropin releasing hormone (CRH)
  • gonadotropin releasing hormone (GRH)
  • thryotropin releasing hormone (TRH)
  • growth hormon releasing hormone (GHRH)
  • somatostatin (SS; GH inhibiting hormone)
  • prolactin releasing hormone (PLRH)
  • dopamine (DA; also PLIH)
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15
Q

posterior pituitary

signalled by

hormones relased

A

hormones made in hypothalamus go to posterior pituitary along nerve axons

hormones relased by PP

  • ADH (vasopressin)
  • oxytocin
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16
Q

cortex hormones from adrenal glands

A

mineralcorticoids e.g. aldosterone

glucocorticoids e.g. cortisol

sex hormones e.g. androgens, oestrogens

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17
Q

medulla of adrenal glands releases

A

adrenaline

modified sympathetic ganglion

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18
Q

pancreatic islets relaseases

A

glucagon - α cells

insulin - β cells

somatostatin - δ cells

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19
Q

pancreatic δ cells release

A

somatostatin

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20
Q

pancreatic β cells release

A

insulin

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21
Q

pancreastic α cells release

A

glucagon

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22
Q

glucagon

A

released in response to low blood sugar

acts to raise blood glucose

actions:

  • when glucose is gone you need glucagon
    • glycohenesis in the liver
    • gluconeogenesis in the liver
    • lipolysis and ketone synthesis
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23
Q

insulin

A

released in response to raised blood glucose concentrations

acts to lower blood glucose

facilitates glucose entry into - muscle cells, adipocytes

gluocse uptake to liver is not insulin dependent

promotes formation of m acromolecules

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24
Q

somatostatin

A

functions as a local hormone, inhibits secretion of both insulin and glucagon

seperate from the action of inhibiting growth hormone release from anterior pituitary

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25
Q

diabetes melliyus

A

abnormality of glucose regulation (lots of sweet pee)

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26
Q

diabetes insipidus

A

abnormality of renal function - watery pee

reduced ADH

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27
Q

type 1 diabetes mellitus

A

insulin defcicient

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28
Q

type 2 diabetes mellitus

A

insulin resistant

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29
Q

type 1 diabetes mellitus

is

A

immune mediated pancreatic β cell destruction

ciculating antibodies present:

  • glutanic acid decarbozylase
  • islet cell antibodies
  • insulin cell antibodies

causes hyperglyceamia (inc blood glucose)

results in ketoacidosis

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30
Q

ketoacidosis

A

type 1 diabetes mellitus

body breaks fdown fats - produce ketone bodies

build up in insulin def and lower blood pH

blood glucose is raised concurrent to this

due to these phenomena there is osmotic diuresis and resultant dehydration

sodium and potassium loss due to leaking out of cells and into urine

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31
Q

signs of ketoacidosis

A

polyuria

polydipsia

tiredness

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32
Q

acute presentation of ketoacidosis

A

hyperglyceamia

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33
Q

type 2 diabetes mellitus is

A

insulin resistance and relative insulin deficiency

metabolic disorder

  • elevataed basal insulin (defect in insulin resistance)
  • decreased overal insulin (β cell response to hyperglycaemia inadequate)
  • basal hepatic glucose increased (insulin fails to supress glucose)
  • insulin stimulated muscle glucose uptake reduced
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34
Q

sigsn of type 2 diabetes

A

glucose intolerance in body

hyperinsulinaemia

hypertension

abdominal obesity

dyslipidaemia (abnormal lipid levels in blood)

procoagulant epithelial markers (causes early platelet adhesions, sticky endothelium)

early and acclerated athersclerosis

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35
Q

typical characteristics of type 1 diabetes

A

younger

thin

family Hx of autoimmune disease

diabetic symptoms

easily get ketosis

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36
Q

typical characteristics of type 2 diabetic

A

older

obese

strong family Hx

present with secondary complications (cardiac etc)

rarley get ketosis

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37
Q

drugs for diabetes

A

oral hypoglucaemic drugs (reduce blood glucose Hyper>Drug=Hypo)

bisguianides

sulfonylureas

carbohydrate absorptiono delayers

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38
Q

bisguanides

A

good drug, lowers blood glucose, reduce gluconeogenesis but doesn’t lead to hypo

e.g. metformin

  • taste distubance
  • lactic acid build up due to taking it - can be fatal
  • insulin sensitisers
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39
Q

sulfonylureas

A

stimulate insulin secretion

risk of causing hypo and weight gain (due to increase macromolecules)

insulin scretagogues

e.g. gliclazide

40
Q

carbohydrate absorption delayers

A

does what it says

e.g. A-carbose

41
Q

type 2 diabetes specific management

A

weight loss

diet restriction

diet pills (orlistat, sibutramine)

gastric bypass

42
Q

type 1 diabetes specific management

A

insulin sub cutaneously

different preparations/regimes - indivualised

ideal sugar 4<7

HbA1C (6<10%) measure of glucose bound to haemoglobin

43
Q

macrovascular complications of diabetes

A

PVD lower limbs

neuropathy (autonomic - impacts small vessels, causes ischaemia and diabetic foot)

cerbrovascular (stroke, TIA)

44
Q

microvascular diabetic complications

A

retinopathy - blindness

nephropathy (backflow from bladder)

45
Q

types of multiple endocrine neoplasia

A

1

2a

2b

46
Q

MEN1

A

multiple endocrine neoplasia

  • parathyroid
  • pancreaitc islets
  • anterior pituitary
47
Q

MEN2a

A

multiple endocrine neoplasia

  • parathyroid
  • medullary thryoid
  • phaechromocytoma
48
Q

MEN2b

A

multiple endocrine neoplasia

  • medullary thyroid
  • pahechormocytoma
  • mucosal neuromas
  • marfanoid appearance
49
Q

pituitary tumours are called

A

adenomas

50
Q

functional adenomas can cause

A

amenorrhea-galactorrhea syndrome

Cushing’s disease

Acromegaly

51
Q

amenorrhea-galactorrhea syndrome

A

hyperprolactinaemia - infertilty, poor breast milk production

52
Q

Cushing’s disease

A

caused by excess of gluocorticoids secodary to adreanl hyperplasia

excess ACTH production

signs

  • moon face
  • buffalo hump
  • central obesity + proximal muscle wasting
  • hirsutism in females

systmic effects

  • cortisol = insulin resistance = impaired glucose tolerance/diabetes
  • mineralcortcoids = salt and water resistance- oedema and HT
53
Q

Cushing’s syndrome

A

non-pitutary

caused by primary adrenal disease

decreased GH

  • growth failure in children
  • metabolic changes in adults - inc fat, reduced vitality

non functional adenomas

54
Q

acromegaly

A

growth hormone excess after epiphyseal plates have fused

if in children known as Gigantism - Test for IGF-1 (insuliln like growth factor 1)

signs

  • coarse facial features
  • visual field defects - bitemporal hemianopia (optic nerve crossover)
  • enlarged tongue
  • denture no longer fitting
  • inc diastema and reverse overbite
  • ankylosis of TMJ
  • hypertension
  • large hands and feet
  • type 2 diabetes
  • nerve pathology - III, IV and VI palsies
  • CVD - ischaemic heart disease, acromegalic cardiomyopathy
55
Q

non-functional adenomas

A

space occupying tumours

visual field defects

hormone deficiencies due to destruction of paraenchyma of pituitary (replaced with tumour)

can be reduced with trans-spehnoidal surgery

56
Q

thryoid hormones

A

T3: tri-iodothyronine (deiodinated form of T4 works once in target cells)

T4 -thyroxine (more numerous than the former)

57
Q

hyperthyroidsim

A

excess T3 and T4

58
Q

hyperthyroidism can cause

A

graves disease

toxic multi-nodular goitre

toxic adenoma

59
Q

graves disease

A

due to hyperthyroidism

  • auto-antibodies stimulate the TSH receptor = more hormone produced in pituitary
  • exopthalmos
  • finger clubbing
  • opthalmopathy
60
Q

toxic multinodular goitre

A

goitre is swelling of thyoid resulting in excess bound hormone (thryotoxicosis)

61
Q

toxic adenoma

A

takes control of hormone release

signs

  • tachycardia
  • atrial fibrilation
  • tremor
  • exopthalmos
  • goitre
    • diffuse multi-nodular? iodine?
    • solitary? caner risk!

symptoms

  • weight loss
  • heat intolerance
  • tremor/irritability
  • emotional
62
Q

tx for toxic adenoma

A

carbimazole > methimazole (anti-thyroid drug), block and replace w T4 as needed

partial thyroidectomy

radioactive iodine

can both lead to hypothyroidsm

63
Q

hypothyroidism aka

A

myxoedema

64
Q

priamry cause of hypothyroidism

A

hashimoti’s thyroiditis

65
Q

Hashimoti’s thyroiditis

A

gradual autoimmune destruction of thyroid gland

  • goitre and hypothyroid features
  • vitiligo
  • type 1 diabetes
  • pernicious anaemia (B12/Folate)
  • Addison’s disease
  • Down’s syndrome

idiopathic atrophy (10x more in female, lymphocyte infiltrate into organs cause organ specific autoimmune disease)

radiodine treatment/thyroidectomy surgery

iodine deficiency (goitre)

caused by drugs used for hyperthryoidism - carbimazole, amiodarone, lithium

congenital

66
Q

secondary cause of hypothyroidism

A

hypothalmic/pituitary disease - don’t release the hormones that act on the thyroid gland

decreased TRH (hypothalamus)

decreased TSH (ant.pit)

67
Q

sigsn of hypothyoidism

A
  • dry coarse skin
  • bradycardia
  • hyperlipidaemia
  • confused state/memory loss
  • goitre (hashimoto’s and iodine def)
  • delayed reflexes
68
Q

symptoms of hypothyroidism

A
  • lethary
  • cold intolerance
  • depression
  • weight gain
  • hoaeseness, puffed face adn extremitis
  • angina
  • hair loss
69
Q

hyperthyroidism tx

A

Carbimazole *TASTE DISTURBANCES

  • Titration
  • block and replace w/ T4

β- blockers
Radioiodine

  • Hypothyroid risk w/time

Partial Thyroidectomy (w/ drug therapy to stabilise)

Graves Opthalmopathy- simple treatments

70
Q

hypothyroidism tx

A

thyroxine

monitor TSH levels

71
Q

dental aspects of thyroid issues

A

Hyperthyroid- Pain, Anxiety problems, don’t treat until controlled

Hypothyroid- if severe avoid sedation!!!

If controlled treat patient as if normal

Goitre is detectable to the dentist

72
Q

thryoid cancer

A

Papillary - good prognosis

Folicular- poor prognosis

Undifferentiated in Elderly

Cold Nodules on radioisotope scan

Can affect TSH- give T4 post op

73
Q

Addison’s disease basic

A

destruction of adrenal tissue

74
Q

Cushing disease/syndrome basic

A

excess adrenal action

75
Q

therapeutic corticosteroids basic issue

A

suppress adrenal action and their adverses affects

76
Q

adrenal gland is

A

op top of kidneys

made of 3 main zones

produces hormones thanks to cholesterol made in the liver

77
Q

3 main zones of adrenal gland

A

zona glomerulosa

zona fasicularis

zona reticularis

78
Q

zona glomerulosa makes

A

aldosterone - mineralcotocoid

RAAS system - BP + Salt/H2O

  • dec BP detected
  • Angiotensin II causes secretion of aldosterone
  • Aldosterone causes increased reabsorption of Sodium and increases water retention to increase blood pressure
  • Increases Pottasium loss

ACE inhibtors affect this hormone but have side effects

  1. cough
  2. angio-oedema
  3. oral lichenoid reaction

AT2 blockers

79
Q

zona fasicularis makes

A

cortisol - glucoroticoid - ACTS ON ANGIOTENSIN

aka “The Stress Hormone”

Breakdown of fat and protein

Reduces osteogenesis

Counteracts Insulin= Higher blood sugar

Decreases amino acid uptake by muscles

lowers immune reactivity

raises blood pressure

Circadian release- Nocturnal peak

80
Q

zona reticularis makes

A

adrenal androgens

DHEA

testosterone precursor

involved in adrenarche a.k.a early maturation puberty etc

81
Q

therapeutic steroids

A

given ‘point values’ based on their potency against naturally occuring Cortisol

cortisol has value of 1

e.g 5mg Prednisalone = 20mg of Hydrocortisone
Hydrocortisone = 1
Prednisalone = 4
Triamcinolone = 5
Dexamethasone = 25
Bethamethasone = 30

Enhance glucorticoid effect- think of what cortisol does normally (x multiplied by factor of steroid potency)

Enhanced mineralcorticoid effect- salt and water retention w/ aldosterone action in RAAS = Hypertension

82
Q

side effects of steroids

A
  • hypertension - aldosterone
  • osteoporosis - cortisol
  • type 2 diabetes - cortisol
  • increased infection risk - cortisol
  • increased cancer risk
83
Q

adrenal disorders

hyperfunction

A

glucoticoids (cortisol) - Cushing’s syndrom

Mineralcorticoids (aldosterone) - Conn’s syndrome

84
Q

Cushing’s syndrome

A

hyperfunction of adrenal (cortisol)

  • arenal tumour (primary)
  • pituitary tumour (secondary) = inc ACTH level
  • ectopic ACTH production from lung tumour (weird)
85
Q

Conn’s syndrome

A

hyperfucntion of adrenal gland - mineralcorticoid (aldosterone)

  • caused by adrenal tunour
  • either hyperplasia/malignancy
  • excess sodium retention - hypertension
  • excessive potassium loss - polyuria and muscle weakness
86
Q

adrenal disorders

hypofunction

A

addison’s disease (primary) - gland destruction

pituitary failure (secondary)

87
Q

Addison’s disease

A

hypofunction of adrenal gland - primary

GLAND DESTRUCTION

surgical/TB/ cancer can cause, but main one is Autoimmune adrenalitis

  • thyroid
  • diabetes mellitus
  • pernicious anaemia (B12 and folate

signs

  • postural hypotension (BP drops upon standing - head rush) - due to salt and water loss
  • weight loss and lethargy
  • hyperpigmentation - scars, mouth, skin creases
  • vitiligo

symptoms

  • weakness
  • anorexia
  • loss of body hair (females)
88
Q

Addison’s disease test will have

A

high ACTH

low cortisol

synacthen - negative

89
Q

addisonian crisis

A
  • hypotension
  • vomitting
  • eventual coma
  • hyponatraemia (low sodium) hence the hypotension
  • hypovolaemic shock (>20% of blood volume lost)

cortisol and fludrocortisone

90
Q

managing addisonian crisis

A

treat the problem

fluid reuscitation

  • saline infusions
  • corticosteroids IV
  • correct hypoglycaemia
  • treat precipitating event (infection)
91
Q

pitituary disease (secondary)

A

causes reduction in secretion of adren-corticotropic releasing hormone

low ACTH

low cortisol

synacthen - positive

92
Q

synacthen

A

tests ACTH stimulation

if ACTH normal = negative result

if ACTH low = positive result

93
Q

adrenal hyperfunction tx

A

Detect Cause

  • pituitary
  • Renal
  • Ectopic (lung)

Surgery follows

  • pituitary
  • Adrenalotomy
  • Adrenalectomy
94
Q

adrenal hypofuntion tx

A

Hydrocortisone- replace cortisol

Fludrocortisone- replace aldosterone

95
Q

steroids in dentistry

A

If someone has stopped prolonged systemic steroids in last 3 months

  • High risk
  • Cover with 100mg IM dose of steroid to cover patient

ALWAYS ASK ABOUT STEROID USE PAST 6 MONTHS

Diabetes and CV disease in Addison’s

Candidiasis in Cushing’s

Oral Pigmentation in Addison’s and Cushing’s

Can be other causes

  • Melanotic Macule
  • Drugs- Minocycline (antibiotic), Azidothymidine (HIV/AIDs), Oral Contraceptive
  • Naevus
  • Pregnancy

REVISION BDS (43 decks)

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