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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what does endocrine mean

A

substance released into the blood and causes an effect

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2
Q

what does paracrine mean

A

substance which acts on cells within same vicinity and causes an effect

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3
Q

what does autocrine mean

A

a cell-produced substance which acts on the cell that produced it to cause an effect

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4
Q

which type of hormones have slow clearance and a long half life

A

fat soluble/steroid

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5
Q

which type of hormones have fast clearance and short half life

A

water soluble/peptide

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6
Q

what is negative feedback

A

stimulus causes a hormone to be released which directly counteracts stimulus

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7
Q

what is positive feedback

A

stimulus causes a hormone to be released which increases the stimulus

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8
Q

what is an exocrine hormone

A

secretions secreted through a duct to site of action

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9
Q

where is a peptide hormone receptor located

A

cell membrane

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10
Q

where is a steroid hormone receptor located

A

cytoplasm

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11
Q

what hormones have a receptor in the nucleus

A

thyroid
oestrogen
vitamin D

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12
Q

where does ANP act

A

in the heart

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13
Q

where is IGF-1 released

A

liver

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14
Q

where is erythropoietin released

A

kidneys

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15
Q

where are gastrin and incretin released

A

in the GI tract

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16
Q

what is appetite

A

desire to eat food

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17
Q

what is hunger

A

need to eat

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18
Q

what is anorexia

A

lack of appetite

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19
Q

what is satiety

A

feeling of fullness/ disappearance of appetite after a meal

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20
Q

what are the BMI values

A 
under 18.5 = underweight
18.5-24.9 = normal
25 - 29.9 = overweight
30 - 39.9 = obese
above 40 = morbidly obese
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21
Q

what is the role of the hypothalamus in hunger

A

lateral hypothalamus = hunger centre

ventromedial hypothalamic nucleus = satiety centre

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22
Q

what do alpha cells of the pancreas secrete

A

glucagon

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23
Q

what do beta cells of the pancreas secrete

A

insulin

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24
Q

what is the main function of insulin

A

suppress hepatic glucose output = decreased gluconeogenesis and glycogenolysis
increase glucose uptake into insulin sensitive tissue
suppress lipolysis and breakdown of muscle

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25
Q

what are the clinical values for diabetes diagnosis

A

plasma glucose more than 11mmol/L

fasting glucose more than 7mmol/L

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26
Q

what are the clinical values for diagnosing type 2 diabetes

A

HbA1c of more than 48mmol/mol

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27
Q

what is mild hypoglycaemia

A

less than 4mmol/L with no symptoms

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28
Q

what is serious hypoglycaemia

A

less than 3mmol/L often symptomatic

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29
Q

what is severe hypoglycaemia

A

less than 2mmol/L symptomatic with impaired cognitive function

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30
Q

why does hypoglycaemia occur

A

increased levels of insulin usually due to insulin injections in diabetics or healthy individuals with insulinomas

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31
Q

how do you treat hypoglycaemia

A

administer 15g fast acting carb
test blood glucose 15 mins after and check its above 4mmol/L
administer long acting carb to prevent recurrence

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32
Q

what is whipples triad

A
  1. symptoms of hypoglycaemia
  2. blood glucose <50mg/dL
  3. relief of symptoms following ingestion of glucose
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33
Q

presentation of pituitary tumours - 3 key things

A
  1. pressure on local structure
  2. pressure on normal pituitary
  3. functioning tumour
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34
Q

cushings disease definition

A

increased secretion of ACTH from the anterior pituitary gland causing chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)

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35
Q

what is cushings syndrome

A

increased cortisol levels

due to a cause not directly acting on the anterior pituitary

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36
Q

what can cause cushing syndrome

A

prescribed glucocorticoid drugs
excess cortisol production from:
- adrenal tumour
- hyperplastic adrenal gland
- adrenal gland with nodular adrenal hyperplasia
ACTH producing tumours e.g. small lung cell cancers
CRH producing tumours

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37
Q

what are the main functioning pituitary tumours

A
  1. prolactinoma
  2. GH producing tumour = can cause acromegaly
  3. ACTH producing tumour = can cause cushings
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38
Q

how do somatostatin analogues work

A

inhibit multiple hormones and shrink tumours
may have side effects
not available orally
e.g. LANREOTIDE

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39
Q

how are dopamine agonists useful

A 
useful for prolactinoma (and GH secreting tumour)
no damage to pituitary 
work quickly
orally available
relatively ineffective
e.g. CABERGOLINE, BROMOCRITINE
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40
Q

how do GH receptor antagonists work

A

act as competative antagonists to GH
doesnt change GH levels but blocks receptors so less IGF1 produced
daily subcutaneous injection
e.g. PEGVISOMANT

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41
Q

what is the circadian rhythm

A

changes in hormone levels through the day
hormone levels peak just after waking then decrease after this until sleep where they rise again
e.g. cortisol

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42
Q

what is primary adrenal insufficiency (addisons)

A

due to impairment at adrenal glands
= destruction of adrenal cortex
= low cortisol but high ACTH (feedback)

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43
Q

what is secondary adrenal insufficiency

A

due to impairment at pituitary and/or hypothalamus
= reduced adrenal cortex stimulation
= low ACTH therefore low cortisol

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44
Q

what is tertiary adrenal insufficiency

A

due to hypothalamic disease and decrease in CRH

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45
Q

what is thyroid peroxidases TPOs

A

antibody found in almost all individuals with autoimmune hypothyroidism
also associated with graves disease = hyperthyroidism
marker in healthy individuals for increased chance of developing autoimmune thyroid diseases

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46
Q

what is the mechanism of thyroid destruction in autoimmune disease

A

cytotoxic T lymphycyte mediated
thyroglobulin and TPO antibodies may cause secondary damage but alone = no effect
rare = antibodies against TSH receptors block effect of TSH

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47
Q

what causes predisposition to autoimmune thyroid disease

A
  1. female
  2. HDL-DR3 and other immunoregulatory genes
  3. environmental factors = stress
  4. high iodine intake
  5. smoking
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48
Q

what autoimmune disease are related to autoimmune thyroid disease

A 
type 1 diabetes
Addisons disease
vitiligo
coeliac disease
pernicious anaemia
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49
Q

what is hyperthyroidism

A

abnormally high T4 and T3 levels

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50
Q

what are the main pituitary mass legions (?)

A

craniopharyngioma
rathke’s cysts
meningioma
lymphocytic hypophysitis

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51
Q

what are the definitive signs of puberty

A 
females = menarche, breast bud presence (depend on oestrogen)
males = first ejaculation, testes over 3mL large
52
Q

what are the female secondary sexual characteristics

A

breast/genitalia growth

pubic/auxiliary hair growth

53
Q

what are the male secondary sexual characteristics

A

external genitalia/auxiliary hair growth

larynx/laryngeal enlargement

54
Q

what is thelarche

A 
breast development = first visible change of puberty
induced by oestrogen = 
ductal proliferation
site specific adipose deposition
enlargement of areola and nipple
55
Q

what is adrenarche

A

developmental process where specialised subset of cells arise forming the zona reticulata
occurs at 2/3 end at 9/10
caused by increased in DHEA and DHEA-s

56
Q

what is pubarche

A

most pronounced clinical result of adrenarche

= appearance of pubic hair

57
Q

what are the indications for late puberty in women

A

lack of breast development by 13
more than 5 years between breast development and menarche
lack of pubic hair by 14
absent menarche by 15-16

58
Q

what are the indications for late puberty in men

A

lack of testicular enlargement by 14
lack of pubic hair by 15
more than 5 years to complete genital enlargement

59
Q

what are the hormone levels in a male with primary hypogonadism

A

raised LH/FSH

low testosterone

60
Q

what is the effect of anabolic steroid use in men

A

low testosterone and suppressed LH

61
Q

what are the hormone levels in primary ovarian failure in women

A

high LH and FSH
FSH is greater than LH
low oestrogen

62
Q

what are the effects of metformin on glucose control

A
  1. increase peripheral insulin sensitivity (?)
  2. increased glucose uptake and use by skeletal muscle
  3. decreased hepatic gluconeogenesis
  4. decreased intestinal glucose absorption
63
Q

what are the side effects of metformin

A 
GI disturbances
nausea
vomiting
lactic acidosis
weight neutral or loss
64
Q

describe the action of sulphonylureas E.G. GLICLAZIDE

A

block potassium channels on pancreatic beta cells = stimulating insulin secretion

65
Q

what are the side effects of sulphonylureas

A

GI disturbances
hypoglyceamia
weight gain

66
Q

describe the action of a DPP4 inhibitor

A

DPP4 = enzyme in vascular endothelial lining which INactivates incretin hormones = DPP4 inhibitor = competitive agonist of DP44 enzyme = result in enhanced incretin effect= more insulin secreted

67
Q

what are the side effects of DPP4 inhibitors

A

GI disturbances

acute pancreatitis

68
Q

describe the action of a GLP-1 receptor agonist

A

GLP1 agonists activate GLP1
GLP1 acts to increase concentration of incretin
also cause delay in gastric emptying

69
Q

what are the side effects of GLP1 agonists

A 
GRUPH
GI disturbances
Respiratory tract infection
UTI
Peripheral oedema
Hepatotoxicity
70
Q

describe the action of thiazolidinediones (TZD) e.g. pioglitazone

A

acts to increase bodies response to own insulin

act to decrease glucose and FFA levels

71
Q

what are the side effects of TZDs

A

weight gain
hypoglycaemia (low risk though)
heptatomegaly
fracture risk

72
Q

describe the action of SGLT2 inhibitors

A

act to inhibit SGLT2 transporter
prevents glucose reabsorption in the PCT of the nephron
= results in increased glucose loss in urine = decrease blood glucose levels

73
Q

what is bariatric surgery

A

acts to decrease stomach size or bypass sections to promote weight loss

74
Q

where is leptin expressed most

A

in white fat cells

75
Q

what is the role of leptin

A

switch off appetite + immunostimulation

lack of leptin = constant appetite

76
Q

what is peptide YY

A

secreted by neuroendocrine cells in the ileum/pancreas/colon in response to food
hormone that binds to neuropeptide Y (NPY) receptor
inhibit gastric motility and therefore reduce appetite

77
Q

what is the role of cholycystokinin CCK in appetite

A

released in response to meal and increased duodenal pH
delays gastric emptying
cause gall bladder contraction
stimulates insulin secretion
stimulates vagus nerve = feeling of satiety

78
Q

what secretes CCK

A

secreted by enteroendocrine cells in the duodenum

79
Q

what is the role of ghrelin

A

cause an increased in growth hormone release
stimulates appetite
increases food intake
promotes fat storage

80
Q

what produces ghrelin

A

stomach

81
Q

name 3 hormones/receptors that suppress your appetite

A

leptin
peptide YY
CCK

82
Q

name a hormone that stimulates appetite

A

ghrelin

83
Q

what is the role of incretins

A

augment insulin secretion from beta cells
(some) inhibit glucagon release from alpha cells
= decrease blood glucose levels
DPP4 = inactivates incretins

84
Q

how does hyperglycaemia stimulate insulin secretion (in 4 steps)

A
  1. hyperglycaemia leads to increase glucose uptake in cells
  2. glucose metabolism = increase ATP = K+ channels close
  3. causes depolarisation of cell membrane = Ca2+ channels open and Ca2+ enter
  4. increased Ca2+ in cell = exocytosis of insulin vesicles
    = insulin released by pancreatic beta cells
85
Q

describe short acting soluble insulins

A

start working within 30-60mins

last for 4-6 hrs

86
Q

describe short acting insulin analogues

A

faster onset and shorter duration of action than soluble

routinely used in DMT1

87
Q

describe longer acting insulin

A

insulin + protamine/zinc
intermediate lasting 12-24hrs
long acting lasting >24hrs

88
Q

when should you avoid doing an HbA1c test

A

type 1 DM
pregnant
children
haemoglobinopathies

89
Q

what is used to treat hypothyroidism

A

levo-thyroxine lifelong treatment

aim = TSH levels >0.5

90
Q

what is used to treat hyperthyroidism

A
  1. betablockers for rapid attacks/tachycardia
  2. carbimazole = antithyroid drug = blocks T3/T4 synthesis (may need levothyroxine to replace lost T3/4)
  3. radioiodine therapy = shrink thryoid gland + decrease number of T3/4 producing cells
    * radioiodine = risk of hypothyroidism
91
Q

what drugs can cause hyperthyroidism/hyperthyroidism

A

amioderone
lithium (rare)
iodine
ipilimumab

92
Q

what 3 things characterise diabetic ketoacidosis DKA

A
  1. hyperglycaemia
  2. raised plasma ketones
  3. metabolic acidosis
93
Q

what investigations are done in DKA

A
  1. blood glucose test >11.0mmol/L
  2. blood ketones = finger prick near patient test
  3. blood pH/carbonate = acidaemia
  4. urine dipstick = heavy glycosuria and ketonuria
  5. Cr and Urea high due to dehydration
94
Q

how is DKA managed

A

fluids
IV insulin - 6 units per hr starting dose
electrolytes (K+)

95
Q

what is hyperglycaemic hyperosmolar state

A
  1. marked hyperglycaemia
  2. hyperosmolality
  3. milds/no ketosis
    most common cause is INFECTION (particularly pneumonia)
    = dehydration
    = decreased consciousness
    = polyuria
96
Q

how is hyperglycaemic hyperosmolar state managed

A

same as for DKA
fluids
insulin 3 units/hour, only if severe
LMWH because hyperosmolality causes blood viscosity to increase = clots, MI, stroke

97
Q

what is a thyroid storm

A 
rare/life-threatening = rapid deterioration of thyrotoxicosis
high fever
tachycardia
extreme restlessness
delirium/coma/death
98
Q

how is a thryoid storm managed

A
  1. propranolol
  2. large doses of carbimazole
  3. potassium iodide = block release of T3/4 from gland
  4. hydrocortisone = inhibit conversion of T4 to T3
99
Q

whats the most common cause of hyperthryoidism

A

graves disease

100
Q

what does IGF1 do

A

stimulate growth by protein synth
increase lipolysis
stimulate hypertrophy and hyperplasia of bone, skeletal muscle
decrease blood glucose

101
Q

symptoms of cushings

A 
Cataracts
Ulcers
Striae
Hypertension and hyperglycaemia
Increase risk infection
Necrosis
Glucosuria
102
Q

what is the first line treatment for acromegaly

A

transphenoidal surgical resection to remove adenoma from pituitary

103
Q

describe the ECG features in hypokalaemia

A

U have no Pot (K+) and no Tea but a long PR and a long QT

  • flat T waves
  • ST depression
  • long PR and QT
  • pathological U waves
104
Q

describe the Tx fro Conns syndrome

A

laproscopic adrenalectomy

aldosterone antagonist = spironolactone

105
Q

what is the commonest cause of primary adrenal insufficiency (addisons) worldwide and in UK

A 
UK = addisons
worldwide = TB
106
Q

what is the Tx for adrenal insufficiency (addisons)

A 
glucocorticoids = hydrocortisone/prednisolone
mineralocorticoids = fludrocortisone
107
Q

describe the pathophysiology of SIADH

A

too much ADH = insertion aquaporin 2 = water retention = blood dilution = hyponatraemia
too much ADH = decreased RAAS-aldosterone = secretion of Na+ = excess water removed WITH Na+ =
hyponatraemia with NORMOVOLAEMIA

108
Q

what drug is used in the Tx of SIADH

A

demeclocycline = inhibit action of ADH on kidney

109
Q

what drugs can cause hyperkalaemia

A 
NSAIDs
ACEi = block aldosterone binding
spironolactone
ciclosporin
heparin
110
Q

what is the blood plasma value for hyperkalaemic and hypokalaemic

A

over 5.5mmol/L
emergency = over 6.5mmol/L
under 3.5mmol/L
emergency = under 2.5mmol/L

111
Q

what is the blood plasma values for hypercalcaemia and hypocalcaemia

A

> 2.6mmpl/L on 2 or more occasions

<2.1mmol/L

112
Q

what is chvosteks sign and what condition would you see it in

A

tapping over facial nerve in parotid gland region = ipsilateral twitch
= hypocalcaemia

113
Q

what is trousseaus sign and what condition would you see it in

A

carpopedal spasm induced by inflation of BP cuff to 20 above systolic
= hypocalcaemia

114
Q

what ECG changes would you see in hyper and hypocalcaemia

A 
hyper = short QT, tented T
hypo = long QT
115
Q

how to work out plasma osmolality

A

(Na x 2) + glucose + urea

116
Q

what antibodies are present in DMT1

A

anti-GAD
pancreatic islet autoantibodies
islet antigen 2 antibodies

117
Q

what drugs are used to lower cortisol

A

metyrapone

ketoconazole

118
Q

what disease causes bulging eyes and why

A

graves disease

swelling and oedema of extra-occular muscles

119
Q

what is kallmans syndrome

A

decreased GnRH causes anaemia
genetic
failure to start or finish puberty

120
Q

what is a pheochromocytoma

A

catecholamine secreting tumour = adrenaline
diagnosed by blood conc of hormones
treat with surgery and alpha blocker then beta blocker

121
Q

what is a prolactinoma

A

prolactin secreting tumour
cause headaches + period changes
check prolactin levels
treat with dopamine agonists (cabergoline)

122
Q

what is hyperparathyroidism

A 
increase PTH
caused by parathyroid adenoma/hyperplasia
primary secondary or tertiary 
bones, groans, stones, psychic moans
primary = high Ca
secondary = low Ca
treat by surgical removal of cancer
calcium correction
treat underlying 
possible bisphosphonates for osteoporosis
123
Q

name a calcium mimetic

A

cinacalcet

124
Q

what is hypoparathyroidism

A

low PTH = rare
symptoms same as hypocalcaemia (chovstek + trousseau)
high phosphate and low calcium
treat with IV calcium + vitamin D analogue

125
Q

name a vitamin D analogue

A

alfacalcidol

126
Q

what is a carcinoid tumour

A

seratonin secreting tumour
pain/weight loss/palpable mass
causes carcinoid syndrome
diagnose with serum 5-Hydroxyindoleacetic acid (seratonin bkd/n product) + liver ultrasound
treat with somatostatin analogue = octreotide

Phase 2a (15 decks)

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