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Phase 2a > Encodrine > Flashcards

Encodrine Flashcards

1
Q

two types of hormones?
difference in cell interactions?
examples?

A

water soluble and fat soluble
water - bind to surface - peptides
fat - diffuse into cell - thyroid hormone

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2
Q

hormones classes?

A

peptides
amines
iodothyronine
cholesterol deriavtives and steroids

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3
Q

where do fat soluble binds to?

A

cytoplasm or nucleus

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4
Q

method of travel for adrenocortical and gonadal steroids?

A

95% protein bound

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5
Q

fate of progesterone in testes or adrenals?

A

adrenals - cortisol
testes - androstenedione - testosterone
ovaries - estrodione

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6
Q

control of hormone action?

A

hormone metabolism - increased metabolism to reduce fundtion
hormone receptor induction
hormone receptor down regulation
synergism - combined effects of two hormones amplified - glucagon with spinepherine
antagosim

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7
Q

pititary growth problems signs

A

tumour mass effects - blindness
hormone excess - tumour producing excess prolactin, GH, TSH
Hormone deficiency - tumour destroys pituiatry tissues

request MRI

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8
Q

half life of T4 ?

A

5 TO 7 DAYS

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9
Q

half life of T3?

A

2 days

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10
Q

function of thryoid hormone?

A

growth rate accelerated
enhances fat metabolism
accelerates food metabolism
increases protien synthesis
increase ventilation rate

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11
Q

stimulation of renin

A

low sodium
drop of blood volume
drop in blood pressure

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12
Q

weight regulation dependant on?

A

envrioment and genes - homeostatic system
adipose tissue sends feedback

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13
Q

leptin?

A

satiety hormone
leptin receptor found in hypothalamus

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14
Q

MAIN ORGAN WHich regulates appetite in brain?

A

hypothalamus

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15
Q

hormones which increase/ decrease appetite in hypothalamus?

A

NPY/ AGRP - INCREASE appetite
POMC - decrease appetite

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16
Q

percentage of ingested glucose goes where?

A

40% to liver
60% to muscle

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17
Q

role of glucagon?

A

increase hepatic glucose output via
- gluconeogenesis
- glycogenolysis
reduced peripheral glucose uptake
stimulate peripheral release of gluconeogenic precursors (amino acids)
- lipolysis

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18
Q

how does diabetes cause morbidity and mortality?

A

causes
diabetic ketoacidosis
hyperosmolar hyperglycaemic state
macrovascualr and microvascular tissue complications
- retinppathy (loss of sight)
- diabetic neuropathy
- stroke
- CV

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19
Q

what other hormones are realeased when blood sugar is low?

A
  • GH
  • cortisol
  • adrenaline
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20
Q

types of diabetes

A

type 1
type 2
MODY - monogenic diabetes
pancreatic diabetes - pancreas stops working (damage from surgery)
endocrine diabetes - cushings syndrome
malnutrition diabetes

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21
Q

hyperosmolar hyperglycaemic state?

A

hyperglycemia but no acidosis
- still enough insulin to prevent lipolysis - excessive production of ketones - no acidosis

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22
Q

why is HBA1C levels used?

A

long term trend of blood sugar
glucose attaches to RBC which have lifespan of 3 months

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23
Q

describe the ideal drug to treat T2 diabetes

A

-reduce appetite and induce weight loss
- preserve beta cells and insulin secretion
- increase insulin secretion at meal times
- inhibit counterregulatory hormones
- not increase rick of hypoglycemia

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24
Q

role of GLP - 1

A

stimulates insulin secretion
reduces appeptite
slows gastric emptying

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25
Q

what counteracts glp -1

A

DPP 4

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26
Q

role of SGLT 2 inhibitors

A

lock reabsorption of glucose in kidnets increasing glucose excretion in urine
lowering blood glucose levels

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27
Q

why does obesity cause T2D?

A

obesity impairs insulin action
excessive adipose issue causes insulin resistance

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28
Q

benefits and risk of tight glucose control?

A

reduces risk of retinopathy but increase risk of hypoglycaemia

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29
Q

basal vs bolus insulin?

A

bolus - quick acting taken before meals
basal - long acting

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30
Q

insulin treatment of T1DM ?

A

pre meal - bolus
adjusted to what is in the meal
between meals and at night - basal
aim to maintain blood sugar between 4-7 mmol/l

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31
Q

levels of hypoglycaemia?

A

level 1 - <3.9 mmol/l - no symptoms
level 2 - <3mmol/l
level 3 - require third party help

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32
Q

what other factors can cause hypoglycaemia?

A

sleep and exercise

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33
Q

impaired awareness of hypoglycaemia?

A

excessive drops in blood glucose - brain stops responding
no symptoms but dangerously low blood sugar

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34
Q

third line of defense for diabetics when blood sugar low?

A

adrenaline
because no insulin and no glucagon storage left

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35
Q

Acromegaly vs gigantism ?

A

Gigantism - excessive GH during childhood and dont go through puberty
Acromegaly - excessive GH from tumour during adulthood

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36
Q

why is a pelvic ultrasound done on pubertal patients?

A
  • mullerian structures present?
  • morphology of uterus
  • morphology of ovaries
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37
Q

maturation of external geniltalia under oestrogens?

A
  • labia majora and minora increase in size
  • rugation and change in color of labia majora
  • Hymen thickens
  • clitoris enlarges
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38
Q

what causes oubic hair in girls?

A

adrenal and ovarian androgens

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39
Q

precocious psuedopuberty?

A

signs of puberty - release of adrenal sex hormones
so low LH and FSH

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40
Q

how many effected with turner syndrome?

A

1 in 2000 girls

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41
Q

otitis media

A

inflammatory infection of middle ear

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42
Q

results FROM primary and secondary hyperthyroidism investogations

A

TFTs:
Primary (negative feedback) – low TSH, high T3/T4
Secondary – high TSH, high T3/T4

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43
Q

antibodies only present in graves disease?

A

TSH receptor antibody (TRAb) – Graves only

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44
Q

signs of drug induced hyperthyroidism?

A

only thyroid hormones is raised

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45
Q

treatment of hyperthyroidism?

A

beta blocker - decreases SNS activation
1st line: Carbimazole – anti-thyroid drug
- Blocks thyroid hormone synthesis
radioiodine - damages hyperplasia thyroid cells
thyroidectomy

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46
Q

complication of hyperthyroidism?

A

thyroid storm - thyroidtoxicty - too much t4
coma, AF, delirium and death
osteoporosis
elphantisis

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47
Q

describe autoimmune thyroiditis causing hypothyroidism?

A

hashimoto thyroiditis
antithyroid autoantibodies (anti tpo antibodies and anti thyroglobulin) cause atrophy of thyroid follicles
CD8 mediated - induce apoptosis

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48
Q

how does amiodarone cause hyper or hypo thyroidism ?

A

Amiodarone
Can cause hyperthyroidism due to high iodine
Can cause hypothyroidism as it inhibits the conversion of T4 to T3

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49
Q

acromegaly def?
gigantism def?

A
  • excessive production of growth hormone occurring in adults after fusion of the epiphyseal plates
  • excessive production of growth hormone occurring in children before fusion of the epiphyses of long bones
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50
Q

what can increase GH secretion?

A

low blood glucose
increased sleep
increased excercise
lack of food
increased stress like trauma

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51
Q

methods limiting gh release?

A
  • increase in GHRH signals hypothalamus to stop producing GH
  • GH causes somatomedins released - ant pit stop producing GH
  • GH signal hypothalamus to produce somatostatin to ant pit to stop GH release
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52
Q

direct effect of GH ?
indirect effect?

A

organ growth
increase in insulin resistance - high blood insulin

IGF-1 IS PRODUCED
increased cellular metaboism

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53
Q

role of dopa mine in prolactin release?

A

overrides thyrotropin releasing hormone which stimulates releases of prolactin
inhibits prolactin release

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54
Q

effect of high levels of prolactin?

A

increase dopamin - inhibits further prolactin release
inhibits release of gonadotropin (grh)

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55
Q

aetiology of prolactinoma?

A

benign adenoma of the pituitary gland producing prolactin
functioning tumour

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56
Q

which part of the kidneys is not under control by pituitary gland?

A

adrenal medulla

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57
Q

where is testosterone mainly produced?

A

In the testicles

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58
Q

WHATS another name for ADH?

A

AVP - arigine vasopressin

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59
Q

main regulation of calcium metabolism

A

parathyroid gand

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60
Q

where is avp produced?

A

hypothalamus because release from post pituitary - post pituitary doesnt synthesize anything

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61
Q

ROLE OF GROWth hormone on which cells and organs and what effect do they have

A
  • liver - gluconeogenesis
    IGF1 synthesised in liver from gh
  • fat cell - lipolysis
  • skeletal muscle - increased amino acid uptake / protein synthesis
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62
Q

receptor for GH

A

growth hormone receptor - enzyme linked receptor

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63
Q

symptoms of excess GH secretion

A

polyuria
sweating
joint pain
headaches
swollen hands n feet

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64
Q

role of DHEA?

A

DHEA (adrostenedione) converted to testosterone

65
Q

hormes secreted in circadian rythems?

A

ACTH
GH
prolactin
cortisol - androgens (TESTOSTERONE)
TSH

66
Q

does t4 follow circadian rythem ?

A

no - but cortisol do follow circadian rhythms
(testosterone, DHEA 17OH progesterone )

67
Q

cortisol defiency features include?

A

HYPOTension
weight loss
muscle aches
lethargy

68
Q

features of hypothyroidism ?

A

weight gain
constipation
menorhagia

69
Q

Which test would you likely want to perform in
a patient with proximal muscle weakness,
purple striae and thin skin?

A

Overnight
dexamethasone - measuring cortisol
suppression test

70
Q

oilgomennorhea vs ammenorhea ?

A

oligomennorhea - infregqient periods
ammenorhea - no periods

71
Q

A 24 year old girl presented with hirsutism,
oligomenorrhoea and acne. What test would you
likely carry out from the ones below?

A

Ultra sound ovaries

72
Q

A 54 year old gentleman presented with
hyponatraemia.what is a definitive presentation of hyponatreamia caused by SIADH?

A

euvolemia with hyponatremia

73
Q

Essential criteria for the diagnosis of
SIADH

A
  • Hyponatraemia < 135 mmol/L
  • Plasma hypo-osmolality < 275 mOsm/Kg
  • Urine osmolality > 100 mOsm/Kg
  • Clinical euvolaemia
  • No clinical signs of hypovolaemia (orthostatic decreases in blood pressure,
    tachycardia, decreased skin turgor, dry mucous membranes)
  • No clinical signs of hypervolaemia (oedema, ascites)
  • Increased urinary sodium excretion > 30 mmol/L with normal salt and
    water intake
74
Q

causes of SIADH ?

A

Lung abscess
Subdural
haemorrhage
Lymphoma
Cerebrovascular
accident
carcinoma
DRUGS:
C- chemo
A - antidepressants - SSRIs
R- recreational drugs MDMA
D- diuretics
I- inhibitors - ace inhibitors
S- sulfonylurea
H - Hormones

75
Q

hormones that suppress appetite

A

cck
peptide YY
GLP1
glucose

76
Q

The main adipose signal to the brain
is

A

leptin

77
Q

A 65 year old lady is diagnosed with SIADH.
Her sodium is 123mmol/l. What is your first
line of management?

A

asympomatic - will treat with fluid
restriction

78
Q

A patient with Addison’s disease
presents with a chest infection. What
do you do?

A

double steroids

79
Q

tests are typical of
secondary hypogonadism

A

low lh low testosterone

80
Q

Typical features of hypogonadism in a
male include

A

decreased sexual drive
joints and muscular aches
decreased hair growth

81
Q

A patient has a noon testosterone level
below the normal range. What will you
do?

A

Repeat the test at
0900h and check for
symptoms

82
Q

satiety def

A

The physiological
feeling of no hunger

83
Q

commonest cause of primary adrenal defiency ?

A

Worldwide - Adrenal TB
UK - ADDISONS disease (adrenalitis)

84
Q

plasma ACTH in levels in primary adrenal insuffcency or secondary?

A

primary - HIGH ACTH with low or normal cortisol confirms primary hypoadrenalism
secondary/ tertiary - LOW ACTH and cortisol indicate secondary or tertiary hypoadrenalism

85
Q

Differential Diagnosis between primary and secondary hyperalodsteronism?

A

primary - adrenal adenoma
secondary - arises when there is excess renin (and hence angiotensin II) which stimulates aldosterone release

86
Q

ECG of hypokalemia ?

A

prolong PR interval
ST depression
shallow t wave
PROMINENT U WAVE
U have no Pot (K+) and no Tea but a Long PR and a Long QT

87
Q

neuroendocrine tumour normally found?

A

GI tract lining most common
lungs
pancreas
liver - common metaizing point
ocaires

88
Q

why flushing in carcinoid syndrome?

A

increase histamine and bradykinin - increased vasodilation

89
Q

effect of increased seratonin in carcinoid syndrome?

A

fibrosis of heart due to excess fibroblast production
broncho constriction
impaired kidney function due to fibrosis
increased gastric motility - diarrhoea

90
Q

test for cushings disease?

A

24 hour urinary free cortisol tests for Cushing’s Disease
cortisol produce in zona fasciculata of adrenal cortex

91
Q

treatement of hypoglycaemia?

A

IV glucagon or IV dextrose

92
Q

Reloationship of glucagon and somatostatin and cortisol?

A

Somatostatin, also known as growth hormone-inhibiting hormone, is produced in the pancreas and inhibits the secretion of insulin and glucagon. Glucagon increases the secretion of somatostatin via the feedback mechanism

Glucagon is known to stimulate ACTH-induced cortisol release.

93
Q

Kallmann’s syndrome hormone levels?

A

low lh, fsh and low testosterone

94
Q

kallmans syndrome presentation?

A

combination of anosmia and cleft palate along with the blood tests suggesting hypogonadotropic hypogonadism points
to kallmans

small testicles

95
Q

medications which increase rick for osteoporosis fractures?

A

Long-term, systemic corticosteroids such as prednislone

96
Q

acronym for appetite regulating hormones?

A

Leptin lowers appetite
Ghrelin Grows appetite

97
Q

role of glicazide?

A

is a sulphonylurea, and it’s main mechanism of action is through stimulating the sulphonylurea-1 receptors on the pancreatic cells to stimulate insulin production.

98
Q

tumour which may cause breast growth in men ?

A

Testicular (e.g. seminoma secreting hCG) may cause gynaecomastia -produces oestrogen

99
Q

metformin drug class?

A

biguanide

100
Q

how does metformin work?

A

INHIBITS gluconeogenesis
Increases insulin sensitivity (GLUT 4)

101
Q

how is metformin excreted in kidneys ?

A

excreted unchanged in urine
doesnt bind to plasma proteins

102
Q

why are SGLT-2 inhibitors used?

A

weight loss and diabetes
inhibit inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule

glucose in excreted instead of being reabsorped

103
Q

role of Sulfonylurea

A

increase insulin production
bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells
block these channels

104
Q

which part of nephron do loop diuretics and thiazides effect?

Effect on potassium?

A

loop diuretics - loop of henle
thiazides - distal tubule

more sodium in collecting ducts
more sodium reabsorbed into principal cells and therefor potassium (from principle cell) released into collecting duct to neutralise all the positive sodium in principle cell.

105
Q

role of corticosteroids with diabetes? example?

A

they have antiinsulin effects so difficult to maintain blood sugar levels
prednisolone

106
Q

essential step for production of steroid hormones? where does this occur?

A

cholesterol to pregnenolone
Pregnenolone is the precursor for all steroid hormone
occurs within mitochondira

107
Q

primary causes of hyporthyroidism?

A

autoimmune - hashimotos thyroiditis
thyroid cell destruction
- reduced t4/ t4 production
- loss of negative feedback inhibition
- increased TSH from ant pit gland
iodine deficiency
thyroidectomy

108
Q

t2dm medication that can cause hypoglycaemia?

A

gliclazide - sulphonylurea stimulates insulin release from pancreatic B cells

109
Q

first line treatment for prolactinoma

A

dopamine agonists

110
Q

electroabnormality from thyroidectomy?

A

hypocalcaemia
thyroid release calcitonin to inhibit osteoclasts - so calcium reabsorption is decreased in bone and kidneys

111
Q

symptoms of t1 dm?

A

weight loss
fatigue
polyruia
polydypsia

112
Q

long term microvascular complication of diabetes?

A

nephropathy
neuropathy
retinopathy

113
Q

tx for dka

A

iv fluids
insulin

114
Q

symptoms for thyrotoxicosis?

A

frequent bowel movement
anxiety
weight loss
increased sweating

115
Q

tft with thyrotoxicosis?

A

high t4/t3
low tsh

116
Q

aeitology of graves disease?

A

autoimmune condition - antibodies bind to TSH receptors in thyroid gland - stimulates production of t4/t3

117
Q

antithyroid medication for graves?

A

carbimazole - 1st line
inhibits synthesis of t4/t3

118
Q

cause of hypoparathyroidism?

A

Autoimmune destruction of parathyroid glands – Di-George syndrome
Vitamin D deficiency - results in less Ca2+
Can cause mild and occasionally severe hypocalcaemia and osteomalacia
Congenital
Parathyroidectomy (secondary)
Magnesium deficiency

119
Q

Chvostek’s sign
Trousseau’s sign

A

Chvostek’s sign - face twitches when touches mandible

Trousseau’s sign - swan formation of hands when blood pressure cuff applied

sign of hypocalceamia

120
Q

signs and symptoms of hypocalceamia and hypopth? mnemoic?

A

SPASMODIC
Spasms – carpopedal spasms = trousseau’s sign
Perioral paraesthesia (around mouth)
Anxious, irritable, irritational
Seizures
Muscle tone increases
Orientation impaired and confusion
Dermatitis
Impetigo herpetiformis – psoriatic pustules
Chvostek’s sign, cataracts, cardiomyopathy

121
Q

tx for hypoparathyroidism?

A

Calcium supplement
Calcitriol (active vitamin D)
Synthetic PTH

122
Q

tx for polymyalgia rheumatia vs GCA?

A

corticosteroids immediatly for GCA to prevent visual loss - prednisolone 60-80mg
lower dose prednisolone 15- 30 mg
aim to reduce over time
oral bisphosphinates in both to prevent osteoporosis?

123
Q

ix for polymaylgia rheumatica?

A

The most indicative investigations are ESR and CRP. The ESR can be markedly raised (>60mm/hr)

The essential investigations are:

FBC
Urea and electrolytes
LFTs
Bone profile
Protein electrophoresis
Thyroid function tests
Creatinine kinase
Rheumatoid factor
Urinalysis

124
Q

ddx polymyalgia rheumatica vs myotisis?

A

Myositis causes bilateral proximal muscle weakness, while pain is either absent or mild.

In polymyalgia rheumatica, bilateral pain and stiffness are prominent, but there should not be muscle weakness on examination (though this may be difficult to confirm as movements may be limited by pain.)

125
Q

Via which mechanism can polyarteritis nodosa cause life-threatening haemorrhage?

A

aneurysms

126
Q

example or hormones using cAMP messaing?

A

ACTH -
calicotonin
epinehprine
gulcagon
pth
ADH

127
Q

tx 1st line and gold standard for prolactinomas?

A

1st line - dopamine angonist - bromocriptine
gold standard - transphnoidal removal of pit tumour

128
Q

ix for pit prolactinoma?

A

mri of head of pituitray tumour

129
Q

how to avoid adrenal crisis during surgery of pheachromocytochromia ?

A

alpha recetpro inhibitor
Give phentolamine (an Alpha receptor blocker)

130
Q

hba1c?

A

Glycated haemoglobin, a form of haemoglobin that is measured to identify the three- month average plasma glucose concentration- accept glycated haemoglobin.

131
Q

apart from metformin name 4 other classes of dm drugs?

A
  • SGLT-2 inhibitor
  • Sulfonylurea e.g. gliclazide
  • glitazone e.g. pioglitazone
  • DPP-4 inhibitor
132
Q

hormone decreased in conns syndrome?

A

renin released from the kidneys

133
Q

tx for hyperalodosteronism?

A

potasssium sparing diuretics
- spirolactinone
surigcal removal of tumour

134
Q

genetic mutation for phaeochromocytoma?

A

MEN 2A or MEN 2B

135
Q

carcinoid tumour? cp?

A

neuroendocrine tumour
SOB
diarhoea
flushing
itching

136
Q

State 3 types of cancers that can cause SIADH.

A

SMAL CELL CARCINOMA OF THE LUNG
PANCREATIC CANCER
PROSTATE CANCER!!

137
Q

ecg of hyperkaleamia?

A

PROLONGED pr interval
flattened p waves
tall t waves
wide QRS
bradycardia

138
Q

symptoms of hyperkealmia?

A

Mmuscle wekaness
U rinary disturbance - little to none
R esp distress
ECG changes
Reflexes- hyperflexive
dysnopnea

139
Q

first line ix for acromegaly ?

A

IGF - 1

140
Q

first line ix for acromegaly?

A

Transsphenoidal resection of the pituitary adenoma

141
Q

second line tx for acromegalY?

A

gh antagonist GH antagonists: Pegvisomant

142
Q

ROLE OF PTH?

A
  • PTH increases bone remodelling and turnover. PTH stimulates osteoclasts to reabsorb bone mineral
    which liberate calcium into blood (breaks down bone).
  • PTH increases the amount of calcium reabsorbed in the kidney which means that less is excreted in
    urine.
  • PTH decreases phosphate reabsorption in the kidney.
  • PTH decreases phosphate reabsorption in the kidney, increasing the amount excreted.
  • PTH increases absorption of Ca2+ in the gut.
    *1,25 (oh)2D3 formation in the kidneys = increases Ca2+ in gut
143
Q

signs of hypocalcemia?

A

Chvostek’s sign - tap over the facial nerve causes spasm of the facial muscles
Trousseau’s sign - inflate the blood pressure cuff to 20mmHg above systolic for 5 minutes and the
hand should form a claw.

144
Q

mech of carbimazole?

A

blocks thyroid perixodase and inhibits iodinsation of tyrosine

145
Q

causes of hyperkaleamia ?

A

NSAIDS
AKI
Addisons
DKA
Spirolactone

146
Q

tx for hyperkaleamia?

A

calcium glutonate - emergency
1st line non urgent - insulin and dextrose

147
Q

cp of hypokaleamia?

A
148
Q

An 81 year old man faints at a party but recovers after a few seconds. He sees his
General Practitioner a few days later and informs her that he has had two further
episodes of dizziness since the party. The doctor finds his blood pressure to be
160/80 mmHg. He has a strong regular pulse at a rate of 30 beats per minute.
An ECG shows regular but broad QRS complexes at a rate of 32 per minute. P
waves are also visible, again regular but at the faster rate of 75 per minute, and
without any discernible relationship between the timing of P waves and QRS
complexes.
Which is the most likely cause of the patient’s symptoms?

A

3rd degree av block complete!
P wave at own rate and QRS at different rates!

149
Q

line of tx for t2dm?

A

1st line metformin
2nd line SGLT 2 inhibitors -
CanagliFLOZIN, dapagliFLOZIN
3rd line sulfonyureas - gliclazide
or DPP4 INHIBITORS - gliptans SITAGLIPTAN
or pioglitazone

150
Q

SIDE EFFECTS of SGLT2 INHIBITORS

A

CANAGLIFLOZIN
UTI due to high sugar in urinary tract
constipation; dyslipidaemia; hypoglycaemia (in combination with insulin or sulfonylurea); increased risk of infection; nausea; thirst; urinary disorders; urosepsis

151
Q

side effects of pioglitazone?

A

weight gain, fluid
retention, liver dysfunction and fractures

152
Q

side effcts of DPP4 inhibitors?

A

DPP4 INHIBITORS
headache + pancreatitis + constipation
NO WEIGHT GAIN!

153
Q

tx for DI?

A

1st line - desmopressin
2nd line - thiazide diuretics

154
Q

features of secondary syphilis ?

A

rash on soles and palms and chest
There is also lymphadenopathy and ulcers present on the mucous membranes. Other less common features include malaise and fever

155
Q

cause of peripheral neuropathy in isonizid?

A

B6 depletion so b6 supplements should be taken

156
Q

CP of rheumatic fever?

A

choreatic movements and complains of pain in her left wrist and right ankle. She is tachycardic and pyrexial.
previous sore throat

157
Q

karposi sarcoma?

A

large purple macular rashes - sign of AIDS

158
Q

first line tx for bacterial meningitis?

A

benzylpenicillin

Phase 2a (9 decks)

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