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Phase 2b > Endocrine revision > Flashcards

Endocrine revision Flashcards

1
Q

what hormones are released from the hypothalamus

A

thyrotropin releasing hormone
dopamine
growth hormone releasing hormone
somatostatin
gonadotrophin releasing hormone
corticotropin releasing hormone
oxytocin
vasopressin

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2
Q

what hormones are released from the anterior pituitary

A

FSH + LH
adrenocorticotrophic hormone
TSH
GH
prolactin

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3
Q

what does GHRH stimulate

A

LH and FSH

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4
Q

what does CTRH stimulate

A

ACTH

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5
Q

what does GHRH stimulate

A

growth hormone

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6
Q

what does TRH stimulate

A

thyroid stimulating hormone

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7
Q

what does dopamine do

A

inhibits prolactin

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8
Q

where does FSH and LH act

A

gonads for germ cell development and hormone secretion

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9
Q

where does TSH act

A

throid to stimulate T3 and T4

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10
Q

where does GH act

A

on cells to control metabolism and growth by stimulating IGF-1 production

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11
Q

where does prolactin act

A

breast tissue/milk ducts to stimulate milk production

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12
Q

what cells does FSH act on

A

sertoli to secrete anti-mullerian hormone
stimulate oestrogen

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13
Q

what cells does LH act on

A

leydig for testosterone production
stimulates progesterone

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14
Q

what can a pituitary tumour result in

A

pressure on local structures (optic chiasm) resulting in bitemporal hemianopia
hypopituitarism
hyperpituitarism (acromegaly, cushings disease, prolactinoma)

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15
Q

how much glucose is used a day

A

200g/day

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16
Q

how much glucose comes from liver

A

90%

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17
Q

what is the major consumer of glucose

A

brain

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18
Q

why is the brain the major consumer of glucose

A

as it cannot use FFA

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19
Q

is the brain insulin dependent

A

no

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20
Q

what chromosome is insulin coded for on

A

chromosome 11

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21
Q

when is muscle/fat insulin dependent

A

in postprandial state

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22
Q

what is the goal of insulin

A

reduce blood glucose

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23
Q

how does insulin affect muscle

A

results in glycogen and protein synthesis

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24
Q

how does insulin affect fat

A

causes fatty acid synthesis

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25
Q

describe the biphasic response of insulin

A

1) blood glucose is increased and insulin stored in B-cells is released to increase peripheral uptake of glucose (=>glycogen)

2) glucose has not decreased enough more insulin is made and secreted, but is a lot slower

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26
Q

what is the goal of glucagon

A

to increase glucose

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27
Q

what is a marker for natural insulin release in the body

A

C-peptide

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28
Q

do you get C-peptide in synthetic insulin

A

no

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29
Q

what is the started molecule for insulin

A

proinsulin

(made of a alpha and beta strand, connected by C-peptide)

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30
Q

what does a GLUT-1 receptor do

A

basal non-insulin stimulated glucose into cells

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31
Q

what does a GLUT-2 receptor do

A

found in B-cells and has a low affinity for glucose, so when it is in high concentrations a lot of glucose is uptaken and sensed and insulin is secreted

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32
Q

where are GLUT-2 receptors found

A

B-cells and renal tubules

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33
Q

what does a GLUT-3 receptor do

A

non-insulin mediated

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34
Q

where are GLUT-3 receptors found

A

brain neurones and placenta

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35
Q

whar does a GLUT-4 receptor do

A

peripheral action of insulin on muscle and adipose to cause glucose uptake

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36
Q

what chromosome is insulin receptor found on

A

chromosome 19

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37
Q

what happens when insulin binds to an insulin receptor

A

tyrosine kinase results in GLUT-4 expression on CSM

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38
Q

what hormones are released by the posterior pituitary

A

oxytocin - paraventricular nucleus
vasopression - supraorbital nucleus

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39
Q

what does oxytocin do

A

milk ejection
labour induction

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40
Q

what does vasopressin do

A

stimulates when BP drops, stress (major factor in RAAS)

vasoconstiction in BVs
increase Aquaporin 2 expression
increases aldosterone

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41
Q

what are the functions of cortisol

A

increase protein and carb breakdown
upregulates alpha 1 on arterioles and increased BP
suppress immune response
increase osteoclast activity = osteoporotic
increase insulin resistance

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42
Q

what are the layers of the adrenal gland

A

zona glomerulosa
zona fasciculata
zona reticularis
adrenal medulla

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43
Q

what is released from each region of the adrenal gland

A

glomerulosa - aldosterone
fasciculata - cortsiol
reticularis - androgens
medulla - NAd, ADr

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44
Q

what are the 4 types of diabetes

A

T1DM
T2DM
MODY
LODA

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45
Q

what is MODY

A

maturity onset diabetes of youth - a rare auto dom T2DM presentation in young patients

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46
Q

what is the treatment for MODY

A

sulfonyurea

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47
Q

what is LADA

A

latent onset of diabetes in adults - T1DM presents in an older patient

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48
Q

what are three secondary causes of diabetes

A

acromegaly and cushings
haemochromatosis
thiazides and corticosteroids

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49
Q

what is T1DM

A

a type 4 hypersensitivity reaction which causes the autoimmune destruction of pancreatic B-cells - an absolute insulin deficiency

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50
Q

what is the epidemiology of T1DM

A

young
thin
north European (Finland)

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51
Q

what are some risk factors for T1DM

A

HLA DR2 DQ3
HLA DR4 DQ8
other autoimmune disease
environmental infection (viral)

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52
Q

what is the patho of T1DM

A

autoimmune B islet destruction leading to absolute insulin deficiency - this results in hyperglycaemia and low cellular glucose which increases lipolysis and gluconeogenesis

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53
Q

what electrolyte disturbance do you get with uncontrolled T1DM

A

hyperkalaemia - insulin is not present to drive K+ into cells

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54
Q

symptoms of T1DM

A

lean young patient with
POLYDIPSIA
POLYURIA/NOCTURIA
WEIGHT LOSS
glycosuria

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55
Q

what initial tests are done for a diagnosis of T1DM

A

random plasma glucose
fasting plasma glucose (8+ hours not eating)

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56
Q

what better test is done to diagnose T1DM

A

HbA1C (taken within three months to see glycated Hb)

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57
Q

what is the normal ranges for RPG and FPG and HbA1C

A

RPG = < 11.1
FPG = < 7
HbA1C = < 48/6.5%

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58
Q

what is the diabetes ranges for FPG, RPG and HbA1C

A

RPG = > 11.1
FPG = > 7
HbA1C = > 48/6.5%

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59
Q

what is the oral glucose tolerance test

A

give 75g of fast acting glucose then measure BG 2hr later, if Bg > 11.1 = diagnostic

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60
Q

treatment for T1DM

A

basal bolus insulin

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61
Q

what is basal bolus insulin

A

basal = long acting - maintain stable insulin levels throughout day
bolus = faster acting - 30 minutes pre-prandial to give insulin spike

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62
Q

what are the 4 types of insulin with examples

A

rapid - novorapid, aspart
short - regular insulin
intermed - NPH
long - glargine, detemir

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63
Q

what is the main complication of T1DM

A

Diabetic ketoacidosis

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64
Q

what is the patho of T1DM

A

there is a decrease in insulin and glucose leaves the cells, which leaves them with no energy resulting in FA oxidation and gluconeogenesis which results in the formation of ketone bodies = acidic and decreased O2 Hb binding

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65
Q

symptoms of DKA

A

kussmaul breathing (deep laboured breaths to blow of CO2)
pear drop breath
reduced tissue turgor
hypotension
tachycardia

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66
Q

diagnosis of DKA

A

blood ketones - >3
hypeglycaemia - > 11.1
blood pH < 7.3 / HCO3- <15

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67
Q

treatment of DKA

A

1st fluids
insulin + glucose
potassium

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68
Q

what is T2DM

A

peripheral insulin resistance with partial insulin deficiency (CHO/lipid/beta amyloid deposits in pancreas)

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69
Q

what is the typical epidemiology of T2DM

A

later in life >30y/o
males
obese

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70
Q

RF for T2DM

A

genetic link (FHx)
smoking
obesity
HTN
sedentary lifestyle

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71
Q

what is T2DM a Rf for

A

HTN
silent MI
nephrotic syndrome
CKD

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72
Q

what is the patho of T2DM

A

peripheral insulin resistance (malfunctional insulin intracellular activation pathway) resulting in decreased GLUT4 expression

leading to hyperglycaemia with an increase in insulin demand from a depleted beta cell population

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73
Q

symtpoms of T2DM

A

obese
HTN
POLYDIPSIA
POLYURIA
GLYCOSURIA
+/- acanthosis nigracans

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74
Q

diagnosis of T2DM

A

same as T1DM

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75
Q

diagnosis of prediabetes

A

impaired glucose tolerance = normal FPG <6 + 2hr OGTT 7.8-11.1

impaired fasting glucose = FPG 6.1-6.9 + 2hr OGTT < 7.8

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76
Q

treatment for T2DM - prediabetic

A

prediabetic - lifestyle changes (diet and exercise and modify RF)

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77
Q

treatment for T2DM

A

1st - metformin
sulfonylurea
DPP4-i
SGLT-2 inhibitor
insulin

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78
Q

what is metformin

A

a biguanide that increases peripheral sensitivity to insulin

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79
Q

what is a sulfonylurea

A

gliclazide - increases amount of insulin your pancreas makes

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80
Q

DPP4-i example

A

sitagliptin - blocks DPP4, an enzyme which destroys incretin so more incretin is present meaning more insulin is produced and less glucose is produced by the liver

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81
Q

SGLT2-i examples

A

dapagliflozin - reduce renal tubular glucose reabsorption (reduce BG w/o stimulating insulin release)

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82
Q

main complication of T2DM

A

hyperosmolar hyperglycaemic state

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83
Q

what is the pathophysiology of hyperosmolar hyperglycaemic state

A

excessive hepatic gluconeogenesis (not totally insulin deficient so ketogenesis doesn’t occur)

glucose is osmotically active therefore causes a hyperosmolar blood state

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84
Q

symptoms of HHS

A

severe T2DM
decreased consciousness (plasma osmolarity)

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85
Q

diagnosis of HSS

A

heavy glycosuria
increased plamsa osmolarity (>3) with hyperglycaemia
NO ketonuria/hyperketonemia

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86
Q

treatment of HHS

A

1st insulin (+ potassium and glucose)
Iv fluid 0.9% saline
LMWH - as pt has thicker blood

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87
Q

macrovascular complications of diabetes

A

MI
ischaemic stroke
PVD

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88
Q

microvascular complications of diabetes

A

retinopathy
neuropathy
nephropathy

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89
Q

complications of DKA

A

coma
hypothermia
hypotension
cerebral oedema

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90
Q

what is the patho of diabetic retinopathy

A

microaneurysms and haemorrhages of retinal vein
microinfarcts
maculopathy - fluid leakage and oedema = central vision loss

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91
Q

diagnosis of diabetic retinopathy

A

fundoscopy
optic CT

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92
Q

treatment for diabetic retinopathy

A

pan-retinal photocoagulation laser
virectomy

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93
Q

patho of diabetic nephropathy

A

hyperglycaemia results in an increased glomerular pressure, which constricts effecrent glomerular arteriole leading to fibrosis and glomerular inflammation and increase in basement membrane width

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94
Q

patho of diabetic neuropathy

A

nerve tissues metabolic and vasculature is disturbed which impairs mitochondria resulting in decreased neutrophic support leading to the injury of neurones

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95
Q

clinical presentation of diabetic neuropathy

A

pain, paraesthesia, burning sensation which is worse at night
autonomic problems - postural hypotension
glove and stocking sensory loss (foot insensitivity and dryness => damage => impaired healing and glucose rich for bacteri and no protection => ulcer => amputation)
mononeuritis multiplex

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96
Q

treatment for pain from diabetic neuropathy

A

pregabalin/gabapentin
amitriptyline

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97
Q

causes of hypoglycaemia

A

diabetes medication - insulin and sulfonylurea
liver failure
addison’s
insulinoma
pituitary insufficiency
non-pancreatic neoplasm

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98
Q

what are the symptoms of hypoglycaemia

A

decreased consciousness
dizziness
may faint

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99
Q

treatment for hypoglycaemia

A

IV glucose
or IM glucagon (if no IV access)

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100
Q

what spinal region does the thyroid sit

A

C5-T1

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101
Q

what connects the two lobes of the thyroid

A

isthmus

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102
Q

what supplies the thyroid

A

superior thyroid artery

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103
Q

what is the superior thyroid artery a branch of

A

external carotid artery

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104
Q

what is the process of forming T3/T4

A

iodine trapped
diffuses into colloid
binds to tyrosine residues on thyroglobulin using TPO enzyme creating T1/T2
TSH secreted by thyrotrophs and there is TSH-R binding which stimulates T1 and T2 release
these bind together to form either T3/T4 and released into general circulation

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105
Q

causes of hyperthyroidism

A

most common = graves disease
toxic multinodular goitre
toxic adenoma
ectopic TSH secretion
de quevain’s thyroiditis
drugs - amiodarone, iodine, lithium

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106
Q

how does toxic multinodular goitre cause hyperthyroidism

A

nodules secrete thyroid hormones

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107
Q

where may an ectopic secretion of TSH come from

A

struma ovarii (ovarian teratoma), mets

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108
Q

clinical presentation of de quervain’s thyroiditis

A

red, swollen, tender goitre post viral infection causes thyroid gland to release hormone into circulation

often causes hypo after

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109
Q

treatment for de quervain’s thyroiditis

A

aspirin

if severe - prednisolone

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110
Q

what is the pathophysiology of graves

A

TSH-R autoantibodies result in the activation of the receptor and hence the stimulation of thyroid hormones

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111
Q

symptoms of hyperthyroidism

A

heat intolerance
diarrhoea
weight loss + hyperphagia
anxiety
oligomenorrhoea

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112
Q

signs of hyperthyoridism

A

goitre
tachycardia
exopthalamous
pretibial myexoedema
muscle wasting
fine tremor

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113
Q

diagnosis of graves

A

positive TSH-R Ab’s

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114
Q

diagnosis of hyperthyroidism

A

thyroid function tests

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115
Q

decreased TSH and increased T4

A

primary hyperthyroidism (graves)

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116
Q

increased TSH and increased T4

A

secondary hyperthyroidism

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117
Q

increased TSH and normal T4

A

subclinical hypothyroid

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118
Q

decreased TSH and normal T4

A

subclinical hyperthyroid

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119
Q

what test can be done to differentiate graves and TMG

A

thyroid USS

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120
Q

what is carbimazole CI in and what would you give as an alternative

A

pregnancy and can give propylthiouracil

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121
Q

other treatments for hyperthyroidism

A

propylthiouracil
in pregnancy may also need to give levothyroxine to prevent fetal iatrogenic hypothyroid
radioactive iodine (131) - CI in pregnancy
surgery

122
Q

S/E of carbimazole

A

agranulocytosis - presents as sore throat

123
Q

complications of hyperthyroidism

A

thyroid storm
heart failure
osteoporosis

124
Q

what is a thyroid storm

A

rapid deterioration of thyrotoxicosis and large amounts of T4 are released
there is sytemic decompensation which may lead to AF, HTN, coma and possible death

125
Q

causes of hypothyroidism

A

hashimoto’s (MC in developed world)
iodine deficiency (MC in developing world)
postpartum thyroiditis
amiodarone
progressed de quervains

126
Q

what is the pathophysiology of hashimotos and postpartum hypothyroidism

A

autoimmune thyroid destruction (anti TPO-Ab’s)

127
Q

why is postpartum thyroiditis different to hashimotos

A

there is an acute phase where it presents during pregnancy and resolves by itself within 1 year of symtpoms

128
Q

symptoms of hypothryoidism

A

cold intolerance
constipation
weight gain
lethargy
menorrhoea

129
Q

signs of hypothyroidism

A

bradycardia
slow reflexes
cold hands
goitre
pretibial myexedema

130
Q

increased TSH and decreased T4

A

primary hypothyroid

131
Q

decreased TSH and decreased T4

A

secondary hypothyroid

132
Q

increased TSH and normal T4

A

subclinical hypothyroid

133
Q

diagnosis of hypothyroidism

A

TFT
anti TPO Ab’s
typically anaemic

134
Q

treatment for hypothyroidism

A

levothyroxine

135
Q

why must levothyroxine be used carefully

A

may cause iatrogenic hyperthyroidism so titrate to effect

136
Q

complications of hypothyroidism

A

myxedema coma (often infection precipitated) from rapidly decreasing T4 - presents with hypothermia, loss of consciousness and heart failure

137
Q

treatment for myxedema coma

A

levothyroixine, ABx, hydrocortisone (until adrenal insufficiency has been ruled out)

138
Q

types of thyroid carcinoma

A

papillary (MC)
follicular
anaplastic
lymphoma
medullary cell

139
Q

what is the most common type of thyroid carcinoma

A

papillary

140
Q

symptoms of thyroid carcinoma

A

thyroid nodules - hard and irregular
local compression = hoarse voice

141
Q

diagnosis of thyroid carcinoma

A

fine needle aspiration biopsy
TFT
thyroid USS

142
Q

differential for hypothyroidism

A

depression
alzheimers dementia
anaemia

143
Q

treatment for papillary and follicular thyroid cancer

A

thyroidectomy and radiodine

144
Q

treatment for anaplastic thyroi cancer

A

palliative

145
Q

mets sites for thyroid cancer

A

lungs = MC
bone
liver
brain

146
Q

what is cushings disease

A

pituitary adenoma secreting excess ACTH

147
Q

what is cushings syndrome

A

to much cortsiol of any cause

148
Q

what causes pseudo-cushings

A

alcohol and will resolve within 1-3 weeks

149
Q

what are the two types of causes of cushings

A

ACTH dependent and ACTH independent

150
Q

what are some examples of dependent cushings syndrome

A

cushings disease (MC) and ectopic ACTH (SCLC)

151
Q

what are some examples of independent cushings syndrome

A

iatrogensis (steroids) (MC overall cause) and adrenal adenoma

152
Q

what is the patho of cushings

A

cortisol has a negative feedback effect on CRH and ACTH.
CRH is typically released with circadian rhythm and is increased in the morning and decreased at night, but in cushings this is lost and patient is left with irregulated CRH, ACTH and cortisol

153
Q

symptoms of cushings

A

moon face
central obesity
purple abdo striae
osteoporosis
plethoric complexion
thin easy bruising skin
+/- easy infection and muscle atrophy

154
Q

diagnosis of cushings

A

rule out oral steroids
random serum cortisol
dexamethasone suppression test
plasma ACTH

155
Q

1st line test for suspected cushings

A

random serum cortisol - meaure at 12am, lowest here so if increased is abnormal

156
Q

what to do if cushings is suspected and patient is on steroids

A

stop them

157
Q

what is the dexamethasone suppression test

A

dexamethasone is essentially cortisol and in a healthy patient should provide negative feedback on HPA axis and decrease cortisol
1) give dexamethasone and mesaure cortisol before dex (00:00)
2) measure cortisol at 08:00am

158
Q

what results might a dexamethasone suppression test show

A

non-cushings - suppression cortisol lvls <50mmol/L
cushings - little to no suppression

159
Q

how can cushings disease be investigated

A

high dose dexamethasone and if there is low cortisol

160
Q

if 1st line is positive what can be meausred next

A

plasma ACTH (after a high dose dexamethasone)

161
Q

what results might be shown with plasma ACTH measurements

A

if increased - dependent cause - look for ectopic ACTH
if decreased - independent consider adrenal adenoma

162
Q

treatment for cushings disease

A

transphenoidal resection
bilateral adenectomy

163
Q

complication of adrenalectomy

A

Nelson’s syndrome

164
Q

what is Nelson’s syndrome

A

pituitary tumour will continue to enlarge as no negative feedback being provided from the adrenals leading to an increase in ACTH and skin hyperpigmentation

165
Q

treatment of adrenal adenoma

A

unilateral adrenalectomy

166
Q

treatment of ectopic ACTH

A

surgical removal (SCLC)

167
Q

complication of cushings

A

osteoporosis and T2DM

168
Q

primary causes of adrenal insufficiency

A

developed world - autoantibodies mediated destruction of adrenals (Addison’s)

developing world - TB (+sarcoidosis)

169
Q

secondary causes of adrenal insufficiency

A

iatrogenic (suppression of HPA axis - steroids)

170
Q

other causes of adrenal insufficiency

A

adrenal mets (lungb liver breast)
adrenal haemorrhage

171
Q

what are autoantibodies targeted against in addison’s

A

21-alpha hydroxylase

172
Q

what is waterhouse-friderichsen syndrome

A

adrenal insufficiency due to adrenal haemorrhage

173
Q

what is the major cause of waterhouse-fridrichsen syndrome

A

meningococcal meningitis

174
Q

what is the patho of primary adrenal insufficiency

A

addison’s destroys adrenal cortex so ACTH increases and adrenal hormones decrease

175
Q

what is the patho of secondary adrenal insufficiency

A

HPA suppression - so decreased ACTH and decreased adrenal hormones

176
Q

difference in presentation of secondary and primary adrenal insufficiency

A

primary = skin hyperpigmentation
secondary = no skin hyperpigmentation

177
Q

why do you get skin hyperpigmentation in primary adrenal insufficiency

A

increased ACTH stimulates POMC which form melanocytes resulting in hyperpigmentation

178
Q

symptoms of adrenal insuffciency

A

lethargy
weight loss
postural hypotension (decreased aldosterone)
vitiligo
change in body hair (decreased androgens)
hyperpigmentation
hypoglycaemia
abdo pain and vomiting

179
Q

diagnosis of adrenal insufficiency

A

short synACTHen test

180
Q

how does the short synACTHen test work

A

it tests adrenal reserves
1) measure basal cortisol at 09:00 (where normally highest)
2) administer synACTHen
3) sample cortisol after 30 mins

181
Q

what result would exclude addisons

A

plasma cortisol >580nmol/L after 30 mins

182
Q

other tests to diagnose addison’s

A

auto 21-alpha hydroxylase Ab’s
blood
CXR (TB suspected)
ACTH 09:00 lvl (primary increased a lot, decreased in secondary)

183
Q

treatment for addison’s

A

hydrocortisone
fludrocortisone

184
Q

what should you do to the dose of a patient on steroids if they have an infection/trauma

A

double it as cortisol is needed for stress response

185
Q

what is an adrenal crisis

A

severe adrenal insufficiency - especially low cortisol

186
Q

symptoms of an adrenal crisis

A

N + V
renal failure
loss of consciousness

187
Q

treatment for adrenal crisis

A

immediate hydrocortisone + IV saline
+/- dextrose if hypoglycaemic

188
Q

what are some differentials for addisons

A

hyperthyroidism
haemochromatosis
anorexia nervosa

189
Q

what is acromegaly

A

excess Human growth hormone

190
Q

what is the difference between acromegaly and gigantism

A

acromegaly is in adults after epiphyseal fusion and gigantism is before epiphyseal fusion in children

191
Q

give a cause of acromegaly

A

functional pituitary adenoma

192
Q

what is the patho of acromegaly

A

GHRH secreted stimulates GH from somatotrophs which causes increased levels of IGF-1 produced from the liver which exerts its effect on ROB

193
Q

symptoms of acromegaly

A

large hands/feet
box jaw
vision change
sleep apnoea
large intradental gaps
carpal tunnel syndrome

194
Q

investigations for acromegaly

A

IGF-1 serum lvl = 1st line
OGTT is impaired - Gold standard

195
Q

treatment for acromegaly

A

transphenoidal surgery
octreotide - SST analogue
bromocriptine - DA agonist
pegvisomat - GH antagonist

196
Q

complications of acromegaly

A

T2DM, sleep apnoea

197
Q

where is prolactin produced from

A

lactotrophs

198
Q

what are the causes of hyperprolactinaemia

A

prolactinoma
drugs - ecstasy

199
Q

what are the symptoms of hyperprolactinaemia

A

amenorrhoea
galactorrhoea + sexual dysfunction
decreased libido
erectile dysfunction
gynaemastacosia
(bitemporal hemianopia)

200
Q

investigations for hyperprolactinemia

A

increased serum prolactin

201
Q

what is the treatment for hyperprolactinemia

A

DA agonist - cabergoline/bromocriptine (can shrink tumour)

202
Q

differentials for hyperprolactinaemia

A

prolactinoma
primary hypothyroidism
iatrogenic - drug
pregnancy

203
Q

what is Conn’s syndrome

A

also known as primary hyperaldosteronism, it is where there is excess aldosterone independent of the RAAS

204
Q

what is secondary hyperaldosteronism

A

too much aldosterone due to excess renin

205
Q

causes of primary hyperaldosteronism (Conns’)

A

2/3 - adrenal adenoma - Conns
1/3 - bilateral adrenal hyperplasia

206
Q

what is the patho of Conn’s

A

increased aldosterone results in increased sodium and decreased potassium resulting in HTN and hypokalaemia

207
Q

symptoms of primary hyperaldosteronism

A

resistant HTN (not fixed with beta-b/ACE-i)
hypokalaemia
muscle weakness
paraesthesia
polydipsia and polyuria

208
Q

investigations for hyperaldosteronism

A

aldosterone:renin increased - 1st line
diagnostic = serum aldosterone not suppressed with 0.9% IV saline (or fludrocortisone)

209
Q

what is the renin level in primary hyperaldosteronism

A

suppressed

210
Q

what might an ECG show in a patient with hyperaldosteronism

A

hypokalaemic - long PR, flate inverted T waves, U waves and ST depression

211
Q

treatment for hyperaldosteronism

A

laproscopic adrenalectomy
spirolonactone (aldosterone antagonist) - use 4 wks pre-op and for bilateral hyperplasia

212
Q

differentials for primary aldosteronism

A

essential HTN
renal artery stenosis
thiazide induced hypoK in pt with essential HTN
Liddle syndrome

213
Q

what is diabetes insipidus

A

inability to concentrate urine resulting in large productions (3L+) of dilute urine a day

214
Q

what are the two types of diabetes insipidus

A

cranial - decreased ADH secretion
nephrogenic - decreased kidney response to ADH

215
Q

causes of cranial DI

A

ADH gene mutation
pituitary adenomas
idiopathic

216
Q

caused of nephrogenic DI

A

renal tubular acidosis
ADH-R mutation
polyuria

217
Q

patho of DI

A

decreased ADH = increased water loss in urine resulting in it being diluted and in high volumes

218
Q

symptoms of DI

A

polyuria
polydipsia
hypernatraemia
lethargy/coma/confusion
severe dehydration

219
Q

what should initiate suspicion of DI

A

3+L urine daily

220
Q

what investigations should be done for DI

A

water deprivation test (8h) + serum and urine osmolarity
IM desmopressin and urine osmolarity

221
Q

what are the normal and DI results for the water deprivation test

A

normally = serum osm stays normal and urine osm increases
DI = serum osm rises while urine is unchanged

222
Q

what are the DI results for the IM desmopressin test

A

cranial - before urine osm = < 300, after >800 = adequate ADH to have effect on kidney

nephrogenic - before urine osm = <300, after <300 = ADH will have no effect on kidney

223
Q

treament for cranial DI

A

desmopressin

224
Q

treatment for nephrogenic DI

A

thiazides (+underlying cause)

225
Q

how do thiazides work to treat nephrogenic DI

A

it will increased water loss at DCT therefore encouraging Na+ uptake (and water retention) which will concentrate urine and increase retention volume

226
Q

differentials for DI

A

psychogenic polydipsia
DM
diuretic use
hypercalacemia

227
Q

what is SIADH

A

where there is an inappropriate amount of ADH secreted leading to dilute euvolaemia

228
Q

what electolyte imbalance may SIADH cause and why

A

hyponatraemia as excess ADH results in more water retention and therefore compensatory Na+ excretion to maintain euvolaemia

229
Q

causes of SIADH

A

tumours - SCLC, pancreatic, pancreatic
trauma to head
infection: TB, pneumonia, meningitis

230
Q

using the pneuimonic SIADH what are the causes of SIADH

A

SCLC
infection/immunocompromised
abscesses
drugs - SSRI’s, sulfonylurea and carbamezapine
head trauma

231
Q

patho of SIADH

A

increased ADH independent of RAAS results in vasoconstriction and increased BP
also increased aquaporin-2 of CD therefore increasing BP by water retention (more dilute blood and sodium loss)

232
Q

symptoms of SIADH

A

hyponatraemia symptoms

233
Q

symptoms of hyponataremia

A

vomiting
headache
decreased GCS
muscle weakness
seizures
brainstem herniation and neurological deficits

234
Q

how does hyponatraemia cause brainstem herniation

A

low sodium means increased compensatory water enters skulls resulting in increased ICP
causes hyponataremic encephalopathy
risk of brainstem herniation through foramen magnum (tentorial herniation)

235
Q

investigations for SIADH

A

serum electrolytes - decreased sodium and normal potassium
urine osm high and serum osm low

give 0.9% saline to ensure it is not sodium depletion, in this case serum will normalise

236
Q

treatment for SIADH

A

fluid restrict + hypertonic solution (conc. blood)
treat cause - excise tumour
chronic cases - furosemide, vasopressin antagonist (tolvaptan)

237
Q

differentials for SIADH

A

pseudohyponatraemia
hypovolaemia
psychogenic polydipsia
renal failure
addison’s disease
hypothyroidism

238
Q

what is carcinoid tumours and syndrome

A

poorly malignant tumours of enterochromaffin cells which produce 5-HT (serotonin)

239
Q

where are carcinoid tumours mostly found

A

gastrointestinal tract at appendix
terminal ileum
(can be in lungs)

240
Q

what is a carcinoid tumour

A

only the neoplastic cells - no symptoms

241
Q

what is carcinoid syndrome

A

when tumour has metastasised to liver and symtpoms begin (secreted amined normally degraded by liver, but when mets present they enter straight into circulation)

242
Q

what are the symptoms of carcinoid syndrome

A

flushing
diarrhoea
tricuspid incompetence

243
Q

investigations of carcinoid syndrome

A

liver USS - mets
increased 5-HIAA (serotonin breakdown)
CT/MRI to locate primary tumour

244
Q

treatment of carcinoid syndrome

A

surgical tumour excision
octeotride (somatostatin analogue) can block tumout hormoned

245
Q

complication of carcinoid syndrome

A

carcinoid crisis - life threatening symtpoms - increase octeotride

246
Q

carcinoid syndrome differentials

A

IBS
Crohns
menopause
asthma

247
Q

what is a phaeochromocytoma

A

an adrenal medullary tumour that secreted catecholamines (NAd, Adr)

248
Q

what are the causes of phaeochromocytoma

A

MEN 2a + 2b (multiple endocrine neoplasia)
neurofibromatosis (tumours deposited along myelin sheath)

249
Q

what are the symptoms of phaeochromocytoma

A

hypertension
pallor
very sweaty
tachycardic

250
Q

investigations for phaeochromocytoma

A

plasma metanephrines and normethanephrines (increased)

(other - urinary catecholamines and CT image tumour)

251
Q

why are metanephrines and normetanephrines better than NAd/Adr

A

have a longer half life and so are more sensitive

252
Q

treatment for phaeochromocytoma

A

alpha blockers first (phenoxybenzamine)
then beta-blockers (atenolol)
excise tumour with surgery if possible

253
Q

what do beta blockers do in treating phaeochromocytoma

A

prevents reactive vasoconstriction

254
Q

complications of phaeochromocytoma

A

HTN crisis (180/120 + BP)
Tx = phentolamine

255
Q

how many parathyroid glands are there and where

A

4 on the posterior aspect of the thyroid

256
Q

what is the parathyroid sensitive to

A

calcium

257
Q

what increases and decreases the released of PTH

A

decreased calcium increases PTH
increased calcitonin decreased PTH

258
Q

where is calcitonin released from

A

parafollicular ‘C’ cells of thyroid

259
Q

differentials for phaeochromocytoma

A

anxiety/panic attacks
hyperthyroidism
illicit substances
carcinoid syndrome
menopause
pre-eclampsia

260
Q

what does PTH do

A

inhibits OPG (osteoprotegerin) which allows RANK-L signalling from osteoblasts => osteoclasts => bone resorption

activates vitamin D to increased calcium and phosphate gut absorption and increases calcium absorption and phosphate excretion in DCT of kidney

261
Q

what is the most common cause of hypercalcaemia in the community

A

hyperparathyroid

262
Q

what is the most common cause of hypercalcaemia in hospital

A

bone malignancies like myeloma

263
Q

what is the most common cause of hypoPTH

A

CKD

264
Q

what is a primary cause of hyperparathyroidism

A

parathyroid adenoma (sometimes hyperparathyroid hyperplasia)

265
Q

cause of secondary hyperparathyroid

A

physiological response to decreased calcium
- there is a compensatory hypertrophy of all glands

266
Q

what is a cause of tertiary hyperparathyroidism

A

occurs after many years of secondary hyperPTH - glands act autonomously and release PTH irregardless of negative feedback

267
Q

symptoms of hypercalcaemia

A

bones - excess resorption = osteopenia
stones - kidney stones
groans - abdo pain and constipation
psych moans - depression and anxiety

268
Q

what is the PTH, Calcium, phosphate and ALP levels in primary hyperPTH

A

PTH = increased
calcium = increased
phosphate = decreased
ALP = increased

269
Q

what is the PTH, Calcium, phosphate and ALP levels in secondary hyperPTH

A

PTH = increase
calcium = decreased
phosphate = increased
ALP = increased

270
Q

what is the PTH, Calcium, phosphate and ALP levels in tertiary hyperPTH

A

PTH = increased
calcium = increased
phosphate = increased
ALP = increased

271
Q

what does an ECG show in hypercalacaemia

A

short QT

272
Q

how do you treat hyperparathyroidism (primary, secondary and tertiary)

A

primary - removal of PTH adenoma / parathroidectomy
secondary/tertiary - treat cause

273
Q

complications of hyperPTH

A

acute severe hypercalacaemia

274
Q

how do you treat acute severe hypercalacaemia

A

IV fluids an bisphosphonates

275
Q

differentials of primary hyperPTH

A

multiple myeloma
sarcoidosis
thyrotoxicosis
thiazide use
immobilisation

276
Q

differential for secondary hyperparathyroidism

A

primary hyperPTH

277
Q

causes of primary hypoparathyroidism

A

PTH gland failure (Di George’s syndrome or idiopathic)

278
Q

causes of secondary hypoparathyroidism

A

after surgery (parathyroid/thyroidectomy)

279
Q

causes of pseudohypoPTH

A

peripheral PTH resistance
short statute and small 4th/5th MTC

280
Q

symptoms of hypocalacaemia

A

convulsions, arrhythmia, tetaniy, numbness

281
Q

signs of hypocalacaemia

A

chvostek (twitching of facial muscles when CN7 tapped over parotid)
trousseau (carpopedal spasm when applying tourniquet to forearm)

282
Q

diagnosis of hypoparathyroidism

A

low PTH
low calcium
increased phosphate

283
Q

treatment for hypoPTH

A

calcium supps
Vit D3
(AdCalD3)

284
Q

what would an ECG show for hypoCa

A

long QT

285
Q

what are some differentials for hypoparathyroidism

A

low Mg
low albumin
CKD
Vit D deficiency

286
Q

causes of hypercalacaemia

A

most common = hyperPTH and bone malignancy
drugs - thiazides
excess Ca intake
hyperthyroid
dehydration

287
Q

what does muscle tone do in increased calcium

A

decreased

288
Q

causes of Hypocalcaemia

A

CKD (as decrease Vit D produced)
severe vit D deficient
hypoparathyroid
drugs - bisphosphonates, calcitonin
acute pancreatitis

289
Q

what does muscle tone do in low calcium

A

increase

290
Q

what is considered hyperkalaemia

A

more than 5.5 (>6.5 is an emergency)

291
Q

causes of hyperkalaemia

A

AKI
drugs - NSAIDS, spironolactone, ACEi
addison’s
DKA (+DM)
increased intake
renal tubular acidosis

292
Q

why is there abnormal heart rhythm in hyperK+

A

increased potassium decreases threshold for action potential and therefore depolarises earlier

293
Q

symptoms of hyperK+

A

fast
irregular pulse
VF risk
myalgia

294
Q

diagnosis of hyperK+

A

absent P waves
prolonged PR
tall tented T waves
wide QRS

increased K+

295
Q

treatment for hyperK+

A

calcium gluconate = urgent
insulin + dextrose = non-urgent

296
Q

what are the parameters for hypokalaemia

A

<3.5 (<2.5 = emergency)

297
Q

causes of hypoK+

A

thiazides + loop diuretics
Conn’s
renal tubular acidosis
GI losses
Decrease intake

298
Q

symptoms of hypoK+

A

hypotonia
hyporeflexia
arrhythmias (esp. AF)

299
Q

diagnosis of HypoK+

A

decreased K+
ECG

300
Q

what would be on an ECG in hypoK+

A

small inverted T waves
prominent U waves
ST depression
PR prolongation

301
Q

treatment of hypoK+

A

K+ replacement
aldosterone antagonist (spironolactone)

Phase 2b (16 decks)

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