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Phase 2a > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

What are water soluble hormones?

A
  • stored in vesicles
    -unbound transport
    -bind to surface receptor
    -fast clearance
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2
Q

What are the types of water hormones?

A

-TRH,LH,FSH

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3
Q

What are fat soluble hormones?

A

-synthesised on demand
-protein bound
-diffuse into cell
-slow clearance

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4
Q

What are the types of fat soluble hormones?

A
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5
Q

What are the types of fat soluble hormones?

A

steroids - cortisol

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6
Q

What are the peptide hormones?

A

TRH, Gonadotrophins

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7
Q

What are the amine hormones?

A

Dopamine
Epinephrine
Noradrenaline
Adrenaline

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8
Q

What hormones does the anterior pituitary gland release?

A

FSH+LH
ACTH
GH
TSH
Prolactin

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9
Q

What is the mechanism of FSH + LH?

A

Hypothalamus- GnRH-AP-FSH/LH- ovaries +testes

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10
Q

What does FSH act on?

A

granulosa cells to produce oestrogen and Sertoli cells to stimulate spermatogenesis

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11
Q

What does LH act on?

A

theca cells to produce androgens and leydig cells to produce testosterone

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12
Q

What is the ACTH mechanism?

A

Hypothalamus - corticotropin releasing hormone- AP- adrenocorticotropic hormone - adrenal cortex (zona fasciulata). -gluccocorticoid -cortisol

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13
Q

What is the function of cortisol?

A
  1. increases protein and carbohydrate breakdown
    2.vasoconstriction
  2. suppresses inflammatory dn immune response
    4.inhibits non essential factors
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14
Q

What is the mechanism of GH?

A

Hypothalamus - Growth hormone releasing hormone - AP - GH- liver- IGF-1 production

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15
Q

How is insulin released?

A

Biphasic - released in two phases
1. Increase peripheral glucose uptake (glucose-> glycogen)
Glucose binds to GLUT2 receptors on pancreas, stimulating insulin release
2. Insulin binds to peripheral insulin receptors - activates intracellular tyrosine kinase + cascade
Result = increased Glut-4 channel expressing on cell membranes to increase peripheral uptake

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16
Q

What is the mechanism for TSH?

A

Hypothalamus - TRH- AP-TSH - T3+T4 - carried in blood bound to thyroglobullin binding protein

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17
Q

What are the functions of T3+T4?

A
  • food metabolism
    -protein synthesis
    -increased sympathetic action
    -heat production
    -needed for growth and development
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18
Q

What is the mechanism of prolactin?

A

Hypothalamus - dopamine - AP - Prolactin - milk production and breast development

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19
Q

What is released at the post pituitary ?

A

Oxytocin - milk ejection + labour induction

Vasopressin - recruited when low blood volume, stress
-vasoconstriction
-increase aldosterone

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20
Q

What does the zona glomerulosa release?

A

aldosterone

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21
Q

What does zone reticualris release?

A

Androgens

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22
Q

What does the adrenal medulla secrete?

A

Adrenaline , noradrenaline

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23
Q

What can pituitary tumours cause?

A
  • press on local structures - optic chiasm
    -hypOpituitarism
    -hypERpituitism - acromegaly, cushings, prolactinoma
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24
Q

What are the types of diabetes?

A

T1Dm
T2DM
MODY- Maturity onset diabetes of the young
LADA- latent autoimmune diabetes in adults

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25
Q

What are secondary causes of diabetes?

A

Acromegaly + cushings
Haemachromatosis
Thiazides/ corticosteroids

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26
Q

What is type 1 diabetes?

A

Type 4 hypersensitivity; autoimmune destruction of pancreatic B cells leading to absolute insulin deficiency

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27
Q

What is the epidemiology of T!DM?

A
  • Young patients
    -lean
    -North European descent
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28
Q

What are the risk factors of T1DM?

A
  • HLA DR3/ HLA DR4
    -other autoimmune diseases
    -environmental infection
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29
Q

What is the pathology of T1DM?

A

Autoimmune beta islet destruction = absolute or very low insulin therefore -hyperglycaemia,
-low cellular glucose so increase in lipolysis and gluconeogenesis
-hyperkalamia even though total body K+ is low as insulin stores K+ into cells via Na+/K+ATPases

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30
Q

What is the presentation of T1DM?

A

Lean young patient with polydipsia, nocturia, polyuria, polyphagia and weight loss
Glycosuria +/- sigs of ketogenesis

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31
Q

What is the diagnosis of T1DM?

A

random blood glucose= >11.1 mol/L = T1DM
Fasted blood glucose = >7mmol/L = T1DM
HbA1C= 48mmol/L or >6.5% = T1DM

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32
Q

What are the normal levels for RBG, FBG and HbA1C?

A

<11.1mmol/L - normal RBG
<6.0mmol/L - normal FBG
<6% - normal Hb1AC

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33
Q

What is the Hb1AC level for pre-diabetes?

A

5.7%- 6.4%

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34
Q

What is the treatment for T1DM?

A

Basal bolus Insulin
Basal = longer acting, to maintain stable insulin levels throughout the days
bolus= faster acting, 30mins pre-prandial to give ‘insulin spike’

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35
Q

What are the different types of insulin?

A

rapid -novorapid
short- regular insulin
intermed- NPH
long- glargine

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36
Q

What is the main complication of T1DM?

A

Diabetic ketoacidosis

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37
Q

What are the causes of DKA?

A

poorly managed T1DM, infection/illnesses

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38
Q

What is DKA?

A

increasing hyperglycaemia and rising ketones

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39
Q

What is the presentation of DKA?

A

10 -years old
-presents to a&e with severe dehydration and a history of T1DM.

Sx:
-kussmaul breathing (deep laboured breaths to blow off CO2)
-Pear drop breath (fruity ketone breath smell)
-Reduced tissue turgor, hypotension and tachycardia

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40
Q

what is the pathology of DKA?

A

Absolute insulin deficiency = unrestrained lipolysis + gluconeogenesis. So much gluconeogenesis that not all glucose is usable so it is converted to ketone bodies(increase in acidic concentration = ketoacidosis)

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41
Q

What is the diagnosis of DKA?

A

Ketones - blood >3mmol/L
Hyperglycemic >11.1mmol/L
Acidosis (met) <7.3pH or >15mmol HCO3-

+Ketonuria, glycosuria and hyperkalaemia

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42
Q

What is the treatment for DKA?

A

ABCDE - emergency
1st line - always fluid - dehydration
then insulin (+glucose to prevent hypoglycaemia and K+ to replenish potassium stores)

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43
Q

What is type 2 diabetes?

A

Peripheral insulin resistance with peripheral insulin deficiency - carbohydrates, lipids and beta amyloid deposits in pancreas

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44
Q

What are the risk factors for T2DM?

A

-FHX
-smoking
-obesity
-HTN
-sedentary lifestyle

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45
Q

What is the pathology of T2DM?

A

peripheral insulin resistance (malfunctional insulin intracellular activation pathway) therefore decrease in GLUT4 expression , and minor destruction to pancreatic islets due to deposition.
Results in hyperglycaemia and increase in insulin demand from depleted B cell population.

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46
Q

What is the presentation of T2DM?

A

obese, hypertensive, older, with polydipsia, polyuria, nocturia, glycosuria
Aconthisis nigricans - dark pigmented skin folds -severe insulin resistance

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47
Q

What is the diagnosis of T2DM?

A

same as T1DM:
FBG: >7mmol/L
RBG >11.1mmol/L
HbA1C >6.5%/ 48<

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48
Q

What are the pre diabetes states?

A

IGT - impaired glucose tolerance test
IFG-impaired fasting glucose

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49
Q

What are the results of IGT?

A

normal FBG >6mmol/L
2hr OGTT - 7.8-11mol/L - pre diabetic

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50
Q

What are the results for IFG?

A

FBG- 6.1-6.9 mmol/L
normal 2hr OGTT <7.8 mmol/L

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51
Q

What are the normal ranges for OGTT?

A

oral glucose tolerance test
normal - <7.8mmol/L
pre-diabetic 7.8-11
diabetic >11.1

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52
Q

what are the normal ranges for FBG?

A

normal - <6
prediabetic 6.1 - 6.9
diabetic >7

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53
Q

What are the ranges for RBG?

A

normal <11.1
Diabetes >11.1

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54
Q

What are the ranges for Hb1AC?

A

normal - <42/<6%
pre-diabetic 42-47/ 6-6.4%
Diabetics >48/ >6.5%

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55
Q

What is the treatment for T2DM?

A

if pre-diabetic = lifestyle changes to diet and exercise
Diabetic =
1. metformin(increase peripheral sensitivity to insulin)
2. If Hb1AC 58+ - add sulfonylureas (gliclazide)
3. Still high - consider 3rd drug - DPP4 inhibitor, SGLT-2 inhibitor
4. Give insulin

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56
Q

Do you gain or lose weight on Metformin, gliclazide, DPP4, glitazones?

A

metformin - lose
gliclazide- gain
DPP4 inhibitors - no change
Glitazones - gain

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57
Q

What is the main complication of T2DM?

A

Hyperosmolar hyperglycaemic state

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58
Q

What is the pathology of HHS?

A

excessive hepatic gluconeogenesis not totally insulin deficient therefore ketosis doesn’t occur
- glucose osmotically active therefore excessive glucose = hyperosmolar blood

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59
Q

What is the presentation of HHS?

A

severe T2DM, low consciousness

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60
Q

What is the diagnosis of HHS?

A

Heavy glycosuria, increase plasma osmolarity(>300mmol/L) with hyperglycaemia - no ketonuria

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61
Q

What is the treatment of HHS?

A
  1. insulin ( and potassium and glucose)
  2. Iv fluid - saline
    -LMWH- anticoagulant as they have thicker blood
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62
Q

What are DM microvascular complications?

A

retinopathy, neuropathy( Charcot foot), nephropathy (nephrotic syndrome, CKD)

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63
Q

What are DM macrovascular complications?

A

Cardiovascular (MI), cerebrovascular (stroke), peripheral arterial disease (PVD)

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64
Q

What is hypoglycaemia ?

A

Abnormally low blood glucose

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65
Q

What are the causes of hypoglycaemia ?

A

often resulting from diabetes drugs; sulfonylureas or insulin
Non diabetic - oral, liver failure, Addisons

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66
Q

What do sulfonylureas do?

A

stimulate increased insulin production and secretion

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67
Q

What is the presentation of hypoglycaemia ?

A

decreased consciousness, dizziness, sometimes will faint

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68
Q

What is the treatment for hypoglycaemia?

A

IV glucose - IM glucagon

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69
Q

Where does the thyroid sit?

A

C5-T1
2 lobes connected with isthmus

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70
Q

Where does the inferior thyroid artery arise from?

A

off thyrocervical trunk

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71
Q

Where does the superior thyroid artery arise from?

A

off external carotid artery

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72
Q

What are the follicular cells?

A

Iodine trapping - from circulation

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73
Q

What is the colloid?

A

Synthesis of T3+T4 - produces thyroglobulin

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74
Q

What is the T3+T4 process?

A
  • iodine trapped diffuses into colloid
    -binds to tyrosine residues on thyroglobulin, using TPO enzyme catalyst
    -T1or T2
    -TSH - Rbinding= stimulates T1+2 release
    T1+T2= T3
    T2+T2 = T4
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75
Q

What is hyperthyroidism?

A

Excess thyroid hormone in the blood

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76
Q

What is the most common cause of hyperthyroidism?

A

Graves disease

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77
Q

What are other causes of hyperthyroidism?

A
  • toxic multinodular goitre
    -ectopic TSH secretion
    -toxic adenoma
    -drugs= amiodarone, iodine
    -de quervains thyroiditis - post viral infection
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78
Q

What is the epidemiology of hyperthyroidism?

A

common in females

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79
Q

What is the pathology of hyperthyroidism?

A

TSH- R autoantibodies - excessively stimulate thyroid

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80
Q

What are the symptoms of hyperthyroidism?

A
  • heat intolerance
    -diarrhoea
    -weight loss
    -hyperphagia
    -anxiety
    -oligomenorrhoea
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81
Q

What are the signs of hyperthyroidism?

A

-Goitre
-tacycardia
-pretibial myxoedema
- muscle wasting
-fine tremor

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82
Q

What is the diagnosis of hyperthyroidism?

A

Graves = TSH-R antibodies positive
Thyroid functioning tests:
-low TSH - High T4= primary hyperthyroid - graves
-high TSH -High T4 = secondary hyper
-High TSH - T4=subclinical hypothyroid
-Low TSH - T4= subclinical hyperthyroid
Anti-TPO Ab’s - more in hypo
Thyroid USS - tmg vs graves

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83
Q

What is the treatment for hyperthyroidism?

A

1st line - carbimazole(CI in pregnancy) + propranolol alongside
-radioactive 131iodine; definitive treatment - destroys excess thyroid tissue (CI in pregnancy)
-surgery

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84
Q

What is a side effect of carbimazole?

A

agranulocytosis - presents as sore throat

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85
Q

what is a complication of hyperthyroidism?

A

thyroid storm - rapid deterioration thyrotoxicosis - high level of T4- systemic decompression;AF,HTN and coma, heart failure, osteoporosis

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86
Q

What is the treatment of Thyroid storm?

A

propylthioruracil + KI

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87
Q

What is graves disease?

A

Autoimmune condition , that causes hyperthyroidism

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88
Q

What is the pathology of graves disease?

A

increased levels of TSH receptor stimulating antibody

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89
Q

What is the presentation of graves?

A
  • opthhalmopathy - bulging eyes
    -Dermopathy - pretibial myxedema
    -characteristic rash - acropachy
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90
Q

What is hypothyroidism?

A

Lack of thyroid hormone

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91
Q

What is the epidemiology of hypothyroidism?

A

women
ageing
postpartum

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92
Q

What is the main cause in the developed world?

A

Hashimotos Thyroiditis

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93
Q

What is hashimotos thyroiditis?

A

Autoimmune thyroid destruction

94
Q

What is the main cause in the developing world?

A

iodine deficiency

95
Q

What are other causes of hypothyroidism?

A

post part rum thyroiditis
-amiodarone
-secondary causes - hypopituitarism

96
Q

What is post part rum thyroiditis?

A

same mechanism as hashimotos but
1- acute - presents during pregnancy
2-resolves by itself after a year of Sx

97
Q

What is the pathology of hypothyroidism?

A

Anti-tpo (thyroid peroxidase) antibodies high vs thyroid

98
Q

What are the symptoms of hypothyroidism?

A

cold intolerance, constipation, weight gain, lethargy , menorrhagia

99
Q

What are the signs of hypothyroidism?

A

bradycardia, slow reflexes, cold hands, Goitre, pretibial myxoedema

100
Q

What is the diagnosis of hypothyroidism?

A

TFTs:
-High TSH - Low T4= primary hypothyroidism
-Low TSH- Low T4 = secondary hypothyroidism
-High TSH - T4 =subclinical hypothyroidism
Anti-TPO antibodies high - in hashimotos
-typically anaemic - any type

101
Q

What is the treatment for hypothyroidism?

A

Levothyroxine(T4) - careful with dose, can cause iatrogenic hyperthyroidism

102
Q

What is a complication of hypothyroidism?

A

Myxoedema coma(often infection precipitated); rapidly decrease T4

103
Q

What is the presentation of myxoedema coma?

A

hypothermia, loss of consciousness , heart failure

104
Q

What is the treatment myxoedema coma?

A

Levothyroxine
Abx + hydrocortisone - until adrenal insufficiency has been ruled out

105
Q

What are the types of thyroid carcinomas?

A

Papillary -mc
Follicular
Anaplastic - mets the most
Lymphoma
medullary cell

106
Q

What is the behaviour, spread and prognosis of papillary ?

A

young
local spread
good prognosis

107
Q

What is the behaviour, spread and prognosis of Follicular ?

A

middle age
Spread to lung/bone
usually good prognosis

108
Q

What is the behaviour, spread and prognosis of anaplastic?

A

aggressive
local spread
very poor prognosis

109
Q

What is the behaviour, spread and prognosis of lymphoma?

A

variable behaviour
usually poor prognosis

110
Q

What is the behaviour, spread and prognosis of medullary cells?

A

familial
Local and metastasises
poor prognosis

111
Q

Where does thyroid carcinomas metastasise to ?

A

Lung -50%
Bone-30%
liver-10%
brain-5%

112
Q

What is the presentation of thyroid carcinomas ?

A

mostly present at thyroid nodules - hard + irregular
- local compression -hoarse voice
-dysphagia
-any metastasises

113
Q

What is the diagnosis of thyroid carcinoma?

A

Fine needle aspiration biopsy
TFts, ultrasound thyroid

114
Q

What is the treatment of thyroid carcinomas?

A

papillary + follicular = thyroidectomy + radioactive given
Anaplastic + lymphoma = palliative mostly

115
Q

What is cushings syndrome?

A

Refers to the abnormalities resulting from excess cortisol from any cause

116
Q

What is cushings disease?

A

Used to describe the clinical state of free circulating glucocorticoids , occurs when a pituitary adenoma secretes excess ACTH

117
Q

What are the ACTH dependent causes of cushings syndrome?

A

Cushing disease - mc
ectopic ACTH - sclc

118
Q

What are the ACTH independent causes of cushings syndrome?

A

steroid use -mc overall cause
adrenal adenoma

119
Q

What is the pathology of cushings syndrome?

A

Corticotrophin releasing hormone typically released with a circadian rhythm (high in morning, low at night)
Here, this rhythm is lost - excessive unregulated CRH, ACTH,Cortisol

120
Q

What is the ACTH mechanism?

A

hypothalamus - crh - pituitary - ACTH - adrenal gland - cortisol

121
Q

What is the presentation of cushings syndrome?

A

moon face
central obesity
purple abdo striae
osteoporosis
thin easy bruising skin
plethoric complexion
easy infections
muscle atrophy

122
Q

What is the diagnosis of cushings?

A

Rule out oral steroids- if on steroids =STOP
FIRST LINE:
-Random serum cortisol high (at 12 am should be at its lowest) then FIRST LINE test:
-Dexamethasone suppression test - in a healthy patient should have negative feedback
-measure cortisol before and after
-if suppressed >50nmol/L= non cushings
-no suppression =cushings
-If first line positive then measure plasma ACTH
-high ACTH = ACTH dependent cause so look for cushings disease on pituitary MRI
-Low ACTH - ACTH independent cause - consider adrenal adenoma

123
Q

What is the dexamethasone suppression test?

A

Dexamethasone = essentially cortisol therefore in a healthy patient should negative feedback HPA axis and lower cortisol
1. measure cortisol level then give dexamethasone measure, over night
2. measure cortisol 8hr after
-non cushings - suppression (>50nmol/L)
-cushings- little/ no suppression

124
Q

What is the treatment for cushings disease?

A

transphenoidal resection or bilateral adrenalectomy

125
Q

What is a complication of bilateral adrenalectomy?

A

Nelson’s syndrome; pituitary tumour will continue to enlarge with no negative feedback from adrenals- increased ACTH + skin hyperpigmentation

126
Q

What is the treatment for adrenal adenoma?

A

unilateral adrenelectomy

127
Q

What is the treatment for ectopic ACTH?

A

surgical removal - SCLC

128
Q

What is a complication of cushings?

A

osteoporosis, secondary DM

129
Q

What is adrenal insufficiency?

A

Autoimmune destruction of the entire adrenal cortex in primary adrenal insufficiency or HPA axis suppression in secondary adrenal insufficiency . Resulting in mineralocorticoid, glucocorticoid and androgen deficiency.

130
Q

What are the primary causes of adrenal insufficiency?

A

main cause in developed world - Addisons
main cause in developing world - TB

131
Q

What are the secondary causes of adrenal insufficiency?

A

Iatrogenic - suppression of HPA axis from steroids

132
Q

What are other causes of adrenal insufficiency?

A

adrenal mets - lung, liver,breast
Adrenal haemorrhage

133
Q

What is the pathology of Addisons?

A

Addison’s destroys adrenal cortex by autoantibodies therefore high ACTH and low adrenal hormones. High ACTH stimulates proopiomelanocortin (melanocytes) resulting in hyperpigmentation

134
Q

What is the pathology of HPA suppression?

A

HPA suppression therefore low ACTH and low Adrenal hormones and no hyperpigmentation

135
Q

What is the presentation of adrenal insufficiency?

A

Lethargy,
weight loss
postural hypotension
vitiligo
change in body hair
hyperpigmentation (1)
hypoglycaemia
Abdo pain + vomiting

136
Q

What is the diagnosis of adrenal insufficiency?

A

Short synACTHen test:
Test adrenal reserve; 1. measure basal cortisol at 9am
2.administer synacthen
3. sample cortisol again after 30 min
If plasma cortisol >580nmol/L after 30 min EXCLUDE Addisons
-Auto 21-d hydroxylase Ab’s
-bloods
-CXR for TB if suspected
-High ACTH(9am) in primary but low in secondary

137
Q

\What is the treatment for adrenal insufficiency?

A

Hydrocortisone, fludrocortisone
If trauma/ infection. Double dose of hydrocortisone

138
Q

What is adrenal crisis?

A

Severe adrenal insufficiency especially hydrocortisolemia, ; N+v, renal failure, level of consciousness

139
Q

What is the treatment for adrenal crisis?

A

immediate hydrocortisone +IV saline + dextrose if hypoglycaemic

140
Q

What is acromegaly?

A

Excess growth hormone- HGH in adults (after epiphyseal fusion)
Gigantism in children (before epiphyseal fusion)

141
Q

What are the causes of acromegaly?

A

Functional pituitary adenoma
or ectopic GH releasing hormone from a carcinoid tumour

142
Q

What is the pathology go acromegaly?

A

Hypothalamus –> GHRH–> anterior pituitary–> GH–> liver-IGF-1 which exerts effects on rest of body
In acromegaly high IGF-1 (produced by liver)

143
Q

What is the presentation of acromegaly ?

A

Large hands/feet, box jaw, change in vision (bitemporal hemianopia), sleep apnoea (increase in larynx soft tissue), large interdental gaps, carpal tunnel syndrome , IGT - risk of T2DM

144
Q

What is the diagnosis of acromegaly?

A

IGF-1 serum level high - always first line screening
Impaired glucose tolerance is gold standard - OGTT

145
Q

What is the treatment of acromegaly?

A

1st line - transsphenoidal surgery
otherwise : somatostatin analogue - octreotide
dopamine agonist - bromocriptine
GH agonist. -pregvisomant

146
Q

What is the complication of acromegaly?

A

T2DM, sleep apnoea

147
Q

What is hyperprolactinemia?

A

Most common in females, high serum prolactin

148
Q

What are the causes of hyperprolactinoma?

A

prolactinoma, drugs(ecstasy) -mc

149
Q

what is the presentation of hyperprolactinoma?

A

Amenorrhoea, galactorrhea, sexual dysfunction, decreased libido, erectile dysfunction, decreased testosterone , bitemporal hemianopia

150
Q

What is the diagnosis of hyperprolactinoma?

A

high serum prolactin

151
Q

What is the treatment fro hyperprolactinoma?

A

dopamine agonists- bromocriptine - shrinks tumour as dopamine inhibitor of prolactin

152
Q

What is conns syndrome - hyperaldosteronism?

A

Excess aldosterone independent of RAAS

153
Q

What is the most common secondary cause of hypertension?

A

hyperaldosteronism

154
Q

What are the causes of hyperaldosteronism?

A

2/3 - adrenal adenoma (Conn’s)
1/3- bilateral adrenal hyperplasia

155
Q

What is the cause of secondary hyperaldosteronim?

A

excess renin which increases aldosterone

156
Q

What is the pathology of hyperaldosteronism?

A

increase in aldosterone = increase in Na+ / H2O and decrease in K+, hypertension with hypokalaemia

157
Q

What is the presentation of hyperaldosteronism?

A

resistant hypertension -unfixable with ACE-i/BB
hypokalaemia; muscle weekness, parasthesia, polydipsia, polyuria

158
Q

What is the diagnosis of hyperaldosteronism?

A

1st line - aldosterone:renin high
Diagnostic = high serum aldosterone not surpassed with Iv saline or fludrocortisone
Hypokalemia - ECG( prolonged PR, ST depression, flat t waves)

159
Q

What is the treatment for hyperaldosteronism?

A

Surgery - laparoscopic adrenelectomy
Spironolactone - aldosterone antagonist

160
Q

What is diabetes inspidus?

A

Tool little ADH from posterior pituitary gland or kidneys aren’t responding to ADH.

161
Q

What are the 2 types of diabetic inspidus?

A

cranial - low ADH secretion
Nephrogenic - decreased kidney response to ADH

162
Q

What are the causes of cranial diabetic inspidus?

A

ADH gene mutation, pituitary adenomas, idiopathic

163
Q

What are the causes of nephrogenic diabetic inspidus?

A

Renal tubular acidosis, ADH-R mutation, polyuria

164
Q

What is the pathology of diabetic insipidus ?

A

Low ADH, increased H2O losses in urine; dilute high volumes

165
Q

What is the presentation of diabetic insipidus?

A

polyuria, polydipsia, hypernatramia, lethargy, confusion, severe dehydration

166
Q

What is the diagnosis of diabetic insipidus?

A
  • 3+ L urine daily = suspect
    1- Water deprivation test(no fluid for 8hr)- Serum osmolality stays normal, urine osmolality high - normally
    Serum osmolality rises while urine is unchanged - DI
    2-Inject IM desmopressin (differentiate cranial + nephrogenic)
167
Q

How do you differentiate between cranial and nephrogenic urine osmolality?

A

Inject IM desmopressin:
Cranial urine osmolality :Before<300= low after High >800 - adequate ADH to have effect on kidney
Nephrogenic urine osmolality before <300 low after <300 low - ADH has no effect on kidney

168
Q

What is the treatment for diabetes insipidus?

A

Cranial - desmopressin
Nephrogenic - thiazides - increase H2O loss at DCT therefore encourages increase Na+ uptake and H2O retention which will concentrate urine and increase retention volume

169
Q

What is syndrome of inappropriate ADH, (SIADH)?

A

Inappropraitely released ADH; dilute euvolemia
-cause of hyponatremia

170
Q

How does SIADH cause hyponatremia?

A

excess ADH = more water retention therefore compensatory Na+ excretion to maintain euvolemia

171
Q

What are the causes of SIADH?

A

S- sclc
I- infection/ immunocompromised -TB
A-abscesses
D- drugs-SSRI,
H-head trauma

172
Q

What is the pathology of SIADH?

A

increased ADH, independent of RAAS- increased vessel vasoconstriction therefore increased BP
-increased ADH increased aquaporins - increases water retention therefore blood volume- excess H2O retained means more dilute blood and more Na+ loss

173
Q

What is the presentation of SIADH?

A

Sx of hyponatremia
- vomiting, headache, low consciousness (decreased GCS), muscle weaknesss
Low Na+ -seizures, neurological complications ;brainstem herniation

174
Q

What causes a brainstem herniation?

A

low Na+ means high compensatory H2O; enters skull = increased ICP
- causes hyponatremic encephalopathy
-risk of brainstem herniating through Forman magnum (tentorial herniation)

175
Q

What is the diagnosis of SIADH?

A

Low Na+ and normal K+ serum
- high urine osmolality - concentrated urine and dilute serum
DDx- Na+ depletion - give IV saline - if serum normalises = Na+ depletion if it doesn’t =SIADH

176
Q

What is the treatment for SIADH?

A

Fluid restrict + hypertonic saline to concentrate blood
Treat underlying cause - tumour excision
Chronic cases - Drugs; furosemide, vasopressin antagonist

177
Q

What is a carcinoid tumour?

A

malignant tumour of enterochromaffin cells which produce 5-HT/serotonin
- only the neoplastic cells no symptoms

178
Q

What is carcinoid syndrome?

A

When carcinoid tumour metastasises to liver, constellation of Sx

179
Q

Where are the carcinoid tumours?

A

Mostly GIT at appendix and terminal ileum- also can be lungs

180
Q

What is the presentation of carcinoid syndrome?

A

Flushing, diarrhoea, tricuspid incompetence (valve lesion)
may have RUQ pain, respiratory problems

181
Q

What is the diagnosis of carcinoid syndrome>

A

Liver USS - positive mets
increase In 5-Hydroxyindoleacetic acid in urine - major 5HT metabolite - GS
CT/MRI to locate primary tumour

182
Q

What is 5HT?

A

5- hydroxytryptamine (serotonin)

183
Q

What is the treatment of carcinoid syndrome?

A

Surgically excise primary tumour - definitive
octreotide (somatostatin analogue) - can block tumour hormones

184
Q

What is a complication of carcinoid syndrome?

A

carcinoid crisis; life threatening Sx constellation

185
Q

What is the treatment for carcinoid crisis?

A

SST analogue - octreotide - high dose

186
Q

What is pheochromocytoma?

A

Adrenal medullary tumour , secretes catecholamines (Adr,NAd)

187
Q

What are the causes of pheochromocytoma?

A

usually inherited associated with
- Men 2a +2b (multiple endocrine neoplasia)
-neurofibromatosis 1 - tumours deposited along nerve myelin sheath

188
Q

What is MEN2?

A

A rare, genetic disorder that affects the endocrine glands and can cause tumors in the thyroid gland, parathyroid glands, and adrenal glands.

189
Q

What is the presentation of pheochromocytoma?

A

hypertension, pallor, very sweaty, tachycardic

190
Q

What is the diagnosis of pheochromocytoma?

A

plasma metanephrines + normetanephrines - diagnostic
- more sensitive readings than NAd/Adr as longer half life
- urinary catecholamines
- CT image tumour

191
Q

What is the treatment of pheochromocytoma?

A

Drugs - alpha blocker first (phenozybenzamine) then beta blocker - atenolol - prevents reactive vasoconstriction
- surgery - excise tumour

192
Q

What are metanephrines?

A

made when your body breaks down hormones called catecholamines
metanephrines and normetanephrines are metabolites of the catecholamines

193
Q

What are the complications of pheochromocytoma?

A

HTN crisis (180/20 + BP)
causes - XR contrast, TCA, opiates
Treat -phentolamine - alpha blocker

194
Q

What is the parathyroid gland?

A

4 glands on posterior aspect of thyroid - very sensitive to change in calcium

195
Q

What is the action of the parathyroid gland?

A
  • Parathyroid hormone released when low calcium, negative feedback by increased calcium and by calcitonin
  • PTH inhibits osteoprotegerin (which competes with Rank-L) therefore allows Rank -L signalling from osteoblasts - osteoclasts - bone resorption
    -PTH acts on kidney to convert 25-hydroxycholecalciferol to its active form1,25 dihydroxyvitamin D -which increases calcium and phosphate gut absorption and decreases calcium and phosphate excretion at DCT
    PTH- increases intestinal calcium absorption and at the kidneys and increases phosphate excretion at kidneys
196
Q

What is hyperparathyroidism?

A

Parathyroid gland produce too much parathyroid hormone

197
Q

What are the primary causes of hyperparathyroidism?

A

excessive PTH secretion usually caused by parathyroid adenoma (or sometimes parathyroid hyperplasia) - mc (hyperparathyroid–> hypercalcaemia

198
Q

What is the secondary cause of hyperparathyroidism?

A

physiological compensatory hypertrophy of all parathyroids in response to hypocalcaemia , vitamin deficiency or chronic kidney disease

199
Q

What is the tertiary cause of hyperparathyroidism?

A

Glands become autonomous, producing excess PTH even after the correction of calcium deficiency. occurs after many years of secondary hyperparathyroidism .

200
Q

What is the malignant cause of hyperparathyroidism?

A

neoplasms (squamous cell lung cancer, breast, renal) secrete PTHrp; ectopically mimics PTH

201
Q

What is the presentation of hyperparathyroidism?

A

Hypercalcemia
- bones (excess resorption therefore osteopenia), stones (kidney stones), Groans(abdo pain and constipation) and psychedelic moans (depression and anxiety)

202
Q

What is the diagnosis for primary hyperparathyroidism?

A
  • high PTH
    -high calcium
    -low phosphate
    -high ALP - alkaline phosphate
203
Q

What is the diagnosis of secondary hyperparathyroidism?

A
  • high PTH
    -low calcium
    -high phosphate
    -high ALP
204
Q

What is the diagnosis of tertiary hyperparathyroidism?

A
  • high PTH
    -high calcium
    -high phosphate
    -high ALP
205
Q

What are other tests needed to diagnose hyperparathyroidism?

A

XRKUB- renal stones
DEXA scan - bone density
U+Es - access renal function
ECG- short QT - hypercalcaemia

206
Q

What is the treatment for hyperparathyroidism?

A

primary = removal of PTH adenoma/ parathyroidectomy of all 4 glands
secondary/tertiary = treat cause
malignant = remove tumour

207
Q

What is a complication of hyperparathyroidism?

A

Acute severe hypercalcemia

208
Q

How do you treat acute severe hypercalcemia?

A
  • give IV fluids + bisphosphonates
209
Q

What is more common hypoparathyroidism or hyperparathyroidism?

A

Hyper most common

210
Q

What is the primary cause of hypoparathyroidism?

A

PTH gland failure
- Di George syndrome –> familial, PTH glands failed to develop
-idiopathic

211
Q

What is the secondary cause of hypoparathyroidism?

A
  • after surgery (parathyroid/ thyroidectomy) - most common
212
Q

What is pseudohypoparathyroidism?

A
  • peripheral PTH resistance
    -short stature + small 4th/5th metacarpals
213
Q

What are the symptoms of hypoparathyroidism?

A
  • hypocalcemia
    -CATS go numb
    -Convulsions, arrhythmia ,tetany, numbness
214
Q

What are the signs of hypoparathyroidism?

A

Hypocalcemia signs:
-Chvostek’s (twitching of facial muscles when CN7 tapped over parotid)
-Trousseau’s - carpopedal spasms when applying tourniquet to forearm

215
Q

What is the diagnosis of hypoparathyroidism?

A
  • low PTH
    -low calcium
  • high phosphate
    -ECG; long QT
216
Q

What is the treatment for hypoparathyroidism?

A
  • calcium supplements + vitamin deficiency supplements -AdCalD3
217
Q

What are the causes of hypercalcemia?

A
  • hyperparathyroid
    -bone malignancy
    -Drugs- thiazides
    -Excess Ca++ intake
    -hyperthyroid
    -dehydration
218
Q

What is the diagnosis for hypercalcemia?

A

-serum calcium >2.6mmol/L
ECG - long QT
- low PTH due to negative feedback except in hyperparathyroid

219
Q

What is the presentation of hypercalcemia?

A

BONES - pain, osteoporosis
STONES - kidney stones
GROANS - abdominal pain + constiaption
PSYCHEDILIC MOANS - anxiety+ depression
+decrased muscle tone + contractions

220
Q

What are the causes of hypocalcemia?

A
  • CKD( low vit D activation)
    -Severe vitamin D deficiency
    -hypoparathyroidism
    -Drugs - bisphosphonates
221
Q

What is the diagnosis for hypocalcemia?

A

Serum calcium <2.1mmol/L
ECG - short QT
-PTH always high except in hypoparathyroidism

222
Q

What is the presentation of hypocalcemia?

A

CATs go numb
- convulsions, arrhythmias, tetany, numbness
Chvosteks signs
Trousseau’s sign
- increased muscle tone + contractions

223
Q

What are the causes of hyperkalemia?

A

-AKI
-Drugs - NSAIDs,Spironolactone, ACEi
-Addisons
-DKA
-increased intake

224
Q

What is the pathology of hyperkalemia?

A

Increased potassium decreases threshold action potential therefore easier depolarisation + abnormal heart rhythms

225
Q

What is the presentation of hyperkalamia?

A
  • fast irregular pulse
    -myalgia - muscle aches and pains
226
Q

What is the diagnosis of hyperkalemia?

A

U+E = >5.5mmol/L - hyper
>6.5mmol/L - medical emergency

ECG:
-absent p waves
-prolonged PR
-Tall tented T waves
-Wide QRS

227
Q

What is the treatment for hyperkalemia?

A

if urgent - calcium gluconate - stabilise cardiac membrane then insulin and dextrose

Non urgent- insulin and dextrose

228
Q

What are the causes of hypokalaemia?

A
  • Thiazides and loop diuretics
    -Conns
    -Renal tubular acidosis
    GI losses
    -decreased intake
229
Q

What is the presentation of hypokalaemia?

A

hypotonia, hyporrefelxia , arrhtymias - AF

230
Q

What is the diagnosis for hypokalemia?

A

U+Es - <3.5mmol/L- hypo
<2.5mmol/L - emergency

ECG:
-small inverted T waves
-prominent u waves
-ST depression
-PR prolongation

231
Q

What is the treatment for hypokalaemia?

A

K+ replacement
-aldosterone agonist - spironolactone

Phase 2a (9 decks)

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