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Endocrine Diseases Flashcards

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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
What are secondary causes of diabetes?
Acromegaly + cushings Haemachromatosis Thiazides/ corticosteroids
26
What is type 1 diabetes?
Type 4 hypersensitivity; autoimmune destruction of pancreatic B cells leading to absolute insulin deficiency
27
What is the epidemiology of T!DM?
- Young patients -lean -North European descent
28
What are the risk factors of T1DM?
- HLA DR3/ HLA DR4 -other autoimmune diseases -environmental infection
29
What is the pathology of T1DM?
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
30
What is the presentation of T1DM?
Lean young patient with polydipsia, nocturia, polyuria, polyphagia and weight loss Glycosuria +/- sigs of ketogenesis
31
What is the diagnosis of T1DM?
random blood glucose= >11.1 mol/L = T1DM Fasted blood glucose = >7mmol/L = T1DM HbA1C= 48mmol/L or >6.5% = T1DM
32
What are the normal levels for RBG, FBG and HbA1C?
<11.1mmol/L - normal RBG <6.0mmol/L - normal FBG <6% - normal Hb1AC
33
What is the Hb1AC level for pre-diabetes?
5.7%- 6.4%
34
What is the treatment for T1DM?
Basal bolus Insulin Basal = longer acting, to maintain stable insulin levels throughout the days bolus= faster acting, 30mins pre-prandial to give 'insulin spike'
35
What are the different types of insulin?
rapid -novorapid short- regular insulin intermed- NPH long- glargine
36
What is the main complication of T1DM?
Diabetic ketoacidosis
37
What are the causes of DKA?
poorly managed T1DM, infection/illnesses
38
What is DKA?
increasing hyperglycaemia and rising ketones
39
What is the presentation of DKA?
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
40
what is the pathology of DKA?
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)
41
What is the diagnosis of DKA?
Ketones - blood >3mmol/L Hyperglycemic >11.1mmol/L Acidosis (met) <7.3pH or >15mmol HCO3- +Ketonuria, glycosuria and hyperkalaemia
42
What is the treatment for DKA?
ABCDE - emergency 1st line - always fluid - dehydration then insulin (+glucose to prevent hypoglycaemia and K+ to replenish potassium stores)
43
What is type 2 diabetes?
Peripheral insulin resistance with peripheral insulin deficiency - carbohydrates, lipids and beta amyloid deposits in pancreas
44
What are the risk factors for T2DM?
-FHX -smoking -obesity -HTN -sedentary lifestyle
45
What is the pathology of T2DM?
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.
46
What is the presentation of T2DM?
obese, hypertensive, older, with polydipsia, polyuria, nocturia, glycosuria Aconthisis nigricans - dark pigmented skin folds -severe insulin resistance
47
What is the diagnosis of T2DM?
same as T1DM: FBG: >7mmol/L RBG >11.1mmol/L HbA1C >6.5%/ 48<
48
What are the pre diabetes states?
IGT - impaired glucose tolerance test IFG-impaired fasting glucose
49
What are the results of IGT?
normal FBG >6mmol/L 2hr OGTT - 7.8-11mol/L - pre diabetic
50
What are the results for IFG?
FBG- 6.1-6.9 mmol/L normal 2hr OGTT <7.8 mmol/L
51
What are the normal ranges for OGTT?
oral glucose tolerance test normal - <7.8mmol/L pre-diabetic 7.8-11 diabetic >11.1
52
what are the normal ranges for FBG?
normal - <6 prediabetic 6.1 - 6.9 diabetic >7
53
What are the ranges for RBG?
normal <11.1 Diabetes >11.1
54
What are the ranges for Hb1AC?
normal - <42/<6% pre-diabetic 42-47/ 6-6.4% Diabetics >48/ >6.5%
55
What is the treatment for T2DM?
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
56
Do you gain or lose weight on Metformin, gliclazide, DPP4, glitazones?
metformin - lose gliclazide- gain DPP4 inhibitors - no change Glitazones - gain
57
What is the main complication of T2DM?
Hyperosmolar hyperglycaemic state
58
What is the pathology of HHS?
excessive hepatic gluconeogenesis not totally insulin deficient therefore ketosis doesn't occur - glucose osmotically active therefore excessive glucose = hyperosmolar blood
59
What is the presentation of HHS?
severe T2DM, low consciousness
60
What is the diagnosis of HHS?
Heavy glycosuria, increase plasma osmolarity(>300mmol/L) with hyperglycaemia - no ketonuria
61
What is the treatment of HHS?
1. insulin ( and potassium and glucose) 2. Iv fluid - saline -LMWH- anticoagulant as they have thicker blood
62
What are DM microvascular complications?
retinopathy, neuropathy( Charcot foot), nephropathy (nephrotic syndrome, CKD)
63
What are DM macrovascular complications?
Cardiovascular (MI), cerebrovascular (stroke), peripheral arterial disease (PVD)
64
What is hypoglycaemia ?
Abnormally low blood glucose
65
What are the causes of hypoglycaemia ?
often resulting from diabetes drugs; sulfonylureas or insulin Non diabetic - oral, liver failure, Addisons
66
What do sulfonylureas do?
stimulate increased insulin production and secretion
67
What is the presentation of hypoglycaemia ?
decreased consciousness, dizziness, sometimes will faint
68
What is the treatment for hypoglycaemia?
IV glucose - IM glucagon
69
Where does the thyroid sit?
C5-T1 2 lobes connected with isthmus
70
Where does the inferior thyroid artery arise from?
off thyrocervical trunk
71
Where does the superior thyroid artery arise from?
off external carotid artery
72
What are the follicular cells?
Iodine trapping - from circulation
73
What is the colloid?
Synthesis of T3+T4 - produces thyroglobulin
74
What is the T3+T4 process?
- 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
75
What is hyperthyroidism?
Excess thyroid hormone in the blood
76
What is the most common cause of hyperthyroidism?
Graves disease
77
What are other causes of hyperthyroidism?
- toxic multinodular goitre -ectopic TSH secretion -toxic adenoma -drugs= amiodarone, iodine -de quervains thyroiditis - post viral infection
78
What is the epidemiology of hyperthyroidism?
common in females
79
What is the pathology of hyperthyroidism?
TSH- R autoantibodies - excessively stimulate thyroid
80
What are the symptoms of hyperthyroidism?
- heat intolerance -diarrhoea -weight loss -hyperphagia -anxiety -oligomenorrhoea
81
What are the signs of hyperthyroidism?
-Goitre -tacycardia -pretibial myxoedema - muscle wasting -fine tremor
82
What is the diagnosis of hyperthyroidism?
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
83
What is the treatment for hyperthyroidism?
1st line - carbimazole(CI in pregnancy) + propranolol alongside -radioactive 131iodine; definitive treatment - destroys excess thyroid tissue (CI in pregnancy) -surgery
84
What is a side effect of carbimazole?
agranulocytosis - presents as sore throat
85
what is a complication of hyperthyroidism?
thyroid storm - rapid deterioration thyrotoxicosis - high level of T4- systemic decompression;AF,HTN and coma, heart failure, osteoporosis
86
What is the treatment of Thyroid storm?
propylthioruracil + KI
87
What is graves disease?
Autoimmune condition , that causes hyperthyroidism
88
What is the pathology of graves disease?
increased levels of TSH receptor stimulating antibody
89
What is the presentation of graves?
- opthhalmopathy - bulging eyes -Dermopathy - pretibial myxedema -characteristic rash - acropachy
90
What is hypothyroidism?
Lack of thyroid hormone
91
What is the epidemiology of hypothyroidism?
women ageing postpartum
92
What is the main cause in the developed world?
Hashimotos Thyroiditis
93
What is hashimotos thyroiditis?
Autoimmune thyroid destruction
94
What is the main cause in the developing world?
iodine deficiency
95
What are other causes of hypothyroidism?
post part rum thyroiditis -amiodarone -secondary causes - hypopituitarism
96
What is post part rum thyroiditis?
same mechanism as hashimotos but 1- acute - presents during pregnancy 2-resolves by itself after a year of Sx
97
What is the pathology of hypothyroidism?
Anti-tpo (thyroid peroxidase) antibodies high vs thyroid
98
What are the symptoms of hypothyroidism?
cold intolerance, constipation, weight gain, lethargy , menorrhagia
99
What are the signs of hypothyroidism?
bradycardia, slow reflexes, cold hands, Goitre, pretibial myxoedema
100
What is the diagnosis of hypothyroidism?
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
What is the treatment for hypothyroidism?
Levothyroxine(T4) - careful with dose, can cause iatrogenic hyperthyroidism
102
What is a complication of hypothyroidism?
Myxoedema coma(often infection precipitated); rapidly decrease T4
103
What is the presentation of myxoedema coma?
hypothermia, loss of consciousness , heart failure
104
What is the treatment myxoedema coma?
Levothyroxine Abx + hydrocortisone - until adrenal insufficiency has been ruled out
105
What are the types of thyroid carcinomas?
Papillary -mc Follicular Anaplastic - mets the most Lymphoma medullary cell
106
What is the behaviour, spread and prognosis of papillary ?
young local spread good prognosis
107
What is the behaviour, spread and prognosis of Follicular ?
middle age Spread to lung/bone usually good prognosis
108
What is the behaviour, spread and prognosis of anaplastic?
aggressive local spread very poor prognosis
109
What is the behaviour, spread and prognosis of lymphoma?
variable behaviour usually poor prognosis
110
What is the behaviour, spread and prognosis of medullary cells?
familial Local and metastasises poor prognosis
111
Where does thyroid carcinomas metastasise to ?
Lung -50% Bone-30% liver-10% brain-5%
112
What is the presentation of thyroid carcinomas ?
mostly present at thyroid nodules - hard + irregular - local compression -hoarse voice -dysphagia -any metastasises
113
What is the diagnosis of thyroid carcinoma?
Fine needle aspiration biopsy TFts, ultrasound thyroid
114
What is the treatment of thyroid carcinomas?
papillary + follicular = thyroidectomy + radioactive given Anaplastic + lymphoma = palliative mostly
115
What is cushings syndrome?
Refers to the abnormalities resulting from excess cortisol from any cause
116
What is cushings disease?
Used to describe the clinical state of free circulating glucocorticoids , occurs when a pituitary adenoma secretes excess ACTH
117
What are the ACTH dependent causes of cushings syndrome?
Cushing disease - mc ectopic ACTH - sclc
118
What are the ACTH independent causes of cushings syndrome?
steroid use -mc overall cause adrenal adenoma
119
What is the pathology of cushings syndrome?
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
What is the ACTH mechanism?
hypothalamus - crh - pituitary - ACTH - adrenal gland - cortisol
121
What is the presentation of cushings syndrome?
moon face central obesity purple abdo striae osteoporosis thin easy bruising skin plethoric complexion easy infections muscle atrophy
122
What is the diagnosis of cushings?
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
What is the dexamethasone suppression test?
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
What is the treatment for cushings disease?
transphenoidal resection or bilateral adrenalectomy
125
What is a complication of bilateral adrenalectomy?
Nelson's syndrome; pituitary tumour will continue to enlarge with no negative feedback from adrenals- increased ACTH + skin hyperpigmentation
126
What is the treatment for adrenal adenoma?
unilateral adrenelectomy
127
What is the treatment for ectopic ACTH?
surgical removal - SCLC
128
What is a complication of cushings?
osteoporosis, secondary DM
129
What is adrenal insufficiency?
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
What are the primary causes of adrenal insufficiency?
main cause in developed world - Addisons main cause in developing world - TB
131
What are the secondary causes of adrenal insufficiency?
Iatrogenic - suppression of HPA axis from steroids
132
What are other causes of adrenal insufficiency?
adrenal mets - lung, liver,breast Adrenal haemorrhage
133
What is the pathology of Addisons?
Addison's destroys adrenal cortex by autoantibodies therefore high ACTH and low adrenal hormones. High ACTH stimulates proopiomelanocortin (melanocytes) resulting in hyperpigmentation
134
What is the pathology of HPA suppression?
HPA suppression therefore low ACTH and low Adrenal hormones and no hyperpigmentation
135
What is the presentation of adrenal insufficiency?
Lethargy, weight loss postural hypotension vitiligo change in body hair hyperpigmentation (1) hypoglycaemia Abdo pain + vomiting
136
What is the diagnosis of adrenal insufficiency?
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
\What is the treatment for adrenal insufficiency?
Hydrocortisone, fludrocortisone If trauma/ infection. Double dose of hydrocortisone
138
What is adrenal crisis?
Severe adrenal insufficiency especially hydrocortisolemia, ; N+v, renal failure, level of consciousness
139
What is the treatment for adrenal crisis?
immediate hydrocortisone +IV saline + dextrose if hypoglycaemic
140
What is acromegaly?
Excess growth hormone- HGH in adults (after epiphyseal fusion) Gigantism in children (before epiphyseal fusion)
141
What are the causes of acromegaly?
Functional pituitary adenoma or ectopic GH releasing hormone from a carcinoid tumour
142
What is the pathology go acromegaly?
Hypothalamus --> GHRH--> anterior pituitary--> GH--> liver-IGF-1 which exerts effects on rest of body In acromegaly high IGF-1 (produced by liver)
143
What is the presentation of acromegaly ?
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
What is the diagnosis of acromegaly?
IGF-1 serum level high - always first line screening Impaired glucose tolerance is gold standard - OGTT
145
What is the treatment of acromegaly?
1st line - transsphenoidal surgery otherwise : somatostatin analogue - octreotide dopamine agonist - bromocriptine GH agonist. -pregvisomant
146
What is the complication of acromegaly?
T2DM, sleep apnoea
147
What is hyperprolactinemia?
Most common in females, high serum prolactin
148
What are the causes of hyperprolactinoma?
prolactinoma, drugs(ecstasy) -mc
149
what is the presentation of hyperprolactinoma?
Amenorrhoea, galactorrhea, sexual dysfunction, decreased libido, erectile dysfunction, decreased testosterone , bitemporal hemianopia
150
What is the diagnosis of hyperprolactinoma?
high serum prolactin
151
What is the treatment fro hyperprolactinoma?
dopamine agonists- bromocriptine - shrinks tumour as dopamine inhibitor of prolactin
152
What is conns syndrome - hyperaldosteronism?
Excess aldosterone independent of RAAS
153
What is the most common secondary cause of hypertension?
hyperaldosteronism
154
What are the causes of hyperaldosteronism?
2/3 - adrenal adenoma (Conn's) 1/3- bilateral adrenal hyperplasia
155
What is the cause of secondary hyperaldosteronim?
excess renin which increases aldosterone
156
What is the pathology of hyperaldosteronism?
increase in aldosterone = increase in Na+ / H2O and decrease in K+, hypertension with hypokalaemia
157
What is the presentation of hyperaldosteronism?
resistant hypertension -unfixable with ACE-i/BB hypokalaemia; muscle weekness, parasthesia, polydipsia, polyuria
158
What is the diagnosis of hyperaldosteronism?
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
What is the treatment for hyperaldosteronism?
Surgery - laparoscopic adrenelectomy Spironolactone - aldosterone antagonist
160
What is diabetes inspidus?
Tool little ADH from posterior pituitary gland or kidneys aren't responding to ADH.
161
What are the 2 types of diabetic inspidus?
cranial - low ADH secretion Nephrogenic - decreased kidney response to ADH
162
What are the causes of cranial diabetic inspidus?
ADH gene mutation, pituitary adenomas, idiopathic
163
What are the causes of nephrogenic diabetic inspidus?
Renal tubular acidosis, ADH-R mutation, polyuria
164
What is the pathology of diabetic insipidus ?
Low ADH, increased H2O losses in urine; dilute high volumes
165
What is the presentation of diabetic insipidus?
polyuria, polydipsia, hypernatramia, lethargy, confusion, severe dehydration
166
What is the diagnosis of diabetic insipidus?
- 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
How do you differentiate between cranial and nephrogenic urine osmolality?
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
What is the treatment for diabetes insipidus?
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
What is syndrome of inappropriate ADH, (SIADH)?
Inappropraitely released ADH; dilute euvolemia -cause of hyponatremia
170
How does SIADH cause hyponatremia?
excess ADH = more water retention therefore compensatory Na+ excretion to maintain euvolemia
171
What are the causes of SIADH?
S- sclc I- infection/ immunocompromised -TB A-abscesses D- drugs-SSRI, H-head trauma
172
What is the pathology of SIADH?
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
What is the presentation of SIADH?
Sx of hyponatremia - vomiting, headache, low consciousness (decreased GCS), muscle weaknesss Low Na+ -seizures, neurological complications ;brainstem herniation
174
What causes a brainstem herniation?
low Na+ means high compensatory H2O; enters skull = increased ICP - causes hyponatremic encephalopathy -risk of brainstem herniating through Forman magnum (tentorial herniation)
175
What is the diagnosis of SIADH?
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
What is the treatment for SIADH?
Fluid restrict + hypertonic saline to concentrate blood Treat underlying cause - tumour excision Chronic cases - Drugs; furosemide, vasopressin antagonist
177
What is a carcinoid tumour?
malignant tumour of enterochromaffin cells which produce 5-HT/serotonin - only the neoplastic cells no symptoms
178
What is carcinoid syndrome?
When carcinoid tumour metastasises to liver, constellation of Sx
179
Where are the carcinoid tumours?
Mostly GIT at appendix and terminal ileum- also can be lungs
180
What is the presentation of carcinoid syndrome?
Flushing, diarrhoea, tricuspid incompetence (valve lesion) may have RUQ pain, respiratory problems
181
What is the diagnosis of carcinoid syndrome>
Liver USS - positive mets increase In 5-Hydroxyindoleacetic acid in urine - major 5HT metabolite - GS CT/MRI to locate primary tumour
182
What is 5HT?
5- hydroxytryptamine (serotonin)
183
What is the treatment of carcinoid syndrome?
Surgically excise primary tumour - definitive octreotide (somatostatin analogue) - can block tumour hormones
184
What is a complication of carcinoid syndrome?
carcinoid crisis; life threatening Sx constellation
185
What is the treatment for carcinoid crisis?
SST analogue - octreotide - high dose
186
What is pheochromocytoma?
Adrenal medullary tumour , secretes catecholamines (Adr,NAd)
187
What are the causes of pheochromocytoma?
usually inherited associated with - Men 2a +2b (multiple endocrine neoplasia) -neurofibromatosis 1 - tumours deposited along nerve myelin sheath
188
What is MEN2?
A rare, genetic disorder that affects the endocrine glands and can cause tumors in the thyroid gland, parathyroid glands, and adrenal glands.
189
What is the presentation of pheochromocytoma?
hypertension, pallor, very sweaty, tachycardic
190
What is the diagnosis of pheochromocytoma?
plasma metanephrines + normetanephrines - diagnostic - more sensitive readings than NAd/Adr as longer half life - urinary catecholamines - CT image tumour
191
What is the treatment of pheochromocytoma?
Drugs - alpha blocker first (phenozybenzamine) then beta blocker - atenolol - prevents reactive vasoconstriction - surgery - excise tumour
192
What are metanephrines?
made when your body breaks down hormones called catecholamines metanephrines and normetanephrines are metabolites of the catecholamines
193
What are the complications of pheochromocytoma?
HTN crisis (180/20 + BP) causes - XR contrast, TCA, opiates Treat -phentolamine - alpha blocker
194
What is the parathyroid gland?
4 glands on posterior aspect of thyroid - very sensitive to change in calcium
195
What is the action of the parathyroid gland?
- 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
What is hyperparathyroidism?
Parathyroid gland produce too much parathyroid hormone
197
What are the primary causes of hyperparathyroidism?
excessive PTH secretion usually caused by parathyroid adenoma (or sometimes parathyroid hyperplasia) - mc (hyperparathyroid--> hypercalcaemia
198
What is the secondary cause of hyperparathyroidism?
physiological compensatory hypertrophy of all parathyroids in response to hypocalcaemia , vitamin deficiency or chronic kidney disease
199
What is the tertiary cause of hyperparathyroidism?
Glands become autonomous, producing excess PTH even after the correction of calcium deficiency. occurs after many years of secondary hyperparathyroidism .
200
What is the malignant cause of hyperparathyroidism?
neoplasms (squamous cell lung cancer, breast, renal) secrete PTHrp; ectopically mimics PTH
201
What is the presentation of hyperparathyroidism?
Hypercalcemia - bones (excess resorption therefore osteopenia), stones (kidney stones), Groans(abdo pain and constipation) and psychedelic moans (depression and anxiety)
202
What is the diagnosis for primary hyperparathyroidism?
- high PTH -high calcium -low phosphate -high ALP - alkaline phosphate
203
What is the diagnosis of secondary hyperparathyroidism?
- high PTH -low calcium -high phosphate -high ALP
204
What is the diagnosis of tertiary hyperparathyroidism?
- high PTH -high calcium -high phosphate -high ALP
205
What are other tests needed to diagnose hyperparathyroidism?
XRKUB- renal stones DEXA scan - bone density U+Es - access renal function ECG- short QT - hypercalcaemia
206
What is the treatment for hyperparathyroidism?
primary = removal of PTH adenoma/ parathyroidectomy of all 4 glands secondary/tertiary = treat cause malignant = remove tumour
207
What is a complication of hyperparathyroidism?
Acute severe hypercalcemia
208
How do you treat acute severe hypercalcemia?
- give IV fluids + bisphosphonates
209
What is more common hypoparathyroidism or hyperparathyroidism?
Hyper most common
210
What is the primary cause of hypoparathyroidism?
PTH gland failure - Di George syndrome --> familial, PTH glands failed to develop -idiopathic
211
What is the secondary cause of hypoparathyroidism?
- after surgery (parathyroid/ thyroidectomy) - most common
212
What is pseudohypoparathyroidism?
- peripheral PTH resistance -short stature + small 4th/5th metacarpals
213
What are the symptoms of hypoparathyroidism?
- hypocalcemia -CATS go numb -Convulsions, arrhythmia ,tetany, numbness
214
What are the signs of hypoparathyroidism?
Hypocalcemia signs: -Chvostek's (twitching of facial muscles when CN7 tapped over parotid) -Trousseau's - carpopedal spasms when applying tourniquet to forearm
215
What is the diagnosis of hypoparathyroidism?
- low PTH -low calcium - high phosphate -ECG; long QT
216
What is the treatment for hypoparathyroidism?
- calcium supplements + vitamin deficiency supplements -AdCalD3
217
What are the causes of hypercalcemia?
- hyperparathyroid -bone malignancy -Drugs- thiazides -Excess Ca++ intake -hyperthyroid -dehydration
218
What is the diagnosis for hypercalcemia?
-serum calcium >2.6mmol/L ECG - long QT - low PTH due to negative feedback except in hyperparathyroid
219
What is the presentation of hypercalcemia?
BONES - pain, osteoporosis STONES - kidney stones GROANS - abdominal pain + constiaption PSYCHEDILIC MOANS - anxiety+ depression +decrased muscle tone + contractions
220
What are the causes of hypocalcemia?
- CKD( low vit D activation) -Severe vitamin D deficiency -hypoparathyroidism -Drugs - bisphosphonates
221
What is the diagnosis for hypocalcemia?
Serum calcium <2.1mmol/L ECG - short QT -PTH always high except in hypoparathyroidism
222
What is the presentation of hypocalcemia?
CATs go numb - convulsions, arrhythmias, tetany, numbness Chvosteks signs Trousseau's sign - increased muscle tone + contractions
223
What are the causes of hyperkalemia?
-AKI -Drugs - NSAIDs,Spironolactone, ACEi -Addisons -DKA -increased intake
224
What is the pathology of hyperkalemia?
Increased potassium decreases threshold action potential therefore easier depolarisation + abnormal heart rhythms
225
What is the presentation of hyperkalamia?
- fast irregular pulse -myalgia - muscle aches and pains
226
What is the diagnosis of hyperkalemia?
U+E = >5.5mmol/L - hyper >6.5mmol/L - medical emergency ECG: -absent p waves -prolonged PR -Tall tented T waves -Wide QRS
227
What is the treatment for hyperkalemia?
if urgent - calcium gluconate - stabilise cardiac membrane then insulin and dextrose Non urgent- insulin and dextrose
228
What are the causes of hypokalaemia?
- Thiazides and loop diuretics -Conns -Renal tubular acidosis GI losses -decreased intake
229
What is the presentation of hypokalaemia?
hypotonia, hyporrefelxia , arrhtymias - AF
230
What is the diagnosis for hypokalemia?
U+Es - <3.5mmol/L- hypo <2.5mmol/L - emergency ECG: -small inverted T waves -prominent u waves -ST depression -PR prolongation
231
What is the treatment for hypokalaemia?
K+ replacement -aldosterone agonist - spironolactone

Phase 2a (9 decks)

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