phase 2 endo Flashcards

1
Q

how to remember addisons symptoms

A

“lean, tanned, tired, tearful”

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2
Q

what Abnormalty is seen in SIADH

A

hyponatraemia

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3
Q

1st line test for acromegaly

A

IGF-1

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4
Q

describe calcium in primary hyperparathyroidism

A

raised

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5
Q

what produces and secretes corticosteroids such as cortisol

A

Zona fasciculata

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6
Q

what does zona glomerulosa produce

A

mineralocorticoids e/g aldosterone

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7
Q

what does zona reticularis produce

A

produces and secretes androgens

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8
Q

what can corticosteroid withdrawal lead to

A

Secondary adrenal insufficiency

because the adrenal glands atrophy

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9
Q

types of cancers that can cause SIADH.

A

Small cell carcinoma
Prostate cancer
Pancreatic cancer
Lymphomas
Cancer of the thymus

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10
Q

hyperkalaemia signs/symptoms

A

Muscle weakness/ Painful cramping / Paraesthesia
Neurological derangement/ irritability/ anxiety
Palpitations
Abdo cramping and diarrhoea
Dyspnoea
Hyperreflexia

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11
Q

what is a loss of peripheral vision called

A

Bitemporal hemianopia – pressure on the optic chiasm from a pituitary adenoma

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12
Q

first line treatment for GH secreting pituitary adenoma

A

Transsphenoidal resection of the pituitary adenoma

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13
Q

how do thyroid adenomas usually present

A

as solitary thyroid nodules

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14
Q

first line test for cushings

A

Overnight dexamethasone suppression test

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15
Q

most common cause of Cushing’s Syndrome?

A

exogenous causes e.g. glucocorticoid use (corticosteroids)

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16
Q

which artery does the superior thyroid artery branch from?

A

) External carotid artery

17
Q

what causes Hypercalcaemia of malignancy

A

by excessive secretion of parathyroid hormone released
peptide (PTHrP)

18
Q

What drug is commonly used to reduce thyroid hormone production? (

A

Carbimazole

19
Q

how does carbimazole work

A

Blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin, this
leads to decreased thyroid hormone production.

20
Q

pathophysiology of Primary hyperthyroidism`

A

TSH-R autoantibodies formed (1) - Autostimulation of thyroid gland(1)`

21
Q

signs of hyperthyroid disease

A

tachycardia, fine tremor, thin hair, ptosis, lid lag, opthalmoplegia, pretibial myxoedema, goitre,

22
Q

medical treatments for hyperthyroidism

A
  • Carbimazole, either titrated to effective dose or given concurrent with thyroxine to prevent iatrogenic hypothyroidism
  • Beta-blockers (eg. propanolol) for rapid symptom control
  • Radioiodine
23
Q

What is HbA1C a measure of, and how often is it usually taken

A

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

24
Q

what hormone is decreased in conns syndrome

A

Renin, produced in the kidneys

25
Q

hypokalameia ecg

A
  • Prolongation of the PR interval
  • T wave flattening and inversion
  • ST depression
  • Prominent U waves (best seen in the precordial leads)
26
Q

two places where alpha adrenorecptors can be found and what it does there

A

Blood vessels; Constricts

Sphincters (e.g bladder neck); Contracts

27
Q

two places where beta adrenergic receptors are found and what they do there

A

Beta 1 - contract heart muscle

Beta 2 - bronchodilation of airways

28
Q

How to avoid hypertensive crisis in surgery for phaechromocytoms

A

Give phentolamine (an Alpha receptor blocker)

29
Q

why does a dopamine blocker cause hyperprolactinoma

A

Prolactin is inhibited by dopamine so the use of a dopamine blocker will cause prolactin levels to increase due to the reduced inhibition

30
Q

first line treatment for hyperprolactinoma

A

a dopamine agonist such as bromocriptine or cabergoline

31
Q

gold standard treatment for hyperprolactinom

A

transsphenoidal surgery and removal of the tumour

32
Q

classic triad of symptoms for t1dm

A

polydipsia, polyuria and weight loss

33
Q
A