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Flashcards in Endocrine Deck (71)
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1

How much of the bodes calcium is bound to albumin?

How is this binding affected by altering pH of the blood?

40% to albumin

Acidotic reduces binding ∴ increased Ca2+
Alkalotic increases binding ∴ reduces Ca2+

2

How is calcium excreted?

Renally
90% prox tubule via Na reabsorption
10% distal tubule via PTH regulation

3

When is PTH secreted and by what cells

Ca low
Vit D low
Phosphate high

Chief cells (parathyroid)

4

What are the 4 diff ways that PTH works

Increases Renal Ca reabsorption
Increases bone Ca resorption
Increases Vit D activation (indirect increase GI absorption)
Increases phosphate excretion (renal)

5

What is the action of Vit D?
Describe the 2 ways of obtaining VitD
Describe the 2 steps of activation

Increases GI absorption of Ca + Phos

Endogenously synth in skin (D3 - cholecalciferol)
Exogenously (D2 - ergocalciferol) (dairy)

1st hydroxylation - Liver
2nd hydroxylation - Kidneys (1,25-(OH)2-D2/3) (ACTIVE)

6

When is Calcitonin secreted and by what cells
What is its action

When plasma Ca low
Parafollicular C cells
Antagonises PTH to reduce Ca

7

List the conditions of:
MEN1 syndrome (3)
MEN2a (3)
MEN2b (3)

Parathyroid (hyperplasia/adenoma)
Pancreatic endocrine (gastrinoma/insulinoma)
Pituitary (adenoma)

Thyroid medullary
PCC
Parathyroid (hyperplasia)

MEN2a minus parathyroid
Mucosal neuroma
Marfanoid appearance

8

What are the 2 main causes of hypercalcaemia

List 7 other less common causes

97%
Primary hyperparathyroid
OR
Malignancy (mets/myeloma/paraneo)

Excess Vit D (exo, granulomas (TB/Sarc), lymphoma tx)
Excess Calcium intake (milk-alkali synd)
Hereditary (hypocalciuric hypercalcaemic)
Drugs (thiazides, lithium)
Severe AKI
Thyrotoxicosis
Addison's

9

What level of Ca is classed as acute hypercalcaemia?
Outline the management

Ca > 3.5 + severe sx

Fluids (3–6L 0.9% in 24hrs) ± diuretics (risk overload)
ABCDE
Agua (above) (1-2x normal maintenance)
Bisphosphonates
Calcitonin
Dialysis (if renal impaired)
Essence of the problem

10

What are the symptoms of hypercalcaemia? (5)

BONES
Bone pain
Patho #

STONES
Renal stones
AKI/CKD

THRONES
Polyuria

GROANS
Abdo pain
Pancreatitis / GI ulcer
Vom / Constipation

MOANS
Depression / Confusion
Tiredness
Mm weakness

11

What Ix are included for a bone profile? (4)

Ca
Phosphate
PTH
ALP

12

What further Ix would you do on someone with hypercalcaemia? (2+3)

ECG (QT narrowing + arrest!)
LFTs (ALP)
±24hr urinary Ca
±DEXA (extent osteoporosis)
±Technetium uptake (localise tumour)

13

What is the management of primary hyperparathyroidism?

Parathyroidectomy (even for asymp)
14d AdCal

NB same for tertiary

14

What are the causes of secondary hyperparathyroidism? (2)
What is the cause of tertiary?

Renal disease
Vit D defc

Tertiary: from longstanding secondary (e.g. CKD)

15

List the differential causes of hypocalcaemia with low PTH

Idiopathic
T: post-op thyroid / neck irrad
A: primary
M: severe hypomagnesia
N: malignancy / sarcoid infil
C: DiGeorge (congenital absence)

16

List the differential causes of hypocalcaemia with high PTH

Alkalosis (increased albumin binding)
Acute pancreatitis (precipitates into abdo)
Acute hyperphosphat (renal failure, rhabdo, tumour lysis)

Bisphosphonates
Calcitonin
vitD Defc

17

What are the features of hypocalcaemia (2+4)

Central irritability:
Seizures
Depression/anxiety

Peripheral irritability:
Tetany /cramps
Carpo-pedal spasms
Perioral anaesthesia
Cataracts

18

What is the treatment for hypocalcaemia?

AdCal
± IV calcium gluconate (for severe) (give as bolus + maintenance)

19

List some causes of HHS (5)

Glucose rich foods
Steroids
Thiazides
B-blockers
Intercurrent illness (infection/MI)

20

What features may present in HHS (4)

Dehydration (v severe > DKA)
No raised ketones but ± mild lactic acidosis
Stupor/coma/seizures
Evidence underlying illness

21

How is HHS Dx?

Calculate osmolality:
2Na + Urea + Glucose (NNUG)
HHS = >320 (normal 280-295)

22

What are the actions of alpha cells in the pancreas in hypoglycaemia (3)

Increase gluconeo
Increase glycogenolysis
Reduce glycogen synthesis

23

Outline the management of hypoglycaemia

If can swallow: liquid glucose + recheck 10mins
If can't: IM glucagon (500mcg/1mg)
Long-acting carb when S+S improve

If no glucagon/no response/alc consumed:
999 + IV gluc (20% 100ml) (upto 3)
IM glucagon if delayed IV

24

List differentials for a diffuse goitre (5)

Iodine req high (physiolog): preg/puberty
Iodine defc (dietary)

Autoimm: Graves/Hashimoto's
Inflamm: DeQuervain's (subacute) / Reidel's

Drugs: anti-thyroid / io excess / amIOdarone / lithium

25

List differentials for a nodular goitre (8)

Solitary:
Thyroid malig
Metastasis
Lymphoma

Multinodular:
Infiltration (TB/Sarcoid)
Toxic goitre
Subacute thyroiditis

26

What Ix are necessary for a thyroid swelling?
Give reasons for each

TFTs - hypo/hyper/eu
Thyroid autoAbs - autoimm
FBC - related anaemia
ESR - thyroiditis/autoimm
USS - solid/cystic
CT Neck/Thorax - if pressure sx
FNAC - benign/malig

27

List some triggers for a thyroid crisis/storm (3)
List the features (5)

Body stress in uncontrolled hyperthyroid:
Childbirth
Infection
Surgery

Hyperpyrexia
Severe tachycardia
Profuse sweating
Vomiting/diarrhoea
Confusion/psychosis

28

How is a thyroid crisis treated?

Propylthiouracil
Propanolol
Sodium iodide
High-dose steroid
ICU/Supportive

29

What Ix help Dx Graves?

TFTs: TSH low / T3-4 high
TSH-R Ab (95% specific)
Technetium uptake scan (if TSH-R Ab not present) - Graves: diffuse (vs toxic 'hot' / thyroiditis cold)
CT/MRI orbit (assess extent eye disease)

30

What treatments are available for thyrotoxicosis

What is done for Graves/non-Graves

Propanolol (non-selective B-blocker) – for sx
Anti-thyroids (carbimazole/propylthiouracil)
Radioactive iodine
Surgery

Graves:
titration of anti thyroids / RAI or surg if no remission
Non-Graves:
1st line RAI/Surg