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Endocrine Flashcards

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1
Q

How much of the bodes calcium is bound to albumin?

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

A

40% to albumin

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

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2
Q

How is calcium excreted?

A

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

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3
Q

When is PTH secreted and by what cells

A

Ca low
Vit D low
Phosphate high

Chief cells (parathyroid)

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4
Q

What are the 4 diff ways that PTH works

A

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

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5
Q

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

A

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)

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6
Q

When is Calcitonin secreted and by what cells

What is its action

A

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

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7
Q

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

A

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

Thyroid medullary
PCC
Parathyroid (hyperplasia)

MEN2a minus parathyroid
Mucosal neuroma
Marfanoid appearance

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8
Q

What are the 2 main causes of hypercalcaemia

List 7 other less common causes

A

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

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9
Q

What level of Ca is classed as acute hypercalcaemia?

Outline the management

A

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
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10
Q

What are the symptoms of hypercalcaemia? (5)

A

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

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11
Q

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

A

Ca
Phosphate
PTH
ALP

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12
Q

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

A 
ECG (QT narrowing + arrest!)
LFTs (ALP)
±24hr urinary Ca
±DEXA (extent osteoporosis)
±Technetium uptake (localise tumour)
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13
Q

What is the management of primary hyperparathyroidism?

A

Parathyroidectomy (even for asymp)
14d AdCal

NB same for tertiary

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14
Q

What are the causes of secondary hyperparathyroidism? (2)

What is the cause of tertiary?

A

Renal disease
Vit D defc

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

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15
Q

List the differential causes of hypocalcaemia with low PTH

A 
Idiopathic
T: post-op thyroid / neck irrad
A: primary
M: severe hypomagnesia
N: malignancy / sarcoid infil
C: DiGeorge (congenital absence)
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16
Q

List the differential causes of hypocalcaemia with high PTH

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

Bisphosphonates
Calcitonin
vitD Defc

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17
Q

What are the features of hypocalcaemia (2+4)

A

Central irritability:
Seizures
Depression/anxiety

Peripheral irritability:
Tetany /cramps
Carpo-pedal spasms
Perioral anaesthesia
Cataracts
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18
Q

What is the treatment for hypocalcaemia?

A

AdCal

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

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19
Q

List some causes of HHS (5)

A 
Glucose rich foods
Steroids
Thiazides
B-blockers
Intercurrent illness (infection/MI)
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20
Q

What features may present in HHS (4)

A

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

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21
Q

How is HHS Dx?

A

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

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22
Q

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

A

Increase gluconeo
Increase glycogenolysis
Reduce glycogen synthesis

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23
Q

Outline the management of hypoglycaemia

A

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

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24
Q

List differentials for a diffuse goitre (5)

A 
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

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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
31
What are the indications for surgical management of hyperthyroid (3) What are the post-op comps (4)
Suspect malig Large toxic goitre Others failed / CI Haematoma Hypothyroid Hypocal (hypoparathy – often transient) Vocal cord paresis
32
``` Commonest causes for hypothyroid (2) Uncommon causes (4) Rare causes (2) ```
Hashimoto's (initial hyper then atrophic thyroiditis) Post-hyperthyroid treatment Iodine defc (commonest worldwide) Thyroiditis Drugs (amiodarone, lithium) Secondary: hypothalamus/pituitary Congenital agenesis Neoplastic infiltration
33
What Ix should be done for suspected hypothy (3+2)
TFTs: high TSH / low T3-4 TPO Abs (Hashimotos) FBC (micro/macrocytic anaemia) CK – mm hypothy (raised) Chol – hepatic hypothy (raised)
34
What are the diff types of thyroid cancer, in order of their frequency?
Papillary (70%) - young females Follicular (20%) Medullary (5%) Aplastic (<5%)
35
How is papillary carcinoma managed?
Dx: hemithyroidectomy (FNAC too sim to adenoma) Radical surgical resection ± radio-iodine Thyroglobulin (post-op tumour marker)
36
What are the features of a non-functioning pituitary adenoma (5)
Bitemporal hemianopia Ocular palsies ICP raised - HEADACHE Hypopituitarism: Fatigue/Myalgia/Hypotension/Insipidus/Hypothy) Hypothal compression sx: Appetite/thirst/sleep-wake
37
What are the features of a functioning pituitary adenoma? (4)
Mass effects as per non-func (Bitemp/Ocular/ICP/Comp sx - appetite/thirst/sleep) Acromegaly Cushings Hyperprolactinaemia NB TSH/FSH/LH secretion in tumours v rare
38
What is the management for a prolactinoma | SEs of this
Lifelong Dopamine agonists (bromocriptine/ropinarole) SEs: Dizzy/N+V/Syncope Fibrosis - pulm/cardiac/retroperitoneal
39
List the features of Acromegaly | List some complications
``` Appearance: Hand/feet enlarge Jaw/supraorbital ridge prominent Interdental separation Macroglossia ``` ``` Systemic: Hypopituitarism (tiredness/myalgia/insipidus/hypothy) Sweating Headaches Bitemporal hemianopia ``` ``` Comps: HTN Diabetes Cardiomyopathy Colorectal cancer ```
40
How is Acromegaly dx? | How is it managed?
IGF-1 raised (indicates GH levels over 24hrs) GTT (should suppress GH) ``` Somatostatin analogues (to shrink) Surgery (transphenoidal) ```
41
What is metabolic syndrome?
T2DM Central Obesity Hyperlipidaemia
42
List the DDx causes of 2º DM
Pancreatic: • CF • Carcinoma • Chronic pancreatitis ``` Endocrine: • Cushing's • Acromegaly • Hyperthyroid • PCC • Glucagonoma ``` ``` Congenital: • Friederich's ataxia • Myotonic dystrophy • Insulin-R abns • Haemochromatosis ``` ``` Drug-Induced: • Thiazides • Corticosteroids • Antipsychotics • Antiretrovirals ```
43
What are the Dx criteria for a DKA How are the diff severities classed
D: Glucose >11 (or previously known DM) K: Ketones >3 (blood) / >2 (urine) A: VBG – pH < 7.35 / HCO3- <15 Mild: pH 7.3 – 7.35 Mod: pH 7.1 – 7.3 Severe: pH <7.1
44
What are the indications for an urgent R/V in DKA (4)
Severe (pH <7.1) Sats/BP unresponsive to Tx Pt unresponsive (drowsy) Pt pregnant
45
Outline (simple terms) the management of DKA | FIPURI
``` A–E inc. Obs + Bloods Once suspect: • Fluid 0.9% (1L in 1hr, 500ml in 10min if SBP<90) • Insulin (50u Actrarapid in 50ml 0.9% at 0.1u/kg/hr) • Potassium consider (if <5.4) • Urgent R/V consider • Reassess / Recommence • Identify cause ```
46
List some causes of HHS (6)
``` Glucose-rich foods Steroids Thiazides B-blockers Infection MI ```
47
Outline (simple terms) management of HHS | FIPPRI
``` A–E inc. Obs + Bloods Once suspect: • Fluids (1L 1hr) • ± Insulin (0.05u/kg.hr) • Potassium consider • Prophylactic LMWH • Reassess (GOOF-UE) / Recommence • Identify cause ```
48
When during a hypoglycaemic episode are pts advised to come into hosp? (4) How are they treated in hospital ?
No response No glucagon available Alc consumed 100ml 20% glucose (upto x3) IM glucagon if delayed access
49
What are the diff types of Diabetic Neuropathy (5)
``` Polyneuropathy symmetrical Mononeuropathy (single/multiplex) Acute painful Autonomic Amyotrophy (rare) – painful quadriceps wasting ```
50
What are the presenting features of: | Diabetic symmetrical polyneuropathy (6)
Initial vibration/deep pain/temp Then glove + stocking "walking on cotton wool" Then proprio ("lose balance when washing face") Ulcers Interosseous wasting Deformity (Charcot's)
51
What are the presenting features of: | Diabetic Acute Painful neuropathy (3)
Painful burning Feet / shins / anterior thigh Worse at night
52
``` What are the common sites of: Diabetic Mononeuropathy (2) ```
``` Ocular palsies (CN3/4/6) Isolated peripheral nn's e.g. nn compressions ```
53
What are the presenting features of: | Diabetic Amyotrophic Neuropathy
Rare Middle-aged men Painful progressive quadriceps wasting
54
What are the presenting features of: | Sympathetic (4) + Parasympathetic (4) autonomic neuropathy in diabetes
``` Sympathetic: • Lack sweating • Post hypo • Horner's • Ejaculatory failure ``` ``` Parasymp: • Holmes-Adie pupil • Constipation • Urinary retention • Erec dysfunc ```
55
How is diabetic nephropathy monitored for / treated?
Monitoring: • Microalb: Early morning urine alb:creatinine (>3) Treatment: • Good BP control • Give ACEi if any micro-albumin (regardless BP)
56
What are 2 CIs to RAI (radioactive iodine) | What 3 things should be advised if undertaking RAI therapy
CI to RAI: • Pregnancy • Active Graves' ophthalmopathy Counsel on: • Small increased risk thyroid cancer • Avoid prolonged child contact 3wks / preg 6m • No effects on fertility / congen malfs / other cancers
57
What are the causes of panhypopituitarism (2; 3+3)
Pituitary destrn: • Surg removal • Squished by tumour • Sheehan's Hypothalamic destrn: • Infarct • Infection • Mass: Sarcoidosis / Craniopharyngioma
58
What are the causes of Cushing's? (4)
Exogenous steroid therapy** Cushing's DISEASE (pituitary ACTH) Paraneoplastic ectopic ACTH Adrenal tumour/hyperplasia (ACTH low)
59
What are the familial causes of PCC (3)
MEN 2a/b NF von Hippel-Lindau
60
How is PCC Dx?
Urinary metadrenaline/normetadrenaline (x3) | CT/MRI/Functional (locate tumour)
61
What is Addison's disease exactly? | What hormones are affected
Primary adrenal insufficiency • Cortisol • Aldosterone • Sex steroids
62
How is Addison's different to hypothalamic-pituitary disease?
Aldosterone (mineralo) is indépendant of HPA (from AT2) Androgens can be independent of HPA Thus HPA (hypothal-pit disease) only on ACTH/Cortisol
63
What are the causes of Addison's (5)
``` V: Adrenal haemorrhage (Waterhouse-Friderichsen) I: TB* (worldwide) T/I: Overwhelming sepsis Autoimmune adrenalitis** (UK) N: lymphoma / metastatic (lung/breast) ```
64
What are the features of Addison's disease (4)
Non-specific: fatigue/myalgia/weakness/wt loss/depression Syncope / Post hypo / Dehydration ``` Pigmentation (hands/scars) Hair loss (androgenic – pubic/axillary) ```
65
What Ix are done to diagnose Addison's? | What Ix are done in identifying the cause?
U+Es inc. Ca/Glucose Short synacthen (ACTH stim) test ± FBC (anaemia) ``` Adrenal autoAbs (21-hydroxylase) (autoimm) If autoAbs –ve: CT / CXR (TB/met) ```
66
What is the treatment for Addison's?
Long-term hydrocortisone Long-term fludrocortisone Precautions: 'steroid card/bracelet' / urgent IM hydro
67
How does an Addisonian crisis present? | How should it be managed?
NB sim to DKA but glucose low ``` Fever N+V Shock Hypogly Hyponat Hyperkal ``` Tx: IV fluids + IV hydrocortisone
68
What is Conn's syndrome exactly? | What are the possible features (6)
Primary hyperaldosteronism ``` Young females Asymp Resistant HTN Headaches Hypokal: • Mm cramps/weakness • Polyuria ```
69
What are the causes of primary hyperaldosteronism (2)
Conn's syndrome (60%) | Bilateral adrenal hyperplasia (30%)
70
What Ix are done into hyperaldosteronism? (2) | What Ix are done to identify the cause (2)
U+Es: Hypokalaemia Raised Aldosterone:Renin (Fludrocortisone supp test) ``` CT (ddx conn's / hyperplasia) Adrenal scintigraphy (radioactive uptake) ```
71
How is Conn's/Hyperaldosteronism treated?
Pre-Op spironolactone (control HTN/hypokal) | Laparoscopic adrenalectomy

CP3 Medicine (7 decks)

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