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CP3 Medicine > Endocrine > Flashcards

Endocrine Flashcards

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
Q

List differentials for a nodular goitre (8)

A

Solitary:
Thyroid malig
Metastasis
Lymphoma

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

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26
Q

What Ix are necessary for a thyroid swelling?

Give reasons for each

A 
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
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27
Q

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

List the features (5)

A

Body stress in uncontrolled hyperthyroid:
Childbirth
Infection
Surgery

Hyperpyrexia
Severe tachycardia
Profuse sweating
Vomiting/diarrhoea
Confusion/psychosis
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28
Q

How is a thyroid crisis treated?

A 
Propylthiouracil
Propanolol
Sodium iodide
High-dose steroid
ICU/Supportive
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29
Q

What Ix help Dx Graves?

A

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
Q

What treatments are available for thyrotoxicosis

What is done for Graves/non-Graves

A

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
Q

What are the indications for surgical management of hyperthyroid (3)
What are the post-op comps (4)

A

Suspect malig
Large toxic goitre
Others failed / CI

Haematoma
Hypothyroid
Hypocal (hypoparathy – often transient)
Vocal cord paresis

32
Q 
Commonest causes for hypothyroid (2)
Uncommon causes (4)
Rare causes (2)
A

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
Q

What Ix should be done for suspected hypothy (3+2)

A

TFTs: high TSH / low T3-4
TPO Abs (Hashimotos)
FBC (micro/macrocytic anaemia)

CK – mm hypothy (raised)
Chol – hepatic hypothy (raised)

34
Q

What are the diff types of thyroid cancer, in order of their frequency?

A

Papillary (70%) - young females
Follicular (20%)
Medullary (5%)
Aplastic (<5%)

35
Q

How is papillary carcinoma managed?

A

Dx: hemithyroidectomy (FNAC too sim to adenoma)
Radical surgical resection ± radio-iodine
Thyroglobulin (post-op tumour marker)

36
Q

What are the features of a non-functioning pituitary adenoma (5)

A

Bitemporal hemianopia
Ocular palsies
ICP raised - HEADACHE

Hypopituitarism:
Fatigue/Myalgia/Hypotension/Insipidus/Hypothy)
Hypothal compression sx:
Appetite/thirst/sleep-wake

37
Q

What are the features of a functioning pituitary adenoma? (4)

A

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
Q

What is the management for a prolactinoma

SEs of this

A

Lifelong Dopamine agonists (bromocriptine/ropinarole)
SEs:
Dizzy/N+V/Syncope
Fibrosis - pulm/cardiac/retroperitoneal

39
Q

List the features of Acromegaly

List some complications

A 
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
Q

How is Acromegaly dx?

How is it managed?

A

IGF-1 raised (indicates GH levels over 24hrs)
GTT (should suppress GH)

Somatostatin analogues (to shrink)
Surgery (transphenoidal)
41
Q

What is metabolic syndrome?

A

T2DM
Central Obesity
Hyperlipidaemia

42
Q

List the DDx causes of 2º DM

A

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
Q

What are the Dx criteria for a DKA

How are the diff severities classed

A

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
Q

What are the indications for an urgent R/V in DKA (4)

A

Severe (pH <7.1)
Sats/BP unresponsive to Tx
Pt unresponsive (drowsy)
Pt pregnant

45
Q

Outline (simple terms) the management of DKA

FIPURI

A 
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
Q

List some causes of HHS (6)

A 
Glucose-rich foods
Steroids
Thiazides
B-blockers
Infection
MI
47
Q

Outline (simple terms) management of HHS

FIPPRI

A 
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
Q

When during a hypoglycaemic episode are pts advised to come into hosp? (4)

How are they treated in hospital ?

A

No response
No glucagon available
Alc consumed

100ml 20% glucose (upto x3)
IM glucagon if delayed access

49
Q

What are the diff types of Diabetic Neuropathy (5)

A 
Polyneuropathy symmetrical
Mononeuropathy (single/multiplex)
Acute painful
Autonomic
Amyotrophy (rare) – painful quadriceps wasting
50
Q

What are the presenting features of:

Diabetic symmetrical polyneuropathy (6)

A

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
Q

What are the presenting features of:

Diabetic Acute Painful neuropathy (3)

A

Painful burning
Feet / shins / anterior thigh
Worse at night

52
Q 
What are the common sites of:
Diabetic Mononeuropathy (2)
A 
Ocular palsies (CN3/4/6)
Isolated peripheral nn's e.g. nn compressions
53
Q

What are the presenting features of:

Diabetic Amyotrophic Neuropathy

A

Rare
Middle-aged men
Painful progressive quadriceps wasting

54
Q

What are the presenting features of:

Sympathetic (4) + Parasympathetic (4) autonomic neuropathy in diabetes

A 
Sympathetic:
• Lack sweating
• Post hypo
• Horner's
• Ejaculatory failure
Parasymp:
• Holmes-Adie pupil
• Constipation
• Urinary retention
• Erec dysfunc
55
Q

How is diabetic nephropathy monitored for / treated?

A

Monitoring:
• Microalb: Early morning urine alb:creatinine (>3)

Treatment:
• Good BP control
• Give ACEi if any micro-albumin (regardless BP)

56
Q

What are 2 CIs to RAI (radioactive iodine)

What 3 things should be advised if undertaking RAI therapy

A

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
Q

What are the causes of panhypopituitarism (2; 3+3)

A

Pituitary destrn:
• Surg removal
• Squished by tumour
• Sheehan’s

Hypothalamic destrn:
• Infarct
• Infection
• Mass: Sarcoidosis / Craniopharyngioma

58
Q

What are the causes of Cushing’s? (4)

A

Exogenous steroid therapy**
Cushing’s DISEASE (pituitary ACTH)
Paraneoplastic ectopic ACTH
Adrenal tumour/hyperplasia (ACTH low)

59
Q

What are the familial causes of PCC (3)

A

MEN 2a/b
NF
von Hippel-Lindau

60
Q

How is PCC Dx?

A

Urinary metadrenaline/normetadrenaline (x3)

CT/MRI/Functional (locate tumour)

61
Q

What is Addison’s disease exactly?

What hormones are affected

A

Primary adrenal insufficiency
• Cortisol
• Aldosterone
• Sex steroids

62
Q

How is Addison’s different to hypothalamic-pituitary disease?

A

Aldosterone (mineralo) is indépendant of HPA (from AT2)
Androgens can be independent of HPA

Thus HPA (hypothal-pit disease) only on ACTH/Cortisol

63
Q

What are the causes of Addison’s (5)

A 
V: Adrenal haemorrhage (Waterhouse-Friderichsen)
I: TB* (worldwide)
T/I: Overwhelming sepsis
Autoimmune adrenalitis** (UK)
N: lymphoma / metastatic (lung/breast)
64
Q

What are the features of Addison’s disease (4)

A

Non-specific: fatigue/myalgia/weakness/wt loss/depression

Syncope / Post hypo / Dehydration

Pigmentation (hands/scars)
Hair loss (androgenic – pubic/axillary)
65
Q

What Ix are done to diagnose Addison’s?

What Ix are done in identifying the cause?

A

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
Q

What is the treatment for Addison’s?

A

Long-term hydrocortisone
Long-term fludrocortisone
Precautions: ‘steroid card/bracelet’ / urgent IM hydro

67
Q

How does an Addisonian crisis present?

How should it be managed?

A

NB sim to DKA but glucose low

Fever
N+V
Shock
Hypogly
Hyponat
Hyperkal

Tx: IV fluids + IV hydrocortisone

68
Q

What is Conn’s syndrome exactly?

What are the possible features (6)

A

Primary hyperaldosteronism

Young females
Asymp
Resistant HTN
Headaches
Hypokal: 
• Mm cramps/weakness
• Polyuria
69
Q

What are the causes of primary hyperaldosteronism (2)

A

Conn’s syndrome (60%)

Bilateral adrenal hyperplasia (30%)

70
Q

What Ix are done into hyperaldosteronism? (2)

What Ix are done to identify the cause (2)

A

U+Es: Hypokalaemia
Raised Aldosterone:Renin (Fludrocortisone supp test)

CT (ddx conn's / hyperplasia)
Adrenal scintigraphy (radioactive uptake)
71
Q

How is Conn’s/Hyperaldosteronism treated?

A

Pre-Op spironolactone (control HTN/hypokal)

Laparoscopic adrenalectomy

CP3 Medicine (7 decks)

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