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MRCP Revision > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Prediabetes Impaired fasting glucose

A

due to hepatic insulin resistance (more likely to develop T2DM than IGT).

fasting glucose 6.1-7.0 (need to do OGTT to rule out T2DM dx)

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2
Q

Impaired glucose tolerance

A

due to muscle insulin resistance.

OGTT 2hrs 7.8 to 11.1

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3
Q

Rx for prediabetes (IFG/IGT)

A

lifestyle mod, yearly f/u, metformin if heading towards T2DM despite participation

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4
Q

Which form of prediabetes (IFG or IGT) is one more likely to develop T2DM with

A

IFG

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5
Q

Dx for T2DM

A

Fasting glucose >7. Random glucose/2hrs post OGTT >11.1. Symptomatic x1, asymptomatic x2

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6
Q

Metformin MOA

A

biguanide, activates AMPK, reduces hepatic gluconeogenesis, increases peripheral insulin sensitivity

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7
Q

How to titrate metformin up

A

slowly (1wk before increasing dose)

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8
Q

What to do if meformin SE unacceptable

A

convert to MR

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9
Q

metformin SE

A

lactic acidosis, reduced B12 absorption, GI upset

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10
Q

Contraix for metformin

A

ckd, tissue hypoxia, iodine contrast, ETOH

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11
Q

Sulfonylurea moa

A

binds to ATP-dependent K (atp) channel on pancreatic beta cells (closes them), increases pancreatic insulin secretion.

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12
Q

sulfonylurea SE

A

hypo, weight gain, SIADH, cholestatic liver dysf, peripheral neuropathy.

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13
Q

Sulfonylurea contraix

A

pregnancy
breastfeeding

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14
Q

Meglitinides MOA

A

like sulfonylureas

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15
Q

When to give meglitinides instead?

A

for erratic lifestyles

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16
Q

Meglitinide SEs

A

weight gain, hypoglycaemia (less than sulfonylureas)

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17
Q

Glitazones SE

A

weight gain, fluid retention, liver dysfunction, fractures

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18
Q

Glitazones MOA

A

PPAR gamma and alpha agonism

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19
Q

Gliptins MOA

A

DPP-4 inhibitor, increases peripheral incretin levels

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20
Q

Gliptins SE

A

pancreatitis

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21
Q

Acarbose MOA

A

intestinal alpha glucosidase inhibitor

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22
Q

Acarbose SE

A

increased delivery of carbs to colon –> flatulence, diarrhoea

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23
Q

GLP-mimetics - when to give and how

A

exenatide (must be given within 60 mins pre-morning/evening meals), liraglutide (just OD). Must be combined with metformin + sulfonylurea.

Indicated if BMI>35, or if insulin is unacceptable

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24
Q

GLP- mimetics SE

A

nausea, vomiting, pancreatitis, renal impairment

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25
Q

Do gliptins cause weight gain?

A

no

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26
Q

Do gliptins cause hypoglycaemia

A

no

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27
Q

SGLT-2 inhibitor action

A

reversible inhibition of sodium glucose contransporter at PCT

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28
Q

SGLT-2 inhibitor SEs

A

urinary/genital infections
Fournier’s gangrene
ketoacidosis
lower-limb amputations
weight loss

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29
Q

Thiazolidinediones MOA

A

PPAR-gamma agonism,

act on intracellular nuclear receptors, reduce peripheral insulin resistance

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30
Q

Thiazoliniediones SE

A

weight gain, LFT derangement, fluid retention (worsened with insulin which itself has potential of causing fluid retention), fractures, bladder Ca

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31
Q

Contraix for thiazolinediones

A

HF

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32
Q

HbA1c % to mmol/mol conversion

A

(Average BM=2*HBA1c (%) -4.5).

6%=42mmol/mol, add 11mmol/mol for every %

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33
Q

What causes lower-than-expected HbA1c?

A

(dependent on RBC lifespan, so anything causing shortened RBC lifespan)

Sickle cell, G6PD def, hereditary spherocytosis, haemodialysis

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34
Q

What causes higher than expected HbA1c?

A

Vit B12/folate def, IDA, splenectomy

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35
Q

At what HbA1c do you add a 2nd drug for pts on metformin?

A

58 (7.5%)

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36
Q

How often do you monitor HbA1c after adding 2nd drug on top of metformin?

A

every 6 months, 3-6 months until stable

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37
Q

What HbA1c target do you go for when on a drug causing hypoglycaemia?

A

53 (7%)

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38
Q

When to give SGLT-2 in T2DM

A

As 2nd line, if QRISK>10%, CVD/IHD, HF

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39
Q

When to give GLP-1 mimetic?

A

4th line in T2DM, switch one of 3 drugs with GLP-1 mimetic

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40
Q

How to start insulin for T2DM on metformin?

A

continue metformin,
start with human NPH insulin (isophane, intermediate-acting), taken at bed-time/twice daily

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41
Q

Rules for metformin during ramadan?

A

metformin doses should be split 1/3 before sunrise, 2/3 after sunset

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42
Q

Rules for sulfonylureas in Ramadan

A

give for after sunset

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43
Q

Food with high glycaemic index

A

white rice, baked potato, white bread

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44
Q

Food with medium glycaemic index

A

couscous, boiled new potato, digestive biscuits, brown rice, porridge

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45
Q

Food with low glycaemic index

A

fruit, veg, peanuts

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46
Q

How to treat peripheral neuropathy

A

Amitriptyline, duloxetin, gabapentin, pregabalin (try 3 other 3 drugs if 1st is ineffective)

Tramadol as rescue therapy for severe neuropathic pain

topical capsaicin for localised pain

pain management clinics

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47
Q

T2DM related gastroparesis sx

A

erratic blood glucose control, bloating, vomiting

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48
Q

Rx for T2DM relatedd gastroparesis

A

metoclopramide, domperidone, erythromycin

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49
Q

Forms of GI autonomic neuropathy in diabetes

A

gastroparesis
chronic diarrhoea (at nigh)
GORD (reduced lower oesophageal sphincter pressure)

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50
Q

Diabetic foot disease Rx

A

screening on annual basis for ischaemia (by palpation of DP, PT pulses) and neuropathy (10g monofilament)

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51
Q

Mortality in HHS

A

20%

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52
Q

precipitants of HHS

A

intercurrentillness
dementia
sedatives

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53
Q

HHS sx

A

over many days, dehydration, polyuria, polydipsia, lethargy, N&V, reduced GCS, focal neuro, hyperviscosity.

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54
Q

Dx for HHS

A

hyperglycaemia (>30),

hyperosmolality (>320)

no ketoacidosis.

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55
Q

HHS Rx

A

fluids
insulin only if BMs don’t fall to IVF
VTE prophylaxis

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56
Q

HHS complications

A

hyperviscosity-related (infarcts etc)

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57
Q

When to add metformin in T1DM?

A

if BMI>25 as likely to have insulin resistance too

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58
Q

how are ketones produced in DKA

A

by uncontrolled lipolysis → excess free fatty acids → ketone bodies (beta hydroxybutyrate, acetoacetate).

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59
Q

Precipitants of DKA

A

infection, missed insulin, MI

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60
Q

DKA sx

A

abdo pain, polyuria, polydipsia, dehydration, Kussmaul respiration, acetone-smelling breath

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61
Q

Dx for DKA

A

glucose>11
pH<7.3
bicarb<15
ketones>3/ketonuria++

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62
Q

Rx for DKA

A

IVF 1st
0.1unit/kg/hr fixed rate insulin
once BM<14, 10% dextrose at 125ml/hr with saline
Monitor K (may need KCL if K 3.5-5.5)

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63
Q

DKA resolution

A

pH>7.3
ketones<0.6
bicarb>15
Eating and drinking
(should resolve within 24hrs)
Switch to SC insulin

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64
Q

Compl of DKA

A

gastric stasis, VTE, arrhythmias (2ndarly to hyperK/hypoK), cerebral oedema (children esp vulnerable with IVF esp 4-12hrs post fluids), hypoK, hypoglycaemia, ARDS, AKI

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65
Q

Causes of hypoglycaemia

A

insulinoma (increased ratio of proinsulin to insulin), insulin/sulfonylureas, liver failure, addison’s, alcohol (exaggerated insulin secretion, effect of alcohol on pancreatic microcirculation, redistribution of pancreatic blood flow from exocrine into endocrine parts), nesidioblastosis (beta cell hyperplasia)

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66
Q

Hormones in response to hypoglycaemia

A

reduced insulin, increased glucagon, GH, cortisol later released, increased SNS.

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67
Q

Rx for hypoglycaemia

A

in community, oral glucose 10-20g/glucogel/dextrogel. In hospital, if alert as community, if unconscious/no swallow, IV 20% glucose or IM/SC glucagon

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68
Q

Insulinoma sx, assx

A

neuroendocrine tumour from pancreatic islets of langerhans cells. Most common pancreatic endocrine tumour. 10% malignant, 10% multiple. 50% MEN1 assx.

Sx: Hypoglycaemia early in morning, just before meal, rapid weight gain, high insulin, raised proinsulin:insulin ratio, high C-peptide.

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69
Q

Dx of insulinoma

A

supervised, prolonged fasting (up to 72hrs)
CT pancreas

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70
Q

Rx for insulinoma

A

surgery
diazoxide, somatostatin if not for surgery

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71
Q

Addison’s sx

A

Sx: lethargy, weakness, anorexia, N&V, weight loss, ‘salt-craving’, hyperpigmentation (palmar creases), vitiligo, loss of pubic hair in women (DHEA deficiency due to loss of functioning adrenal tissue and androgen deficiency), hypotension, hypoglycaemia, hypoNa, hyperK

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72
Q

Causes of Addison’s

A

autoimmune 80% in UK.

Primary: TB, mets, meningococcal septicaemia (Waterhouse-Friderichsen syndrome), HIV, antiphospholipid, Nelson’s syndrome (post-b/l adrenalectomy)

Secondary: pituitary disorders (tumours, irradiation, infiltration). Exogenous steroids.

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73
Q

Addisonian crisis sx:

A

collapse, shock, pyrexia

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74
Q

Causes of Addisonian crisis

A

sepsis/surgery, adrenal haemorrhage (Waterhouse-Friderichsen), steroid withdrawal.

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75
Q

Addisonian crisis Rx

A

IV/IM Hydrocortisone 100mg 6hrly until stable then oral replacement after 24hrs, Fluids.

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76
Q

List steroids from Most MR/least GR activity to least MR/most GR activity

A

fludrocortisone, hydrocortisone, prednisolone, dexamethasone/betmethasone

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77
Q

SE of steroids

A

DM, weight gain, hirsutism, hyperlipidaemia, Cushing’s, osteoporosis, proximal myopathy, avascular necrosis of femoral head, infection, TB reactivation, psychosis, depression, mania, insomnia, peptic ulcers, pancreatitis, glaucoma, cataracts, growth suppression, intracranial HTN, neutrophilia, fluid retention, HTN.

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78
Q

When to do gradual withdrawals for steroids

A

if >40mg OD for >1wk/ >3wks Rx/ repeated courses

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79
Q

How common is a pituitary adenoma

A

10% of pop

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80
Q

How to classify pituitary adenomas

A

Micro <1cm, macro >1cm.

Functioning/non-functioning.

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81
Q

Rx for pituitary adenomas

A

dopamine agonists for prolactinomas
somatostatin analogues for GH-secreting adenomas
cortisol synthesis inhibitors for ACTH-secreting adenomas.
Transsphenoidal surgery, radiotherapy.

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82
Q

Where is prolactin produced

A

anterior pituitary

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83
Q

What inhibits prolactin

A

dopamine

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84
Q

Causes of high prolactin

A

prolactinoma, pregnancy, oestrogens, physiological (stress, exercise, sleep), acromegaly (⅓), PCOS, primary hypothyroidism (TRH stimulates prolactin release), dopaminergic antagonists (metoclopramide, domperidone), antipsychotics (phenothiazines, haloperidol), SSRIs, opioids

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85
Q

Acromegaly sx

A

coarse facial features, spade-like hands, increased shoe size, macroglossia, prognathism, interdental spaces, excessive sweating, oily skin (sweat gland hypertrophy), features of pituitary tumour, raised prolactin in ⅓ (with galactorrhoea), 6% MEN1.

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86
Q

Acromegaly complications

A

HTN, DM (>10%), CDM, colorectal Ca (colonoscopy at 40 + surveillance)

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87
Q

Acromegaly ix

A

IGF-1 levels,

then OGTT to confirm diagnosis (GH should be suppressed in normal, but no suppression in acromegaly, IGT also assx with acromegaly)

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88
Q

Acromegaly Rx:

A

trans-sphenoidal surgery.

somatostatin analogue (octreotide, directly inhibits GH release, effective 50-70%, as adjunct to surgery or used if inoperable)

pegvisomant OD SC (GHr antagonist, reduces IGF-1 levels in 90%, no size reduction)

dopamine agonists (bromocriptine, only in minority), external irradiation (for older patients)

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89
Q

MODY inheritance pattern

A

autosomal dominant

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90
Q

Dx of MODY

A

genetic testing

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91
Q

MODY Rx

A

sulfonylureas

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92
Q

MODY 3

A

(60%): HNF1A, progressive, higher risk for complications, Rx: low-dose sulfonylureas

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93
Q

MODY1

A

HNF4A, progressive, reduced endogenous insulin secretion, higher risk for complications

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94
Q

MODY 2

A

(20%): GCK, stable, fasting hyperglycaemia. Rx: none required

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95
Q

MODY4 gene

A

PDX1

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96
Q

MODY5 gene

A

HNF1B

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97
Q

LADA sx + dx

A

often misdiagnosed as t2dm, presents younger in life, without increased body habitus, insulin not required in early stages. Often with other autoimmune diseases.

Dx: Glutamic acid decarboxylase autoantibodies.

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98
Q

Causes of cranial DI

A

idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis

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99
Q

Causes of nephrogenic DI

A

genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel

electrolytes
hypercalcaemia
hypokalaemia

lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts

demeclocycline

tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

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100
Q

Rx for nephrogenic DI

A

thiazides, low salts

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101
Q

What does prolactin do

A

stimulates breast development, milk production, reduces GnRH pulsatility at hypothalamus, blocks action of LH on ovary/testes.

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102
Q

What is prolactin stimulated by

A

TRH, pregnancy, oestrogen, breastfeeding, sleep, stress, metoclopramide, antipsychotics

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103
Q

PTH actions

A

increases Ca, reduces PO4, increases renal Ca reabsorption, osteoclast activity (indirectly), renal 1 alpha hydroxylation of 25-hydroxycholecalciferol, reduces renal PO4 reabsorption

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104
Q

1, 25 dihydroxycholecalciferol actions

A

increases Ca, PO4, increases renal tubular reabsorption, gut absorption of Ca, increases osteoclast activity, increases renal PO4 reabsorption in proximal tubule

105
Q

1,25 dihydroxycholecalciferol actions

A

increases Ca, PO4, increases renal tubular reabsorption, gut absorption of Ca, increases osteoclast activity, increases renal PO4 reabsorption in proximal tubule

106
Q

Where is calcitonin from?

A

C cells in thyroid

107
Q

Calcitonin actions

A

inhibits osteoclasts
inhibits renal tubular Ca absorption

108
Q

Sx of hypoCa

A

Tetany, perioral paraesthesia, depression, cataracts, prolonged QTc, Trosseau’s sign (95%), Chvostek’s sign (70%) (Trousseau’s more sensitive)

109
Q

Causes of hypoCa

A

Vit D def, CKD, hypoPTH (post-surgery), pseudohypoparathyroidism (target cells insensitive to PTH), rhabdomyolysis (initial stages), hypoMg (end-organ PTH resistance), massive blood transfusions, acute pancreatitis
Hungry Bone Syndrome:

110
Q

What is hungry bone syndrome

A

rare, post-parathyroidectomy. Long-standing hyperPTH → high pre-op PTH levels → constant osteoclast activity + hyper Ca, bone demineralisation → parathyroidectomy + PTH falls rapidly → bones re-mineralise rapidly → hypoCa

111
Q

How to treat for hypoCa

A

IV Ca Gluconate (10ml 10% 10mins) if severe with sx, with ECG changes

112
Q

Causes of hyperCa from malignancy

A

PTHrP from tumour (eg squamous cell lung ca)
Bone mets
Myeloma (osteoclastic bone resorption by cytokines released from myeloma cells)

113
Q

Comonest cause of hyperCa in hospitalised and non-hospitalised

A

hospitalised: primary hyperPTH
non-hospitalised: malignancy

114
Q

causes of hyperCa

A

HyperPTH
Malignancy
granulomas (sarcoidosis, TB, histoplasmosis)
vit D intoxication
acromegaly
thyrotoxicosis
addison’s
milk-alkali syndrome
chronic Paget’s (with prolonged immobilisation)
dehydration
thiazides
calcium-containing antacids

115
Q

Rx of hyperCa

A

rehydration with saline (3-4l/day), then bisophosphonates (max effect at 7 days), consider calcitonin (quicker than bisphosphonates), steroids (if sarcoidosis), furosemide (esp if cannot tolerate fluid rehydration)

116
Q

Causes of primary hyperPTH

A

85% solitary adenoma, 10% hyperplasia, 4% multiple adenoma, 1% carcinoma

117
Q

Assx of primary hyperPTH

A

HTN, MEN I and II, peptic ulceration (hyperCa stimulates gatrin secretion, increases gastric acid production)

118
Q

Ix of primary hyperPTH

A

low PO4
urine calcium:creatinine clearance ratio>0.01
technetium-MIBI subtraction scan

XR: pepperpot skull, osteitis fibrosa cystica

119
Q

Rx for primary hyperPTH

A

Surgery (total parathyroidectomy) if: Ca>1 above normal, calciuria>400, creat clearance <30% of normal, life threatening hyperCa, nephrolithiasis, age<50, neuromuscular sx, bone mineral density reduction in femoral neck, lumbar spine, distal radius with T score <-2.5

Give cinacalcet if not for surgery (calcimimetic with allosteric activation of Ca-sensing receptor)

120
Q

PO4 and vitD levels in secondary hyperPTH

A

high PO4, low vit D

121
Q

Indications for surgery in secondary hyperPTH

A

bone pain
persistent pruritis
soft tissue calcifications

122
Q

What happens in tertiary hyperPTH

A

ongoing hyperplasia of PTH glands after correction of underlying renal disorder.

123
Q

PO4 in primary hyperPTH vs tertiary hyperPTH

A

PO4 low in primary, high in tertiary

124
Q

Rx for tertiary hyperPTH

A

allow 12 months post-transplant for resolution by itself, then consider surgery

125
Q

Benign familial hypocalciuric hypercalcaemia

A

Aut Dom
urine Ca:creatinine clearance ratio <0.01

126
Q

Cause of hypoPTH

A

2ndary to surgery

127
Q

Rx for hypoPTH

A

alfacalcidol

128
Q

PseudohypoPTH - what causes it

A

target cells insensitive to PTH, due to G protein abnormality

Aut Dom.

129
Q

Types of pseudohypoPTH

A

Type I: complete receptor defect
Type II: receptor still intact

130
Q

Sx for pseudohypoPTH

A

low IQ
short stature
shortened 4th, 5th metacarpals
obesity
round face
low Ca
high PO4
high PTH

131
Q

Dx and Ix for peudohypoPTH

A

urinary cAMP, PO4 levels post PTH infusion. Rises in true hyperPTH. PseudohypoPTH type I: neither cAMP/PO4 rises. PseudohypoPTH type II: cAMP rises

132
Q

PseudopseudohypoPTH

A

normal biochemistry but just phenotypes of pseudohypoPTH

133
Q

Hashimoto’s

A

(chronic autoimmune thyroiditis), may be acutely transiently hyperthyroid. 10x more common in women. Sx: firm, non-tender goitre. anti-TPO and thyroglobulin abs. Assx: autoimmune, MALT lymphoma

134
Q

Riedel’s thyroiditis

A

rare, dense fibrous tissue replacing normal parenchyma. Sx: hard, fixed, painless goitre, middle-aged women, retroperitoneal fibrosis

135
Q

Pendred’s syndrome genetics

A

aut rec, SLC26A4 mutation in PDS gene, Chr 7.

136
Q

Pendred’s syndrome sx

A

Defect in iodine organification. b/l sensorineural deafness, progressive, delay in academic progression, exacerbated by head trauma (avoid contact sports). Mild hypothyroid/euthyroid with goitre.

137
Q

Ix for pendred’s syndrome

A

perchlorate discharge test (TFTs often normal), genetic testing, auudiometry, MRI (one and a half turns in cochlea instead of two and a half turns).

138
Q

Rx for Pendred’s syndrome

A

Thyroid hormones
Cochlear implants

139
Q

Subclinical hypoThyroidism TFTs

A

raised TSH
normal T3, T4

Risk of progressing to hypothyroidism, which is increased with presence of autoantibodies

140
Q

Rx for subclinical hypothyroidism

A

If TSH>10: Start levothyroxine if TSH >10 on 2 separate occasions 3 months apart.

If TSH 5.5-10:
6-month trial of levothyroxine on 2 separate occasions 3 months apart + age <65yrs + symptomatic
Age >65yrs watch and wait
Asymptomatic → observe + rpt TFTs in 6 months

141
Q

When to start levothyroxine on lower starting doses (25mcg OD) in hypothyroidism

A

elderly
IHD

142
Q

How often do you check TFTs when treating for hypothyroidism

A

8-12 wks

143
Q

In pregnancy how much do you increase levothyroxine dose

A

at least 25-50mcg

144
Q

SE of levothyroxine

A

hyperthyroidism, reduced bone mineral density, angina worsening, A fib. Iron, calcium carbonate reduces absorption so give at least 4 hrs apart.

145
Q

Skin manifestations of hypothyroidism

A

dry (anhydrosis), cold, yellowish skin, non-pitting oedema, dry, coarse scalp hair, loss of lateral aspect of eyebrows, eczema, xanthomata, pruritis (in hyperthyroid too)

146
Q

Commonest cause of hyperthyroidism

A

Grave’s

147
Q

Grave’s disease sx

A

most common, 30-50 yr old women. Triad: eyes (exopthalmos, opthalmolplegia), shins (pretibial myxoedema), Acropachy (clubbing, soft tissue swelling of hands/feet, periosteal new bone formation).

148
Q

Abs in Grave’s

A

anti-TSH receptor (90%), anti-TPO (75%).

149
Q

Ix in Grave’s

A

thyroid scintigraphy shows diffuse, homogenous, increased uptake

150
Q

Thyroid eye disease sx

A

25-50%, due to anti-TSHr → inflammation

Sx: exophthalmos, conjunctival oedema, optic disc swelling, ophtalmoplegia, exposure keratopathy

151
Q

RF for thyroid eye disease

A

Smoking, radioiodine.

152
Q

Rx for thyroid eye disease

A

stop smoking
topical lubricants
steroids
radiotherapy
surgery

153
Q

Compl of thyroid eye surgery

A

exposure keratopathy (commonest)
optic neuropathy (most serious, compression of optic nerve at apex of orbit by extraocular muscles, requiring urgent intervention)
strabismus
diplopia

154
Q

When to get urgent ophthalm r/v in thyroid eye disease

A

(3Ds, 3Cs) deterioration in vision, disc swelling, de-eye (eye pop out), corneal opacity, cornea visible when eye closed, colour vision change.

155
Q

Rx for Grave’s disease

A

propanolol initially for sx control

anti-thyroid drug therapy
block-and-replace
radioiodine

156
Q

Describe Anti-thyroid drug therapy

A

start carbimazole 40mg OD, reduce gradually, for 12-18 months
fewer SE than block-and-replace

157
Q

Describe Block-and replace therapy

A

carbmazole 40mg OD, thyroxine added when euthyroid, lasts 6-9 months

158
Q

When to use radioiodine for Grave’s?

A

if relapse/resistant to ATD

159
Q

Contraix for radioiodine

A

pregnancy (avoid conception 4-6 months post Rx)
Age<16yrs
Thyroid eye disease (relative contraix)

160
Q

Carbimazole MOA

A

blocks TPO from coupling and iodinating tyrosine residues on thyroglobulin

161
Q

carbimazole SE

A

agranulocytosis
crosses placenta

162
Q

Toxic multinodular goitre

A

autonomously functioning nodules.

Ix: nuclear scintigraphy showing patchy uptake.

Rx: radioiodine.

163
Q

subacute (de quervain’s) thyroiditis:

A

post-viral infection, raised ESR

4 phases: Hyperthyroid (3-6wks) → euthyroid (1-3wks) → hypothyroid (wks-months) → normal.

Ix: scintigraphy shows globally reduced uptake.

Rx: self-limiting. Steroids if severe (esp if hypothyroid). aspirin/NSAIDs for pain

164
Q

Thyroid storm precipitants

A

thyroid/non-thyroidal surgery, trauma, infection, acute iodine load (eg contrast)

165
Q

Sx of thyroid storm

A

fever, tachycardia, confusion, N&V, HTN, HF, jaundice, LFTs deranged

166
Q

Rx for thyroid storm

A

treat underlying + IV propranolol + propylthiouracil/methimazole + Lugol’s iodine + IV dexamethasone (4mg QDS)/hydrocortisone (blocks T4 conversion to T3)

167
Q

Sick euthyroid syndrome TFTs

A

Either all TSH, T4, T3 low or TSH normal + others low

168
Q

Forms of thyroid cancer

A

Papillary 70%
Follicular 20%
Medullary 5%
Anaplastic 1%
Lymphoma

169
Q

Papillary thyroid cancer

A

70%, young females, excellent prognosis. Mixture of papillary and colloidal filled follicles. Histology: papillary projections, pale empty nuclei. Seldom encapsulated. LN mets predominate, haematogenous mets rare. Rx: total thyroidectomy + radioiodine, yearly thyroglobulin levels

170
Q

Follicular thyroid cancer

A

May be macroscopically encapsulated, microscopically capsular invasion seen (adenoma has no capsular invasion). Vascular invasion predominates. Rare multifocal disease. Rx: total thyroidectomy, radioiodine, yrly thyroglobulin levels

171
Q

Follicular thyroid adenoma

A

Follicular adenoma - usually solitary thyroid nodule, need histological assessment to exclude carcinoma

172
Q

Medullary thyroid cancer

A

C cells (parafollicular) from neural crest (not thyroid tissue), raised calcitonin, MEN2 assx (familial 20%). Both LN + haematogenous mets. Nodal disease - poor prognosis.

173
Q

Anaplastic thyroid cancer

A

Elderly females. Local invasion common. Often Not responsive to chemo, can cause pressure sx. Rx by resection. Palliation via isthmusectomy, radiotherapy. Histology: spindle, giant cells

174
Q

Thyroid lymphoma

A

rare, Hashomito’s assx (chronic infiltration of thyroid gland with B-lymphocytes, which undergo clonal proliferation, predisposing to MALT thyroid lymphoma). Histology: extranodal marginal B-cells

175
Q

Thyroid changes in pregnancy

A

increased TBG, causing increased total thyroxine (free thyroxine unaffected)

176
Q

HCG action on TSHr

A

can activate, causing transient gestational hypothyroidism

HCG falls in 2nd/3rd trimester

177
Q

Rx fo thyrotoxicosis in pregnancy

A

propylthiouracil in 1st trimester
carbimazole in 2nd trimester
T4 should be kept in upper third of normal
Thyrotrophin receptor stimulating abs should be checked at 30-36 wks

Radioiodine and block-and-replace regimes contraindicated

178
Q

Is thyroxine safe in pregnancy and breastfeeding?

A

yes to both

179
Q

How to screen for hypothyroidism in pregnancy

A

TSH measured each trimester and 6-8 weeks post-partum

180
Q

How much more thyroxine is required in pregnancy

A

by up to 50% as early as 4-6 wks

181
Q

How common is gestational DM

A

1 in 20 pregn

182
Q

RF for gestational DM

A

BMI <30, previous macrosomic baby >4.5kg, previous gestational diabetes, 1st deg relative with diabetes, ethnicity (South Asian, black Caribbean, Middle Eastern).

183
Q

How to screen and dx gestational dm

A

GTT (women with past GDM get OGTT after booking + at 24-28wks, others get it at 24-28wks).

Dx: 5678 fasting glucose >5.6, 2-hr glucose >7.8.

184
Q

Rx of gestational DM

A

if fasting glucose <7, diet → metformin if target not met within 1-2 wks → insulin. If fasting glucose >7, insulin. If 6-6.9 but complications such as macrosomia/hydramnios, give insulin. Glibenclamide as alternative to insulin

185
Q

Targets for BM management in gestational DM

A

Targets: (7.8 becomes post-1hr, add .3, .4 to 5,6 for fasting + post-2hrs) fasting 5.3, 1hr post meal 7.8, 2hrs post meal 6.4

186
Q

Rx for pre-existing diabetes in pregnancy

A

weight loss if BMI>27, stop oral hypoglycaemics, start insulin. Folic acid 5mg/day from pre-conception to 12 wks, detailed anomaly scan at 20 wks (including 4-chamber view of heart and outflow tracts), tight glycaemic control, treat retinopathy

187
Q

Hypertriglyceridaemia causes

A

DM, obesity, ETOH, Chronic renal failure, thiazides, non-selective beta blockers, unopposed oestrogen, liver disease

188
Q

Hypercholesterolaemia causes

A

nephrotic syndrome, cholestasis, hypothyroid

189
Q

When to assess for familial hypercholesterolaemia

A

cholesterol >7.5 or PMHx/1st deg FHx of premature IHD (<60yrs), if children of affected parents.

190
Q

Mutation in familial hypercholesterolaemia

A

Aut Dom. Mutations in LDL receptor protein mutations

190
Q

Dx of familial hypercholesterolaemia

A

Simon Broome criteria (cholesterol>7.5 + LDL-C>4.9, cholesterol>6.7 + LDL>4 in children, + possible/definite FHx

191
Q

Rx for familial hypercholesterolaemia

A

lipid clinic, high dose statins, screening for 1st deg relatives.

192
Q

Remnant hyperlipidaemia

A

rare cause of mixed hyperlipidaemia (high cholesterol + triglycerides) (Friedrickson type III hyperlipidaemia/broad-beta disease/dysbetalipoproteinaemia)

assx with apo-e2 homozygosity.

High IHD, PVD rates.

Impaired removal of intermediate density lipoprotein from circulation by liver.

Sx: yellow palmar creases, palmar xanthomas, tuberous xanthomas.

Rx: fibrates

193
Q

Hyperuricaemia assx

A

hyperlipidaemia
HTN
metabolic syndrome

194
Q

Causes of hyperuricaemia

A

Increased synthesis: Lesch-Nyhan, myeloproliferative disorders, purine-rich diet, exercise, psoriasis,cytotoxics

Reduced excretion: low-dose aspirin, diuretics, pyrazinamide, pre-eclampsia, ETOH, renal failure, lead

195
Q

Klinefelter’s

A

47 XXY, taller than average, lack of secondary sexual characteristics, small, firm testes (no cryptorchidism), infertile, gynaecomastia (breast Ca risk), elevated gonadotrophin levels, low testosterone. Dx by karyotype

196
Q

Kallman’s

A

X recessive. Failure of GnRH neurons to migrate to hypothalamus. Sx: delayed puberty, hypogonadism, cryptorchidism, anosmia, low sex hormones, low gonadotrophins, normal/above-average height, cleft lip/palate, visual/hearing defects. Rx: testosterone and gonadotrophin supplementation

197
Q

RF for urinary inncontinence

A

age, past pregnancy/childbirth, high BMI, hysterectomy, FHx.

198
Q

Ix for urinary incontinence

A

bladder diaries 3 days, vaginal exam, urine dip + MSU, urodynamic studies

199
Q

Describe urge incontinence

A

detrusor overactivity, urge followed by uncontrollable leakage from few drops to complete emptying

200
Q

Rx for urge incontinence

A

bladder retraining 6 wks min. Antimuscarinics - oxybutynin, (immediate release, contraix in frail, due to risk of delirium, impairment of daily functions), tolterodine (immediate release), darifenacin (OD preparation). Mirabegron (beta 3 agonist, caution in frail)

201
Q

Describe stress incontinence

A

leakage when coughing/laughing

202
Q

Rx for stress incontinence

A

pelvic floor training >8 contractions TDS min 3 months, surgical (retropubic mid-urethral tape procedures), duloxetine (SNRI, increases synaptic conc of noradrenaline and serotonin within pudendal nerve, → increases urethral striatal muscle stimulation in sphincter → enhanced contraction)

203
Q

what causes overflow incontinence

A

bladder outlet obstruction

204
Q

Functional incontinence

A

comorbidities impair ability to get to bathroom in time. Causes: dementia, sedation, injury/illness affecting ambulation

205
Q

Autoimmune polyendocrinopathy syndromes

A

Type 1: Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC), Aut rec AIRE1 gene mut, Chr 21. ⅔ of Chronic mucocutaneous candidiasis (in young child), Addison’s, primary hypoparathyroidism

Type 2: Schmidt’s syndrome, more common, polygenic, HLA DR3/4 assx, Addison’s + T1DM + autoimmune thyroid.

206
Q

Multiple Endocrine Neoplasia

A

MEN Type I: MEN1 gene, hyperCa most common presentation. 3Ps: hyperPTH (95%), Pituitary tumours (70%), Pancreatic tumours (50%, insulinoma/gastrinomas), adrenal, thyroid tumours

MEN Type IIa: RET oncogene, 1 M, 2Ps: Medullary thyroid Ca (70%, papillary also assx), hyperPTH, Phaeochromocytoma

MEN Type IIb: RET, 2Ms, 1P: Medullary thyroid Ca, Marfanoid body habitus, Phaeochromocytoma

207
Q

Phaeochromocytoma assx

A

MEN II
NF
von Hippel-Lindau

208
Q

Phaeo sx

A

10% rule: bilateral, malignant, familial, extra-adrenal (most common site: organ of Zuckerkandl, adjacent to aortic bifurcation)
Sx: HTN (90%), headaches, palpitations, sweating, anxiety

209
Q

Phaeo dx

A

24-hr urinary metanephrines

210
Q

Rx for phaeo

A

alpha (phenoxybenzamine) then beta blockade + surgery

211
Q

Dynamic pituitary function testing

A

: Give insulin, TRH, LHRH, record glucose, cortisol, GH, TSH, LH, FSH, sometimes prolactin. Rises: GH>20, cortisol>550, TSH>2, LH, FSH double

212
Q

Insulin stress test

A

to investigate hypopituitarism. IV insulin → measure GH, cortisol (should rise normally, due to hypoglycaemia).

Contraix: epilepsy, IHD, adrenal insufficiency

213
Q

Causes of hyponatraemia with urinary Na >20

A

Hypovolaemic: thizides, loop diuretics, Addison’s, diuretic stage of renal failure

Euvolaemic: SIADH, hypothyroidism

214
Q

SIADH causes

A

Cancer (small cell lung, pancreas, prostate), Neuro (stroke, SAH, SDH, meningitis/encephalitis/abscess), Infections (TB, pneumonia), Drugs (VASCC - Vincristine, anti-depressants (TCAs, SSRIs), sulfonylureas, carbamazepine, cyclophosphamide), PEEP, prophyrias.

215
Q

Ix for SIADH

A

high urinary Na + osmol

216
Q

Rx for SIADH

A

slow correction, fluid restrict, demeclocycline (reduces collecting tubule responsiveness to ADH), ADH receptor antagonists

217
Q

How to Rx for hypoNa

A

Chronic without severe sx: fluids if hypovolaemic. Fluid restrict if euvolaemic, + democlocycline, vaptans (V2 antagonists). Fluid restrict + diuretics/vaptans if hypervolaemic.
Acute with severe (<120)/symptomatic: HDU monitoring, hypertonic saline (3% NaCl)

Compl: central pontine myelinolysis: astrocyte apoptosis, demyelination. Locked in syndrome

218
Q

Causes of hypoNa with urinary Na<20

A

Extra-renal losses: diarrhoea, vomiting, sweating, burns, rectal adenoma
Water excess (Hypervolaemic): HF, cirrhosis, nephrotic syndrome, IV dextrose, psychogenic polydipsia

219
Q

Causes of hypoK with HTN

A

Cushing’s
Primary hyperaldosteronism
Liddle’s
11 beta hydroxylase def

220
Q

Causes of hypoK without HTN

A

diuretics
GI loss
RTAs
Bartter’s
Gitelman’s

221
Q

Causes of hypoK with alkalosis

A

vomiting
diuretics
Cushing’s
Conn’s

222
Q

Causes of hypoK with acidosis

A

diarrhoea
RTA
acetazolamide
patially treated DKA

223
Q

Causes of Cushing’s syndrome

A

ACTH-dependent: Cushing’s disease (80% - ACTH secreting pituitary tumour), ectopic (5-10%, small cell lung ca commonest cause, with very low K levels)
ACTH-independent: iatrogenic (commonest, steroids), adrenal adenoma (5-10%), adrenal carcinoma (rare), micronodular adrenal dysplasia

224
Q

Pseudo-Cushing’s

A

mimics Cushing’s, due to ETOH excess/severe depression, false +ve dexamethasone suppression test/24hrs urinary free cortisol. Ix: insulin stress test required

224
Q

Carney’s syndrome

A

cardiac myxoma with pituitary adenoma

225
Q

Ix for Cushing’s syndrome

A

low-dose (overnight) dexamethasone suppression test (no suppression in Cushing’s syndrome), 24-hr urinary cortisol x2, bedtime salivary cortisol x2.

Localisation tests:
9am and midnight plasma ACTH + cortisol levels: if ACTH suppressed, non-ACTH dependent cause likely

High-dose dexamethasone suppression test: If cortisol suppressed, Cushing’s disease (pituitary adenoma). If ACTH suppressed, Ectopic ACTH syndrome. If ACTH suppressed but cortisol not suppressed, Cushing’s syndrome due to other causes (eg adrenal adenomas)

CRH stimulation: if pituitary source, cortisol rises. If ectopic/adrenal then no change
Petrosal sinus sampling of ACTH to differentiate between pituitary and ectopic ACTH secretion

Insulin stress test: differentiate between Cushing’s and pseudo-Cushing’s

226
Q

Causes of primary hyperaldosteronism

A

b/l idiopathic adrenal hyperplasia (60-70%), adrenal adenoma (Conn’s - 20-30%), unilateral hyperplasia, familial hyperaldosteronism, adrenal carcinoma

227
Q

Ix for primary hyperaldosteronism

A

high aldosterone/renin ratio (-ve feedback due to Na retention lowers renin), high-res CT abdo, adrenal being sampling (differentiates unilateral and b/l sources).

228
Q

Rx for primary hyperaldosteronism

A

surgery for Conn’s, spironolactone for b/l adrenocortical hyperplasia

229
Q

Liddle’s syndrome

A

aut dom, DCT epithelial Na channel defect causing increased Na reabsorption, hyperNa, hypoK, alkalosis, HTN. Low renin+low aldosterone.

Rx: amiloride/triamterene (K-sparing)

230
Q

What kind of acidosis does RTA cause?

A

hyperchloraemic metabolic acidosis, with normal AG

231
Q

Type 1 RTA

A

(A for ACID) cannot generate acid urine in distal tubule. hypoK. Compl: nephrocalcinosis/stones (Ca PO4 stones have increased tendency to be deposited at higher pHs). Causes: (A for Autoimmune causes) idiopathic, Rh arth, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

232
Q

Type 2 RTA

A

(B for BICARB) reduced HCO3- reabsorption in proximal tubule. hypoK. Compl: (B for Bones) osteomalacia. Causes: idiopathic, Fanconi’s syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors

233
Q

Type 3 RTA

A

mixed. Extremely rare, carbonic anhydrase II deficiency. HypoK

234
Q

Type 4 TA

A

hyperK. Reduced aldosterone → reduced proximal tubular ammonium excretion. Causes: hypoaldosteronism, DM

235
Q

Barrter’s syndrome

A

Aut rec, defective Cl absorption at Na/K/Cl co-transporter (NKCC2) in ascending loop of Henle (like furosemide) Sx: normotensive, childhood presentation, polyuria, polydipsia, hypoK, weakness

236
Q

Gitelman’s

A

aut rec, def in thiazide-sensitive Na/Cl transporter in DCT (like thiazides). Sx: normotension, hypoK, hypocalciuria, hypoMg, metabolic alkalosis

237
Q

Bartter’s vs Gitelman’s sx

A

Bartter’s has more polyuria, polydipsia, Gitelman’s has more hypoMg, hypocalciuria (with hyperCa)

238
Q

ECG for hyperK

A

tented T, small P, broad QRS, sinsoidal pattern, asystole.

239
Q

Causes of hyperK

A

AKI, K sparing diuretics, ACEi, ARBs, ciclosporin, beta blockers, heparin (inhibits aldosterone), metabolic acidosis, Addison’s, rhabdomyolysis, massive transfusions. Foods (bananas, oranges, kiwi fruit, avocado, spinach, tomatoes)

240
Q

Pseudohyperkalaemia

A

excessive K leakage from cells during or after blood being taken.

Causes: haemolysis during venepuncture (excessive vacuum, prolonged tourniquet use, needle gauge too small), delay in processing specimen, high platelet, leukocyte, RBC count, familial.

Rx: get ABG or request slow spin

241
Q

Galactosaemia

A

Aut rec. Galctose-1-phosphate uridyl transferase absence → galactose-1-phosphate. Sx: jaundice, failure to thrive, hepatomegaly, cataracts, hypoglycaemia post galactose exposure, Fanconi’s syndrome. Dx: urine reducing substances. Rx: galactose-free diet

242
Q

Primary amenorrhoea definition

A

no periods by 15yrs with normal 2ndary sexual characteristics/13yrs with no 2ndary sexual characteristics

243
Q

Causes of primary Amenorrhoea

A

gonadal dysgenesis (Turner’s)
Androgen insensitivity syndrome
Congenital genital tract malformations
Functional hypothalamic amenorrhoea
Congenital adrenal hyperplasia
Impeforate hymen

244
Q

Androgen insensitvity syndrome

A

X recessive. 46XY.

Sx: primary amenorrhoea, little/no axillary/pubic hair. Groin swellings. Breast development.

Dx: buccal smear/chromosomal analysis. High-normal testosterone for post-pubertal.

Rx: counselling, b/l orchidectomy (increased testicular Ca risk), oestrogen therapy

245
Q

Congenital adrenal hyperplasia

A

aut rec disorders. Low cortisol, high ACTH, high androgens. 21-hydroxylase def (90%), 11-beta hydroxylase def (5%, HTN due to excess deoxycorticosterone), 17-hydroxylase def (very rare, low androgens, mineralocorticoid excess). Sx: virilization, salt-wasting (75%), precocious puberty, infertility. Dx: ACTH stimulation testing (increased 17-hydroxyprogesterone). Rx: steroid replacement

246
Q

Rx for primary amenorrhoea and SE

A

Hormone replacement therapy (HRT)

SE: nausea, breast tenderness, fluid retention, weight gain.

Compl: breast Ca risk (increased with progestogen), endometrial Ca (reduced with progestogen), VTE (increased with progestogen), stroke, IHD

247
Q

Secondary amenorrhoea definition

A

periods stop for 3-6 months with normal menses/6-12 months with oligomenorrhoea

248
Q

Causes of secondary amenorrhoea

A

hypothalamic (2ndary to stress/excessive exercise)
PCOS
Hyperprolactinaemia
premature ovarian insufficiency
hypo/hyperthyroid
Sheehan’s
Asherman’s

249
Q

PCOS Rx

A

Rx: weight reduction, COCP.

Hirsutism/acne Rx: COCP, topical eflornithine, spironolactone, flutamide, finasteride under supervision.

Infertility Rx: weight loss, clomifene, metformin (esp if obese), gonadotrophins

250
Q

Premature ovarian insufficiency

A

elevated gonadotrophins, low oestradiol, menopausal sx, pre-40yrs, 1 in 100 women. Causes: idiopathic (most common, FHx assx), b/l oophorectomy, radiotherapy, chemotherapy, infection (mumps), autoimmune, resistant ovary syndrome (FSH receptor abnormalities). Rx: HRT/COCP until menopause age

251
Q

Metabolic syndrome

A

likely due to insulin resistance. Dx: waist circumference (men>102, women>88cm), high triglycerides (>1.7mmol/L), reduced HDL (<1.03 men, <1,29 women), raised BP (>130/85/HTN), fasting BM >5.6/T2DM.

Other assx: microalbuminuria, raised uric acid, PCOS, NAFLD

252
Q

HypoPO4 causes

A

ETOH, liver failure, DKA, refeeding syndrome, hyperPTH, osteomalacia.

253
Q

HypoPO4 consequences

A

haemolysis, WBC/pltlt dysfunction, muscle weakness, rhabdo, CNS dysfunction

254
Q

DVLA HGV licensing in relation to BM control

A

HGV licence possible if they are hypo aware, no hypos in last yr, demonstrate adequate control with regular BM monitoring at least BD and at times relevant to driving, demonstrate hypo risk awareness, no debarring complications

255
Q

Orlistat

A

pancreatic lipase inhibitor. SE: faecal urgency/incontinence/flatulence

256
Q

Evolocumab

A

prevents PCSK9-mediated LDLr degradation

MRCP Revision (10 decks)

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