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Endo 7.5 Flashcards

1
Q

What is type 3c diabetes?

A

2ry to pancreatic disease e.g. inflammation

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2
Q

When to consider bariatric surgery for people with severe obesity?

A
  • BMI >40 OR
  • BMI >35 with other significant disease that could be improved by weight loss
    AND:
  • all non-surg measures have failed to achieve/maintain adequate beneficial weight loss at least 6m
  • intensive specialist Rx
  • gen fit for anaesthesia & surgery
  • they commit to need for long-term follow-up
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3
Q

When to consider bariatric surgery as a 1st line?

A

BMI > 50 & sugical intervention appropriate

- consider orlistat before if waiting time is long

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4
Q

What are the types of bariatric surgery?

A

1rily restrictive: laparoscopic adjustable gastric banding (LAGB) or sleeve gastrectomy
- LAGB less weight loss than the others but fewer complications, so usually 1st line if vmi 30-39

1rily malabsorptive: classic biliopancreatic diversion (BPD) but with duodenal switch - usually reserved for v obese

mixed: Roux-en-Y gastric bypass surgery

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5
Q

Causes of thyrotoxicosis?

A 
Graves (50-60%)
toxic nodular goitre
acute phase of subacute de Quervain's thyroiditis
acute phase of post-partum thyroiditis
acute phase of Hashimoto's thyroiditis
amiodarone Rx
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6
Q

How do thiazolidinediones work?

A

PPAR-gamma agonists

  • reduce peripheral insulin resistance
  • intracellular nuclear receptor - it’s natural ligands are free fatty acids & thought to control adipocyte differentiation & function
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7
Q

Adverse effects of thiazolidinediones ?
C/I?
increased risk of what?

A
  • weight gain
  • liver impairment - monitor LFTs
  • fluid retention - therefore C/I in heart failure
  • increased risk of fractures
  • increased risk bladder cancer with pioglitazone
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8
Q

Causes of Cushing’s syndrome?

A

ACTH-dependent:
Cushing’s disease
ectopic ACTH

ACTH-independent:
steroids commonest
adrenal adenoma
adrenal carcinoma - rare
Carney complex: syndrome inc cardiac myxoma
micronodula adrenal dysplasia - v. rare

Pseudo-Cushing’s

  • mimics often etoh XS or severe depression
  • causes false +ive dexamethasone suppression/24h urinary free cortisol
  • insulin stress test can be used to differentiate
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9
Q

Causes of 1ry hyperaldosteronism - what is the commonest?

A

70% BL idiopathic adrenal hyperplasia
adrenal adenoma (Conn’s)
adrenal carcinoma - extremely rare

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10
Q

Features of 1ry hyperaldosteronism?

A

HTN
hypokalaemia (muscle weakness etc)
alkalosis

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11
Q

1st line Ix in suspected 1ry hyperaldosteronism?

A

plasma aldosterone:renin ratio

  • high aldosterone
  • low renin
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12
Q

How to differentiate between UL & BL sources of aldosterone XS?

A

high-resolution CT abdomen

adrenal vein sampling

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13
Q

Management of 1ry hyperaldosteronism?

A

adrenal adenoma -> surgery

BL adrenocortical hyperplasia -> AA e.g. spironolactone

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14
Q

1ry site of absorption of iron & calcium?

A

duodenum

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15
Q

1st line antihypertensive in PHaeochromocytoma?

A

PHenoxybenzamine

= non-selective alpha blocker

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16
Q

Associations of a phaeochromocytoma?

A

MEN type II
neurofibromatosis
von-Hippel-Lindau syndrome

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17
Q

Features of phaeochromocytoma?

A 
episodic
HTN
headaches
palpitations
sweating
anxiety
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18
Q

Most sensitive test for phaeochromocytoma?

A

24h urinary metanephrine collection

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19
Q

Rx of phaeochromocytoma?

A
  • alpha-blocker phenoxybenzamine
  • then beta-blocker propranolol
  • surgery when stable
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20
Q

Features of metabolic syndrome?

A
  • inc waist circumference/central obesity
  • raised triglycerides
  • reduced HDL cholesterol
  • HTN
  • impaired fasting glucose/T2DM
  • microalbuminuria
  • raised uric acid levels
  • nafld
  • pcos
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21
Q

Test to confirm / screen for Cushing’s syndrome?

A

OVERNIGHT dexamethasone suppression test (LOW dose) = most sensitive = DIAGNOSTIC
24h urinary free cortisol - screen

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22
Q

1st line localisation test for Cushing’s syndrome?

A

9am & midnight plasma ACTH & cortisol levels

- if ACTH suppressed then a non-ACTH dependent cause is likely e.g. adrenal adenoma

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23
Q

What does high-dose dexamethasone suppression test confirm?

A

If it suppresses cortisol, then it confirms a pituitary source of Cushing’s (it can’t suppress adrenal/ectopic cortisol)

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24
Q

What does CRH stimulation test show in Cushing’s syndrome?

A

It it shows a rise in cortisol then confirms a pituitary source
If no change in cortisol, it is ectopic/adrenal

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25
Q

How differentiate ectopic ACTH & pituitary ACTH?

A

Petrosal sinus vein sampling

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26
Q

Which gland secretes prolactin?

What is the 1ry prolactin releasing Inhibitory factor?

A

Anterior pituitary

Dopamine so DA agonists can be used to control galactorrhoea

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27
Q

Features of XS prolactin?

A

M: impotence, galactorrhoea, loss of libido
F: amenorrhoea, galactorrhoea

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28
Q

Drugs causing raised prolactin?

A

metoclopramide, domperidone
phenothiazines
haloperidol
v rarely: SSRIs, opioids

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29
Q

Causes of raised Prolactin?

A 
Pregnancy
Prolactinoma
Pcos
Primary hypothyroid (TRH stimulates prolactin release)
Phys: stress, exercise, sleep
Oestrogens
Acromegaly (1/3)
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30
Q

Definite Ix for suspected Addison’s disease?

A

short synACTHen test
- measure plasma cortisol

  • can also check adrenal autoAb e.g. anti-21-hydroxylase
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31
Q

9am cortisol in Addison’s?

A

<100 abnormal think Addisons
100-500 borderline - do synacthen test
>500 normal, Addisons v unlikely

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32
Q

Electrolyte abnormalities in Addison’s?

A

hyponatraemia
hyperkalaemia
HYPOGLYCAEMI
metabolic Acidosis

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33
Q

Side-effects of mineralocorticoids?

A

HTN

fluid retention

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34
Q

Side-effects of glucocorticoids?

A

MSK: osteoporosis, proximal myopathy, AVN femoral head
immunosuppression: inc infections risk, TB reactivation
endocrine: impaired glucose, increased appetitie/weight gain, hirsutism, hyperlipidaemia, Cushing’s syndrome
GI: peptic ulcers, acute pancreatitis
psych: insomnia, mania, depression, psychosis
ophthalmic: glaucoma, cataract
intracranial HTN
growth suppression in children

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35
Q

MoA of Mirabegron?

A

Beta-3 agonist used for urge incontinence if others have failed or C/I

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36
Q

Urge incontinence Rx

A
  • minimum 6wks bladder retraining
  • 1st line antimuscarinic as a bladder stabiliser; oxybutynin IR (avoid in frail older women), tolterodine IR or darifenacin OD
  • If above fail, mirabegron (beta3 agonist)
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37
Q

Stress incontinence Rx?

A

pelvic floor muscle training: Min 3months of 8 contractions 3x/day
surgery: retropubic mid-urethral tape procedures

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38
Q

MEN type 1

  • features?
  • gene?
  • most common presentation?
A 
Parathyroid 95% (hyperplasia)
Pituitary 70%
Pancreas 50% e.g. insulinoma, gastrinoma (rec peptic ulcers)
- MEN1 gene
- hypercalcaemia
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39
Q

MEN type IIa

  • features?
  • gene?
A

Medullary thyroid ca 70%
Parathyroid 60%
Phaeochromocytoma
- RET oncogene

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40
Q

MEN type IIb

  • features?
  • gene?
A 
Medullary thyroid cancer
Phaeochromocytoma
Marfinoid body habitus
Neuromas
- RET oncogene
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41
Q

Causes of 1ry hyperPTH?

A

solitary adenoma 80%
hyperplasia 15%
multiple adenoma 4%
carcinoma 1%

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42
Q

Features of 1ry hyperPTH?

A 
polydipsia, polyuria
peptic ulcer, constipation, pancreatitis
bone pain/fracture
renal stones
depression
hypertension
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43
Q

Xray showing pepper pot skull - Dx?

A

hyperparathyroidism

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44
Q

Ix in 1ry hyperPTH?

A
  • low phosphate, high Ca
  • PTH raised or normal
  • technetium-MIBI subtraction scan
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45
Q

Rx for 1ry hyperPTH?

A
  • definitive = total parathyroidectomy
  • cons Rx ok if Ca++ < 0.25 above ULN + pt>50yrs + no evidence of end-organ damage
  • calcimimetics e.g. Cinacalcet can be used if surgery unsuitable
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46
Q

Indications for considering parathyroidectomy in 1ry hyperparathyroidism?

A
  • age < 50
  • adj Ca2+ 0.25+ above ULN
  • eGFR<60
  • renal stones/nephrocalcinosis
  • osteoporosis/osteoporotic fracture
  • Sx disease
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47
Q

Pt with HTN + low K + metabolic alkalosis - what is the Dx? best Ix?

A

1ry hyperaldosteronism

renin:aldosterone

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48
Q

What is an insulinoma?

A

= most common pancreatic endocrine tumour; is a neuroendocrine tumour mainly derived from islets of Langerhans
- 10% malignant, 10% multiple (1/2 of which have MEN-1)

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49
Q

Dx of insulinoma?

Rx?

A
  • supervised, prolonged fasting upto72h
  • can do insulin & C-peptide levels DURING attack
  • CT pancreas but doesn’t always show up
  • surgery
  • Diazoxide & Somatostatin if pts not candidates
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50
Q

Features of insulinoma?

A
  • hypo usually ***early in AM or just before meals
  • rapid weight gain
  • high insulin, raised proinsulin:insulin ratio
  • high C-peptide
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51
Q

high renin & high aldosterone think ?

A

BL renal artery stenosis

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52
Q

MoA of Acarbose?

commonest side effect?

A
  • inhibitor of intestinal alpha-glucosidases -> decreased absorption of starch & sucrose
  • therefore increased carb load delivered to colon where bacteria digest complex carbs -> GI side-effects e.f. flatulence & diarrhoea
  • XS flatulence
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53
Q

What is measured in an insulin stress test?
When is it used?
What would happen normally?
What are the contraindications?

A
  • IV insulin -> measure GH & cortisol
  • Ix hypopituitarism
  • GH & cortisol should rise with normal function
  • C/Is = epilepsy, IHD, adrenal insufficiency
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54
Q

Which drugs can cause false negative renin:aldosterone ratio results in 1ry hyperaldosteronism?

A

ACE-I
ARBs
direct renin inhib e.g. aliskiren
AAs

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55
Q

What is acromegaly?

A

XS growth hormone
95% pituitary adenoma
minority ectopic GHRH or GH production by tumours e.g. pancreatic

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56
Q

Features of acromegaly?

A
  • coarse facies, spade hands, inc shoe size
  • large tongue, prognathism, interdental spaces
  • XS sweating (gland hypertrophy), oily sin
  • features of pituitary tumour e.g. hypopituitarism, headaches, bitemporal hemianopia
  • 1/3 raised prolactin -> galactorrhea
  • 6% MEN-I
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57
Q

Complications of acromegaly?

A
  • HTN
  • diabetes >10%
  • CARDIOmyopathy
  • BOWEL ca (initial colonoscopy age 40, then surveillance)
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58
Q

Definitive test for acromegaly?

Screening/monitoring?

A

OGTT with serial GH measurements

  • IGF-1 may be used as a screening test, & sometimes for monitoring
  • MRI pituitary may show a tumour
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59
Q

OGTT in acromegaly?

A
  • in acromegaly, there is no GH suppression (may also show impaired glucose tolerance)
  • normally, GH is suppressed < 2 with hyperglycaemia
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60
Q

Acromegaly Rx:
what is 1st line Rx?
what may be used in older pts or following failed medsurg Rx?

A

1st line: trans-sphenoidal surgery

if everything fails external irradiation sometimes used

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61
Q

Medical Rx options in acromegaly?

A

SOMATOSTATIN analogue e.g. OCTREOTIDE (50-70% efficacy) 1st line
- can be used as an adjunct to surgery

Dopamine agonist e.g. BROMOCRIPTINE - 1st effective med Rx, effective in only a minority

GH receptor antagonist that prevents dimerisation of the GH receptor e.g. PEGVISOMANT OD SC

  • v effective, reduces IGF-1 levels in 90% to normal
  • surgery still needed if mass effect because doesn’t reduce tumour volume
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62
Q

Features of Addison’s disease?

A
  • lethargy, weakness, anorexia, N&V, weight loss, ‘salt craving’
  • hyperpigmentation (esp palmar creases), vitiligo, loss of pubic hair in women, hyPOtension
  • crisis: collapse, shoch, pyrexia
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63
Q

Causes of Hypoadrenalism/Addison’s?

A

80% autoimmune destruction of adrenal glands

1ry: TB, mets, meningococcal septicaemia, HIV, antiphospholipid syndrome
2ry: pituitary disorders

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64
Q

Causes of Addisonian crisis?

A
  • sepsis/surgery causing an acute exacerbation of an chronic insufficiency
  • adrenal haemorrhage e.g. fulminant meningococcaemia Waterhouse-Friderichsen syndrome
  • steroid withdrawal
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65
Q

Rx of Addisonian crisis?

A
  • 100mg IM/IV hydrocortisone
  • 1L fluid over 30-60mins
  • cont hydrocortisone 6hrly if pt stable
  • oral replacement can start after 24h and be reduced to maintenance over 3-4days
  • hydrocortisone has weak mineralocorticoid action
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66
Q

Causes of 1ry amenorrhoea?

A
  • Turner’s syndrome
  • Testicular feminisation
  • CAH
  • congenital malformations of genital tract
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67
Q

Causes of 2ry amenorrhoea i.e. when menses has previously occurred but has not stopped for 6+months?

A

(after excluding pregnancy)

  • hypothalamic amenorrhoea e.g. stress, XS exercise
  • PCOS
  • hyperPRL
  • premature ovarian failure
  • thyrotoxicosis(/hypothyroid)
  • Sheehan’s syndrome
  • Asherman’s syndrome
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68
Q

Initial Ix in amenorrhoea?

A
  • exclude pregnancy
  • TFTs, prolactin
  • oestradiol, androgen levels
  • gonadotrophins (if low often hypothalamic cause, if high then suggests ovarian problem)
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69
Q

What is androgen insensitivity syndrome?
What are the features ?
How do you Dx?
Rx?

A
  • X-linked recessive condition due to end-organ resistance to testosterone causing genotypical males to have a female phenotype (46XY)
  • testicular feminisation syndrome = complete andogen insensitivity
  1. ‘1ry amenorrhoea’
  2. undescended testes causing groin swellings
  3. breast development may occur (testosterone converted to estradiol)

Dx = buccal smear or chromosomal analysis (46XY)

Rx =

  • counselling (raise as female)
  • oestrogen therapy
  • BL orchidectomy (undescended testes increases risk of testicular cancer)
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70
Q

How is hyperaldosteronism, caused by cortisol activating the mineralocorticoid nuclear receptor, prevented?

A

cortisol -> inactive cortisone

by 11-hydroxysteroid dehydrogenase type 2 at the renal parenchyma

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71
Q

What is apparent mineralocorticoid XS?

A

often inherited
autosomal recessive
mutation in 11-hydroxysteroid dehydrogenase type 2 (which normally converts cortisol to inactive cortisone)

rarely, XS liquorice can inhibit this enzyme -> xs cortisol -> AME

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72
Q

What is autoimmune polyendocrinopathy/polyglandular syndrome: APS?
What can occur in both types?

What is type 1 (v rare)?
What is type 2?

A
  • Where addison’s disease/autoimmune hypoadrenalism is associated with other endocrine deficiencies (10%)
  • Vitiligo in both

APS type 1 aka MEDAC = multiple endocrine deficiency autoimmune candidiasis

  • V. rare a. recessive
  • mutation of AIRE1 gene on chr 21
  • Need 2/3 of:
    1. Addison’s disease
    2. 1ry hypoPTH
    3. chronic mucocutaneous candidiasis (typically 1st feature as young child)
APS type 2 - much more common
- polygenic inheritance linked to HLA DR3/DR4
Addison's disease
\+ T1DM OR
\+ autoimmune thyroid disease
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73
Q

What is Bartter’s syndrome?
‘think lots of furosemide’
What are the features?

A
  • usually inherited cause of severe HYPOKALAEMIA due to defective chloride absorption at the Na/K/2Cl- cotransporter (NKCC2) in ascending loop of Henle
  • failure to thrive in childhood (presentation)
  • polyuria, polydipsia
  • hypokalaemia
  • weakness
  • NORMOtension (unlike conns/cushings/liddles)
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74
Q

What are the 3 enzyme deficiencies that can cause congenital adrenal hyperplasia, and what are their features?

A

21-hydroxylase deficiency:

  • virilisation of female genitalia
  • precocious puberty in males
  • !60-70% pts have a salt-losing crisis at 1-3weeks of age

11-beta hydroxylase deficiency:

  • virilisation of female genitalia
  • precocious puberty in males
  • hyPOkalaemia, HTN

17-hydroxylase deficiency:

  • Non-virilising in females
  • inter-sex in boys
  • HTN
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75
Q

Which steroids have the highest glucocorticoid activity with minimal mineralocorticoid?

A

Dexamethasone

Betmethasone

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76
Q

Which steroid has very high mineralocorticoid activity with minimal glucocorticoid?

A

Fludrocortisone

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77
Q

Which steroid is predominantly glucocorticoid, with low mineralocorticoid activity?

A

Prednisolone

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78
Q

Which steroid has high mineralocorticoid activity, with some glucocorticoid activity?

A

Hydrocortisone

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79
Q

What is a dynamic pituitary function test for?
What is given?
What is measured at intervals?
What would be normal?

A

Used to assess pts with suspected 1ry pituitary dysfunction

  • > Given insulin, TRH & LHRH
  • > Measure glucose, cortisol, GH, TSH, LH, FSH +/- PRL
Normally
GH rises > 20
Cortisol rises > 550
TSH rises > 2 from baseline
LH &amp; FSH double
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80
Q

Disorder of sex development:
46XX or 47XXY
both ovarian & testicular tissue present
v rare

A

True hermaphroditism

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81
Q

Disorder of sex development:
46XX
ovaries present but male/ambiguous external genitalia (virilised)
may be 2ry to CAH

A

Female pseudohermaphroditism

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82
Q

Disorder of sex development:
46XY
testes present but external genitalia are female/ambiguous
may be 2ry to androgen insensitivity syndrome

A

Male pseudohermaphroditism

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83
Q 
Disorder of sex development:
46XY
ambiguous genitalia in newborn period
hypospadias common
virilisation in puberty
autosomal recessive
results in inability of males to convert testosterone -> DHT
A

5-alpha-reductase deficiency

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84
Q

Disorder of sex development:
46XY
genotypical male has a female phenotype
rudimentary vagina & testes present but no uterus
elevated testosterone, oestrogen & LH
X-linked recessive

A

Androgen insensitivity syndrome

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85
Q

RFs for endometrial cancer?

A
  • nulliparity, early menarche, late menopause
  • unopposed oestrogen (adding a progestogen reduces risk, eliminates it if prog given continuously)
  • Tamoxifen (ER+ breast ca)
  • obesity, DM, PCOS
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86
Q

Ix for endometrial cancer?

A

1st line TVUS: normal endometrial thickness <4mm has a high NPV

if thick will probably have hysteroscopy with endometrial biopsy

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87
Q

Rx of endometrial cancer?

A

Localised -> TAH with BSO
If high-risk, may have post-op RT
Progestogen Rx sometimes used in frail elderly not suitable for surgery

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88
Q

What is Gitelman’s syndrome?

What are the features?

A

Defect in thiazide-sensitive Na/Cl transporter in the dct

Low K & Mg
Low Ca2+ in urine
NORMOtension
Metabolic ALKAlosis

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89
Q

Causes of gynaecomastia inc drugs?

Usually caused by increased oestrogen:androgen

A
  • phys: puberty
  • liver disease
  • syndromes with androgen deficiency: Kallman’s, Klinefelter’s
  • testicular failure e.g. mumps
  • testicular ca e.g. seminoma secreting hCG
  • ectopic tumour secretion
  • hyperthyroidism
  • haemodialysis

Drugs:

  • spironolactone commonest
  • digoxin
  • cimetidine
  • cannabis
  • finasteride
  • gonadorelin analogues e.g. goserelin, buserelin
  • oestrogens, anabolic steoirds
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90
Q

What is HRT composed of?

A

Small dose of oestrogen

(WITH progestogen in women with a uterus) to help alleviate menopausal vasomotor Sx

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91
Q

Side effects of HRT?

Potential complications/increased risks?

A
  • nausea
  • breast tenderness
  • fluid retention & weight gain
  • increased risk of VTE, stoke, & IHD (10yrs after menopause)
  • increased risk of breast & endometrial ca

Adding a progestogen increases risk of breast cancer & VTE further, but reduces risk of endometrial cancer

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92
Q

Causes of hypercalcaemia?

A
  • 1ry hyperPTH
  • Malignancy: bone mets, myeloma, PTHrP, any ca
  • in malignancy, 80% due to PTHrP, remaining due to osteolysis, some due to calcitriol-mediated high Ca & ectopic PTH secretion

Others:

  • dehydration
  • drugs: thiazides, vitamin d toxicity, calcium-containing antacids
  • endocrine: acromegaly, thyrotoxicosis, addison’s disease
  • granulomas: sarcoid, TB
  • milk-alkali syndrome
  • can occur with prolonged immobilisation in Paget’s bone disease
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93
Q

What is 1ry hypoPTH?
Cause?
Rx?

A
  • decrease in PTH secretion leading to low Ca, high phosphate
  • e.g. 2ry to thyroid surgery
  • Rx with Alfacalcidol
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94
Q

Sx of hypoPTH?

A

usually 2ry to hypocalcaemia

tetany - muscle twitch, cramp, spasm
perioral paraesthesia
Trousseau: carpal spasm if brachial artery occluded by maintaining BP cuff above systolic
Chvostek: tapping parotids causes facial muscle twitch
ecg - prolonged QT interval
chronic - depression, cataracts

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95
Q 
What is pseudohypoPTH?
type I?
type II?
features?
how to Dx?
A
  • target cells are insensitive to PTH, due to mutation in a G protein, leading to high PTH, low Ca, high phosphate

I: complete receptor defect
II: cell receptor intact

  • low IQ
  • short stature
  • short 4th & 5th metacarpals
  • obesity, round face
  • Dx: PTH infusion -> measure urinary cAMP & phosphate levels
    (hypoPTH will cause increase in cAMP & phosphate)
  • In pseudohypoPTH type I, neither increase; in type II cAMP rises
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96
Q

What is pseudopseudohypoPTH?

A

similar phenotype to pseudohypoPTH but normal biochemistry

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97
Q

What is Kallmann’s syndrome?

A

Failure of GnRH-secreting neurons to migrate to the hypothalamus
X-linked recessive
Cause of delayed puberty 2ry to hypogonadotrophic hypogonadism

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98
Q

Features of Kallmann’s syndrome?

A
  • ‘delayed puberty’
  • hypogonadism, cryptorchidism (undesc testes)
  • anosmia
  • low sex hormone levels
  • LH & FSH inappropriately low/normal
  • pts typically of normal/above average height
  • sometimes cleft lip/palate & visual/hearing defects
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99
Q

What is Klinefelter’s syndrome?
Dx?
Features?

A

Karyotype 47XXY
Dx by chromosomal analysis

  • often taller than average
  • lack of 2ry sexual characteristics
  • small, firm testes
  • infertile
  • gynaecomastia - inc incidence of breast ca
  • elevated gonadotrophin levels
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100
Q

What is Liddle’s syndrome?

Rx?

A
  • rare a dominant condition causing HTN & hypokalaemic alkalosis
  • thought to be caused by disordered sodium channels in distal tubules -> inc reabsorption of sodium

Rx with amiloride/triamterene

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101
Q

What is neuroblastoma?

Features?

A
  • childhood malignancy median onset 20m
  • tumour arises from neural crest tissue of adrenal medulla & sympathetic nervous system

Features:

  • abdo mass
  • pallor, weight loss
  • bone pain, limp
  • hepatomegaly
  • paraplegia
  • proptosis
102
Q

Ix of neuroblastoma:
urine?
AXR?

A
  • raised urinary VMA & HVA
  • calcification can be on AXR
  • can Bx the tumour
103
Q

What is MoA of Orlistat?
What are the adverse effects?
What are the NICE criteria for using it?

A

Pancreatic lipase inhibitor
Fecal urgency/incontinence, flatulence

Should only be prescribed as part of an overall plan for managing obesity in adults with:
- BMI 28+ with ass RFs or
- BMI 30+ 
- cont'd weight loss e.g. 5% at 3months
It is normally used <1yr
104
Q

What is MoA of Sibutramine?
Why was it withdrawn in 2010?
What are the adverse effects?
When is it C/I?

A

Centrally acting appetite suppressant (inhibits uptake of serotonin & noradrenaline at hypothalamic sites that regulate food intake)

  • Withdrawn due to increased risk of cardiovascular events
  • HTN, constipation, headache, dry mouth, insomnia, anorexia
  • C/I: in psych illness, HTN, IHD, stroke, arrythmias
105
Q

Commonest cell type of ovarian cancers?

A

70-80% serous carcinomas (90% are epithelial in origin)

106
Q

Clinical features for ovarian cancer?

RFs?

Rx?

A
  • abdo pain, pelvic pain
  • abdo distension, bloating, diarrhoea, early satiety
  • urinary Sx
  • FHx: BRCA1 & 2 gene mutations
  • many ovulations

Rx usually combo of surgery & platinum-based chemo

107
Q

What is PID?
What is the commonest causative organism?
What are the complications of it?

A

= infection & inflammation of female pelvic organs inc uterus, fallopian tubes, ovaries & surrounding peritoneum
Commonest cause = chlamydia trachomatis

Complications:

  • chronic pelvic pain
  • infertility (10-20% after single episode)
  • ectopic pregnancy
108
Q

Features of PID?

Rx?

A
  • lower abdo pain, fever
  • deep dyspareunia
  • vaginal/cervical discharge
  • cervical excitation
  • dysuria & menstrual irregularities can happen
  • perihepatitis: Fitz-Hugh Curtis syndrome (RUQ pain)

Have low threshold for Rx
po OFLOXACIN + po METRONIDAZOLE
or im CEFTRIAXONE + DOXYCYCLINE po + METRONIDAZOLE po
If mild, IUCD can be left in but removal should still be considered (better short term clinical outcomes)

109
Q

What is Pendred’s syndrome?
Features?

Dx?
Rx?

A
  • a recessive disorder of
    1. BL sensorineural deafness
    2. mild hypothyroidism
    3. goitre
  • pts tend to present with progressive HL & delay in academic progression
  • often head trauma makes the HL worse so avoid contact sports
  • defect in iodine organification -> dyshormonogenesis
  • but thyroid Sx often mild, can be clinically euthyroid with goitre, TFTs often normal requiring perchlorate discharge test to aid Dx

Dx via genetic testing (PDS gene chr 7), audiometry & MRI to look for characteristic 1.5 turns in cochlea (vs normal 2.5)

Rx with thyroid hormone replacement & cochlear implants

110
Q

How to classify pituitary adenomas?
Commonest types?
DDx?

A
  1. Size (micro adenoma <1cm & macro adenoma >1cm)
  2. Hormonal status (secretory/functioning adenoma that secretes XS of a hormones vs non-secretory/functioning)

Incidence 10% of people, usually aSx, 10% of adult brain tumours

Prolactinomas = commonest
then non-secreting adenomas
then GH-secreting
then ACTH-secreting

DDx = pituitary hyperplasia, craniopharyngioma, meningioma, brain mets, lymphoma, hypophysitis, vasc malformation

111
Q

How do pituitary adenomas cause Sx?
Ix?
Rx?

A
  • XS hormone
  • depletion of hormone (compression of pituitary)
  • stretching dura within/around pituitary fossa (headaches)
  • optic chiasm compression (bitemporal hemianopia)
  • bloods inc GH, PRL, ACTH, FH, LSH, TFTs
  • formal visual field testing
  • MRI brain with contrast

Rx with combo of:

  • hormonal Rx (e.g. bromocriptine for prolactinoma)
  • surgery
  • RT e.g. transsphenoidal transnasal hypophysectomy
112
Q

PCOS:
aetiology?
features?
Ix?

A
  • not well understood but hyperinsulinaemia & high levels LH are seen, and some overlap with metabolic syndrome
  • menstrual disturbance: oligo/amenorrhoea
  • acne, hirsutism (hyperandrogenism)
  • obesity
  • subfertility & infertility
  • acanthosis nigricans (insulin resistance)

Ix:

  • pelvic US: multiple cysts on ovaries
  • FSH, LH, prolactin, TSH, testosterone. Can have raised LH:FSH, PRL can be normal/mildly raised, testosterone is normal/mildly raised
  • check impaired glucose tolerance
113
Q

Rx of PCOS?

A

Gen - weight reduction, cocp can help regulate cycle

Acne & hirsutism:

  • 3rd gen cocp or co-cyprindiol (anti-androgen) but both increase risk of VTE
  • topical eflornithine
  • spironolactone/flutamide/finasteride under specialist supervision

Infertility: weight reduction
- anti-oestrogen e.g. clomifene to help stimulate ovulation
- &/or metformin, esp in obese
- gonadotrophins
Nb potential risk of multiple pregnancies with anti-oestrogen therapies, which work by occupying hypothalamic oestrogen receptors without activating them -> interferes with binding of estradiol -> preventing negative feedback inhibition of FSH secretion

114
Q

What is premature ovarian failure?
Causes?
Features?

A
  • menopausal Sx & elevated gonadotrophins in <40yrs. 1/100 women
  • idiopathic commonest
  • chemo
  • autoimmune
  • radiation
  • climacteric Sx
  • infertility
  • 2ry amenorrhoea
  • raised FSH, LH
115
Q

What is remnant hyperlipidaemia?
What are the features?
What is the Rx?

A

aka broad-beta disease, dysbetalipoproteinaemia
= rare cause of mixed hyperlipidaemia (raised cholesterol & triglyceride levels)
- thought to be caused by impaired removal of intermediate density lipoprotein from circulation by the liver
- ass with apo-e2 homozygosity
- high incidence IHD & PVD

  • yellow palmar creases
  • palmer xanthomas
  • tuberous xanthomas

Rx 1st line Fibrates

116
Q

What is Sheehan’s syndrome?

What are the features?

A

Postpartum pituitary necrosis caused by hyopituitarism due to hypovolaemia with postpartum haemorrhage

  • failure to lactate
  • breast involution
  • amenorrhoea
117
Q

Rx of papillary & follicular thyroid cancer?

A
  • total thyroidectomy
  • then radio iodine (I-131) to kill residual cells
  • yearly thyroglobulin levels to detect early recurrent disease
118
Q

Commonest thyroid cancer, often young females, v good prognosis?

A

Papillary carcinoma

  • usually contains a mixture of papillary & colloidal filled follicles
  • histologically: papillary projections & pale empty nuclei
  • seldom encapsulated
  • LN metastasis predominate
  • haematogenous metastasis rare
119
Q

Thyroid growth that usually presents as a solitary thyroid nodule, and malignancy can only be excluded on formal histological assessment?

A

Follicular adenoma

120
Q

2nd commonest thyroid cancer, where vascular invasion predominates?

A

Follicular carcinoma

  • multifocal disease is rare
  • macroscopically encapsulated, microscopically capsular invasion is seen (without this, it would be adenoma)
121
Q

Thyroid cancer of parafollicular C cells that secrete calcitonin, and is part of MEN-2?

A

Medullary carcinoma

  • C cells derived from neural crest (not thyroid tissue)
  • raised serum calcitonin
  • familial 20%
  • both lymphatic & haem metastasis can be seen; nodal disease ass with v poor prognosis
122
Q

Commonest thyroid cancer in elderly females, where local invasion is a common feature causing pressure Sx?

A

Anaplastic carcinoma

  • Rx by resection where possible
  • palliation through isthmusectomy & RT
  • chemo ineffective
  • not v responsive to Rx
123
Q

Rarest thyroid cancer, ass with Hashimoto’s?

124
Q

Ix for diabetes insipidus?

Features?

A
  • high plasma osmolality
  • low urine osmolality
  • can do a water deprivation test
  • polyuria, polydipsia, nocturia, dehydration
125
Q

What is cranial diabetes insipidus?

Causes?

A

Deficiency of ADH/vasopressin

  • reduced circulating ADH
  • so kidneys excrete lots of dilute urine (low urine osmolality)
  • mutation
  • idiopathic
  • post-HI trauma
  • pituitary surgery
  • meningitis
  • tumours
  • histiocytosis X
  • DIDMOAD: DI, DM, optic atrophy & deafness
126
Q

What is nephrogenic diabetes insipidus?

Causes?

A

Anything which leads to insensitivity to ADH/interferes with binding

  • mutation: in the receptor gene, more common than gene encoding aquaporin 2 channel
  • metabolic: hypercalcaemia, hypokalaemia
  • drugs: lithium, demeocycline
  • CKD
  • tubulo-interstitial disease: post-obstructive uropathy, sickle cell, pyelonephritis
127
Q 
Water deprivation test - how is it done?
what happens it it is normal?
psychogenic polydipsia?
cranial DI?
nephrogenic DI?
A
  • give fluid overnight -> measure plasma & urine osmolality -> deprive of water for at least 8h -> measure urine osmolality -> administer vasopressin/ADH -> measure again
    normal: normal plasma osmolality, then urine osmolality >600, again >600 after ADH
    psychogenic: low starting pl. osmolality, then urine ism >400 after deprivation, and >400 after ADH

cranial DI: high pl osmolality, urine osm < 300 after deprivation, urine osm > 600 after ADH

nephrogenic DI: high pl osmolality, urine osm < 300 after deprivation, urine osm < 300 after ADH (can’t respond to any ADH)

128
Q

Dx of diabetes with fasting & OGTT:
Sx?
aSx?

A

fasting glucose 7.0+
OGTT/random glucose 11.1+

If aSx, then 2x separate readings

129
Q

Dx of diabetes with HbA1c:
Sx?
aSx?

A

HbA1c 48+ or 6.5%+
If without Sx, then repeat to confirm Dx
- HbA1c less than this doesn’t exclude diabetes (i.e. less sensitive than fasting etc sample)

130
Q

What can lead to misleading lower HbA1c result?

Conditions where HbA1c can’t be used for Dx?

A

Increased red cell turnover
- e.g. blood loss, sub/clinical haemolysis, Hbopathies & red cell disorders like sickle cell, myelodysplastic disease

  • above, untreated IDA, suspected gestational DM, children, HIV, people on steroids etc
131
Q

MoA of Metformin?

C/I?

A
  • increases insulin sensitivity & decreases hepatic gluconeogenesis
  • 1st line in T2DM but C/I if eGFR < 30
132
Q 
MoA of sulfonylureas?
On a molecular level?
Common adverse effects?
When to avoid?
Rare adverse effects?
A
  • stimulate pancreatic beta cells to secrete insulin therefore only effective if functional B cells present
  • they bind to an ATP-dependent K+ channel on the cell membrane of the pancreatic beta cells
  • hypos & weight gain
  • avoid in pregnancy & breastfeeding

Rarely:

  • SIADH/low Na
  • BM suppression
  • cholestatic liver damage
  • peripheral neuropathy
133
Q

MoA of thiazolidinediones?

A
  • activate PPAR-gamma receptor in adipocytes to promote adipogenesis & fatty acid uptake
134
Q

MoA of DPP-4 inhibitors i.e. gliptins?
How is it given?
When might it be preferable to pioglitazone?
What do they increase the risk of?

A
  • increase incretin levels -> inhibit glucagon secretion
  • oral, well tolerated, no increased risk of hypo, no weight gain
  • preferable to pioglitazone if further weight gain would cause significant problems, it is C/I or pt has had poor response
135
Q

MoA of SGLT-2 inhibitors i.e. gliflozins?

A
  • they reversibly inhibit sodium-glucose co-transporter 2 in the renal pct to inhibit glucose reabsorption, and increase glycosuria
136
Q

MoA of GLP-1 agonists i.e.-tides?

A
  • incretin mimetic -> inhibits glucagon secretion & increases insulin secretion
137
Q

What is impaired fasting glucose?

What should people be offered if they have impaired fasting glucose?

A

6.1 =< fasting glucose < 7.0
Offer ogtt to rule out Dx

Due to hepatic insulin resistance

138
Q

What is impaired glucose tolerance?

A

fasting glucose < 7.0 AND After OGTT:
7.8 =< glucose < 11.1

Due to muscle insulin resistance

139
Q

What is pre diabetes?

A

Impaired fasting glucose i.e.
HbA1c 42-47 (6-6.4%) or
fasting glucose 6.1-6.9

140
Q

Abs & Ag involved in T1DM?

What about in LADA?

A
  • HLA DR4 > HLA DR3
  • Ab against beta cells of pancreas
  • anti-IAA: islet-ass Ag Ab, anti-GAD: glutamic acid decarboxylase
141
Q

T1DM:
HbA1c target & monitoring?
self-monitoring or blood glucose?
BG targets?

A
  • monitor HbA1c every 3-6m, target 48mmol/6.5% or lower where possible
  • do BG at least 4x/day inc pre-meals & pre-bed; more frequent if having hypos, unwell, sports, pregnancy etc
  • BG target 5-7 on waking, otherwise 4-7
142
Q

T1DM in adults:
what is insulin regimen of choice?
what is an example?
what type of insulin should be offered for mealtime replacement?

when can you consider adding metformin in T1DM adults?

A
  • basal-bolus regimens
  • e.g. insulin detemir/levemir BD, or can be OD, or glargine OD
  • rapid-acting insulin Analogues before meals
  • If BMI 25+, can add metformin
143
Q

HbA1c target if:
lifestyle+/- metformin Rx?
if on any drug that may cause hypoglycaemia?
if on Rx but HbA1c has risen to 58mmol/7.5%?

A
  • 48mmol/6.5%
  • 53mmol/7.0%
  • 53mmol/7.0%
144
Q

T2DM Drug Rx if someone can tolerate Metformin?

A
  1. Metformin if HbA1c 48/6.5% +
  2. Add 2nd drug if HbA1c 58/7.5% + : sulfonylurea/gliptin/pioglitazone/SGLT2inhibitor
  3. Triple therapy if HbA1c rises/still 58/7.5% + :
    - sulfonylurea can have any of the other drugs added/vice versa
    - or metformin + pioglitazone + SGLT2inhibitor
    - or insulin Rx should be considered
145
Q

What are the criteria for GLP1 mimetic e.g. exenatide in T2DM if triple therapy not effective/tolerated/C/I?

A

The combo of metformin + sulfonylurea + GLP1 mimetic if:
1. BMI 35+ & specific med/psych problem ass with obesity OR
2. BMI < 35 & in whom insulin would have significant occupational implications/weight loss would benefit other significant obesity-related conditions
AND
3. ONLY continue if there is a reduction of at least 11mmol/1.0% HbA1c AND weight loss 3% in 6months

146
Q

T2DM Rx if someone cannot tolerate Metformin or C/I?

A
  1. If HbA1c 48/6.5% then: sulfonylurea/gliptin/pioglitazone
  2. If HbA1c rises to 58/7.5% then double therapy combo of any 2 of the 3 is ok
  3. If it persists at 58/7.5% then consider insulin Rx
147
Q

Starting with insulin Rx in T2DM:
what should be continued?
what insulin can be started initially?

A
  • > Continue metformin. Others would be reviewed for continued need
  • > Start with human NPH insulin (=isophane, intermediate-acting). ON or BD according to need
  • > can add a short-acting insulin if HbA1c v high e.g. 75mmol/9%
  • > use insulin deter/glargine as alternative to NPH if pt needs assistance with injection or lifestyle warrants it if it reduces frequency of injections
148
Q

What is target BP in people with T2DM?
What is 1st line antihypertensive?
When to offer anti platelets?
When to offer a statin & what?

A
  • target BP < 140/80
  • <130/80 if end-organ damage
  • ACE-I 1st line
  • anti-platelets only if existing CVD
  • 1ry prevention atorvastatin 20mg od if Qrisk 10% + (uptitrtte if non-HDL doesn’t fall by at least 40%)
  • 2ry prevention atorvastatin 80mg od (ihd/cvd/pad)
149
Q

Which groups to offer lipid-modification Rx i.e. statin without a formal risk assessment, and what are the criteria?

A

CKD (All, i.e. eGFR < 60 &/or ACR >3)
Familial hypercholesterolaemia
T1DM 1ry prevention atorvastatin 20 if:
- aged 40+
- has had DM for > 10 yrs
- has established nephropathy or
- has other CVD RFs e.g. obesity & HTN
- for all other adults, still consider it… & 80mg if 2ry prevention

150
Q

If a pt with T2DM decides to fast during Ramadan:

  • what should they eat before sunrise/suhoor?
  • monitoring?
  • metformin dose adjustment?
  • sulfonylurea dose adjustment?
  • pioglitazone dose adjustment?
A
  • before sunrise eat meal with long-acting carbs
  • BG monitor to use, esp if they feel unwell
  • 1/3 metformin before sunrise, 2/3 metformin after sunset/iftar
  • take sulfonylura after sunset. if BD prep e.g. gliclazide, take larger proportion of dose after sunset
  • pioglitazone no adjustment needed
151
Q

Precipitating factors of DKA?

Clinical features?

A
  • infection, infarction, iatrogenic (missed insulin), ischaemia
  • abdo pain
  • polyuria, polydipsia, dehydration
  • Kussmaul resp (deep hyperventilation)
  • acetone-smelling breath
152
Q

Dx criteria for DKA?

A
  • hyperglycaemia of glucose > 11/known DM
  • ketonaemia > 3 or ketonuria ++
  • acidaemia: pH < 7.3, bicarb < 15
  • N.b. if anion gap not raised, consider another cause for the acidosis
153
Q

DKA Rx: 4 things?

fluid rate?
electrolyte replacement?

A
  • IV fluids (most deplete at least 5L)
  • IV insulin fixed rate 0.1unit/kg/h - can start 5% dextrose when glucose < 15
  • correction of hypokalaemia
  • Rx underlying cause!!!
  • rate can be 1L bags over 1/2/2/4/4/6hrs etc, slower if young adult <26yrs as greater risk of cerebral oedema… 1:1 nursing, neuro-obs etc - usually occurs 4-12h after Rx but can be any time. If concerned consider CT head & get senior r/v

K level in first 24h:

  • > 5.5, no KCl
  • 3.5-5.5 give 40mmol KCl
  • < 3.5 senior review for additional KCl
154
Q

Complications of DKA and its Rx?

A
  • thromboembolism
  • gastric stasis
  • AKI
  • ARDS
  • arrhythmias 2ry to hyperkalaemia/iatrogenic hypokalaemia
  • iastrogenic inc: cerebral oedema, hypokalaemia, hypoglycaemia (if no glucose bag ran alongside insulin!)
155
Q

Diabetic foot disease occurs 2ry to which 2 main factors?
How to screen for both?
What are their presentations?

What are complications?

A
  1. neuropathy: loss of protective sensation, Charcot’s arthropathy, dry skin
    - 10g monofilament at least annually
    - loss of sensation
  2. peripheral arterial disease: micro & macrovascular ischaemia
    - palpate both distal pulses at least annually
    - absent pulses, intermittent claudication, reduced ABPI

Complications inc: calluses, ulceration, Charcot’s, cellulitis, osteomyelitis, gangrene

156
Q

How to risk stratify diabetic foot disease:
low?
moderate?
high?

A

Low risk: no RFs except callus

Moderate risk:
- deformity/neuropathy/non-critical limb ischaemia

High risk:

  • previous ulceration/amputation or
  • on RRT or
  • neuropathy + non-critical ischaemia or
  • neuropathy + callus/deformity or
  • non-critical ischaemia + callus/deformity
    i. e. 2 of 3 or RRT or previous critical ischaemia

All mod/high risk pts should have regular F/u in local diabetic foot centre

157
Q

Diabetic neuropathic pain Rx ladder?
localised?
rescue?
resistant?

A
  1. duloxetine/amitriptyline/pregabalin/gabapentin
  2. if 1st doesn’t work, trial 1 of the other 3

localised neuropathic pain e.g. post-herpetic neuralgia: Topical Capsaicin

rescue therapy/exacerbations: Tramadol

If resistant: pain clinic

158
Q

Sx & Rx for Gastroparesis as a result of diabetic neuropathy?

A
  • erratic BMs, bloating, vomiting

Rx = prokinetics e.g. metoclopramide/domperidone/erythromycin

159
Q

DVLA rules of diabetes:
Driving HGV if on insulin/hypoglycaemics?

Driving a car (group 1) on insulin/hypoglycaemics?
if on exenatide/other tablets/diet-controlled?

A

HGV driver on insulin/hypoglycaemics:
- no severe hypo in last 12m, driver has hypo awareness, adequate BM monitoring, driver understands risks of hypo, no other debarring complications

Car driver on insulin/hypos:
- can drive if they have awareness, max 1 episode of hypo requiring assistance in past 12m, no relevant visual impairment
on exenatide/tablets/diet:
- no need to inform dvla

160
Q

HbA1c = glycosylated Hb
How is it produced?
What is it dependent on?

Equation for calculating plasma glucose from HbA1c?

A
  • Produced by glycosylation of Hb at a rate proportional to glucose conc

Depends on:

  1. RBC lifespan
  2. average blood glucose concentration

average plasma glucose = (2 X HbA1c) - 4.5

161
Q

What conditions can lead to lower than expected HbA1c?

A

Reduced RBC lifespan i.e. increased red cell turnover e.g.

  • sickle cell
  • GP6D deficiency
  • hereditary spherocytosis
162
Q

What conditions can lead to higher than expected HbA1c?

A

Increased RBC lifespan e.g.

  • vit B12/folic acid deficiency
  • IDA
  • splenectomy
163
Q

Important adverse effects of SGLT2 inhibitors?

A
  • urogenital infections 2ry to glycosuria
  • increased risk DKA!!! - euglycaemic
  • nb they increase total cholesterol (HDL & LDL), significance unclear
164
Q

5 RFs for gestational DM?

Screening for gestation DM?

A
  1. BMI > 30
  2. prev macro baby 4.5kg +
  3. prev gestational DM
  4. 1st degree relative with DM
  5. family origin with high prevalence
  • if pre gest DM then OGTT asap after booking + at 24-28wks if normal - can also self-monitor early
  • OGTT at 24-28wks if any other RF
165
Q

Dx thresholds for gestational DM?

Targets for self-monitoring of pregnancy women (inc those with pre-existing DM)?

A

fasting glucose 5.6+
OGTT 2h glucose 7.8+

fasting target max 5.3
1h post-meal 7.8 or
2h post-meal 6.4

166
Q

Management of pre-existing diabetes during pregnancy:

  • conservative?
  • medicines?
  • supplement?
  • monitoring?
A
  • if BMI > 27 then weight loss
  • stop oral hypoglycaemics, continue metformin, start insulin
  • folic acid 5mg OD from pre-conception to week 12/40
  • wk 20/40 detailed anomaly scan inc 4 chamber view of heart & outflow tracts
  • treat retinopathy (can worsen during pregnancy)
  • tight glycaemic control reduces complication rates
167
Q 
Management of gestational diabetes:
Cons?
When to start metformin?
When to start insulin?
When to offer Glibenclamide?
A

Cons:

  • joint diabetes & antenatal clinic within 1wk, teach self-monitoring of BG, diet & exercise advice
  • trial diet & exercise if fasting glucose < 7

Start metformin:
- if glucose targets not met within 1-2wks of altering diet/exercise

Start insulin if:

  • fasting glucose 7+ at time of Dx
  • fasting glucose 6-6.9 + evidence of complications e.g. macrosomia/hydramnios
  • glucose target not met by diet/exercise/metformin

Only offer glibenclamide if:

  • can’t tolerate metformin or
  • BG target not met by metformin, and declines insulin Rx
168
Q

What is MODY?
inheritance?
features?

A
  • T2DM development in <25yrs old typically
  • autosomal dominant, >6 different genetic mutations identified, usually FHx of early onset DM
  • insulin not usually necessary
  • ketosis not a feature at presentation
169
Q

MODY 3 prevalence?
gene defect?
increased risk of what?

A
  • 60% of MODY cases
  • defect in HNF-1 alpha gene
  • inc risk of hepatocellular cancer
170
Q

MODY 2 prevalence?

gene defect?

A
  • 20% of MODY cases

- defect in glucokinase gene

171
Q

What are meglitinides?
When are they usually used?
Adverse effects?

A

e. g. repaglinide, nateglinide
- insulin secretagogues that bind to ATP-K+ channel like sulfonylureas
- pts with erratic lifestyle
- weight gain & hypo (less than sulfonylureas)

172
Q

Commonest causes of hypoglycaemia?

A
  • insulin/sulfonylureas
  • etoh, liver failure
  • Addison’s disease
  • insulinoma, increased pro:insulin

Sulfonylureas are long-acting anti-glycaemics so can cause recurrent hypoglycaemia

Low glycogen stores in chronic alcoholism prevents glucagon from being an effective Rx for hypoglycaemia
Wernicke’s encephalopathy

173
Q

Hyperosmolar hyperglycaemic state:
presentation?
complications?

A
  • often in elderly T2DMs where hyperglycaemia results in severe dehydration, osmotic diuresis & electrolyte deficiencies. HHS often occurs over days, so disturbances more extreme
  • higher mortality than DKA, and can be complicated by e.g. MI, stroke, peripheral arterial thrombosis
  • uncommon but documented tic: seizures, cerebral oedema, CPM
174
Q

Pathophysiology of HHS?

A
  • hyperglycaemia -> osmotic diuresis with ass loss of Na & K
  • severe volume depletion -> significantly raised serum osmolarity > 320 -> hyper viscosity of blood
  • hypertonicity leads to preservation of intravascular volume so pt usually doesn’t look as severely dehydrated as they are
175
Q

Dx of HHS?

Clinical features?

A
  1. hypovolaemia
  2. marked hyperglycaemia > 30 without significant ketonaemia/acidosis
  3. significantly raised serum osmolarity > 320

Gen: fatigue, lethargy, nausea & vomiting
Neuro: altered GCS, headaches, papilloedema, weakness
Haem: hyper viscosity that can result in MIs, stroke, peripheral arterial thrombosis
CVS: dehydration, hypotension, tachycardia

176
Q

3 goals of HHS Rx?

Fluid replacement?

Monitoring response?

A
  1. normalise osmolality gradually
  2. replace fluid & electrolyte losses
  3. normalise BG gradually
  • estimated fluid losses 100-220ml/kg
  • caution rehydration rate in elderly/comorbidities
  • hypotonic 0.9% NaCl
  • aim of Rx should be to replace at least 3-6L or 50% of losses by 12h, remaining losses within next 12h
  • key parameter is osmolality to which glucose & Na are the main contributors (rapid change in osmolality can lead to CV collapse & CPM)
  • plot osmolarity, Na & glucose on a graph initially hourly
  • rough best of serum osmolarity = 2Na + glucose + urea
  • fluid replacement gradually lowers glucose which will reduce osmolality
  • fall in osmolarity -> shift of water into intracellular space -> rise in Na of 2.4 for every fall in BG of 5.5
  • safe rate of fall of glucose if 4-6mmol/hr
  • target BG 10-15
  • normalisation of electrolytes & osmolality may take 72h
177
Q

Insulin in HHS?

A

ONLY if significant ketonaemia, is insulin indicated e.g. mixed DKA/HHS e.g. fixed rate 0.05u/kg/h
- otherwise, insulin can lead to rapid decline of serum glucose, therefore osmolarity, and if before fluids can cause CV collapse as water moves out the intravascular space -> fall in intravascular volume

178
Q

Potassium in HHS?

A
  • HHS pts are K deplete but less acidotic than DKA
  • can have hyperkalaemia with AKI
  • pts on diuretics may be profoundly hypokalaemic
  • therefore K monitoring & fixing as nec is required
179
Q

What is GLP-1?

A

glucagon-like peptide-1

  • hormone released by the small bowel in response to an oral glucose load
  • an oral glucose load results in a greater release of insulin than if the same load is given IV = incretin effect; this effect is largely mediated by GLP-1, and known to be decreased in T2DM
180
Q

How is Exenatide (a GLP-1 mimetic) administered?

Advantage of Liraglutide (another GLP-1 mimetic) over exenatide?

A

SC within 60minutes before Am & evening meal - should NOT be given after a meal

Liraglutide only OD

181
Q

Main side effects of GLP-1 mimetics?

What adverse effect has exenatide been linked to in some patients?

A

Nausea & vomiting

Severe pancreatitis

182
Q

Overweight taxi driver has started Metformin, HbA1c has come down but still high at 75 - next step?

A

Add DPP-4 inhibitor e.g. sitagliptin (no risk of hypo - driver - and weight neutral)

183
Q

What is MoA of Pegvisomant?

A

GH receptor antagonist

  • used in Acromegaly
  • effectively decreases IGF-1 levels in 90% but doesn’t shrink tumour
184
Q

What is the chromosomal abnormality ass with Klinefelter’s syndrome?

185
Q

Hashimoto’s thyroiditis is associated with which thyroid cancer?

186
Q

What is the most abundant circulating adrenal steroid?

A

DHEA: dehydroepiandrosterone

Adrenals are main source of DHEA in females therefore in Addison’s, Sx can be as a result of androgen deficiency

187
Q

When would you start Metformin in pre diabetes?

A

For high risk adults e.g. ‘whose blood glucose measure (fasting plasma glucose or HbA1c) shows they are still progressing towards type 2 diabetes, despite their participation in an intensive lifestyle-change programme’
e.g. their BT is in pre-diabetes range despite lifestyle interventions

188
Q

What does endometrial histology show during menstrual cycle:
follicular phase?
luteal phase?

A 
Follicular = endometrial proliferation
Luteal = endometrium changes to secretory lining under influence of progesterone
189
Q

What does ovarian histology show during menstrual cycle:
follicular phase?
luteal phase?

A

Follicular: follicles develop; one becomes dominant around mid-follicular phase
Luteal: becomes the corpus luteum

190
Q

What happens to hormone levels during menstrual cycle:
follicular phase?
luteal phase?

A

Follicular:

  • FSH rise -> follicular development -> secrete Oestradiol
  • when egg has matured, it secretes enough estradiol to trigger acute release of LH
  • LH surge leads to ovulation

Luteal:

  • Progesterone secreted by corpus lute rises throughout the luteal phase
  • Corpus luteum degenerates if fertilisation doesn’t happen -> progesterone levels fall
  • Oestradiol levels also rise again
191
Q

What happens to the cervical mucus during menstrual cycle:
follicular phase?
luteal phase?

A

Follicular: after menses, mucus is thick, forming a plug at the external os
- just before ovulation it becomes clear, acellular, low viscosity & stretchy (‘spinnbarkeit’)

Luteal: becomes thick, scant, tacky under influence of progesterone

192
Q

Hypoglycaemia with raised insulin, normal proinsulin, & low C-peptide levels?

A

Insulin abuse

193
Q

How do non-functioning pituitary tumours usually present?

A

Hypopituitarism & pressure effects

194
Q

2ry amenorrhoea with lower FSH, PRL & estradiol?

A

hypothalamic causes e.g. stress/exercise

195
Q

What causes overactive bladder/urge incontinence?

A

Detrusor over-activity

196
Q

1st line for overactive bladder/urge incontinence in older man?

A

Tolterodine

oxybutynin greater risk of confusion

197
Q

What happens biochemically in DKA?

A

Low insulin stimulates lipolysis -> production of ketone bodies, beta-hydroxybutyrate & acetoacetate for metabolic fuel

198
Q

Which type of thyroid cancer is ass with RET oncogene?

A

Medullary mainly
(also papillary)
RET oncogene encodes tyrosine kinase receptor ass with MEN type 2

199
Q

MoA of Carbimazole?

How is it usually dosed?

Adverse effects?

A
  • blocks thyroid peroxidase from coupling & iodinating the tyrosine residues on thyroglobulin -> reducing thyroid hormone production

Usually high doses for 6wks until pt is euthyroid then reduced

Agranulocytosis
- crosses placenta, ok in low doses in pregnancy

200
Q

Features of congenital hypothyroidism?

A
  • prolonged neonatal jaundice
  • delated mental & physical milestones
  • short stature, puffy face, macroglossia, hypotonia
  • irreversible cognitive impairment if not Dx & Rx within first 4wks
201
Q

Graves’ disease:
Presentation?
Specific signs limited to it?

A
  • features of thyrotoxicosis in females aged 30-50
  • commonest cause of thyrotoxicosis in pregnancy
  • 25-50% risk of developing eye disease
  • eye signs 30%: exophthalmos, ophthalmoplegia
  • pretibial myxoedema
  • thyroid acropachy
202
Q

Commonest autoAb in Graves’ disease?

2nd commonest?

A

TSH receptor stimulating Ab 90%

anti-thyroid peroxidase Ab 75%

203
Q

Anti-thyroid drug Rx in Graves’ disease?

A

Carbimazole high dose 40mg at least 6wks until euthyroid then reduced gradually to maintain

  • typically continued 12-18months
  • fewer side-effects than block&replace regime
204
Q

Block & replace Rx in Graves’ disease?

A

Carbimazole 40mg started to block

  • Thyroxine added when pt is euthyroid
  • usually lasts 6-9months
205
Q

Radioiodine Rx in Graves’ disease:
what are the contra-indications?
Thyroxine supplementation?

A

C/I:

  • age < 16yrs
  • pregnancy (avoid conception 4-6m after Rx)
  • relative: thyroid eye disease as it may worsen

Majority will require thyroxine after 5yrs
(hypothyroidism is most likely side effect)

206
Q

What is Hashimoto’s thyroiditis?
who does it typically affect?
What are the clinical features
Which Ab may be present?

A

Autoimmune disorder typically associated with hypothyroidism; there may be a transient thyrotoxicosis in acute phase

  • 10x more common in women
  • commonest cause of hypothyroidism
  • ass with other AI disease e.g. IDDM, Addisons, pernicious anaemia
  1. firm, non-tender goitre
  2. hypothyroidism features
  3. anti-thyroid peroxidase Ab
  4. anti-Tg Ab
207
Q

Causes of 2ry hypothyroidism?

A

Rare

  • pituitary failure
  • Downs, Turners syndromes, coeliac disease
  • Give steroids before thyroxine
208
Q

Causes of 1ry hypothyroidism?

A
  1. Hashimoto’s thyroiditis
  2. Subacute thyroiditis (de Quervain’s)
  3. Riedel thyroiditis
  4. After thyroidectomy/radioiodine Rx
  5. Drug Rx
  6. Dietary iodine deficiency
209
Q

Features of hypothyroidism?

A

Gen: weight gain, lethargy, cold intolerance
Skin: dry, cold, yellow skin
- non-pitting oedema
- dry, coarse scalp hair, loss of lateral aspect eyebrows
GI: constipation
Gynae: menorrhagia
Neuro: reduced deep tendon reflexes, carpal tunnel

210
Q

4 Side effects of thyroxine therapy?

Interaction?

A
  1. reduced bone mineral density
  2. worsening of angina
  3. AF
  4. hyperthyroidism due to overRx

Iron reduces absorption of levothyroxine, so take at least 2h apart

211
Q

Starting dose of thyroxine?
When should initial dose be reduced?
When to check TFTs after a change in thyroxine dose?
What is the therapeutic goal?

A
  • 50-100mcg OD
  • Lower e.g. 25mcg od in over 50s, severe hypothyroidism, & those with IHD
  • check 8-12wk after change
  • normalisation of TSH e.g. 0.5-2.5
212
Q

Hypothyroidism in pregnancy:
thyroxine dose?
when to measure TSH?

A
  • many women require increased thyroxine dose in pregnancy, it is safe in breastfeeding as well
  • measure TSH each trimester (aim low-normal) & 6-8wks postpartum
213
Q

What happens to thyroxine level in pregnancy?

A

Pregnancy increases levels of thyroxine-binding globulin -> increase in levels of total thyroxine (but NO effect in free thyroxine level)

214
Q

What are the 3 risks of untreated thyrotoxicosis in pregnancy?

A
  1. inc risk fetal loss
  2. premature labour
  3. maternal heart failure
215
Q

What is transient gestational hyperthyroidism?

A

When HCG activates the TSH receptor

- HCG levels fall in 2nd & 3rd trimester

216
Q

Rx of thyrotoxicosis in pregnancy:
what is the antithyroid regimen of choice?
free thyroxine level target?
which Ab should be checked & when?

A
  • Propylthiouracil in 1st trimester (because carbimazole has inc risk of congenital abnormalities)
  • Switch back to Carbimazole at start of 2nd trimester (as propylthiouracil has inc risk of severe hepatic injury
  • keep maternal free thyroxine levels in upper 1/3 limit of normal to avoid fetal hypothyroidism
  • check thyrotrophin-receptor stimulating Ab at wks 30-36/40 gestation to help determine risk of neonatal thyroid problems
217
Q

What is Riedel’s thyroiditis?who does it usually affect?
clinical features?
main association?

A

Rare cause of hypothyroidism characterised by DENSE FIBROUS tissue replacing the normal thyroid parenchyma
- usually seen in middle-aged women

  1. hypothyroidism features
  2. hard, fixed, painless goitre

Ass with retroperitoneal fibrosis

218
Q

What is sick euthyroid syndrome?

What is shown on bloods?

A

Non-thyroidal illness, reversible on recovery from a systemic illness

  • low T3 & thyroxine
  • low/normal TSH
219
Q

Skin manifestations of hypothyroidism?

A
  • dry, cold, yellow skin
  • non-pitting oedema
  • dry, coarse scalp hair, loss of lateral 1/3 eyebrow
  • eczema
  • xanthomata
  • pruritus (both)
220
Q

Skin manifestations of hyperthyroidism?

A
  • increased sweating
  • scalp hair thinning
  • thyroid acropachy: clubbing
  • pretibial myxoedema: erythematous, oedematous lesions above lateral malleoli
  • pruritus (both)
221
Q

What is subacute de Quervain’s (granulomatous) thyroiditis?

What are the 4 phases?

A

Thyroid imbalance thought to over after a viral infection, usually presenting with hyperthyroidism

  1. 3-6wks of hyperthyroidism, painful goitre, raised ESR
  2. 1-3wks euthyroid
  3. wks-months of hypothyroid
  4. thyroid structure & function back to normal
222
Q

Ix of subacute de Quervain’s thyroiditis?

A

Globally reduced uptake on iodine-131 scan

223
Q

Rx of subacute de Quervain’s thyroiditis?

A
  • usually self-limiting, not requiring Rx
  • aspirin/nsaids for thyroid pain
  • steroids if severe- esp if hypothyroidism develops
224
Q

What is subclinical hyperthyroidism?

What are the causes?

Why is it important to recognise it?

Rx?

A
  • low TSH < 0.1
  • but normal T3 & free thyroxine
  1. multinodular goitre, esp in elerly females
  2. XS thyroxine can give a similar biochemical picture

Due to the potential adverse effects on heart & bone. Can also impact QoL & inc risk of dementia.

Rx:

  • e.g. therapeutic trial low-dose anti-thyroid agent for 6months to try reduce remission
  • BUT TSH often normalises - so levels should be persistently low to warrant intervention
225
Q

What is subclinical hypothyroidism?

What is the significance?

A
  • raised TSH
  • normal T3, T4
  • no obvious Sx
  • risk of progressing to overt hypothyroidism 2-5%/yr, esp men
  • risk increased by presence of thyroid autoAb
226
Q

Rx of subclinical hypothyroidism:
- if TSH is 4-10 & free thyroxine level normal?

  • if TSH>10 & free thyroxine normal?
A

TSH 4-10, normal thyroxine:

  • <65yrs with Sx, trial levothyroxine, but if no improvement then stop
  • in older esp >80yrs, watch & wait gen avoiding hormonal strategy
  • if aSx, observe & repeat thyroid function in 6months

TSH > 10, normal thyroxine:

  • =<70 yrs start Rx with levothyroxine, even if aSx
  • in older eso >80yrs, again watch & wait
227
Q

What is the basic feedback loop of the hypothalamus-pituitary-end organ system that produces thyroxine hormones?

A

Hypothalamus secretes Thyrotropin-RH

  • > stimulates anterior pituitary to secrete TSH
  • > acts on thyroid gland inc T4 & T3 (triiodothyronine), the main hormones
  • > they act on a wide variety of tissues helping to regulate use of energy sources, protein synthesis & controlling boys sensitivity to other hormones
228
Q

How to classify hypothyroidism problems?

A

Congenital: problem with thyroid dyshormonogenesis/dysgenesis

1ry: problem with thyroid gland
2ry: usually disorder or pituitary, or lesion compressing pituitary

229
Q

Painful goitre + raised ESR + recent viral illness?

A

Subacute de Quervain’s thyroiditis

230
Q

Features of hyperthyroidism?

A

Gen: weight loss, ‘manic’/restlessness, heat intolerance
Cardiac: palpitations/arrhyhtmis e.g. AF
Skin: sweating, pretibial myxoedema, acropachy
GI: diarrhoea
Gynae: oligomenorrhoea
Neuro: anxiety, tremor

231
Q

TSH-receptor Ab?

A

90-100% of Graves’ disease pts

232
Q

anti-TPO Ab?

A

90% of Hashimoto’s thyroiditis pts

233
Q

Nuclear scintigraphy: patchy uptake?

A

Toxic multinodular goitre

234
Q

What drug is often given initially to block adrenergic effects in Graves’?

A

Propranolol

e.g. for tremor

235
Q

Low TSH, normal free T4?

A

Subclinical hyperthyroidism
OR
Steroid Rx

236
Q

Causes of thyrotoxicosis?

A

Graves’
Toxic multinodular goitre
Amiodarone
Acute phases of: subacute thyroiditis, post-partum thyroiditis, or Hashimoto’s thyroiditis

237
Q

What is the pathophysiology of thyroid eye disease?

How to prevent it?

A

Autoimmune response against an autoAg, possibly the TSH-receptor

  • > retro-orbital inflammation
  • > glycosaminoglycan & collagen deposition in the muscles
  • Smoking = most important modifiable RF
  • Radioiodine can worsen the inflammatory Sx - Prednisolone may help reduce this risk
238
Q

Features of thyroid eye disease?
Rx?

What features would need urgent ophthalmology review?

A
  • pt thyroid status can be low/eu/high
  • exophthalmos, conjunctival oedema
  • optic disc swelling, ophthalmoplegia
  • sore, dry eyes if they can’t close eyelids

Rx with topical lubricants (corneal inflammation)

  • steroids
  • RT, surgery

Urgent R/V:

  • unexplained deteriorating vision
  • awareness of change in intensity/quality of colour vision in 1/both eyes
  • Hx of eye suddenly ‘popping out’ = globe subluxation
  • obvious corneal opacity
  • cornea still visible when eyelids closed
  • disc swelling
239
Q

What are the clinical features of a thyroid storm?

Rx?

A

Life-threatening complication of thyrotoxicosis; rarely presenting feature or due to iatrogenic thyroxine

  • nausea & vomiting, confusion & agitations
  • fever > 38.5, tachycardia, hypertension
  • abnormal LFTs
  • heart failure
  • Sx Rx e.g. paracetamol
  • Rx underlying precipitant
  • Propranolol
  • anti-thyroid drugs e.g. propylthiouracil/methimazole
  • Lugol’s iodine
  • dexamethasone e.g. 4mg IV qds - blocks conversion of T4 -> T3
240
Q

What is a toxic multi nodular goitre?
Ix of choice?
Rx of choice?

A

Thyroid gland containing a number of autonomously functioning thyroid nodules -> hyperthyroidism

Ix: nuclear scintigraphy reveals patchy uptake

Rx: Radioiodine Rx

241
Q

What is the pathophysiological mechanism is causing apparent mineralocorticoid excess?

A

11-hydroxylase dehydrogenase type 2 inhibition

242
Q

HTN not responding to drugs + hypokalaemia metabolic alkalosis?

A

1ry hyperaldosteronism

243
Q

Hypothyroidism + hard, fixed, painless goitre?

A

Riedel thyroiditis

244
Q

Hypothyroidism + firm non-tender goitre?

A

Hashimoto’s thyroiditis

245
Q

Myxoedemic Coma/thyrotoxic storm: confusion, bradycardia, hypotension
initial Rx?

A

Hydrocortisone (to Rx adrenal insuffienciency)
& levothyroxine (to replace low thyroid hormone levels causing pts Sx)
- beta blocker if tachycardia

  • Risk of hypopituitarism due to the location of the lesion -> therefore treat as presumed adrenal insufficiency until it has been ruled out.
246
Q

autosomal dominant disorder that mimics hyperaldosteronism, resulting in hypokalaemia associated with hypertension?

A

Liddle’s syndrome

247
Q

Causes of hypokalaemia with hypertension?

A

Cushing’s syndrome
Conn’s syndrome (1ry hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency

248
Q

Causes of hypokalaemia without hypertension?

A
  • diuretics
  • GI loss
  • renal tubular acidosis type 1 & 2
  • Bartter’s syndrome
  • Gitelman syndrome
249
Q

what class of drugs are chlorpropamide & tolbutamide?

A

sulfonylurea

250
Q

When to offer HPV vaccine to men?

A

MSM under age of 45 to protect against anal, throat & penile cancers

EXAM (21 decks)

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