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Finals PACES > Endo > Flashcards

Endo Flashcards

1
Q

Secondary causes of DM

A

Drugs: steroids, ART, antipsychotics, thiazides
Pancreatic: CF, chronic pancreatitis, pancreatic cancer
Endo: phaeo, Cushings, acromegaly, thyrotox
Other: glycogen storage diseases, PCOS

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2
Q

Metabolic syndrome

A 
Central obesity and two of:
increased triglycerides
decreased HDL
HTN
Hyperglycemia (DM, IGT, IFG)
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3
Q

Diabetes lifestyle management

A

DELAAYS
Diet - increased complex carbs and soluble fibre, reduced fat and sodium
Exercise
Lipids - statins
ABP - reduce sodium and EtOH and keep BP <130/80 with ACEi doing this best (B-b masks hypos and thiazide increases glucose)
Aspirin - for all > 50 or under 50 and have CV RF
Yearly / 6 monthly follow-up
smoking cessation

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4
Q

Diabetes management

A
  1. DELAAYS
  2. Metformin (C/I: GFR<30, tissue hypoxia (sepsis/MI as lactate increases), morning before GA and contrast)
  3. Metformin + sulfonylurea (gliclazide taken with breakfast)
  4. can add insulin OR sitagliptin/exenatide if obese or employment/social issues with insulin
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5
Q

Insulin regimes

A

BD Biphasic Regime
 BD insulin mixture 30min before breakfast and dinner
 Rapid-acting: e.g. actrapid
 Intermediate- / long-acting: e.g. insulatard
 T2 or T1 DM with regular lifestyle: children, older pts.
 Assoc, with fasting hyperglycaemia

Basal-Bolus Regime
 Bedtime long-acting (e.g. glargine) + short acting
before each meal (e.g. lispro)
 Adjust dose according to meal size
 ~50% of insulin given as long-acting
 T1DM allowing flexible lifestyle
 Best outcome

OD Long-Acting Before Bed
 Initial regime when switching from tablets in T2DM

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6
Q

Diabetic retinopathy

A

Background Retinopathy
 Dots: microaneurysms
 Blot haemorrhages
 Hard exudates: yellow lipid patches

Pre-proliferative Retinopathy
 Cotton-wool spots (retinal infarcts)
 Venous beading
 Haemorrhages

Proliferative Retinopathy
 New vessels
 Pre-retinal or vitreous haemorrhage

Maculopathy
 ↓ acuity may be only sign
 Hard exudates w/i one disc width of macula

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7
Q

Diabetic neuropathy

A

Peripheral Neuropathy:
Includes absent ankle jerk which is treated paracetamol/ amitriptyline/ gabapentin/ baclofen

Mononeuritis multiplex:
e.g. CN3/6 palsies

Femoral Amyotrophy:
 Painful asymmetric weakness and wasting of quads with loss of knee jerks
 Dx: nerve conduction and electromyography

Autonomic Neuropathy
 Postural hypotension – Rx: fludrocortisone
 Gastroparesis → early satiety, GORD, bloating
 Diarrhoea: Rx c¯ codeine phosphate
 Urinary retention
 ED

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8
Q

Causes of hypos

A 
EXPLAIN
 Exogenous drugs (insulin or sulphonyl)
 Pituitary insufficiency
 Liver failure
 Addison’s
 Islet cell tumours (insulinomas)
 Immune (insulin receptor Abs: Hodgkin’s)
 Non-pancreatic neoplasms: e.g. fibrosarcomas
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9
Q

Cause from Ix for hypo

A

Look at ketones, C-peptide and insulin

Hyperinsulinaemic hypoglycaemia
 Drugs: ↑ C-pep = sulfonylurea; normal C-pep = insulin
 Insulinoma (MEN1)

↓ insulin, no ketones
 Non-pancreatic neoplasms
 Insulin receptor Abs

↓ insulin, ↑ ketones
 Alcohol binge with no food
 Pituitary insufficiency
 Addison’s

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10
Q

Hypo Mx

A

Alert and Orientated: Oral Carb
 Rapid acting: lucozade
 Long acting: toast, sandwich

Drowsy / confused but swallow intact: Buccal Carb
 Hypostop / Glucogel
 Consider IV access

Unconscious or Concerned re Swallow: IV dextrose
 100ml 20% glucose (50ml 50% dextrose: not used)

Deteriorating / refractory / insulin-induced / no access:
 1mg glucagon IM/SC
 Won’t work in drunks + short duration of effect (20min)
 Insulin release may → rebound hypoglycaemia

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11
Q

Thyroid storm Rx

A
  1. Fluid resuscitation + NGT
  2. Bloods: TFTs + cultures if infection suspected
  3. Propranolol PO/IV
  4. Digoxin may be needed
  5. Carbimazole then Lugol’s Iodine 4h later to inhibit thyroid
  6. Hydrocortisone
  7. Rx cause
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12
Q

Causes of hypothyroidism

A

Primary:

  1. Atrophic thyroiditis: most common in UK; antibodies but no goitre, associated with pernicious anaemia, vitiligo
  2. hashimoto’s thyroiditis: TPO +ve with goitre
  3. Iodine deficiency
  4. Post de quervain’s thyroiditis

Post-surgical
Secondary to hypopituitarism

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13
Q

Myxoedema coma features

A 
 Looks hypothyroid
 Hypothermia
 Hypoglycaemia
 Heart failure: bradycardia and ↓BP
 Coma and seizures
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14
Q

Myxoedema coma Mx

A

 Bloods: TFTs, FBC, U+E, glucose, cortisol
 Correct any hypoglycaemia
 T3/T4 IV slowly (may ppt. myocardial ischaemia)
 Hydrocortisone 100mg IV
 Rx hypothermia and heart failure

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15
Q

Plummer’s vs multinodular goitre

A

Multinodular goitre evolves from simple goitre caused by iron deficiency or autoimmune; it usually is euthyroid or subclinical hyperthyroidism

Plummer’s is a toxic multinodular goitre where one of the nodules becomes toxic, so can cause thyrotox and will show uneven uptake on hot nodule

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16
Q

Graves Ab

A

anti-TSH (T2 hypersensitivity)

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17
Q

Hashimoto’s thyroiditis Ab

A

anti-TPO, anti-Tg (T2 and T4 hypersensitivity)

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18
Q

de Quervain’s Ag

A

usually caused by Coxsackie virus; shows reduced iodine uptake

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19
Q

Subacute lymphocytic thyroid disease

A

Diffuse painless goitre
May occur post-partum
Thyrotoxicosis → hypo→eu

20
Q

Riedel’s thyoiditis

A

Hard fixed thyroid mass
Mass effects only (dysphagia, obstruction etc)
Assoc. with retroperitoneal fibrosis

21
Q

Follicular adenoma

A

Single thyroid nodule ± thyrotoxicosis (majority are cold); treat with hemi-thyroidectomy

22
Q

thyroid cyst

A

Solitary thyroid nodule
Asympto or pressure symptoms
Can → localised pain due to cyst bleed
Rx: aspiration or excision

23
Q

Thyroid cancer

A

Papillary is most common, mainly affects 20-40y.o., which spreads to jugulodigastric lymph node or lung
Follicular (bones or lung mets) and papillary stem from follicular cells and have Tg as tumour marker

Medullary associated with MEN2, so must do phaeo screen pre-op. Stem from parafollicular C-cells and use CEA snd calcitonin as tumour markers

Anasplastic are undifferentiated follicular cells that are sen in elderly (>60) and have rapid aggressive growth

24
Q

Risk factors for malignancy in thyroid nodules

A 
 Solitary
 Solid
 Younger
 Male
 Cold (non-functional)
 Risk factor: e.g. radiation exposure
25
Q

Complications of thyroid surgery (usually a collar incision)

A

Early
 Reactionary haemorrhage → haematoma (<1%)
 Laryngeal oedema
 Recurrent laryngeal nerve palsy (0.5%) (Right RLN more common - oblique ascent)
 Hypoparathyroidism (2.5%) → ↓ Ca2+ → Chvostek’s and Trousseau’s
 Thyroid storm - Rx: propranolol, antithyroid drugs, Lugol’s

Late:
 Hypothyroidism
 Recurrent hyperthyroidism
 Keloid scar

26
Q

Ix and Rx for primary hyperparathyroidism

A

 ↑Ca2+ + ↑ or inappropriately normal PTH, ↑ALP, ↓PO4
 ECG: ↓QTc → bradycardia → 1st degree block
 X-ray: osteitis fibrosa cystica → phalangeal erosions
 DEXA: osteoporosis

Treat hypercalcaemia with:  ↑ fluid intake
 Avoid dietary Ca2+ and thiazides (↑ serum Ca)
Can remove adenoma but risk of hypoparathyroidism and recurrent laryngeal nerve palsy

27
Q

Hypoparathyroidism Causes

A

 Autoimmune
 Congenital: DiGeorge (CATCH22)
 Iatrogenic: Surgery; radiation

Rx: ca supplements and calcitriol

28
Q

Pseudohypoparathyroidism

A

 Failure of target organ response to PTH
 Symptoms of hypocalcaemia
 Short 4th and 5th metacarpals, short stature
 Ix: ↓Ca, ↑PTH
 Rx: Ca supplements + calcitriol

29
Q

ACTH independent causes (low ACTH)

A 
 Iatrogenic steroids: commonest cause
 Adrenal adenoma / Ca: carcinoma often → virilisation
 Adrenal nodular hyperplasia
 Carney complex: LAME Syndrome
 McCune-Albright
30
Q

ACTH dependent causes (high ACTH)

A

Cushing’s disease:
 Bilat adrenal hyperplasia from ACTH-secreting
pituitary tumour (basophilic microadenoma)
 Cortisol suppression occurs with high-dose dex

Ectopic-ACTH: excise tumour and give metyrapone
 SCLC
 Carcinoid tumour
 Skin pigmentation, metabolic alkalosis, wt. loss,
hyperglycaemia
 No suppression with any dose of dex

31
Q

Nelson’s syndrome

A

 Rapid enlargement of a pituitary adenoma following
bilateral adrenelectomy for Cushing’s syndrome
 Not typically performed nowadays

Presentation:
 Mass effects: bitemporal hemianopia
 Hyperpigmentation

32
Q

Primary hyperaldosteronism causes; Ix; Rx

A

High BP and hypokalaemia

Bilateral adrenal hyperplasia
Adrenocortical adenoma (Conn's)

Aldosterone:renin ratio elevated; adrenal CT/MRI needed

Conn’s: laparoscopic adrenelectomy
Hyperplasia: spironolactone

33
Q

Secondary hyperaldosteronism

A

Due to ↑ renin from ↓ renal perfusion

Causes
 RAS
 Diuretics
 CCF
 Hepatic failure
 Nephrotic syndrome

Ix
 Aldosterone:renin ratio: normal

34
Q

Bartter’s syndrome

A

 Autosommal recesive
 Blockage of NaCl reabsorption in loop of Henle (as if
taking frusemide)
 Congenital salt wasting → RAS activation →
hypokalaemia and metabolic alkalosis + hyponatraemia
 Normal BP

35
Q

Secondary Adrenal insufficiency

A

Causes
 Chronic steroid use → suppression of HPA axis
 Pituitary apoplexy / Sheehan’s
 Pituitary microadenoma

Features
 Normal mineralocorticoid production
 No pigmentation (ACTH ↓)

36
Q

Phaeo

A

Rule of 10s
 10% malignant
 10% extra-adrenal (found by aortic bifurcation)
 10% bilateral
 10% part of hereditary syndromes: MEN2a and 2b; Neurofibrimatosis; Von Hippel-Lindau: RCC + cerebellar signs

Ix: 
 Plasma + urine metadrenaline
 Also vanillylmandelic acid
 Abdo CT/MRI
 MIBG (mete-iodobenzylguanidine) scan
37
Q

Hypertensive crisis Rx

A

 Phentolamine 2-5mg IV (α-blocker) then labetalol 50mg IV
 Repeat to safe BP (e.g. 110 diastolic)
 Phenoxybenzaime 10mg/d PO when BP controlled
 Elective surgery after 4-6wks to allow full α-blockade
and volume expansion

38
Q

MEN1

A

 Pituitary adenoma: prolactin or GH
 Parathyroid adenoma / hyperplasia
 Pancreatic tumours: gastrinoma or insulinoma

39
Q

MEN2

A

 Thyroid medullary carcinoma
 Adrenal phaeochromocytoma
 A) Hyperthyroidism
 B) Marfanoid habitus

40
Q

Carney Complex/LAME Syndrome

A

LAMES
Lentigenes - spotty skin pigmentation (Peutz Jehgers is DDx)
Atrial Myxoma
Endocrine tumours (pituitary, adrenal hyperplasia)
Schwannomas

41
Q

Peutz-Jeghers

A

 Mucocutaneous freckles on lips, oral mucosa and palms /
soles
 GI hamartomas: obstruction, bleeds
 Pancreatic endocrine tumours
 ↑ risk of cancer: CRC, pancreas, liver, lungs, breast

42
Q

Von Hippel-Lindau

A 
 Renal cysts
 Bilateral renal cell carcinoma
 Haemangioblastomas - Often in cerebellum → cerebellar signs
 Phaeochromocytoma
 Pancreatic endocrine tumours
43
Q

Neurofibrimatosis

A 
 Dermal neurofibromas
 Café-au-lait spots
 Lisch nodules
 Axillary freckling
 Phaeochromocytoma
44
Q

Autoimmune polyendocrine syndrome

A

Type 1: AR - Addison’s, candidiasis, hypoparathyroidism

Type 2 (schmidt’s syndrome): polygenic - Addison’s, thyroid disease, T1DM

45
Q

Craniopharyngeoma

A

 Originates from Rathke’s pouch
 Commonest childhood intracranial tumour → growth failure
 Calcification seen on CT/MRI

46
Q

DI causes

A 
Cranial
 Idiopathic: 50%
 Congenital: DIDMOAD
 Tumours
 Trauma
 Vascular: haemorrhage (Sheehan’s syn.)
 Infection: meningoencephalitis
 Infiltration: sarcoidosis
Nephrogenic
 Congenital
 Metabolic: ↓K, ↑Ca
 Drugs: Li, demecleocycline, vaptans
 Post-obstructive uropathy
47
Q

Waterhouse-Friedrichsen syndrome

A

Adrenal failure with haemorrhage from N meningitidis

Finals PACES (12 decks)

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