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CSIM > Endocrine > Flashcards

Endocrine Flashcards

1
Q

PC hyponatremia

A

N/V, anorexia, confusion, muscle cramps , seizures, coma

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2
Q

Causes of hypovolemic hyponatremia

A

Pre-renal : Burns, D/V, pancreatitis
Renal: Diuretics, Addisons, nephropathy, osmotic diuresis

Salt loss in excess of H20 loss

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3
Q

Causes of euvolemic hyponatremia

A

Dilutional hypoantremia due to intake of water in excess of kidneys ability to excrete.

SIADH, severe hypothyroidism, fluid overload, psychogenic polydipsia

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4
Q

Causes of hypervolemic hyponatremia

A

Water excess = HF, cirrhosis, renal failure

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5
Q

Functions of kidney

A

Secrete epo and renin. Regulate levels of Na+, K+, Cl-, phosphate, HCO3. Regulate acid base balance

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6
Q

Pseudohyponatremia

A

hyperglycaemia, hyperlipidemia, hyperprolactinemia

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7
Q

MOA bisphosphonates

A

Accumulate in bone matrix inhibit osteoclast action by blocking HMG-reductase. Reduced bone reabsorption and calcium uptake

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8
Q

Indications for bisphosphonates

A

osteoporosis, hypercalcemia, metastasis/Pagets

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9
Q

SE of bisphosphonates

A

Oesophageal irritation, headache, osteonecrosis of the jaw, hypocalcemia

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10
Q

Osteomalacia

A

Inadequate mineralisation of bone. Due to vit D deficiency (CKD, poor diet, malabsorption

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11
Q

PC osteomalacia

A

diffuse joint/bone pain, weakness, bowing of legs, compressed vertebrae, #NOF

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12
Q

Signs of osteomalacia

A

Inv - low Ca2+, high PTH, high Alk phos

X-ray - craniotabes, cupped epiphyses

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13
Q

Rapid correction of sodium

A

Pontine demyelinosis - demyelination and necrosis of central pons and corticospinal tracts leading to quadriplegia, ophthalmoplegia, pseudo bulbar palsy and coma

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14
Q

Inv for hyponatremia

A

rule out pseudo causes - BM, cholesterol
TFT’s to rule out hypothyroid
U+E’s - Addisons (high K+, low Na+)
Urine osmolality - SIADH

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15
Q

Mx hyponatremia

A

Stop all diuretics, SSRI’s
SIADH - fluid restriction, levels of sodium are normal just diluted
Acute + symptomatic = 3% hypertonic saline 150ml IV over 15 mins to rapidly replace ( don’t increase by over 10mmol/L in 24hrs)
Find the causes!!

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16
Q

Severe acute hyponatremia

A

Cerebral oedema leading to brainstem herniation due to h20 shift from blood vessels to interstitial space.

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17
Q

SIADH

A

Inappropriate ADH levels leads to fluid retention and hyponatremia. ADH acts to increase aquaporin insertion at the distal convoluted tubule. This leads to low osmolality. As the body retains h20 aldosterone is released to facilitate Na+ loss hence facilitation h20 loss down its concentration gradient.

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18
Q

SIADH Inv

A

low Na+ and plasma osmolality
high urinary Na+ and urinary osmolality
normal thyroid function, no evidence of Addisons

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19
Q

Mx SIADH

A

fluid restrict
ADH receptor antagonist - demeclocycline
find the cause!!

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20
Q

Causes of SIADH

A 
Ectopic ADH - SCLC
Hypothyroidism
Infections - pneumonia, TB, lung abcess, meningitis
SAH, trauma, stroke, 
Drugs - SSRI's, carbamazepine,
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21
Q

Hypernatremia PC

A

Na+ >145 Pc - thirst, polydipsia, polyuria, dehydration leading to weakness, seizures and coma

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22
Q

Causes of hypernatreamia

A

hypovolemic - vomiting, sweating, burns = dehydration
euvolemic - diabetes insipidus (mass water loss)
hypervolemic - hyperaldosteronism, Cushing’s

Much rarer almost exclusively due to h20 deficit

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23
Q

Causes of hypokalemia

A

reduced intake - malnutrition, chronic alcoholism
increased losses - vomiting, diarrhoea
Conn’s, cushings
diuretics, insulin OD, alkalosis, Bblocke

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24
Q

Ranges of potassium

A

hypo < 3.5 moll/l

hyper > 5.5 moll/l

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25
Q

Potassium physiology

A

98% intracellular maintained by Na+/K+ pump. approx 87% absorbed @ proximal convulted tubule and thick ascending limb. Leaves 13 % variable for distal consulted reabsorption via aldosterone. Aldosterone = Na+ reabsorption and K+ excretion

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26
Q

PC hypokalemia

A

asymptomatic, hypotonia, hyporeflexia, cramps + tetany

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27
Q

ECG changes in hypokalemia

A

flattened t waves, increased PR and Qt interval , low volume QRS, ST depression

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28
Q

Potassium modulators

A

B2 agonists ie salbutamol stimulate Na+/K+ pump
Insulin drives K+ intracellularly
Alkalosis - low H+ levels in blood leads to H+/K+ exchange to increase blood H+ levels

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29
Q

Mx hypokalemia

A

mild + moderate (2.5 - 3.9) - oral K+ supplements

severe (<2.5) IV 40mmol KCL in 1l 0.9 % Nacl (max 20mmol per hr)

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30
Q

Causes of hyperkalemia

A 
rhabdomylosis, tumour lysis syndrome
Addison's , hypoaldosteronism
ACEi, potassium sparing diuretics, B blockers
Renal failure
Metabolic acidosis, DKA
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31
Q

PC hyperkalemia

A

tachycardia, palpitations - arrhythmias

flaccid paralysis and weakness

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32
Q

ECG signs of hyperkalemia

A

Tall tented t waves, wide QRS, small p waves - risk of VF

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33
Q

Mx of hyperkalemia (>6.5)

A

IV calcium gluconate 10% 10ml - stabalise cardiac membrane
Nebulised salbutamol
IV 20% glucose and 10 Units insulin infusion

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34
Q

Posterior pituitary

A

ADH and oxytocin

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35
Q

1 vs 2 endocrine disease

A 
1 = dysfunction of target organ
2 = pituitary dysfunction
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36
Q

Congenital adrenal hyperplasia

A

21 hydroxylase deficiency 46xxF leads to development of male characteristics muscle bulk, body hair and deep voice. Due to increased circulation androgens

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37
Q

Mineralocorticoid

A

Aldosterone produced by zona glomerulosa. Acts vasoconstrictor the efferent renal arteriole to increase filtration. Increases sodium retention and potassium excretion. Stimulates ADH release and thirst reflex

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38
Q

Glucocorticoids

A

Cortisol produced by the zona fasiculata. Causes gluconeogensis leading to hyperglycaemia. Protein catabolism leading to muscle wasting. Reduced calcium uptake - osteoporosis. Reduced immune response

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39
Q

Testing the pituitary

A

short synacthen - stimulate using acth

dexamethasone suppression - halt cortisol secretion via -ve feedback

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40
Q

Causes of hypopituitarism

A 
Iatrogenic - surgery, irradiation 
Vascular - apoplexy, sheenans syndrome
Infiltrative - sarcoidosis, haemochromatosis 
Neoplastic - metastasis, adenoma
Infective - TB, abcess
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41
Q

Function of oestrogen

A

2ndary sexual characteristics, inhibits bone reabsorption, alters lipid profile

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42
Q

Function of progesterone

A

maintains uterine lining, reduced contractility of uterine SM, reduced skin elastic

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43
Q

Apoplexy

A

Infarction of pituitary due to haemorrhage or schema linked to presence of pituitary adenoma. Increased risk in DM, DIC and anticoagulation.

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44
Q

PC of apoplexy

A

PC - severe onset headache, vomiting, meningism
visual loss and opthalmaplegia
(cavernous sinus compression)

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45
Q

Mx of apoplexy

A

confirm diagnosis with MRI, IV steroids and fluids to replace. V hard to differentiate from SAH

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46
Q

Sheenhan’s syndrome

A

haemorrhage infarction of pituitary. Often due to post partum haemorraghe

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47
Q

Mass effect of pituitary adenoma

A

Classically gradual vision loss tunnel vision due to optic chiasm compression. Bitemporal hemianopia
Headache and nausea. Possible hyper/hypopituitary

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48
Q

Hyperpituitary problems

A

SIADH, acromegaly, Cushings syndrome, hyperthyroid, hyperprolactinemia

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49
Q

Causes of Cushings syndrome

A 
ACTH dependent - Cushing's disease (benign adenoma)
ectopic ACTH (SCLC, thymic/pancreatic carcinoid)

ACTH independent - bilateral hyperplasia, adrenal adenoma

Exogenous steroids - inhalers, steroids

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50
Q

PC Cushings

A

central obesity - moon face, buffalo hump, wt gain
proximal muscle wasting
straie, easy bruising, fragile skin, acne and hirsutism
impotence, depression and insomnia

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51
Q

Complications of Cushings

A

HTN, DM, osteoporosis, metabolic syndrome

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52
Q

Investigation Cushings

A

24hr urinary cortisol
high Na+, low K+ (due to high aldosterone levels
high BP, high glucose
CT scan to look for adrenal/pituitary adenoma. CXR
dexamethasone supression - failure to suppress. ACTH levels for 1 vs 2

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53
Q

Mx Cushings

A

Transsphenodial surgery for pituitary adenoma
Reduce exogenous steroids
Bilateral adrenalectomy
Treatment of ectopic

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54
Q

Causes adrenal insufficiency

A

1st - Addisons

2nd - AI, TB and AIDS, Malignancy - breast, lung and kidney, Infarction, Waterhouse fredreich ( meningoccal sepeticima) . Amyloidosis and haemochromatosis. Post radiotherapy/ surgery

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55
Q

Adrenal crisis

A

Medical emergency PC hypovolemic shock, abdominal pain, hypoglycaemia, hypotension, confusion, dysarthria

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56
Q

Mx adrenal crisis

A

IV fluids 0.9% NaCl, 100mg IV hydrocortisone, correct hypoglycaemia. ECG to check for arrhythmias due to low K+

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57
Q

Inx adrenal insufficiency

A

low Na+, high K+
high ESR, urea
serum cortisol @ 9am >580nmol
short synacthen test failure to respond.

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58
Q

PC adrenal

A

hypoglycaemia, postural hypotension, N/V, abdo pain, wt loss, malaise, weakness, low Na+, K+
hyper pigmentation of buccal mucosa due to high ACTH

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59
Q

Differentiation of 1st and 2nd adrenal failure

A

1st - high acth, high renin, low cortisol

2nd - low acth, low renin

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60
Q

Causes of hyperaldosteronism

A

1 - Conn’s syndrome (adrenal adenoma), bilateral adrenal hyperplasia, adrenal adenoma

2 - chronically increased renin levels due to HF, cirrhosis, renal artery stenosis, nephrotic syndrome

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61
Q

PC hyperaldosteronism

A

asymptomatic - hypertension, low K+, high Na+, metabolic alkolosis

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62
Q

Inv hyperaldosteronism

A

CT of kidneys looking for adenoma/ hyperplasia
fludrocortisone suppression test
renin:aldosterone (high in 2ndary disease) low renin due to -ve feedback in 1 disease

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63
Q

Mx hyperaldosteronism

A

potassium sparing diuretics

adrenal adenalectomy for Conn’s

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64
Q

Causes of hypothyroid

A 
AI - atrophic thyroid, Hashimotos
Iodine deficiency 
Infection 
Sarcoidosis, neoplasm
Post surgery, radioiodine, drug induced - amiodarone, lithium
65
Q

PC hypothyroid

A

wt gain, depression, cold intolerance, fatigue, weakness, low IQ, hypertension, pleural effusions, anaemia
dry hair, skin, loss of our 1/3rd eyebrow
bradycardia, constipation, carpal tunnel syndrome
SIADH, peripheral oedema

66
Q

Hashimotos

A

AI condition antiTPO +ve. Progressive lymphocytic infiltration and fibrosis of thyroid tissue leads to dysfunction. PC = firm rubbery goitre

67
Q

TFT’s hypothyroid

A

1 - high TSH, low T4
2 - low TSH, low T4

subclinical disordered TFTs asymptomatic pt

68
Q

Mx hypothyroid

A

levothyroxine used to replace titrate up using
1 - TSH levels
2 - T4 level @ upper limit

69
Q

PC hyperthyroid

A

sweating, wt loss, increased appetite, tachycardia, AF
altered mood, irritable,
diarrhoea, polyuria, fine tremor
palmar erythema, congestive HF, muscle wasting, palmar erythema

70
Q

Causes of hyperthyroid

A

Graves, toxic multi nodular goitre, toxic adenoma,

TSHoma

71
Q

Graves specific

A 
thyroid acropatchy - clubbing
dermapathy @ pre tibal sites
exophthalmus and lid retraction 
gritty eye movement and periorbital oedema
\+ve TRab antibodies
72
Q

SE of carbimazole

A 
common = urticaria and rash 
rare = agranulocytosis 2-8wks post commencement of treatment
73
Q

Mx hyperthyroid

A

Graves = block and replace carbimazole and levothyrozxine
TSHoma - transphenoidal surgery
TMN - radioactive iodine

propanolol for symptomatic relief

74
Q

Thyroid storm PC

A

PC - tachycardia, high output HF, hyperthermia, vomiting and diarrhoea, jaundice, renal failure, arrhythmias

75
Q

PCOS

A

irregular menses, sub fertility, 12+ cysts on USS, acne and hirsutism

76
Q

PC hypogonadism

A

Males - erectile dysfunction, osteopenia, low body hair, libido and muscle bulk

Females - infertility, amenorrhea, osteoporosis

77
Q

Male hypogonadism

A

1 - Kleinfelters, Noonans, orchitis post mumps, trauma
2 - Kallman syndrome, increased stress, exercise,
Prader willi, haemochromatosis

Iatrogenic - anabolic steroid use

78
Q

Subclinical thyroid disease

A

asymptomatic, deranged TFT’s

79
Q

Causes of hyperprolactinaemia

A

Dopamine inhibits prolactin secretion. High oestrogen and TRH levels stimulate its production from the pituitary.

  • Physiological = pregnancy, lactation, stress
  • Pathological

drugs - metaclomprimide, COCP, TCA, methyldopa,dopamine antagonists,

cirrhosis, renal failure, hypothyroidism, prolactin secreting pituitary adenoma

80
Q

PC hyperprolactinaemia

A

F - galactorrhea, anovulatory amenorrhoea

M - gynecomastia, erectile dysfunction

81
Q

Mx prolactinoma

A

dopamine agonists - bromocriptine lead to reduced secretion and shrinkage of tutor. surgery only needed id symptoms of mass effect

serum prolactin > 500

82
Q

Acromegaly

A

99% caused by GH producing pituitary adenoma

83
Q

PC acromegaly

A

gradual and progressive sweating, tiredness and fatigue
facial features - frontal bossing, enlarged nose, macro glossia, wide dental spacing, coarse features
soft tissue swelling, large hands and feet
organomegaly
OA and carpal tunnel

84
Q

Complications of acromegaly

A

HTN and DM - increased CVD risk
visual field defects
high risk of CRC and breast cancer
obstructive sleep aponea

85
Q

Inv and Mx Acromegaly

A

high IGF-1, OGTT = failure to suppress GH <1ml
MRI of brain
high glucose, calcium and phosphate
transphenoid surgery / somastatin analogues

86
Q

PC diabetes insipidus

A

PC - polyuria, polydipsia, dehydration

hypernatremia

87
Q

Pathophysiology of DI

A

Lack of ADH leads to low levels of aquaporin channels inserted into collecting ducts. This gives rise to a failure to concentrate urine hence excessive diuresis

88
Q

Causes of DI

A

Cranial - Trauma, pituitary tumors, Sheenan’s syndrome, meningitis. All lead to reduced production of ADH from post pituitary

Nephrogenic (poor response to ADH) PCKD, amyloidosis, CKD, low K+, high ca2+

Dipsogenic - over consumption of h20

89
Q

Mx DI

A

synthetic ADH analogue (desmopressin) only effective for cranial causes.

90
Q

Inv DI

A

fluid deprivation test can rule out dipsogenic causes

desmopressin trial will lead to normalisation of urine output in those with a cranial cause

91
Q

Calcium physiology

A

Low ca2+ is detected stimulating PTH release from parathyroid. This stimulate osteoclast activity to increase Ca2= reabsorption. It also increase absorption in the proximal and distal collecting tubules. Allows calcitriol to convert vit D to 1,25 dihydroxy to increase Ca2+ absorption from the gut

High Ca2+ parafollicular cells produce calcitonin to reduce absorption from the kidney and gut, and suppress osteoclast activity.

92
Q

Hypercalcemia PC

A 
thirst, polyuria - renal stones
weakness, myalgia - bone pain
anorexia and constipation - abode groans
mood change, confusion - psych moans
pathological #

Some of the symptoms are due to Na+ channels on synapses being less likely to open leading to reduced excitability. To compensate calcium is excreted in the urine and can precipitate to form stones

93
Q

Causes of hypercalcemia

A 
Malignancy - myeloma, PTHrp secretion
Renal failure
Sarcoidosis
Hyperparathyroidism
Addisons, phaechromocytoma, hypothyroid
Drugs - thiazide diuretics
94
Q

Inv hypercalemia

A

high PTH - hyperparathyroid, PTHrp
low PTH - secondary causes
- normal ALP = myeloma, sarcoid
- high ALP = bone mets, hyperthyroid

95
Q

Acidosis and hypoalbuminea

A

In acidosis high concentration of H+ in blood leads to albumin repelling Ca2+ reducing albumin bound calcium

In hypoalbuminemic states leads to reduced total calcium as apporx 50% is protein bound

96
Q

Hyperparathyroidism

A

Post menopausal women, 50-70 y/o
Always look for link to MEN 1 and 2
85% benign parathyroid adenoma

97
Q

PC hyperpararthyroid

A

asymptomatic for long periods
HTN due to renal calcification
stones, moans, groans and bones

98
Q

Secondary hyperparathyroidism

A

vit D deficiency, chronic renal failure

99
Q

Complications of hyperparathryoid

A 
Osteoporosis @ hip/wrist
Renal stones and nephrocalcinosis
corneal calcification
pseudo gout
CVD and IHD due to calcification and renal failure
100
Q

Inv hyperparathyroid

A

high PTH, Ca2+, ALK phos, low phosphate

CT scan of parathyroid

101
Q

Mx hyperparathyroid

A

Surgical removal
hydration and monitoring
calcinmet - Ca2+ receptor agonist

102
Q

Osteitis fibrosis cystica

A

Advanced hyperparathyroidism leads to loss of bone mass and replacement with fibrous tissue formation of cyst like brown tumors. Characteristic on X-ray

103
Q

Hypercalcemia of malignancy

A

Poor prognosis - 6 months.
20% - Local invasive osteolytic lesions this can present with bone pain, pathological # and MSCC. Due to myeloma, metastatic breast and lung cancer

80% - Humoral hypercalcemia due to production of PTHrp. This antagonises PTH binding to its receptors leading to increases osteoclast activity and hence CA2+ levels in the blood. Imvx - low PTH and vit D activity
Caused by squamous cell cancers, renal cervix, lung, bladder and oesophageal

104
Q

Myeloma

A

Cancer arising from B cells uncontrolled production of paraprotein. Produces osteoclast activation factors which leads to increase osteoclast activity and hence bone weakness.
PC - CRAB, high Po4, high Ca2+, normal ALP

105
Q

Hyperviscosity syndrome

A

increase blood viscosity due to polycythemia, myeloma or leukaemia. PC - epistaxis, gum bleeding, headaches, visual changes and hearing loss

106
Q

Hypocalcemia PC

A

parathesia or extremities, carpopedal spasm, seizures, muscle twitching, anxiety and irritability. increased muscle tone - colic, dysphagia, stridor

Due to voltage gated Na+ depolarising more easily leading to involuntary muscle contraction

107
Q

Causes of hypocalcemia

A

Chronic renal failure, osteoporosis, vit D defiency, hypoparathyroidism, rhabdomylosis, drug induced - bisphosphanates

Alkalosis leads to pseudo hypocalcemia due to less H+ ions so negatively charged albumin binds to Ca2+

108
Q

Signs of hypocalcemia and Mx

A

Trousseaus - muscle cramps and twitching on application of BP cuff
Chvostek’s - facial twitch when tapped over parotid gland
ECG - prolonged QTc
low Ca2+
Mx - vit D replace, calcium gluconate

109
Q

Causes of hypoparathyroidism

A

Surgical removal
Di george - congenital abnormality of pharyngeal pouch formation
AI
Haemochromatosis

110
Q

Renal failure and hypocalcemia

A

failure to hydroxylate vit D = reduced Ca2+ absorption from gut
failure to excrete phosphate which binds to Ca2+

111
Q

Inv hypoparathyroid

A

low PTH, low Ca2+, low Po4

112
Q

Osteoporosis

A

T score 2.5 = diagnostic. reduced bone mass with normal architecture seen clinically with low impact fragility fractures.

113
Q

Bone mineral density

A

Measured with DEXA scan. Z score = age matched. T score = race, sex of peak adult

114
Q

Risk factors for osteoporosis

A

1 - age, female, smoking + alcohol, low BMI,

2 - renal failure, drugs - steroids, heparin, malabsorption - coeliac, endocrine - cushings, high PTH, hypogonadism

115
Q

PC fractures in osteoporosis

A

colles fracture - wrist outstretched hand
#NOF
wedge vertebral fracture

116
Q

Mx osteoporosis

A

increase wt bearing exercise - tia chi, swimming
loose wt, stop smoking, reduce alcohol
Ca2+ and vit D supplementation
bisphosphanates

117
Q

Diagnosing T2DM

A

symptoms - wt loss, polyuria, polydypsia +

  • random glucose >11.1
  • fasting glucose >7.0
  • 2hr OGTT > 11.1
  • Hba1c > 48

If no symptoms 2 x samples over 2 weeks

118
Q

When not to use HbA1c

A

Renal failure/ haemolytic anaemia due to improper glycosolation of Hb
Acutely unwell
Rapidly changing, gestational or young

119
Q

Risk factors for T2DM

A

FHx, obesity, PCOS, low exercise, low socioeconomic status, asian, HTN, hyperlipidemia

120
Q

PC T1DM

A

wt loss, polyuria, polydipsia, DKA, BMI<25, often adolescent (before 50y/o)
6% chance of son T1DM if father

121
Q

Pathogenesis DKA

A

inability to produce insulin due to destruction of the B islet cells in the pancreas. This lead to reduced glucose utilisation by tissue so levels in the blood increase. Proteolysis and lipolysis occur to find an alternative source for glucose, the break down of lipid yield free fat acids which give rise to ketones causing acidosis. High levels of glucose lead to an osmotic diuresis and hence volume depletion and electrolyte disturbance

122
Q

Autoantibodies T1DM

A

Only used if unusual presentation, appear before onset 95% of children are +ve for GAD,ICA
C peptide - breakdown product of insulin can be used a surrogate marker of insulin production

123
Q

Gestational diabetes

A

randome plasma glucose > 5.6
fasting glucose > 7.8

Screening with OGGT for those with BMI>30, PHx of gestational diabetes, macrocosmic baby, FHx,

124
Q

Risks of gestational diabetes

A

Preg - eclampsia, still birth after 37wks, congenital abnormalities, IUGR, macrosomia
Mum - PPH, C-section/instrumental delivery, traumatic birth
Baby - hypothermia, hypoglycaemia, jaundice, shoulder dystocia,

125
Q

MODY

A

PC - young age of onset, often incidental hypoglycaemia, lack of metabolic syndrome, can present with classical DM presentation

  • Glucokinase (32%)
  • Transcription factors (68%)
126
Q

Insulin secretion

A

High levels of glucose reacts with the glucose receptor on the surface of the B islet cell. The enter the cell and are converted to glucose 6 phosphate by glucokinase. This provides ATP for K+ channels to open allowing insulin secretion to lower glucose levels.

127
Q

Glucokinase MODY

A

Loss of function impairs glucose sensing by increasing threshold needed for insulin secretion.
PC - incidental findings/gestational diabetes, persistent high fasting glucose, no microvascular complications or extra pancreatic features

Mx - test parents/family

128
Q

Transcription factor MODY

A

Role of B cell development genes

  • HNF-1a and HNF-4a
  • HNF-1B
129
Q

HNF-1a and HNF-4a

A

PC - normoglycemia in childhood, develop hyperglycaemia in adolescent years, poor control can lead to complications

Mx - low dose sulponhylurea - glicazide

130
Q

HNF-1B

A

PC renal cysts and diabetes, often co existing pancreatic and genitourinary abnormalities.

Mx - 50% may need dialysis, insulin

131
Q

DIDMOAD

A

diabetets insipidus, diabetes mellitus, optic atrophy and deafness

132
Q

Genetic conditions linked to DM

A

Downs
Turners - AI T1DM
Prader-willi - obesity and insatiable appetite
Kleinfelters - high truncal fat and insulin resistance

133
Q

Neonatal diabetes

A

PC - birth to 6 months, often with IUGR, high glucose levels or DKA. Low C-peptide. Mutation @ B islet cells with the K+/ATP channel

134
Q

Permanent neonatal diabetes

A

More severe form complete failure of insulin release K+ channel permanently open preventing insulin release. Need precise insulin therapy from birth. Often neurological involvement.

135
Q

PC insulin resistance syndromes

A

persistent hyperglycaemia, acanthosis nigricans, PCOS,

136
Q

Lipodystrophy syndromes

A 
FPLD1= Loss of limb fat, increased truncal fat 
FPLD2= loss of fatty tissue from the torso, buttocks, and limbs and a buildup of fat in the face, neck, shoulders and abdomenn
137
Q

HIV and diabetes

A

4x increased risk in those related with HAART. Increased incidence of insulin resistance and diabetes

138
Q

Small cell vs NSCLC

A

Small cell - ectopic ACTH, ADH, lamber eaton mesenteric syndrome

NSCLC - clubbing, hypercalcemia (PTHrp), hypertrophic osteoarthropathy

139
Q

Differential of a neck lump

A 
Lymphoma/ metastasis
Lymphadenopathy - infection 
Thyroid cancer
goitre
thyroglossal cyst
140
Q

Premature ovarian failure

A

low AMH, HRT essential until 50y/o to prevent osteoporosis. Progesterone replacement to prevent endometrial hyperplasia.

141
Q

Phaechromocytoma

A

adrenal medullary catecholamine secreting tumour
PC hypertension, heat intolerance, sweating
headache palpitations, chest pain

142
Q

Inv and Mx phaechromocytoma

A

plasma metanephrines, CT renal.
?MEN
alpha blockers to reduce symptoms
surgery to resect tumour - v tricky high vascular and can lead to mass adrenaline release

143
Q

HAART and Cushings

A

CYP450 inhibitors leading to reduced breakdown of steroids can induce Cushings syndrome

144
Q

Adrenal crisis

A

Anyone on long term steroids who is unwell PC hypotension, reduced GCS and abod pain. IV hydrocortisone stat. Fluids won’t improve due to lack of ADH and angiotensin II

145
Q

De Quervains thyroiditis

A

PC - sore throat, tremor, painful swollen neck
triggered by viral illness - mumps, influenza

Initial phase = follicular destruction - hyperthyroid T4 release. 2ndary hypothyroid due to inflammation and -ve feedback. globally reduced uptake on DAT

146
Q

Differentials of goitre

A

De quervians - painful goitre
TMN - nodular goitre widespread nodular uptake on sean
Toxic adenoma - hot spot on scan
Thyroglossal cyst - tethered moves forward on tongue protrusion
Graves - diffuse goitre +/- bruit, Graves eye signs, acropatchy, pre tibal dermopathy

147
Q

MEN 1

A

parathyroid neoplasia, pituitary adenoma (often prolactinoma), pancreatic tumours - zollinger elision etc

148
Q

MEN 2A

A

medullary thyroid cancer, parathyroid hyperplasia, phaechromocytoma

149
Q

MEN 2B

A

medullary thyroid cancer, phaechromcytoma, marfainoid body habitus + muscosal neuromas

150
Q

PC thyroid cancer

A

often euthyroid, lump in neck often painless, cervical lymphadenopathy. symptoms of mass effect i.e. SVC obstruction, dysphagia

151
Q

Anaplastic thyroid cancer

A

very poor prognosis, rare rapid undifferentiated growth local lymph and blood spread

152
Q

Papillary thyroid cancer

A

80% of cancer linked to radiation exposure, FAP and cowden syndrome. 20-40y/o Mx total thyroidectomy 95% 5yr survival

153
Q

Bartter syndrome

A

Consists of a metabolic alkalosis, hypokalemia, hypercalciuria and occasionally hypomagnesaemia. Presents clinically similar to treatment with loop diuretics

Defect in the Na+/K+/Cl- cotransporter in thick ascending loop of Henle. The Na+ loss leads to volume depletion and RAS activation, increased aldosterone = K+ secretion hence hypokalemia and metabolic alkalosis (increased H+ loss)

154
Q

Gietlman syndrome

A

Consists of a metabolic alkalosis, hypokalemia, hypocalciuria and hypomagnesaemia. Present clinically similar as treatment with thiazide diuretics.

Defective Na+/Cl- cotransporter. As with Bartter syndrome increase Na+ delivery to the collecting duct leads tot RAS activation, increased aldosterone production and a reflex hypokalemia and metabolic alkalosis

Hypocalciuria due to continued Cl- efflux hyperpolarises the basolateral membrane leading to Ca2+ reabsorption

155
Q

MODY gluokinase

A

lack of extrapancreatic features and symptoms, mild fasting hyperglycaemia family history of a similarly mild diabetic illness. These patients mostly do not require treatment.

GCK - glucokinase

156
Q

Hypogonadotrophic hypogonadism

A

Caused by structural (adenoma), infiltrative -haemochromatosis, Kallman’s - no GnRH, functional gonadotrophin deficiency due to stress, excess exercise,

157
Q

Hypergonadotrophic hypogonadism

A

Turners , kleinfelters. Primary abnormalities with the testes. Mumps, infections

158
Q

Congenital Generalised Lipodystrophy

A

Autosomal recessive and very rare. Presents with a generalised absence of adipose tissue, increased appetite, absence of leptin and DM develops within 10-20 years. Is most common in females who can present with acanthosis nigricans, hepatomegally, PCOS and insulin resistance.

CSIM (12 decks)

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