Endocrine Flashcards

1
Q

definition of hypoglycemia

A

< 3.3

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2
Q

what is Whipple’s triad for hypoglycaemia

A

symptoms of hypoglycemia, blood glucose level low, resolve of symptoms after blood glucose level back to normal

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3
Q

causes of hypoglycemia in known diabetes

A

hypoglycaemia (using sulphonylureas eg gliclazide, insulin)

dec glucose delivery (missed meal, fasting)

inc glucose utilisation (exercise)

dec endogenous glucose production (alcohol)

inc insulin sensitivity (weight loss)

dec insulin clearance (renal failure)

pregnancy - tight control

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4
Q

causes of hypoglycemia in non-diabetes

A

pituitary insufficiency - low ACTH

Addison’s disease - low BP, low NA, high K, low aldosterone and ACTH

exogenous drugs (quinine, chloroquine, B-blocker overdose, valproate, aspirin, insulin)

post-meal hypoglycemia

liver disease

Immune Hypo (anti-insulin Ab, or Hodgkins)

non-pancreatic neoplasm (small cell, fibroma, sacroma)

NIPH syndrome - noninsulinoma pancreatogenous hypoglycaemia (islet cell hyperplasia)

starvation + malnutirition

hypothyroidism (myxoedema coma)

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5
Q

symptoms of hypoglycaemia

A
lethergy 
weakness 
sweating 
shaking
tingling lips and tongues
uhnger 
palpitations 
headache
double visions 
difficulty concentrating 
slurred speech
confusion 
change in behavior 
coma
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6
Q

what scale is used to represent the symptoms of hypoglycaemia

A

Edinburgh hypo scale - 11 most common hypoglycaemic symptoms

Autonomic nervous system

  • sweat
  • palpitation
  • shaking
  • hunger

Neuroglycaemic

  • confusion/drowsy
  • dec GCS
  • slurred speech
  • odd behaviour
  • incoordination

General

  • malaise
  • Nausea
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7
Q

what are the investigations for hypoglycaemia

A
  • blood glucose < 3.3
  • Bloods: FBC/UE/LFT, blood glucose, HBA1c, serum insulin
  • C peptide (elevated if endogenous insulin production – either insulinoma or sulfonylurea use)
  • Beta-hydroxybutyrate - < 2.7 mmol/L, low = diagnosis of mesenchymal tumour
  • serum sulfonylurea
  • TSH – hypothyroidism can cause hypoglycaemia
  • serum cortisol – pituitary insufficiency
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8
Q

management of hypoglycemia if GCS is 15

A

If GCS15:

  1. Fast acting sugar: 7/8 jelly babies (not chocolate), 10-20g dextrogel. and
  2. Long acting: 2 toast/ cereal
  3. Check BG after 15mins- aim for 5- repeat x3 above management until normal
  4. BM<3 then 1mg IM glucagon.

GCS<15: assume they cant swallow or IV access cannot rapidly established

  1. 75ml 20% glucose / 150ml 10% glucose IV or 1mg IM glucagon.
  2. Check after 15mins- aim for 5 x3 until normal.
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9
Q

pathophysiology of DKA

A
  • Ketoacidosis occurs in starvation states and produces acetone.
  • In DM a lack of insulin means that glucose cannot be used, pushing the body into the starvation state.
  • A lack of insulin stimulates the release of glucagon from the alpha cells which stimulate glycogen breakdown, gluconeogenesis, release of free fatty acid which are converted by the liver to ketones. = HIGH KETONES.
  • Excess glucose excreted by kidneys due to osmotic diuresis = HIGH URINE GLUOCSE.
  • lipolysis  ketogenesis and metabolic acidosis = METBAOLIC ACIDOSIS.
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10
Q

what are the clinical features of the first presentation of DKA in a T1DM?

A
sudden onset 
weight loss 
ployuria 
polydipsia 
non-specific abdo pain 
drowsy 
confusion 
Kussmauls' breathing 
Ketoci breath
N+V 
dehydration 
inc urination (osmotic diuresis) 

usually due to alcohol intake (because alcohol inc insulin in the blood stream and so less insulin to get glucose into cells)

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11
Q

what are some of the causes of DKA

A

4Is

infection - UTI, RTI, skin
Infarction - MI, stroke, GI tract, peripheral vasculture
INsufficient insulin
intercurrent illness - many underlying conditions precipitate or aggravate DKA

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12
Q

what are the diagnostic criteria for DKA

A

BLood glucose > 11
Ketone - urine 2+ or blood > 3mmol/L
Metabolic acidiosis - pH < 7.3 +/- HCO < 15mmol/L

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13
Q

what are some investigations for DKA

A
FBC - WCC 
U&amp;E - inc urea, creatinine, dehydration 
LFT 
CRP 
amylase 
blood glucose 
blood culture 
HbA1c. 

ABG/VBG - metabolic acidosis, dec bicarb

Urine dip +/- MCS - for infection, ketones, protein, glucose

find infection 
ECG (exclude MI, tall tented in hyperK) 
CXR - RTI infection 
MSU 
Pregnancy test

beware of pseduohyponatreamia - for every 4mmol dec of glucose –> 1 mmol dec in Na+

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14
Q

what are the 9 steps for treating DKA

A

ABCDE
• SpO2, ECG, BP/HR, 2 large bore cannulas

1) diagnosis – pH, Ketones, BM

2) immediate treatment
a. 1L 0.9% NaCl over 1 hour if BP > 90
b. If BP < 90, 500ml bolus stat, max 2L  if BP still low, call criteria outreach
c. start IV insulin – 50 unites quick releasing insulin in 49.5 ml NaCl 0.9% to give 0.1 unit/ml solution via syringe driver at 0.1units/kg/hour
d. call diabetes speciliast team

3) call critical care for review if
a. venous bicarb < 5 or pH < 7.1
b. drowsy (GCS < 12 or abnor AVPU)
c. pregnant
d. heart failure
e. oliguria or anuria
f. sat < 92% on air
g. persistent hypotension < 90 systolic after 2 L
h. K+ < 3.5mmol/L on admission

4) Essential investigations – as mentioned above
5) Insulin – fixed rate insulin (0.1 unites/kg/hour) + continue long acting insulin

6) IV fluids
a. 1L NaCl 0.9% over 1 hour then
b. 1L NaCl 0.9% over 2 hours then
c. 1L NaCl 0.9% over 2 hours then
d. 1L NaCl 0.9% over 4 hours
e. when glucose < 14 mmol/L  continue IVI +/- KCL + 10% glucose 125ml/Hour

7) potassium (start after 2nd IV fluids not resus fluid)
a. if <3.5  senior review (>40 mmol/litre maybe necessary)
b. 3.5-5.5  40mmol KCl per litre of NaCl
c. >5.5 – none

8) Monitoring
a. re-assess hourly for first 4-6 hours
b. check vital signs hourly
c. consider catheter if clinical evidence of poor LV or renal function
d. consider NGT if drowsy
e. treat underlying causes for DKA
f. give LMWH to all (thromboprophylaxis)
g. treatment target
i. blood glucose falls of >3mmol / L / hour until < 14
ii. cap ketones fall of at least 0.5mmol / litre / hour until <0.6
iii. venous bicarbonate rises of > 3 mmol/ litre . hour until > 15
iv. if not improving, inc rate of insulin infusion by 1 unit / hour every hour

9) After recovery
a. transfer to SC insulin if pt able to eat and drink well and pH > 7.3 or blood ketones < 0.6 mmol/L

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15
Q

what is the function of insulin

A

it moves glucose from bloodstream into cells for energy consumption

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16
Q

which cells is destroyed in T1DM

A

beta cells of islet of Langerhans in the pancreas

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17
Q

symptoms of T1DM

A

acute onset
25-50% present with DKA
thin (low BMI)
4Ts - thirst, toilet, thinner, tired

genital itchy or frequent episodes of thursh
wounds heal slowly, boils
recurrent/prolonged infections

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18
Q

what is the investigation regimen of suspect T1/2DM with symptoms

A

singe episode of test of the following:

fasting blood glucose > 7 or
random blood glucose >11.1 or
2 hour fasted glucose > 11.1 (after 75g of glucose) or
HbA1c of 48

also

1) HbA1c
2) FBC - chronic anaemia, elevated WCC
3) U&Es - baseline renal function
4) TFTs
5) LFT
6) tissue transglutaminase (tTG)

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19
Q

what is the investigation regimen of suspect T1/2DM without symptoms

A

2 sperate episodes of testing (2 wk apart) of the following:

fasting glucose > 7 or
random glucose > 11 or
HbA1c > 48 on 2 occasions

also

1) HbA1c
2) FBC - chronic anaemia, elevated WCC
3) U&Es - baseline renal function
4) TFTs
5) LFT
6) tissue transglutaminase (tTG)

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20
Q

differentials for T1DM

A

LADA - latent autoimmune diabetes of adulthood
MODY - Maturity Onset Diabetes of the Young
T2DM
dibaetes insipidus
UTI

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21
Q

what are the different treatment regimen of T1DM

A

basal-bolus
insulin pump
2 injections per day
1 injection per day

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22
Q

when will basal-bolus (multiple daily injections) regimens be beneficial for patients

A

good physiological management

can be flexible to those with varied meal/exercise

only for those who can do multiple injections per day

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23
Q

when is insulin pump insulin treatment regimen used

A

when MDI fails

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24
Q

when is 2 injections per day regimen used?

A

rarely used nowadays

good for those unable to give multiple injections

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25
what is the SICK day rule for Diabetes?
management of blood glucose during sickness 1) Sugar - sugar measurement inc, frequency every 2-3 hrs 2) I - Insulin = keep taking it 3) C - keep taking carbohydrate and fluids 4) K = measure ketones (4 hours) drink at least 3 L of fluid
26
what is the essential mechanism for T2DM
peripheral resistance to insulin --> blood unable to break down glucose into energy properly
27
clinical features of T2DM
* Gradual Onset * Polydipsia (thirst) * Polyuria, esp nocturia * Often obese (high BMI) * Lethargy, blurred vision * Genital itching (pruritius vulvae), frequent episodes of thrush, UTI * unintentional weight loss * DKA rare * Wounds that heal slowly, boils * Recurrent/prolonged infections
28
Treatment for T2DM
• 1st step  lifestyle + aim for HbA1c of < 48 • 2nd step  metformin if HbA1c > 48 + aim for < 48 • 3rd step/1st intensification  if HbA1c > 58  dual therapy & aim for HbA1c < 53 o metformin + DPP-4i o metformin + pioglitazone o metformin + SU o metformin + SGLT-2i • 4th step/2nd intensification  if HbA1c > 58  triple therapy & aim for HbA1c < 53 o metformin + SU + DDP-4i or pioglitazone or SGLT-2i o metformin + SU + GLP-1  if not tolerate the above combination and have BMI > 35 and specific psychological and other medical problems associated with obesity  BMI >35 and insulin would not be suitable  BMI < 30 and South Asian • 5th step/3rd intensification  Insulin (refer for this)
29
complications of T2DM
``` HHS microvascular disease Macrovascular disease inc BP cataracts fatty liver disease ```
30
When is the management for ACR > 2.5 in men or 3.5 in women?
ACEi or ARB and maintain BP <130/80
31
pathophysiology of diabetic foot disease
diabetes causes nerve damage - causes infection and charcoat's diabetes causes PVD - ulcers and gangrene
32
what are the 3 main types of diabetic foot disease?
1) Charcoat's Arthropathy - refers to progressive degeneration of the weight-bearing joint, a process marked by bony destruction, bone resorption and eventually deformity due to loss of sensation 2) diabetic foot infection - caused by repetitive foot trauma which becomes infected 3) diabetic foot ulcer - caused by repetitive foot trauma due to lack of sensation
33
clinical features of charcoat's arhtorpahty
``` pain redness swelling deformity (skin intact) maybe associated with foot ulcer ```
34
clinical features of diabetic foot infections
``` fever pain red swollen hot to touch purulence ``` maybe able to see some break in the skin
35
clinical features of diabetic foot ulcers
eroded ulcer commonly found on pressure points can results in dry or wet gangrene
36
when will you refer a patient with diabetic foot disease
for all diabetic foot pathology refer within 1 day life-threatening limb injury (refer immediately) - ulceration with fever - ulceration with limb ischaemia - concern of osteomylitis - gangrene
37
investigation for charcot's foot
weight bearing X-ray of foot and ankle | consider MRI
38
investigation for diabetic foot infection
FBC + blood glucose soft tissue or bone sample from base of the debrided wound if this cannot be obtained take a deep swab consider X-ray
39
investigation for diabetic foot ulcer
``` assess using SINBAD Size ischaemia neuropahty Bacterial infection area depth ```
40
management of charcoat's foot
acute - monitor treatment usinf foot skin temperature difference in both feet and serial X-rays 1st line - non-removable offloading device 2nd line - removable offloading device
41
management of diabetic foot infection
start abx reassess in 1-2 days when improvement should be seen consider x-ray to assess full extend of the body
42
management of diabetic foot ulcer
nonremovable casting off loading control infectio n and ischemia wound debridement wound dressing
43
management of limb ischaemia
refer to vascular revascularisation - bypass angioplasty stent
44
what are the causes of hyperthyrodisim
grave's disease toxic multi-nodular goitre amiodarone
45
what are the causes of hypothyroidism
7 in total ``` Hashimoto's thyroiditis Subactue Hypothyroditis - *de Quervain's Iodine deficiency lithium Riedel's thyroiditis postpartum thyroiditis amiodarone ```
46
definition of Graves' Disease
Autoimmune hyperthyroidism causes by stimulation of the thyroid by TSH receptor antibodies.
47
Aetiology of Graves' Disease
• Autoimmune: reason for autoimmunity is unknown, 80% genetics and 20% environmental
48
RF for Graves' Disease
female Fhx tobacco use
49
clinical features of Graves' Disease
Systemic - heat intolerance - sweating - weight loss - palpitations - tremor - tachycardia - anxiety/depression - SOB - hair loss - moist, smooth skin - dirrhoea Eye - upper lid retraction - exophthalmos - optic neuropathy other - irregular menstruation, often amenorrhea - loss of libido - oncycholysis - detachment of nail from nailbed - cardiac flow murmur - due to inc flow of blood through the heart valve - palmar erythema - proximal muscle weakness - toxic diffuse goitre - thyroid acropachy - pretibial myxoedema
50
Investigation for Graves' Disease
TSH (suppressed) serum free or total T4 - elevated serum free or total T3 - elevated thyroid isotope scan - diffuse uptake radioactive iodine/technetium uptake - elevated TSH receptor antibodies - +ve thyroid USS - goitre/enlarged CT/MRI of orbit – may show muscle thickening Skin biopsy – may show thyroid dermopathy
51
management of acute thyroid storm of Graves' Disease
High dose antithyroid (carbimazole or polythiouracil or thiamazole ) corticosteroids (Hydrocortisone) beta-blocker (propranolol - congestive heart failure) iodine solution with supportive care. +/- Cholestyramine (bile acid to reduce enterohepatic circulation of thyroid hormones) lithium – to reduce thyroid hormone reduce • supportive care  cooling, correction of volume, resp support
52
what is acute thyroid storm?
volume depletion, congestive heart failure, confusion, N+V
53
when can acute thyroid storm occur
after radioactive iodine therapy due to release of stores of thyroid hormone or at any time
54
management of non-acute Graves' Disease
* 30% spontaneous remission * block and replace therapy - carbimazole titration/carbimazole + levothyroxine replacement * +/- propranolol * Definitive Rx: radioactive iodine or thyroidectomy +/- prednisolone + levothyroxine after surgery/iodine * +/- methylprednisolone (for orbitopathy) * +/- Triamcinolone acetonide topical (for dermopathy)
55
SE of antithyroid meds
agranulocytosis - leukopenia
56
what is another name for Adrenocortical insufficiency?
Addison's Disease - where adrenal glands do not produce enough steroids (cortisol and aldosterone)
57
what is secondary adrenal insufficiency
inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release. this is a result of loss or damage to the pituitary gland common cause = Sheehan syndrome
58
what are the most common causes of primary adrenal insufficiency?
Addison's Disease in developed countries - Autoimmune in endemic countries - TB
59
what are the most common causes of tertiary adrenal insufficiency?
steriods uses - steriod causes the suppression of hypothalamus and so less corticotrophic releasing hormone is released to stimulate the pituitary gland which intern stimulates the adrenocorticotrophic hormone to stimulate the adrenal glands to produce cortisol and alderstone
60
what are some of the less common causes of Addison's Disease
1) infection - Pesudomonas aeruginosa, meningococcal infection, systemic fungal infection secondary to HIB infection 2) malignancies - lung, breast, stomach, colon, melanoma and lymphoma
61
clinical features of Addison's Disease
``` fatigue anorexia reduced libido abdo pain cramps ``` salt craving Bronze hyperpigmentation to skin - ACTH stimulate melanocytes to produce melanin hypotenison
62
investigation of Addison's Disease
* U&E : hyponatraemia, hyperkalaemia, hypercalcaemia * blood urea – elevated due to hypovolaemia * FBC – anaemia * Early morning cortisol * Short syancthen (ACTH) test: synathcen given to patient and blood cortisol measured at baseline, 30 mins and 60 minutes. A failure of cortisol level to rise (double or remain below <497) indicates primary adrenal insufficiency (Addison’s) * Addison’s : ACTH (high), cortisol level low * ACTH level (> 22) * plasma aldosterone (reduced) * plasma renin activity – elevated * 80% autoimmune: Adrenal cortex antibodies and 21 hydroxylase antibodies * CT/MRI adrenals – after biochemical diagnosis has been confirmed
63
management of acute addisonian crisis
hydrocortisone - replaces cortisol
64
on-going management of Addison's Disease
replace cortisol - hydrocortisone or prednisolone or cortisone replace aldosterone - fluticasone in periods of illness/stress - double dose (normally the body produce more cortisol during period of stress) carry steroid card and emergency ID dehydroepiandrosterone - replace androgen in women with dec libido
65
a complication of Addison's disease?
Addisonian crisis - potentially life-threatneing presentation - triggered by infection or trauma - can be 1st presentation - reduced consciousness, hypotension, hypoglycaemia, hyponatraemia, hyperkalemia - treat without Ix - rex - IV hydrocortisone 100mg stat then 100mg every 6 hr - correct hypoglycaemia careful monitoring of electrolytes and fluid balance
66
what are the causes of primary hypothyroidism
hashimoto's thyroiditis -autoimmmune Sub-acute de Quervain thyroiditis - viral Postpartum thyroiditis underdevelopment ecoptic hypoplastic gland seondary to hyperthyroidism treatment - carbimazole, lithium and amiodarone radiation iodine deficiency - added to food such as table salt
67
what are the causes of secondary hypothyroidism - hypothalamic disorder
``` giloma surgery radiotherapy infarction infiltrative - TB, syphilis, sarcoid, hemochromatosis retinods ```
68
what are the causes of secondary hypothyroidism - pituitary disorder
``` pituitary adenoma surgery radiotherapy infarction Sheehan's syndrome infiltrative - TB, syphilis, sarcoid, amyloidosis, hemochromatosis ```
69
what are the RF for hypothyrodisim
``` female middle age FHx autoimmune disorders down syndrome primary pulmonary hypertensions MS ```
70
clinical features of hypothyroidism
``` weight gain fatigue cold intolerance menorrhagia constipation depression - poor concentration bradycardia / low BP dry skin carpal tunnel syndrome coarse hair and hair loss loss of material 1/3 of the eyebrow goitre fluid retention (oedema, pleural effusion, ascites) proximal myopathy myxoedema - severest form as mucoplysaccharides accumulate below the skin and cause facial features to thicken hyporeflexia ```
71
investigation for hypothyroidism
``` serum TSH serum T3/T4 serum cholesterol - elevated FBC - normocytic anaemia fasting blood glucose - elevated serum creatine kinase - elevated Hashimotos- antithyroid peroxidase antibodies and anti-Tg antibodies ```
72
management of hypothyroidism
* Levothyroxine (synthetic T4) – dose titrated till TSH levels are normal * Measure TSH levels monthly till stable, then check 4-6 weeks, then annually
73
what is primary hyperparathyroidism
it is when the parathyroid glands secrete too much parathyroid hormone which causes derangement of Ca2+
74
what is secondary hyperparathyroidism
it is when any disorder that causes an initial low state of Ca2+ which causes excretion of parathyroid hormone from parathyroid glands
75
what is the function of parathyroid glands
regulates serum calcium and phosphate levels also play a part in bone metabolism
76
how does PTH hormone affect serum calcium and calcium phosphate
when Ca2+ is low, PTH is released from the pararthyriod gland PTH acts on kidney, bone and small intestine kidney - PTH causes the release of Calcitriol ( 1,25-(OH)2D) which acts on the kiney to reduce excretion of Ca2+ Bone - PTH and calcitorol both causes releases of Ca2+ and phosphate Small intestine - PTH and Calcitriol in absorption of Ca2+ the over results - inc serum Ca2+ - dec serum phosphate
77
what is tertiary hyperparathyroidism?
occurs after prolong secondary hyperparathyroidism. Glands become autonomous to producing excessive PTH due to hyperplasia of the gland, even after cause of hypocalcemia has been corrected.
78
what are the causes of primary hyperparathyroidism
parathyroid adenoma - 85% carcinoma - small cell lung cancer MEN1/MEN 2a external neck irradiation
79
what are the causes of secondary hyperparathyroidism
CKD malabsorption Vit D deficiency others - crohn's coeliac, following bypass surgery, chronic pancreatitis, fat malabsorption.
80
clinical features of primary hyperthyroidism
Bones, stones, abdominal groans, psychic moan, thrones - excessive Ca2+ resoprtion - osteopenia/osteoporosis - excessive Ca2+ excretion - renal calculi - hypercalcemia - proximal myopathy, anorexia, N+V, abdo pain, constipation - polyuria, polydipsia, dehydration - depression, dementai, confusion, inability to concentrate, memory problems
81
clinical features of secondary hyperthyroidism
o features of chronic renal failure – discoloured skin, bruising, pruritis, evidence of fluid overload (lung rales, pericardial rub and peripheral), elevated BP, fatigue, náusea, poor concentration and myoclonus o featutes of malabsorption o muscle cramps and bone pain o perioral tingling or paresthaesia in fingers or toes o Chvostek’s sign – tapping on the face just anterior to the ear and seeing a twitching of muscles around the mouth – neuromuscular excitability o Trousseau’s sign - Inflating blood pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyper extension of the fingers and flexions of the thumb - neuromuscular excitability o features of rickets in children – bowed legs or knock knee o fratures
82
investigation for hyperparathyroidism
* Albumin adjusted serum calcium- supressed secondary, raised in primary and tertiary (+ renal failure) * PTH – elevated. (measure if calcium is indicative) * Phosphate – supressed primary, raised in secondary and tertiary * 24-hour urinary calcium excretion – high in primary and low in secondary * 25-hydroxyvitamin D (25(OH)D) – low * UE- assess kidney function. * DEXA – risk of osteoporosis * XR – salt and pepper pot skull * Tc-99m sestamibi scanning + USS – to locate the parathyroid mass and to plan for surgery
83
differential for hyperparthyroidism
familial hypocalciuric hypercalcaemia hyperclacaemia of malignancy multiple myeloma sarcoidosis osteomalacia osteoporosis paget's disease
84
management of primary hyperthyroidism
``` surveillance if mild check serum creatinine and calcium level every 6 months 3 sites DEXA study - 1-2 years U&e every 6 months BP - every 6 months correct it ```
85
treatment for primary hyperparathyroidism
 Surveillance if mild  Check serum creatinine and calcium levels every six months  3 site DEXA study – 1-2 years  UE- every six months  Blood pressure – every six months  if symptomatic (kidney, renal calcali, bone disease) parathyroidectomy  if asymptomatic + age < 50 or dec eGFR, bone density < -2.5, 24 hour urinary Ca2+ > 400  parathyroidectomy  bisphosphonate as adjunct  Correct vitamin D deficiency.  Avoid dehydration  Avoid thiazide diuretics
86
treatment for secondary hyperparathyroidism
 Treat underlying disease  Correct vitamin D deficiency – ergocalciferol (Vit D + Ca2+)  treat malabsorption with supplement  Treat CKD: calcium supplementation, correction of vitamin D deficiency  Phosphate restriction +/- phosphate binders (sevelamer, lanthanum, calcium acetate)  Vitamin D analogues  Calcimimetics (e.g. cinacalcet) – stop the production of PTH.  Bisphosphonates – reduced fracture risk. • last resort - parathyroidectomy
87
what can cause malignant hypercalcaemia
``` occurs in 10-20% of cancer due to imbalance between bone resorption + Ca2+ excretion most common cancers - breast - prostate - squamous cell - NSCLC lung - kidney - multiple myeloma - causes punched out lesion - lytic - lymphoma ```
88
pathophysiology of malignant hypercalcaemia
1) Transforming growth factor Alpha (TGFA) - cell growth stimulator and replication that is produced by many tumour cells. It is a powerful stimulator of bone resorption (Osteoclasts) 2) Parathyroid hormone related peptides (PTHrP) - tumour associated protein that mimics PTH, stimulating bone absorption and inc plasma Ca2+ - breast cancer
89
symptoms of malignant hypercalcaemia
* Boans (pain, fractures), moans (lethargy), groans (abdo pain, vomit), thrones (constipation, polyuria), stone * General: dehydration, weakness, fatigue/malaise, drowsiness * CNS: hyporeflexia, confusion, seizure, proximal neuropathy, coma * GIT: weight loss, nausea, vomiting, constipation, ileus, dyspepsia, polydipsia (thirst) * GU: Polyuria * Cardiacbradycardia, short QT, wide T wave, prolonged PR, arrhythmia (HTN), arrest * Late  Confusion, Drowsiness, Fits, Coma
90
INvestigations for malignant hypercalcaemia
* GCS * Bloods: Serum Ca corrected for albumin, U&E, Alk Phos, PTH level, serum PTHrP, serum phosphorus. serum calcitriol, serum 25-hydroxyvitamin D * ECG: Qt shortening
91
Mx of malignant hypercalcaemia
• Saline 1L 4hrly for 24hrs then • 1L 6hrly for 48-72hrs with K+ and mild dose furosemide if risk of fluid overload. About 3L per day. • IV bisphosphonates (pamidronate 60-90mg/zoledronic acid) • If arrythmias/ seizures: calcitonin (normal physiological hormone to reduce absorption of Ca2+ in kidney + inc osteoblast activity) + corticosteroids (this combination help lower serum Ca) o SC/IM calcitonin at 4units/kg 12hrly with oral prednisolone 40mg PO
92
what level of serum Ca2+ will you consider aggressive treatment of malignant hypercalcemia
Ca2+ < 3 = rehydrate with IVI Ca2+ > 3 = 3L of fluids, consider fureosemide and stop thiazide diuretics
93
causes of hyperlipidaemia
can be acquired or genetics disorder - diets - DM - obesity - lack of exercise - CKD - hypothyroidism - pregnancy - FHX - drugs - steriods
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clinical features
mostly asymptomatics but can also presents in acute blockage of vessels eg MI and strokes 1) tendon xanthoma - yellow deposits of cholesterol near joints 2) Xanthelasma - yellow deposition of cholesterol underneath the skin 3) corneal arcus
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investigation for hyperlipidaemia
lipid panel - over cholesterol > 5 mmol/L - HDL cholesterol (bad cholesterol) > 1 mmol/L in men, > 1.2 in female - LDL (good cholesterol) > 3 Non- HDL cholesterol > 4 TC:HDL > 6 if want to find out causes - fasting glucose, TSH, U&Es, serum albumin/LFT
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management of hyperlipidaemia
primary prevention - atorvastatin 20mg | secondary prevention - atorvastatin 80mg