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chemical pathology Flashcards

1
Q

formula for osmolarity

A

osmolarity = 2(Na + K) + urea + glucose

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2
Q

normal range for Na+

A

135-145 mmol/L

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3
Q

symptomatic hyponatraemia clinical presentation

A

medical emergency!
- nausea and vomiting (<134 mmol/L)
- confusion (<131 mmol/L)
- seizures, non-cardiogenic pulmonary oedema (<125 mmol/L)
- coma (<117 mmol/L) and eventual death

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4
Q

causes of hyponatraemia depending on serum osmolality

A

high osmolality
- glucose/mannitol infusion

normal osmolality
- spurius
- drip arm sample
- pseudohyponatraemia (hyperlipidaemia/paraproteinaemia)

low osmolality
- true hyponatraemia

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5
Q

what is TURP syndrome?

A

hyponatraemia from irrigation absorbed through damaged prostate
- glycine 1.5% used to irrigate during TURP
- clinical presentation due to metabolism of glycine and hyponatraemia caused by dilution

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6
Q

causes of hyponatraemia based on hydration status and urinary Na
i. hypovolaemia
ii. euvolaemia
iii. hypervolaemic

A

i. hypovolaemia
> 20 = renal
- diuretics, addison’s, salt-losing nephropathies (kidney is failing to reabsorb sodium so water lost as well)
< 20 = non-renal
vomiting, diarrhoea, excess sweating, third space losses (ascites, burns). kidney is doing its job holding onto sodium

ii. euvolaemia
> 20
- SIADH, severe hypothyroidism, glucocorticoid deficiency

iii. hypervolaemic
> 20 = renal
- AKI, CKD (kidneys not retaining sodium)
< 20 - non-renal
- cardiac failure, cirrhosis, inappropriate IV fluid

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7
Q

management of hyponatraemia in hypovolaemia, euvolemic and hypervolaemic

A

hypovolaemia
- treat the cause - e.g., antiemetics
- supportive - replace deplete fluid slowly with regular checking of sodium to ensure not rising too fast

euvolaemic
- SIADH:fluid restriction and treat the cause, demeclocycline (increases ADH resistance) and tolvaptan can induce a state of diabetes insipidus that may help to correct the SIADH although the cost is prohibitive. if severe, can consider giving slow IV hypertonic 3% saline
- hypothyroid - levothyroxine, addison’s - hydrocortisone +/- fludrocortisone

hypervolaemic
- fluid restrict +/- diuresis
- cirrhosis usually will require specialist input

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8
Q

risk of rapid hyponatraemia correction

A

can lead to central pontine myelinolysis (pseudobulbar palsy, paraparesis locked-in syndrome) therefore aim to increase Na+ by no more than 8-10 mmol/L per 24 hrs

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9
Q

SIADH - diagnostic criteria

A
  • true hyponatraemia (<135) + low plasma/serum osmolality (<270) + high urine sodium (>20) + high urine osmolality (>100) + no adrenal/thyroid/renal dysfunction
  • clinically euvolaemic
  • SIADH is characterised by inappropriate ADH secretion (not in response to a stimulus)
  • increased ADH -> increased water reabsorption -> low plasma Osm (secondary to dilution) -> less water is excreted in the urine -> urine Osm is high
  • confirming the diagnosis requires a normal 9am cortisol and normal TFTs (i.e., diagnosis of exclusion)
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10
Q

SIADH causes

A
  • malignancy - small cell lung cancer (most common), pancreas, prostate, lymphoma (ectopic secretion)
  • CNS disorders - meningoencephalitis, haemorrhage, abscess (pretty much any CNS pathology)
  • chest disease - TB, pneumonia, abscess
  • drugs - opiates, SSRIs, TCAs, carbamazepine, PPIs
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11
Q

SIADH treatment

A
  • fluid restriction and treat the cause
  • demeclocycline (increases ADH resistance) and tolvaptan can induce a state of diabetes insipidus that may help to correct the SIADH although it is cost prohibitive
  • if severe, can consider giving slow IV hypertonic 3% saline
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12
Q

investigations for hypernatraemia

A

raised urea, albumin and PCV

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13
Q

risk of rapid correction of hypernatraemia

A

cerebral oedema

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14
Q

cause of hypernatraemia in hypovolaemia

A

low urinary sodium:
- GI loss: vomiting, diarrhoea
- skin loss: excessive sweating, burns

high urinary sodium >20 - renal losses:
- loop diuretics
- osmotic diuresis (uncontrolled DM, glucose, mannitol) following initial hyponatraemia
- diabetes insipidus
- renal disease (impaired concentrating ability)

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15
Q

cause of hypernatraemia in euvolaemia

A

respiratory (tachypnoea)
skin (sweating, fever)
diabetes insipidus

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16
Q

cause of hypernatraemia in hypervolaemia

A

mineralocorticoid excess (Conn’s syndrome)
inappropriate saline

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17
Q

clinical features of diabetes insipidus

A
  • hypernatraemia (lethargy, thirst, irritability, confusion, coma, fits)
  • clinically euvolaemic
  • polyuria and polydipsia
  • urine: plasma osmolarity is <2 (urine is dilute despite concentrated plasma)
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18
Q

cranial vs nephrogenic diabetes insipidus

A

cranial:
(>50% increase in osmolarity after ADH analogue administered):
- lack of/no ADH production
- causes: surgery, trauma, tumours (craniopharyngioma), autoimmune hypophysitis (from CTLA-4 ipilimumab)
- treatment: desmopressin

nephrogenic:
receptor defect - insensitivity to ADH
causes:
- inherited channelopathies
- drugs: lithium, demeclocycline
- electrolyte disturbances: hypokalaemia, hypercalcaemia
treatment:
- thiazide diuretics

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19
Q

investigations for suspected diabetes insipidus

A
  1. serum glucose (to exclude diabetes mellitus)
  2. serum K+ (exclude hypokalaemia)
  3. serum Ca (exclude hypercalcaemia)
  4. plasma and urine osmolality
  5. diagnostic: 8-hour water deprivation test
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20
Q

water deprivation test - interpretation of results

A

normal
- urine osmolality >600 mOsmol/kg
- U:P ratio > 2 (normal concentrating ability)

primary polydipsia
- urine concentrates but less than normal e.g., >400-600 mOsmol/kg

cranial DI
- urine osmolality increases to >600mOsmol/kg only after desmopressin (if equivocal an extended water deprivation test may be tried; no drinking from 18:00 the night before)

nephrogenic DI
- no increase in urine osmolality even after desmopressin

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21
Q

normal range for potassium

A

3.5-5.5 mmol/L

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22
Q

causes of hypokalaemia (<3.5 mmol/L)

A

either depletion or shift into cells (very rarely decreased intake):
1. GI loss
- vomiting, diarrhoea

  1. renal loss
    - hyperaldosteronism (consider in a patient with high BP and low K), iatrogenic excess cortisol
    - increased sodium delivery to distal nephron (thiazide and loop diuretics)
    - osmotic diuresis
  2. redistribution into the cells
    - insulin, beta-agonists, metabolic alkalosis, refeeding syndrome
  3. rare causes
    - rare tubular acidosis type 1 &2, hypomagnesaemia
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23
Q

clinical features of hypokalaemia

A

muscle weakness, cardiac arrhythmias, polyuria and polydipsia (nephrogenic DI)

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24
Q

hypokalaemia treatment

A
  1. serum K 3.0-3.5 mmol/L = oral KCl, recheck serum K
  2. serum K <3.0 mmol/L (risk of cardiac arrest) = IV KCl (max rate 10mmol/h otherwise risk of arrhythmia; insert central line if higher)
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25
Q

causes of hyperkalaemia (>5.5 mmol/L)

A

excessive intake
- oral (fasting)
- parenteral
- stored blood transfusion

transcellular movement (ICF>ECF)
- acidosis
- insulin shortage (DKA)
- tissue damage/catabolic state (rhabdomyolysis)

decreased excretion
- acute renal failure (oliguric phase)
- chronic renal failure (late)
- drugs: K sparing diuretics (spironolactone), NSAIDs, ACEi, ARBs
- mineralocorticoid deficiency (Addison’s)
- type 4 renal tubular acidosis

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26
Q

ECG changes associated with hyperkalaemia

A
  1. loss of P waves
  2. tall, tented T waves
  3. widened QRS
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27
Q

hyperkalaemia treatment

A

repeat bloods if K>6.5 (possible haemolysis)
1. 10mls 10% calcium gluconate (this is cardioprotective, it does nothing to lower the serum potassium)
2. 100mls 20% dextrose and 10 units of short-acting insulin such as Actrapid
3. nebulised salbutamol is a useful adjunct as well
4. in some cases: consider calcium resonium 15g PO or 30g PR
5. always treat the cause

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28
Q

formula to calculate anion gap and normal range

A

anion gap = Na + K - (Cl + HCO3)

normal range = 14-18 mmol/l

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29
Q

mnemonic for elevated anion gap metabolic acidosis

A

KULT
K - ketoacidosis (DKA, alcoholic, starvation)
U - uraemia (renal failure)
L - lactic acidosis
T - toxins (ethylene glycol, methanol, paraldehyde, salicylate)

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30
Q

formula for osmolar gap
normal range
when is it raised

A

osmolality (measured) - osmolarity (calculated)

normal osmolar gap: <10

  • an elevated osmolar gap provides indirect evidence for the presence of an abnormal solute
  • the osmolar gap is increased by extra solutes in the plasma (e.g., alcohols, mannitol, ketones, lactate)
  • can be raised in advanced CKD due to retained small solutes
  • helpful in differentiating the cause of an elevated anion gap metabolic acidosis
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31
Q

AST, ALT raised - potential causes

A

(hepatic) hepatitis/transaminitis
- ALT > AST = chronic liver disease (inc. NASH), chronic Hep C, hepatic obstruction, advanced fibrosis/cirrhosis (AST:ALT ratio >0.8 in absence of EtOH)
- AST:ALT 2:1 supportive of EtOH liver disease
- AST:ALT 1:1 supportive of viral hepatitis

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32
Q

raised GGT and ALP causes

A

cholestatic/obstructive picture

GGT raised in chronic EtOH use, bile duct disease and metastases - used to confirm hepatic source of raised ALP

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33
Q

isolated raised ALP causes

A
  1. physiological:
    - pregnancy
    - childhood (growth spurt)
  2. pathological:
    - >5x ULN = bone (Paget’s disease - osteoblasts), osteomalacia, liver (cholestasis, cirrhosis)
    - <5x ULN = bone (primary tumours e.g., sarcoma, fractures, osteomyelitis), liver (infiltrative disease, hepatitis), renal osteodystrophy

caveat: plasma cells suppress osteoblasts, hence ALP is normal in myeloma

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34
Q

low albumin causes

A

chronic liver disease, malnutrition, protein-losing enteropathy, nephrotic syndrome, sepsis (3rd spacing)

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35
Q

low urea causes

A

severe liver disease (synthesised in liver), malnutrition, pregnancy

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36
Q

raised urea (x10 ULN) causes

A
  1. upper GI bleed (or large protein meal)
  2. dehydration/AKI (urea excreted renally)
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37
Q

stool colour in post-hepatic jaundice

A

pale

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38
Q

causes of prehepatic jaundice

A
  1. haemolytic anaemia
  2. ineffective erythropoiesis e.g., thalassaemia
  3. congestive cardiac failure
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39
Q

hepatic causes of jaundice

A
  1. hepatocellular dysfunction (viral, alcoholic, hepatitis)
  2. impaired conjugation/BR excretion, BR uptake (Gilbert syndrome, Crigler Najjar syndrome)
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40
Q

post-hepatic causes of jaundice

A

obstruction of biliary tree:
1. intraluminal (stones, strictures)
2. luminal (mass/neoplasm, inflammation e.g., PBC, PSC)
3. dextra-luminal (pancreas/cholangio Ca)

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41
Q

hepatomegaly with smooth vs craggy border causes

A

smooth:
- viral hepatitis, biliary tract obstruction, hepatic congestion secondary to HF (Budd Chiari)

craggy:
- hepatic metastatic disease, polycystic disease, cirrhosis (will shrink)

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42
Q

types of acute porphyrias

A
  1. plumboprophyria
  2. acute intermittent porphyria
  3. hereditary corpoporphyria
  4. variegate porphyria
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43
Q

Plumboporphyria

A

type of acute porphyria

enzyme affected: PBG synthase

  • autosomal dominant
  • extremely rare
  • leads to accumulation of ALA
  • abdominal pain (most important feature)
  • neurological symptoms (coma, bulbar palsy, motor neuropathy)
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44
Q

what are porphyrias?

A

7 disorders caused by deficiency in enzymes, involved in haem biosynthesis, leading to build up of toxic haem products

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45
Q

acute intermittent porphyria

A

enzyme affected: HMB synthase

neurovisceral attacks ONLY:
- GI symptoms (abdo pain, vomiting, constipation)
- neurological (polyneuropathy, seizures)
- bladder dyfunction + red/brown urine
- autonomic dysfunction (tachycardia + hypertension)
- psychiatric (hallucinations, anxiety and insomnia)

important: no skin symptoms

Dx: raised urinary PBG and ALA

management:
- IV haem arginate (1st line)
- IC carbohydrate loading
- avoid attacks (adequate nutrition, avoid precipitants)

precipitating factors:
- ALA synthase inducers (steroids, ethanol, barbiturates)
- stress (infection, surgery)
- reduced caloric intake and endocrine factors (e.g., premenstrual)

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46
Q

hereditary coproporphyria

A

type of acute porphyria

enzyme affected: corpoporphyrinogen oxidase

  • autosomal dominant
  • acute neurovisceral attacks
  • photosensitivity lesions (blistering, skin fragility - classically on back of hands after sun exposure)

increased urine/stool porphyrins + urinary PBG

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47
Q

variegate porphyria

A

type of acute porphyria

enzyme affected: protoporphyrinogen oxidase

  • autosomal dominant
  • acute attacks with skin lesions

increased urine/stool porphyrins + urinary PBG

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48
Q

types of non-acute porphyrias

A
  • congenital erythropoietic porphyria
  • porphyria cutanea tarda
  • erythropoietic protoporphyria
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49
Q

congenital erythropoietic porphyria

A

type of non-acute porphyria

enzyme affected: uroporphyrinogen III synthase

NON-BLISTERING lesions
photosensitivity, burning, itching, oedema following sun exposure

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50
Q

porphyria cutanea tarda

A

type of non-acute porphyria

enzyme affected: uroporphyrinogen decarboxylase

  • MOST COMMON TYPE
  • formation of vesicles on sun-exposed areas of skin crusting, superficial scarring and pigmentation

Dx: increased urinary oroporphyrins and coproporphyrins (pink red fluorescence with Wood’s lamp), often increased ferritin, abnormal LFTs

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51
Q

enzyme affected in erythropoietic porphyria

A

ferrochetolase

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52
Q

hypothalamic hormones and their action on pituitary hormones

A
  1. GHRH
    - stimulates GH
  2. GnRH
    - stimulates LH/FSH
  3. TRH
    - stimulates TSH
    - stimulates prolactin
  4. dopamine
    - inhibits prolactin
  5. CRH
    - stimulates ACTH
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53
Q

combined pituitary function test (CPFT): indications, contraindications, side effects

A

indications:
- assessment of all components of anterior pituitary function used particularly in pituitary tumours or following tumour treatment

contraindications:
- ischaemic heart disease
- epilepsy
- untreated hypothyroidism (impairs the GH and cortisol response)

side-effects:
- sweating, palpitations, loss of consciousness (all the adrenergic effects of hypoglycaemia)
- rarely - convulsions with hypoglycaemia
- patients should be warned that with the TRH injection they may experience transient symptoms of a metallic taste in the mouth, flushing and nausea

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54
Q

combined pituitary function test (CPFT): summary of process, procedure

A

summary:
- administration of LHRH (GnRH), TRH and insulin
- then measure the 0-minute, 30-min, 60-min, 90-min and 120-min levels of the pituitary hormones

procedure:
1. fast patient overnight, ensure good IV access, weight patient
2. mix into 5ml syringe: insulin dose (0.15 units/kg), TRH 200 mcg, LHRH 100mcg –> give IV
3. bloods: basal thyroxine plus glucose, cortisol, GH, LH, FSH, TSH, prolactin every 30min for 1 hour
4. glucose, cortisol, GH up to 2 hours
5. replacements: urgent hydrocortisone, T4, oestrogen, GH

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55
Q

interpretation of combined pituitary function test (CPFT) results

A

interpretation of 3 aspectes

  1. insulin tolerance test (hypoglycaemia <2/2 mmol/L) - increased ACTH + GH (metabolic stress)
    - adequate cortisol response: cortisol increase > 170 nmol/l to above 500 nmol/l
    - adequate GH response: GH increase > 6mcg/L
  2. thyrotrophin releasing hormone test: increased TSH + prolactin
    (dopamine suppress prolactin production, high prolactin -> hypothyroidism)
    - the normal result is a TSH rise to >5mU/i (30-min value > 60-min value)
    - hyperthyroidism = TSH remains suppressed
    - hypothyroidism = exaggerated response
    - with the current sensitive TSH assays basal levels are now adequate and dynamic testing is not usually needed to diagnose hyperthyroidism
  3. gonadotrophin releasing hormone test: increased LH/FSH
    normal peaks can occur at either 30-min or 60-min
    - LH should > 10U/l
    - FSH should >2 U/l
    inadequate response = possible early indication of hypopituitarism
    gonadotrophin deficiency is diagnosed on the basal levels rather than the dynamic response
    - males = low testosterone in the absence of raised basal gonadotrophins
    - females = low oestradiol without elevated basal gonadotrophins and no response to clomiphene
    - prepubertal children should have no response of LH/FSH to LHRH
    (NB: if sex steroids are present (i.e., precocious puberty), the pituitary will be “primed” and will therefore respond to LHRH. priming with steroids MUST NOT occur before this test)
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56
Q

prolactinaemia causes - mild elevation (<1000 miu/l), moderate (1000-5000 miu/l), extreme (>5000 miu/l)

A

mild (<1000):
- stress
- recent breast examination
- vaginal examination
- hypothyroidism
- PCOS

moderate (1000-5000):
- hypothalamic tumour
- non-functioning pituitary tumour compressing the hypothalamus
- microprolactinoma
- PCOS
- drugs e.g., domperidone, phenothiazides

extreme (>5000):
- macroprolactinoma

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57
Q

prolactinoma - findings, management

A

findings: extremely raised prolactin (>6000), no increase in GH (>10) and cortisol (>550nM)

1st line Mx:
- replacements (hydrocortisone, T4, oestrogen, GH), dopamine agonists (cabergoline, bromocriptine)
2nd line Mx:
- transsphenoidal excision (if visual/pressure Sx not responding to medical Tx)

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58
Q

non-functioning pituitary adenoma - findings, management

A

findings: moderately raised prolactin (1000-5000)

Mx:
-cabergoline/bromocriptine; watch and wait if asymptomatic
- can do nothing if not causing any Sx

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59
Q

acromegaly - findings, management

A

findings:
- rise in GH (even before baseline)
- increase in prolactin
- no increase in cortisol

management:
1. transsphenoidal surgery (best)
2. pituitary radiotherapy
3. cabergoline
4. ocreotide (expensive): somatostatin analogue (can’t stop once started)
5. GH antagonist - pegvisomant

F/u: yearly GH, IGF-1 +/- OGTT, visual fields, vascular assessment, BMI, photos

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60
Q

anterior pituitary hormones

A

ADH
oxytocin

61
Q

causes of excess ADH and effect

A

lung
- lung paraneoplasias: usually small cell lung cancer, pneumonia

brain
- traumatic brain injury, meningitis, primary or secondary tumours

iatrogenic
- SSRIs, amitriptyline, carbamazepine, PPIs

effect: SIADH - euvolaemic hyponatraemia

62
Q

causes of ADH failure

A

diabetes insipidus
- increased diuresis due to either failure of production or insensitivity to ADH, leads to decreased urine osmolarity and increased serum osmolality

neurogenic
- failure of production - 50% idiopathic

nephrogenic
- commonly iatrogenic - lithium, also hypercalcaemia, renal failure

dipsogenic
- failure/damage to hypothalamus and thirst drive, hypernatraemia without increased thirst response

63
Q

thyroid storm

A
  • an acute state that presents as shock, with pyrexia, confusion, vomiting
  • must be treated with HDU/ITU support, usually require cooling, high dose anti-thyroid medications, corticosteroids and circulatory and respiratory support
64
Q

hyperthyroidism causes - high uptake

A
  • graves (high diffuse uptake)
  • toxic multinodular goitre (high uptake hot nodules)
  • toxic adenoma (1 area of uptake)
65
Q

hyperthyroidism causes - low uptake

A
  • subacute De Quervains thyroiditis
  • postpartum thyroiditis
  • ectopic: trophoblastic tumour, struma ovarii (excessive hCG)
66
Q

types of thyroidneoplasia

A
  • papillary (75-85%)
  • follicular (10-20%)
  • medullary (5%)
  • anaplastic
  • lymphoma
67
Q

papillary thyroidneoplasia

A

75-85%
20-40 yrs, female
associated with irradiation
very good prognosis

  • painless cervical lymphadenopathy, no obvious clinical abnormality of thyroid
  • tumour marker: thyroglobulin
  • spread: lymph nodes and lung
  • histology: psammmoma bodies (foci of calcification), empty appearing nuclei with central clearing (Orphan Annie eyes)
  • mx: surgery +/- radioiodine, thyroxine (to lower TSH)
68
Q

follicular thyroidneoplasia

A

10-20%
40-60 yrs

  • well-differentiated but spreads early
  • tumour marker: thyroglobulin
  • spread: blood&raquo_space; lungs, bone, liver, breast, adrenals
  • histology: fairly uniform cells forming small follicles, reminiscent of normal thyroid
  • Mx: surgery + radioiodine + thyroxine
69
Q

medullary thyroidneoplasia

A

5%
50-60 yrs
80% sporadic, 20% familial MEN2

  • neuroendocrine neoplasm derived from parafollicular C cells secreting calcitonin
  • tumour marker: CEA, calcitonin
  • histology: sheets of dark cells, amyloid deposition within tumour (calcitonin broken down to amyloid)
  • Mx: screen for phaeochromocytoma pre-op + surgery + node clearance
70
Q

anaplastic thyroidneoplasia

A

elderly
rare, most die within 1 yr

  • early and wide metastases common
  • spread: very aggressive –> local, lymph nodes, blood
  • histology: undifferentiated follicular, large pleomorphic giant cells, spindle cells with sarcomatous appearance
71
Q

lymphoma thyroidneoplasia

A

MALToma
risk factor: chronic hashimoto’s (lymphocyte proliferation)
good prognosis

72
Q

what is multiple endocrine neoplasia? 3 types

A

these are a group of 3 inherited disorders (autosomal dominant), whereby there is a predisposition to develop cancers of the endocrine system

3 forms:
1. MEN1 (3Ps)
pituitary, pancreatic (e.g., insulinoma), parathyroid (hyperparathyroidism)

  1. MEN2a (2Ps, 1M)
    parathyroid, phaeochromocytoma, medullary thyroid
  2. MEN2b (1P, 2Ms)
    phaeochromocytoma, medullary thyroid, mucocutaneous neuromas (& marfanoid)
73
Q

addison’s - causes, symptoms&signs, investigations, treatment

A

causes:
- autoimmune (1st europe), TB (1st worldwide)
- tumour mets
- adrenal haemorrhage (meningococcus)
- amyloidosis
- sudden steroid withdrawal

symptoms & signs:
- raised K+, low Na+, low glucose
- postural hypotension
- skin pigmentation
- lethargy
- depression/psychosis
- can progress to Addisonian crisis

investigations:
- synACTHen test

treatment:
- hormone replacement - hydrocortisone/fludrocortisone if primary adrenal lesion

74
Q

cushing’s syndrome - causes, symptoms&signs

A

ACTH dependent (raised ACTH):
- pituitary tumour - “Cushing’s disease” (85%)
- ectopic ACTH producing tumour (5%. small cell lung cancer, carcinoid tumour)

ACTH independent:
- adrenal adenoma/cancer (10%), adrenal nodular hyperplasia, iatrogenic steroid use

[NB: remember CAPE. cushing’s disease, adrenal adenoma, paraneoplastic, exogenous steroids]

symptoms & signs:
- moon face
- buffalo hump
- central obesity
- striae
- acne
- hypertension
- diabetes
- muscle weakness (proximal myopathy)
- hirsutism
- bruising

75
Q

cushing’s syndrome - investigations, treatment

A

investigations:
- 1st line: overnight dexamethasone suppression test or 24h urinary free cortisol. +ve suggests true Cushing’s syndrome

2nd line: low-dose 0.5mg or high-dose 2mg dexamethasone suppression test (NB: meeran no longer recommends, use inferior pituitary personal sinus sampling instead due to FP rate 20% i.e., ectopic ACTH can be suppressed by high-dose dex)

low dose dex will fail to suppress cortisol in all of these, but high dose will succeed in pituitary cushings

3rd line: CT/PET scan to identify source of ectopic ACTH

treatment:
- treat underlying disease; surgical removal of lesion

76
Q

conn’s syndrome - causes, symptoms&signs, investigations, treatment

A

causes:
- adrenal adenoma

symptoms & signs:
- uncontrollable hypertension
- raised Na, low K
- generally young patient

investigations:
- raised aldosterone:renin ratio

treatment:
- aldosterone antagonists/potassium sparing diuretics - spironolactone, eplerenone, amiloride
- if > 4cm consider surgical excision

77
Q

phaeo - causes, symptoms&signs, investigations, treatment

A

causes:
- adrenal medulla tumour = increased adrenaline

symptoms & signs:
triad:
- headaches
- hypertension
- hyperhidrosis
arrhythmias
death if untreated

investigations:
- plasma and 24h urinary metadrenaline measurement/catecholamines & VMA

treatment:
ABC
- alpha blockade (1st)
- beta blockade
- cut out - surgery when BP well controlled

78
Q

phenytoin - signs toxicity, signs under treatment, interactions and cautions, treatment

A

signs toxicity:
- ataxia and nystagmus

signs under treatment:
- seizures

interactions and cautions:
- at high levels liver becomes saturated -> surge in blood levels

treatment:
- treatment mainly supportive. no specific antidote

79
Q

digoxin - signs toxicity, signs under treatment, interactions and cautions, treatment

A

signs toxicity:
- arrhythmias, heart block, confusion, xanthopsia (seeing yellow-green)

signs under treatment:
- arrhythmias

interactions and cautions:
- levels increased with hypokalaemia. reduce dose in renal failure and in elderly

treatment:
- digibind (digoxin immune Fab)

80
Q

lithium - signs toxicity, signs under treatment, interactions and cautions, treatment

A

signs toxicity:
- tremor (early), lethargy, fits, arrhythmia, renal failure

signs under treatment:
- relapse of mania in bipolar disorder

interactions & cautions:
- excretion impaired by hyponatraemia, reduced renal function and diuretics

treatment:
- treatment mainly supportive. osmotic or forced alkaline duresis/ if Li > 3mmol/L haemodialysis may be used

81
Q

aminoglycosides inc.gentamicin and vancomycin - signs toxicity, signs under treatment, interactions and cautions, treatment

A

signs toxicity:
- tinnitus, deafness, nystagmus, renal failure

signs under treatment:
- uncontrolled infection

interactions & cautions:
- mostly use single daily dosing. monitor peak and trough level before next dose

  • treatment:
  • omit/reduce dose
82
Q

theophylline and aminophylline (which contains theophylline) - signs toxicity, signs under treatment, interactions and cautions, treatment

A

signs toxicity:
- arrhythmias, convulsions, anxiety, tremor

signs under treatment:
- bronchial smooth muscle does not relax - asthma/COPD worsens/does not improve

interactions and cautions:
- variation t1/2; e.g., 4 hrs smokers 8hrs non-smokers, 30hrs liver disease. level increases by erythromycin, cimetidine and phenytoin

treatment:
- omit/reduce dose

83
Q

normal plasma range for calcium

A

2.2 - 2.6 mmol/l

84
Q

calcium metabolism hormones

A
  1. PTH (parathyroid hormone):
    - increases tubular 1a hydroxylation of vitamin D (25(OH)D)
    - mobilises calcium from bone through osteoclast activation
    - increases renal calcium reabsorption
    - increases renal phosphate excretion
  2. 1,25 (OH)2D (calcitriol) - active form of Vit D
    - increases calcium and phosphate absorption from the gut
    - bone remodelling
85
Q

primary hyperparathyroidism causes

A
  • 80% single parathyroid adenoma
  • 15% hyperplasia and multiple adenomas
  • 0.5% carcinomas (most carcinomas non-functional)
  • Men1 (adenoma) and 2 (hyperplasia)
86
Q

secondary hyperparathyroidism causes

A
  • CKD
  • vitamin D deficiency
  • malabsorption syndromes
87
Q

tertiary hyperparathyroidism causes

A
  • prolonged secondary hyperparathyroidism causing unregulated secretion of PTH
  • kidney transplant
88
Q

hypoparathyroidism causes

A
  • postsurgical (most common)
  • postradiation
  • autoimmune
  • iron deposition in people with thalassaemia
  • hypo/hypermagnesaemia
  • pseudohypoparathyroidism (resistance to parathyroid hormone)
  • DiGeorge syndrome
89
Q

Albright Hereditary Osteodystrophy

A
  • hereditary pseudohypoparathyroidism
  • resistance to PTH -> low Ca -> high PTH
  • Sx include short 4th/5th metacarpal
90
Q

commonest cause of hypercalcaemia (>= 2.6mmol/L)

A

community: primary hyperparathyroidism
hospital: malignancy

91
Q

hypercalcaemia symptoms

A
  • stones (renal)
  • bones (pain)
  • groans (psych)
  • moans (abdo pain)
  • thrones (polyuria)
  • muscle weakness
92
Q

hypercalcaemia treatment

A

treat the cause
- dehydration
- hyperparathyroidism
- cancer
- sarcoidosis
- milk alkali syndrome
- thyrotoxicosis
- hypervitaminosis D

93
Q

hypocalcaemia symptoms

A
  • perioral paraesthesia
  • carpopedal spasm
  • anxious/irritable
  • orientation impairment
  • increased smooth muscle tone
  • neuromuscular excitability (Trousseau’s and Chvostek’s sign)
  • dermatitis/impetigo herpetiformis
  • long QT
94
Q

hypocalcaemia treatment

A

if symptomatic or calcium <1.875 mmol/L
- parenteral calcium
- 10% calcium gluconate IV

asymptomatic/chronic/mild hypocalcaemia
- oral calcium supplementation e.g., SandoCal (taken not at meal times)
- if low PTH/vit D: vit D supplementation
- CKD: alfacalcidol
- other patients inc those with liver disease: vit D2 (ergocalciferol) or vit D3 (cholecalciferol)

95
Q

causes of hypocalcaemia

A

artefact
- e.g., hypoalbuminaemia

with high phosphate:
- CKD
- hypoparathyroidism (inc post thyroid surgery)

with normal/low phosphate:
- osteomalacia
- acute pancreatitis
- overhydration
- respiratory alkalosis (reduced ionised/active Ca)

96
Q

renal stones (nephrolithiasis) risk factors

A
  • dehydration
  • abnormal urine pH (e.g., meat intake, renal tubular acidosis)
  • increased excretion of stone constituents
  • urine infection (treat infection)
  • anatomical abnormalities (e.g., meat intake, renal tubular acidosis)
  • increased excretion of stone constituents
  • urine infection (treat infection)
  • anatomical abnormalities
97
Q

calcium stones - causes, preventative management

A
  • most patients are NORMO calcaemic
    results from:
  • hyperoxaluria (increased intake, absorption etc)
  • hypercalciuria (increased intake, renal leak)

preventative management: avoid dehydration, reduce oxalate intake, maintain normal Ca intake, thiazides –> hypocalciuric, citrate (alkalinise urine)

98
Q

investigation and treatment for renal stones

A

1st line investigation: urgent (within 24 hrs of presentation) imaging should be offered (low-dose non-contrast CT for most adults; USS for pregnant women, children and young people)

management:
- IM diclofenac (analgesia)
- stones <5mm in diameter: conservative management
- stones 6-20 mm: lithotripsy/ureteroscopy
- stones > 20mm: percutaneous nephrolithotomy

investigations for recurrent stones:
- serum: Cr, bicarb, Ca, phosphate, urate, PTH (if hypercalcaemic)
- stone analysis
- spot urine: pH, MCS, amino acids, albumin
- 24 hr urine: volume (>2.5L), Ca, oxalate, urate, citrate

99
Q

raised levels of amylase

A

high serum levels in acute pancreatitis (usually >10x upper limit of normal, >3x upper limit of normal required for diagnosis)

non-specific - raised in the following (not an exhaustive list):
- renal insufficiency
- intestinal infarct/peritonitis
- cholecystitis
- salpingitis
- ectopic pregnancy
- abdominal cancers

100
Q

raised lipase

A

if >3x the upper reference range then highly indicative of acute pancreatitis

more specific than amylase but can be raised in:
- renal insufficiency
- small intestinal ischaemia/obstruction
- sepsis
- DKA
- cholecystitis

101
Q

raised creatine kinase

A

most widely used as a marker of muscle damage (CK-MM = skeletal muscle, CK-MB (1&2) = cardiac muscles)

raised levels due to:
- physiological: afro-carribean (<5x upper limit of normal)
- pathological: Duchenne Muscular Dystrophy (>10x ULN), MI (>10x ULN), rhabdomyolysis, statin related myopathy (spectrum of myalgia to rhabdomyolysis occurring secondary to taking statins. RF: high dose, genetic predisposition, previous history of myopathy with another statin. causes rise in CK. reversible with cessation of statin)

NB: MI: not very specific but has a short half life so if suspected reinfarction then use CK as troponin can stay high for days. AST also raised in acute MI.

102
Q

where is ALP found

A

liver, bone, intestine, placenta

103
Q

causes of raised ALP

A

physiological: pregnancy (3rd trimester), childhood (during growth spurt)

pathological:
>5x ULN
- bone (Paget’s, osteomalacia)
- liver (cholestasis, cirrhosis)

<5x ULN
- bone (tumours, fractures, osteomyelitis)
- liver (infiltrative disease, hepatitis)

104
Q

BNP, NT-proBNP

A

BNP:
- brain natriuretic peptide - hormone that is primarily released from the ventricles in the heart
- released in response to ventricular stretch, has roles in seducing systemic vasoconstriction, sodium retention and renal sympathetic activity
- levels of <100 are highly specific for excluding heart failure, >400 is highly sensitive for heart failure. confounding factors to interpretation include CKD

NT-proBNP
- more sensitive than BNP and has greater prognostic value

105
Q

troponin

A

troponin I/T = myocardial injury biomarker
- not an enzyme but a protein which forms part of the contractile apparatus in cardiomyocytes, released during MI
- measure at 6 hours and then at 12 hours post onset of chest pain (100% Se and 98% Sp at 12-24 hours)
- remains elevated for 3-10 days therefore poor indication of reinfarction
- also raised in: coronary spasms, coronary dissection, post PCI, myocarditis, PE, HF, cardiomyopathies, sepsis, cardiac surgery, chest trauma, defibrillation

106
Q

primary hypercholesteraemia diseases

A

familial hypercholesteraemia (type II)
- AD: LDLR, apoB, PCSK9
- AR: LDLRAP1

polygenic hypercholesteraemia
- several polymorphisms

familial hyper-alpha-lipoproteinaemia
- CETP deficiency

phytosterolaemia
- ABC G5 & G*

107
Q

primary hypertriglyceridaemia diseases

A

familial type I
- lipoprotein lipase or apoC II def

familial type V
- apoA V def (sometimes)

familial type IV
- increased synthesis of TG

108
Q

primary mixed hyperlipidaemia diseases

A
  • familial combined hyperlipidaemia
  • familial dysbetalipoproteinaemia
  • familial hepatic lipase deficiency
109
Q

hypolipidaemia diseases

A

Ab- lipoproteinaemia
- MTP def

hypobeta-lipoproteinaemia
- truncated apoB protein

tangier disease
- HDL def

hypoalpha-lipoproteinaemia
- apoA-I mutations (sometimes)

110
Q

lipoproteins in order of density

A

chylomicron < FFA < VLDL < LDL < IDL < HDL

111
Q

PCSK9

A
  • binds LDLR and promotes its degradation
  • gain of function of mutation of PCSK9 -> increased LDL levels
  • novel form of LDL-lowering therapy is Anti-PCSK9 Mab = ebolocumab
112
Q

management of hyperlipidaemia

A
  • 1st line is always conservative - dietary modification and exercise (although dietary intake of cholesterol correlates poorly with actual triglyceride levels)
  • statin therapy:
    HMG-CoA reductase inhibitor
    reduces intrinsic synthesis of cholesterol in the liver
    side effects - myopathy/rhabdomyolysis, fatigue
    other agents more rarely used Ezetimibe
113
Q

management of obesity

A
  1. conservative measures
  2. medical
    no medication has been safely proven to provide sustained weight loss
    - orlistat (a pancreatic lipase inhibitor) [SE: profound flatus and diarrhoea]
    - rimonabant (a cannabinoid antagonist) was trialled and discontinued from use as there was an increased risk of suicide

surgical:
- barriatric surgery is indicated in patients with a BMI > 40 or >35 with a comorbidity associated with obesity
- to be considered requires extensive screening and must commit to long term follow up usually

114
Q

vitamin A (retinol) - deficiency, excess, test

A

deficiency:
- colour blindness (retinitis pigmentosa)

excess:
- exfolitation hepatitis

test:
- serum

115
Q

vitamin D (cholecalciferol) - deficiency, excess, test

A

deficiency:
- osteomalacia/rickets

excess:
- hypercalcaemia

test:
- serum

116
Q

vitamin E (tocopherol) -deficiency, test

A

deficiency:
- anaemia/neuropathy/IHD

test:
- serum

117
Q

vitamin K (phytomenadione) - deficiency, test

A

deficiency:
- defective clotting

test:
- PT

118
Q

which are the fat soluble vitamins

A

A, D, E, K

119
Q

which are the water soluble vitamins

A

B1, B2, B3, B6, B12, C, folate

120
Q

vitamin B1 (thiamine) - deficiency, test

A

deficiency:
- Beri Beri –> wet = CVS, dry = neuro
neuropathy
Wernicke syndrome

test:
- RBC
- transketolase

121
Q

vitamin B2 (riboflavin) - deficiency, test

A

deficiency:
- glossitis

test:
- RBC glutathione reductase

122
Q

vitamin B3 (niacin) - deficiency

A

pellagra - 3Ds
dementia, dermatitis, diarrhoea

123
Q

vitamin B6 (pyridoxone) - deficiency, excess, test

A

deficiency:
- dermatitis/anaemia - sideroblastic

excess:
- neuropathy

test:
- RBC AST activation

124
Q

vitamin B12 (cobalamin) - deficiency, excess, test

A

deficiency:
- pernicious anaemia, sub-acute cord degeneration

test:
- serum B12

125
Q

vitamin C (ascorbate) - deficiency, excess, test

A

deficiency:
- scurvy

excess:
- renal stones

test:
- plasma

126
Q

folate - deficiency, test

A

deficiency:
- megaloblastic anaemia
- neural tube defect

test:
- RBC
- folate

127
Q

zinc excess

A

dermatitis

128
Q

UK screening via the Guthrie blood spot test at 6 days of age

A

phenylketonuria, congenital hypothyroidism, cystic fibrosis, sickle cell disease, MCAD (medium chain acylCoA dehydrogenase) deficiency

NB: the newborn screening programme measures chemicals in the blood spot, it doesn’t involve any genetics. an abnormal chemical level doesn’t always mean that there is a genetic disorder!

129
Q

define specificity

A

specificity is the probability (in %) that someone without the disease will correctly test negative
- TN/(FP+TN)

130
Q

define sensitivity

A

sensitivity is the probability that someone with the disease will correctly test positive
- TP/(TP+FN)

131
Q

what is the positive predictive value

A

PPV is the probability that someone who tests positive actually has the disease
- TP/(TP+FP)

132
Q

what is the negative predictive value

A

NPV is the probability that someone who tests negative actually doesn’t have the disease
- TN/(TN+FN)

133
Q

diagnosis of diabetes mellitus

A

if symptomatic (polydipsia/polyuria/blurred vision/unexplained weight loss/recurrent infections/tiredness) then one of the below is adequate to diagnose:
- HbA1c > 48
- fasting glucose >7
- random glucose > 11.1
- IGTT > 11.1

if asymptomatic then need to arrange repeat testing, preferrably with the same test

IGTT of >7.8 but <11.1 = impaired glucose tolerance

fasting glucose >6.1 but <7.0 is classified as impaired fasting glucose

134
Q

DKA (+ symptoms, management)

A

pH<7.3, plasma glucose > 11mM, blood ketones > 3mM (2+ in urine)
rapid onset, medical emergency

symptoms: confusion, Kussmaul breathing, abdominal pain, nausea, vomiting
precipitants: infection, surgery, missed insulin doses, trauma

management:
A to E approach (call for senior help early)
1. fluids
- 0.9% saline
- SBP <90: give 500ml in 15 mins - RESUS fluids
- SBP >90: give 1 litre over 1 hour. if K+ 3.5-5.5 then add KCl to 2nd litre of fluids
2. insulin (stops ketogenesis)
- only started after fluids
- ensure K+ not <3.5 -> insulin drive K+ into cells and lowers K+
- 0.1u/kg/h fixed rate regimen
3. early senior review +/- ITU involvement
4. monitoring
- monitor glucose and potassium hourly
- catheterisation aiming for urine output >0.5ml/kg/hr
- resolution is when ketones <0.6 and pH>7.3

135
Q

hyperosmolar hyperglycaemic syndrome (HHS)

A

pH>7.3, osmolarity > 320 mOsm, blood glucose > 30mM
HHS develops over few days
patients present acutely unwell with confusion and clinical dehydration

management:
A to E approach
1. fluid replacement
- 0.9% saline over 1 hr
2. IV insulin
- only if >1 mmol/L ketones
- 0.05u/Kg/he fixed rate
3. monitoring
- serial U+Es and glucose readings

136
Q

causes of hypoglycaemia

A

hyperinsulinaemic hypoglycaemia:
- insulin overdose
- sulfonylurea excess
- insulinoma

hypoinsulinaemic hypoglycaemia:
i. +ve ketones
- alcohol binge with no food
- pituitary insufficiency
- addison’s
- liver failure
ii. -ve ketones
non-pancreatic neoplasms:
- fibrosarcomata
- fibromata

non-islet tumour hypoglycaemia
- reduced glucose, insulin, C-peptide, FFA and ketones
= tumours that cause a paraneoplastic syndrome, secreting ‘big IGF-2’, which binds to IGF-1 and insulin receptor

137
Q

common problems in low birth weight

A
  • respiratory distress syndrome
  • retinopathy of prematurity
  • intraventricular haemorrhage
  • patent ductus arteriosus
  • necrotising enterocolitis (inflammation of bowel wall, necrosis and perforation)
138
Q

hyponatraemia causes in newborns

A

first 4-5 days of life:
- excess total body water usually due to excessive intake
- rarely may be SIADH secondary to infection (pneumonia/meningitis) or intraventricular haemorrhage

after first 4-5 days:
- usually loss of sodium due to immature tubular function in patients on diuresis

factitious (i.e. Na+ normal but appears low) e.g., hyperglycaemia

congenital adrenal hyperplasia - 21 alpha hydroxylase deficiency
- addisonian presentation
- usually identified on Guthrie spot

139
Q

urine examination

A

single sample:
- dipstick testing
- microscopic examination
- proteinuria quantification (protein:creatinine ratio (PCR))

24-hour collection:
- proteinuria quantification (superseded by PCR above)
- creatinine clearance estimation
- electrolyte estimation
- stone forming elements

urine microscopy:
- crystals (stones)
- red blood cells (stones, UTI)
- white blood cells (UTI, glomerulonephritis)
- casts (glomerulonephritis)
- bacteria (UTI)

140
Q

define AKI

A

AKI is defined as:
- rise in serum creatinine > 26 within 48 h
- a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- a fall in urine output to less than 0.5mL/kg/hour for more than 6 hours (NB: prostate and bladder pathology can cause this too)

141
Q

causes of AKI

A

pre-renal
- hallmark is reduced renal perfusion with no structural abnormality of the kidney; however, it can become renal if the ischaemia leads to necrosis. responds to volume replacement.

renal
- vascular, glomerular, tubular or interstitial

post-renal
- characterised by obstruction to urinary flow, glomerular filtration requires a pressure gradient, reversal can lead to scarring and permanent renal impairment

142
Q

indications for dialysis as an emergency

A

remember it as the vowels A, E, I, O, U
1. acidosis (metabolic)
2. electrolyte disturbance (e.g., refractory hyperkalaemia)
3. intoxication e.g., lithium, aspirin
4. overload (fluid) e.g., pulmonary oedema
5. uraemic encephalopathy

143
Q

stages of chronic kidney disease (CKD)

A

1 - kidney damage with normal GFR
- GFR > 90 ml/min

2 - mild GFR
60 - 89

3 - moderate GFR
30 - 59

4 - severe GFR
15 - 29

5 - end-stage kidney failure
<15 or dialysis

144
Q

commonest causes of CKD

A
  • diabetes - most common
  • atherosclerotic renal disease
  • hypertension
  • chronic glomerulonephritis
  • infective or obstructive uropathy
  • polycystic kidney disease
145
Q

consequences of chronic kidney disease

A
  1. progressive failure of homeostatic function
    - acidosis
    - hyperkalaemia
  2. progressive failure of hormonal function
    - anaemia (loss of EPO synthesis)
    - renal bone disease (secondary hyperparathyroidism due to low Vit D)
  3. cardiovascular disease
    - vascular calcification and subsequent atherosclerosis (biggest mortality in CKD)
    - uraemic cardiomyopathy
  4. uraemia and death
146
Q

haemodialysis vs peritoneal dialysis

A

haemodialysis
- done via a tunnelled central line (Tessio line) or an arteriovenous fistula
- usually done around 3x/week depending on the patient’s individual circumstances
- not ideal for those who are still at work as requires several hours hooked up to a machine at the hospital

peritoneal dialysis
- undertaken via a Tenckoff catheter
- uses the peritoneum as the dialysis membrane, insert dialysate through the catheter, leave for a few hours then drain
- can be done at home
- increased risk of peritoneal infections

147
Q

renal replacement therapy - transplant

A

kidney transplant is the only definitive cure. requires lifelong immunosuppression with agents like tacrolimus or ciclosporin

transplanted kidney is usually in the RIF:
- rutherford morrison (hockey stick scar)
- right mesocolon is not fixed therefore easier to access the iliac vessels to connect the transplant

148
Q
A

Pathology (5 decks)

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