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My Year 5 Pathology > Chemical Path > Flashcards

Chemical Path Flashcards

1
Q

What are the 2 main roles of calcium in the body?

A

1) Skeleton

2) Metabolic - e.g. action potentials and IC signalling

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2
Q

What are the normal plasma ranges of calcium?

A

2.2 - 2.6mmol/l

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3
Q

How is calcium distributed in the blood?

A

40% bound to albumin (so affected by the level of albumin - must use corrected level)

50% ionised (free - active)

10% complexed - citrate/phosphate

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4
Q

What 2 main hormones are involved in calcium metabolism?

A

1) PTH

2) 1,25(OH)2D - Calcitrol

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5
Q

Give 4 functions of PTH

A

1) mobilises Ca from bone
2) increases renal calcium reabsorption
3) increases renal phosphate excretion
4) increases tubular 1alpha hydroxylaton of vit D (25(OH)D)

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6
Q

How do you work out corrected calcium?

A
  • dependent on the amount of albumin

- Serum (Ca2+) + 0.02 X (40-serum albumin in g/L)

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7
Q

What % of calcium is actually in the serum

A

1% - the 99% left in the bones

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8
Q

What is the corrected calcium if the albumin level is 30 and total calcium is 2.2

A

(2.2 + (0.02 X (40 - 30)) = 2.4 mM

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9
Q

Why must normal plasma calcium level be maintained?

A

for nerve and muscle function

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10
Q

What is hypocalcaemia detected by?

A

the parathyroid gland

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11
Q

What 3 sources does the PTH get Ca2+ from/

A

1) Bone
2) gut (absorption)
3 Kidneys (resorption AND 1 alpha hydroxylase activation)

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12
Q

how is vitamin D synthesised? Draw the 4 step process

A

7-dehydrocholesterol –> (SUN/SKIN –> cholecalicferol (D3) —> liver) —> dihydrocholecalciferol –> (PTH) –> 1,25 dihydrocholecalciferol

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13
Q

What is the other namefor vitamin D3 and where is it synthesised?

A

cholecalciferol - in the skin (SUN)

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14
Q

What enzyme in the kidney activates vitamin D3, and what does it become?

A

1 alpha hydroxylase

1,25-(OH)2 D3
aka 1,25-dihydrocholecalciferol

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15
Q

Where are 25 hydroxylase enzymes found and what do they do/

A

in the liver - convert cholecalciferol (D3) to 25-hydroxycholecalciferol (te inactive and stored version of vitamin D3)

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16
Q

Give 4 risk factors for vitamin D deficiency

A

1) malabsorption
2) Dark skin
3) lack of sunlight exposure
4) diet

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17
Q

What 3 things would you see in the biochem to indicate osteomalacia?

A

1) Low Ca
2) Low Pi
3) Raised ALP

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18
Q

What are Looser’s zones?

A

pseudofractures seen in osteomalacia. airline incomplete stress fractures. Most commonly found on pelvic rami, humeral ad femoral necks, and the axillary edge of the scapulae

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19
Q

what is the significance of a patient coming in with bone pain and eats loads of chappatis?

A

chapatis contain phytic acid –> high dietary intake of phytic acid is known to cause hypocalcaemia as it disrupts absorption and so increases risk of viramin D deficiency and osteomalacia / rickets

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20
Q

What clnical features might you see in rickets in children/

A

1) bowed legs
2) costochondral swelling
3) widened epiphyses at the wrists
4) myopathy

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21
Q

name a class of drug which is known to have an effect on vitamin D levels?

A

anticonvulsants e.g. phenytoin –> induce breakdown vitD so risk of bone disease

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22
Q

what is the difference between osteoporosis and osteomalacia/

A

Osteomalacia –> demineralisation due to low Ca / vitamin D deficiency

Osteoporosis –> redcution in bone density (normal mineralisation) so noral biochemistry

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23
Q

How would you diagnose osteoporosis and what score would you get?

A

DEXA scan: T-score of < -2.5

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24
Q

What would a T score of -1 and -2.5 indicate?

A

osteopenia

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25
Q

What would a T-score f < -2.5 indicate?

A

osteoporosis

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26
Q

Give as many causes of osteoporosis as you can

A

1) Normal - normal age related decline in bone mass
2) Endocrinologoical - early menopause, hyperprolactinaemia, thyrotoxicosis, cushings
3) Drugs - steroids
4) lifestyle - sedentary, smoking, low BMI

5- others: genetic, prolonged illness / childhood illness

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27
Q

wHAT IS THE tX FOR OSTEOPOROSIS

A

Lifestyle - weight bearing exercise, stop smoking, reduce EtOH

Drugs- Vit D/C
Bisphosphonates - e.g. alendronate

Strontium

SERMs e.g. raloxifene

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28
Q

How do bisphosphonates work and give an example of one

A

alendronate

they encourage apoptosis of osteoclasts

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29
Q

What is the most common electrolyte abnormality in inpatients?

A

hyponatraemia

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30
Q

What is the normal range for serum sodium?

A

135 - 145mmol / L

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31
Q

Where is ADH released from?

A

Posterior pituitary

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32
Q

What receptors does ADH act upon, where are they, and wht does this achieve?

A

V2 receptors in the collecting duct of the nephron, insertion of aquaporins

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33
Q

ADH action on V1 receptors has what effect?

A

Vasoconstriction of vascular smooth muscle

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34
Q

What are the 2 main stimuli for ADH secretion?

A
  1. high serum osmolality

2. low blood volume / pressure

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35
Q

what detects the blood volume/pressure resulting in ADH secretion?

A

baroreceptors in the carotids, atria, aorta

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36
Q

what is the 1st step in the clinical assessment of a hyponatraemic patient?

A

fluid status

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37
Q

what are the clinical signs of hypovolaemia?

A
  • tachycardia
  • postural hypotension
  • dry mucous membranes
    reduced tissue turgor
  • confusion / drowsiness
  • reduced urine output
  • low urine Na+ (<20)
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38
Q

what are 3 clinical signs of hypervolaemia

A

raised JVP
bibasal crackles
peripheral oedema

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39
Q

If you suspect a patient is hypovolaemic and hyponatraemic, what 4 differentials must you think of?

A

vomiting
diarrhoea
diuretics
salt losing nephropathy

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40
Q

what are 3 causes of hyponatraemia in a hypervolaemic patient

A

cardiac failure
cirrhosis
renal failure

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41
Q

Why do you get hypervolaemia and hyponatraemia in heart failure?

A

reduced cardiac output, reduced blood pressure due to failing heart, causing increased ADH release due to baroreceptor stimulation, resulting in increased water retention and low sodium

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42
Q

why does liver cirrhosis result in hypervolaemic hyponatraemia?

A

increased NO, vasodilation, reduced BP, sensed by baroreceptors, ADH secretion, water retention

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43
Q

what are the 3 causes of hyponatraemia in a euvolaemic patient?

A
  1. hypothyroidism
  2. adrenal insufficiency
  3. SIADH
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44
Q

What investigations would you like to do in a patient with euvolaemic hyponatraemia?

A
  1. TFTs (hypothyroidism)
  2. Short synacthen test (ACTC - see cortisol rise, or NOT if Adrenal insufficiency)
  3. plasma and urine osmolality (if SIADH - will have low plasma ad high urine osmolality)
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45
Q

How do you diagnose SIADH? (4 steps)

A
  1. ensure not hypovolaemic - clinically and ask about vomiting/diarrhoea
  2. check TFTs (hypothyroidism)
  3. Rule out adrenal insufficiency
  4. Check urine and plasma osmolality - in SIADH serum Os = Low and urine = high

would also check for tumours with CT etc and chest

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46
Q

What is the serum and urine osmolality in SIADH?

A 
serum = low 
urine = high
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47
Q

how would you manage a euvolaemic patient wth hyponatraemia?

A
  • fluid restriction

- treat the underlying cause

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48
Q

what should you think about using to treat a severely hyponatraemic patient who is seizing and low GCS?

A

Hypertonic saline (3%)

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49
Q

What is the most important thing to remember when correcting hyponatraemia?

A
  • NEVER correct serum Na >8-10mmol/L in the first 24 hours because there is a massive risk of osmotic demyelinaton (central pontine myelionlysis)
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50
Q

What is an iatrogenic cause of central pontine myelinolysis?

A

Increasing serum sodium too fast: should never be more than 8-10 mmol/L in the 1st 24h

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51
Q

what 2 drugs can you consider to treat SIADH?

A
  1. Demeclocycline

2. Tolvaptan

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52
Q

which is consistent wit SIADH:

  1. reduced plasma osmolality & urine osmolality
  2. reduced plasma osmolality and increased urine osmolality
A

2!!

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53
Q

What are the main causes of hypernatraemia

A
  1. unreplaced water loss - GI, sweat, renal (diuretics, reduced ADH release, diabetes insipidus)
  2. patient cannot control intake e.g. children, elderly
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54
Q

What investigations would you order in a patient with suspected diabetes insipidus?

A
  • serum glucose (DM)
  • serum potassium (hypokalaemia)
  • serum calcium (hypercalcaemia)
  • plasma and urine osmolality
  • water deprivation test
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55
Q

What would the plasma and urine osmolality look like in diabetes insipidus?

A

less water reabsorbed due to inadequate ADH

urine = low 
plasma = high
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56
Q

Why can low potassium and high calcium cause diabeted insipidus?

A

causes resistance to ADH - nephrogenic DI

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57
Q

what happens in a water deprivation est to a DI patient

A

don’t drink - urine normally becomes more concentrated but in DI urine will remain dilute due to non secreton of ADH so urine osmolality will remain low

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58
Q

what is the correct treatment of hypernatraemia?

A

water replacement with 5% dextrose, and correct ECF volume depletion with 0.9% saline

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59
Q

What are the 4 routes of entry of CNS infection

A
  1. haematogenous
  2. direct implantation
  3. local extension - secondary to esstablished infection
  4. PNS into CNS - viruses
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60
Q

what is the most common route of CNS infection?

A

local extension - secondary to established infection …. nasopharyngeal spread

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61
Q

what are the major causative agents of meningitis?

A
  • neisseria meningitides
  • strep pneumoniae
  • H. influenzae
  • TB
  • viruses
  • cryptococcus neoformans
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62
Q

Is meningococcal meningitis classified as acute, chronic or aseptic?

A

Acute

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63
Q

What is the number 1 cause of meningitis?

A

Neisseria meningitides

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64
Q

What are the 2 most commonly identified organisms in aseptic meningitis?

A

Coxsackievirus group B & echoviruses

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65
Q

What’s the difference between meningitis and meningoencephalitis?

A

meningitis = inflammation of meninges & CSF

Menigoencephalitis = inflammation of meninges & brain parenchyma

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66
Q

what are the 2 most common viral causes of encephalitis?

A

HSV (1 & 2)

enteroviruses (coxsackie A & B, echovirus, polio)

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67
Q

What virus is becoming a leading and deadly ause of encephalitis internationally?

A

West Nile Virus

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68
Q

what species have a hign salt tolerance and can reside on contact lensess, potentially leading to abcesses & meninigits?

A

Acanthamoeba

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69
Q

what are the 2 main routes of brain abscesses occurring?

A
  1. ear infections/otitis media spreading medially e.g. streptococci
  2. staph. aureus flicking off heart valves (endocarditis) and spreading haematogenously
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70
Q

what investigations should you consider for CNS infections?

A 
MRI 
CT 
LP (NOT if septic) 
brain biopsy 
Blood culture 
Throat Swab 
Blood PCR
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71
Q

CSF report shows 2500 neutrophils, and is turbid - what is the likely diagnosis?

A

pyogenic (bacterial) meningitis - ? neisseria meningitides, pneumococcus, listeria

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72
Q

CSF sample is clear, has a high protein level of 5g/L and contains 300 lymphocytes, negative gram stain

A

TB

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73
Q

Gram positive diplococci causing neck stiffness and headache in 21 year old student?

A

Strep pneumoniae

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74
Q

18 year old with headache and neck stiffness, CSF shows gram negitive diplococci>

A

Neisseria meningitides

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75
Q

treatment for meningitis (generic)

A

Ceftriaxone IV 2 bd

if >50 yrs / immunocompromised + amoxicillin Iv g 4hourly

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76
Q

Tx for generic meningoencephalitis?

A

Aciclovir 10mg/kg IV tds

Ceftriaxone IV 2g bd

if >50 / immunocompromised + amoxicillin IV 2g 4 hourly

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77
Q

What is a major clinicl way of differentiating between meningitis and meningo-encepalitis?

A

both have neck stiffness etc but meningo-encephalitis also presents with confusion

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78
Q

what should be the main things you want to do quickly in clinical assessment and initial Ix and Tx of patent presenting with headache fever and neck stiffness

A
  • full history
  • are they immunocompromised??
  • get LP
  • give Abx
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79
Q

how to you calculate the anion gap?

A

na + K - Cl - bicarb

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80
Q

what is the normal anion gap?

A

18mM

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81
Q

What 2 substances are thee most common causes of a high anion gap?

A

ketones and lactate

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82
Q

what causes a respiratory alkalosis?

A

primary hyperventilation - e.g anxiety

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83
Q

Whymight a hyperventilating patient get carpal spasm?

A

pH gets higher and higher due to low CO2, respiratory alkalosis, which increases the binding of calcium to albumin, reducing free ionised calcium, resulting in paralysis

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84
Q

how do you calculate osmolality?

A

2(Na + K) + Glucose + Urea mosm/kg

85
Q

why do patients become unconscious if they are in a hypermolar hyperosmotic state?

A

Draws water out of the brain - becomes very dehydrated

86
Q

low CO2 and low pH means…..

A

metabolic acidosis

87
Q

What can an overdose of metformin cause?

A

Lacic acidosis (because i inhibits conversion of lactate back to glucose, resulting in it bulding up in the blood- akalosis)

88
Q

What is the basic test to diagnose diabetes

A

fasting glucose >7 mM

89
Q

If glucose is <7mM but you are still suspicious that a patient has diabetes, what test would you consider?

A

glucose tolerance test

- give 75g glucose at time 0 and check plasma glucose after 2 hours - if >11.1mM then iabetes

90
Q

Which LFT is markedly elevated in bile duct obstruction / obstructive jaundice?

A

ALP

91
Q

what are 3 major reasons for a low albumin?

A
  1. low production - chronic liver disease, malutrition
  2. loss - e.g. gut / kidneys (nephrotic syndrome)
  3. sepsis - 3rd space loss
92
Q

What does AFP test for?

A

hepatocellular carcinoma - but also raised in pregnancy, and testicular cancer

93
Q

When looking at LFTs, what does a normal albumin level suggest?

A

preserved synthetic function

94
Q

what drug is a commo cause of cholestatic jaundice?

A

augmentin

95
Q

what is Courvoisier’s sign ad what does it indicate?

A

painless palpable gall bladder in the presence of jaundice - unlikely to be gall stones

96
Q

which hepatitis is the commmonest cause of acute hepatitis and jaundice and diarrhoea

A

Hep A

97
Q

What do you treat a paracetamol overdose with

A

N-acetyl cystine an potentially liver transplant

98
Q

Which hormone causes the hypotension in Addison’s disease

A

Aldosterone

99
Q

what 2 hormones does TRH stimulate?

A

TSH AND prolactin

100
Q

what 6 hormones are released by the anterior pituitary?

A
  1. prolactin
  2. GH
  3. LH
  4. FSH
  5. TSH
  6. ACTH
101
Q

If you suspect a macroadenoma, what clinical sign should you look for?

A

bitemoporal hemianopia

102
Q

What is the diagnosis if prolactin is >6000

A

always a prolactinoma - so huigh that cells must be making prolactin

103
Q

What should be your next main investigation if we suspect a prolactinoma and already know that prolactin levels are >6000

A

Pituitary function test

104
Q

What does a pituitary function test involve

A

administer “stress” with insulin to induce hypoglycaemia, + GnRH + TSH

105
Q

What are the 2 major contraindication for the combined pituitary function test’?

A
  1. cardiac risk factors are present e.g. IHD, angina and abnormal ECG –> highly likely to have a MI
  2. No history of epilepsy
106
Q

What is the term for a patient who’s glucose is <1.5nM and unconscus

A

neuroglycopenia

107
Q

When is it legal to publically restrain someone

A

If they are diabetic, having a hypo, confused and aggressive, and you tackle and force them to eat something - legally fine!

108
Q

how do you treat a patient who becomes severely hypoglycaemic during a combined pituitary function test?

A

50ml of 20% dextrose

109
Q

What level of glucose should you aim to achieve during a combined pituitary function test?

A

<2.2mM - if it does not get this low then should administer more insulin

110
Q

Why might you get high prolactin in a non functioning adenoma>

A

adenoma presses on the pituitary stalk, causing pit failure and also preventing dopamine reaching pituitary resulting in increased prolactin

111
Q

what tests should you consider if suspecting Acromegaly

A
  1. bloods - GH
  2. Glucose tolerance test - will not suppress GH in acromegaly
  3. IGF-1
112
Q

what is the best treatment for acromegaly?

A 
pituitary surgery - best outcomes
OR 
- cabergoline 
- octerotide 
- pit radiotherapy
113
Q

Which part of the adrenal makes cortisol?

A

Zona reticularis

114
Q

Which part of the adrenals make adrenaline?

A

Medulla

115
Q

which part of the adrenals makes aldosterone

A

zona glomerulosa

116
Q

In patients with primary hypothyroidism, what are thy also likely to have

A

aDDISONS DISEASE

117
Q

what test should you do to confirm addisons?

A

Synacthen test - synthetic ACTH administered IM and measure cortisol - if it remains low then shows adrenal insufficiency

118
Q

WHAT ARE THE 3 DIFFERENTIALS YOU SHOULD THINK ABOUT when a patient presents with HTN and an adrenal mass?

A
  1. phaeochromocytoma
  2. Conns
  3. Cushings
119
Q

What is the treatment of phaeochromocytoma?

A
  1. alpha blockade URGENTLY (to prevent arrythmias/cardiac arrest) - phenoxybenzamine
  2. add beta blocker
  3. surgery
120
Q

what is the likely diagnosis: 33 year old with HTN and hypokalaemia. Plasma aldosterone raised and plasma renin suppressed

A

Conn’s syndrome

121
Q

What is the most common cause, apart from oral steroids, of Cushing’s?

A

85% due to pituitary dependent cushing’s disease

122
Q

What are 2 less common causes of cushings? (10% and 5%)

A

10% caused by adrenal adenoma

5% caused by ectopic production of ACTH from lung cancer

123
Q

What should be the next investigation if you have already done a dexamethasone suppression test (0.5mg 6 hoourly) which indicates cortisol suppression and s Cushing’s?

A

High dose dexamethasone suppression test (2mg every 6 hours for 48 hours) to help you determine the cause of cushing’s –> if suppressed to 50% of baseline then you can be sure the diagnosis is pituitary dependent cushings

124
Q

What would be your next investigation if you have performed a high dose dexamethasone suppression test which has shown 50% suppression of cortisol?

A

Pituitary MRI –> suspect pituitary dependent cushings disease and so look for a microadenoma which you would then consider removing with surgery

125
Q

What are the clinical lab criteria for SIADH?

A
  • euvolaemic hyponatraemia
  • inappropriately high urine osmolarity (should be keeping the Na)
  • increase Na excretion >20mmol/l
  • normal renal, crida, thyroid and adrenal function
  • Diagnosis of exclusion
126
Q

What is the most common malignant cause of SIADH

A

small cell lung cancer (secreting ADH ectopically)

127
Q

What lab findings are there with Diabetes insipidus

A

Euvolaemic Hypernatraemia
very dilute urine (low osmolality)
May have

128
Q

What investigations would you want to do for diabetes insipidus?

A

Serum glucose (DM)
blood potassium (hypo) and Calcium (hyper) - as these can cause nephrogenic DI
blood and urine osmolarity
water deprivation test (8h)

129
Q

How can you tell between cranial and nephrogenic Diabetes insipidus?

A

In a water deprivation test, neither will concentrate urine naturally.
If you give DESMOPRESSIN - cranial DI will be treated and urine can be concentrated, but nephrogenic DI lacks the receptors so urine still remains dilute

130
Q

How would you treat hypernatraemia?

A

treat underlying cause

fluid replacement

131
Q

What is the normal potassium range

A

3.5-5.5 mmol/L

132
Q

What is the normal Sodium range>

A

135-145mmol/L

133
Q

Does acidosis cause potassium to increase or decrease and why

A

acidosis or dropping pH causes potassium to rise - due to the tight link between H+ and K+ where if pH drops by 0.1 then K+ rises by 0.7 as it moves out of the cells

134
Q

is potassium mainly intra or extracellular?

A

K+ is predominantly INTRACELLULAR

135
Q

Which liver enzyme is most raised in alcohol cirrhosis

A

AST

136
Q

what are the main causes of elevated ALP?

A
  • cholestasis (intra or extra hepatic, obstructive jaundice)
  • bone disease (metastatic)
  • Pregnancy ++
137
Q

what causes a raised GGT?

A
  • chronic alcohol use
  • bile duct disease
  • hepatic metastasis
138
Q

What causes a low albumin

A
  • reduced production - e.g. in chronic liver disease, malnutrition
  • increased loss - e.g. gut/kidney
  • sepsis - 3rd space loss
139
Q

which tumour marker helps the diagnosis of hepatocellular cancer?

A

AFP - alpha-feto protein

140
Q

which liver enzyme is very raised in pregnancy?

A

ALP

141
Q

Which enzyme is faulty in Gilbert’s syndrome

A

glucuronyltransferase

142
Q

Gilbert’s syndrome causes a build up of which type of bilirubin
/

A

unconjugated

143
Q

Which gene is responsible for Gilbert’s syndrome

A

UGT1A1 gene on Ch2

144
Q

If a jaundiced patient has very high ALP, but on USS there is no dilatation, what is the likely cause of the raised bilirubin?

A

drug induced cholestasis e.g. by augmentin following an infection

145
Q

What is courvoisier’s sign?

A

in the presence of a painless palpable gallbladder, jaundice is unlikely to be caused by gallstones

146
Q

What are the 3 components of the combined pituitary function test?

A
  1. Metabolic stress test: Administer insulin (0.15units/kg) to induce hypoglycaemia must be <2.2mM - to stimulate cortisol
  2. TRH test to stimulate TSH –> should be higher at 30 mins >60 mins
  3. gonadotrophin releasing hormone test –> LHRH to stimulate LH and FSH, if reduced will be an early sign of hypopituitarism
147
Q

Where is ALP present?

A

Bone, liver, placenta, Liver

148
Q

What are the 3 creatinine kinase forms?

A

CK-MM (skeletal muscle)
CK- MB (cardiac muscle)
CK-BB (brain)

149
Q

what are some pathological causes of raised CK?

A 
MI 
Myopathy e.g. Duchenne's muscular dystrophe 
muscle damage 
statin related myopathy 
severe exercise
150
Q

A 64 year old man who smokes and has a family history of cardiovascular disease has recently been started on atorvastatin. Three weeks after commencing the tablet, he complains of generalised muscle pain. What is the working clinical diagnosis?

A

statin related myopathy

151
Q

A 64 year old man who smokes and has a family history of cardiovascular disease has recently been started on atorvastatin. Three weeks after commencing the tablet, he complains of generalised muscle pain. What enzyme will help with the diagnosis?

A

CK

152
Q

which type of creatinine kinase is most useful for MI?

A

CK-MB

153
Q

when should you measure troponin after chest pain?

A

6H AND 12H

sensitivity rises from 17% to 92%

154
Q

What is the unit of measurement for plasma enzyme activity ?

A

U/L

155
Q

Which type of vitamin D do we commonly measure?

A

25-hydroxy vitamin D (deactivated) - gives an indication of storage

156
Q

What does vitamin B3 or Niacin deficiency cause?

A

Remember the 3 D’s

dementia, diarrhoea, dermatitis

157
Q

What can an excess of vitamin C cause?

A

renal stones

158
Q

What can a deficiency of vitamin cause?

A

colour blindness

159
Q

What is the average GFR?

A

120 ml/min 0r 7.2 L per hour

160
Q

What is the equation for calculating the kidney clearance?

A

C= (Urine conc x vol)/plasma conc

161
Q

What is the gold standard measure of GFR

A

Inulin clearance - but only really used for research

162
Q

What 3 characteristics must markers of GFR have?

A
  • not bount to proteins
  • freely filtered by the glomerulus
  • not modified by tubules
163
Q

Which factor(s) limit(s) the use of serum creatinine as a marker of GFR?

It is influenced by intake of fat
It is lower in the black population
It is related to muscle mass
It is reabsorbed by the renal tubules
All of the above
A

Related to muscle mass

164
Q

How much age related decline is there in renal GFR?

A

1ml/hr/year

165
Q

what is an alternative endogenous marker to creatinine?

A

Cystatin C

166
Q

what is a more paractical way of measuring proteinura than a 24h urine collection

A

Protein:creatinine ration

167
Q

A 50 year old, known alcoholic, presents generally unwell, seemingly intoxicated, with acute kidney injury. Urine microscopy reveals calcium oxalate crystals, what diagnosis do you suspect?

A

ethylene glycol poisoning

168
Q

You admit a 28 year old man who you suspect has a renal stone, what is your first choice of imaging?

a) Plain KUB
b) CT
c) Ultrasound KUB
d) IVU
e) MRI

A

nowadays CT KUB is the investigation of choice - mush more accessible

169
Q

what is the hallmark of pre-renal AKI?

A

reduced renaal perfusion

170
Q

What is the most common cause of pre-renal AKI

A

True volume depletion

171
Q

Causes of pre-renal AKI

A
  • true volume depletion
  • renal ischaemia ie renal artery stenosis
  • Hypotension
  • oedema
  • Drugs (decreasing renal blood flow)
172
Q

Which class of drugs may predispose patients to developing pre-renal AKI?

A

a) NSAIDs - decrease afferent arteriolar dilatation
b) Calcineurin inhibitors - decrease afferent arteriolar dilatation
c) ACEi or ARBs - decrease efferent arteriolar constriction
d) Diuretics

173
Q

what is the hallmark of post-renal aki?

A

phsical obstruction to the urine flow

174
Q

Causes of post-renal AKI?

A

blocked catheter
prostate/urethral blockage
ureter blockage (causing bilateral)

175
Q

Give 3 exampkles of long term injuries the kidneys can get due to prolonged obstruction?

A
  1. tubular damage
  2. Glomerular ischaemia
  3. long term interstitial scarring
176
Q

what are exogenous and endogenous causes of tubular injury causing intrinsic AKI?

A

endogenous: myoglobin + immuoglobulins
Exogenous: Contrasts, acyclovir, aminoglycosides

177
Q

What two measures do we use to define severity of acute kidney injury?

A

urine output

Creatinine

178
Q

What are the 3 most common causes of CKD?

A

1) diabetes
2) atheroslerotis
3) HTN

179
Q

How can you treat a patient with anaemia due to chronic kidney disease/

A

ESA (erythropoietin stimulating agent) e.g. EPO alpha/beta or Darbopoietin (Aranesp)

180
Q

What types of ESA are there

A

EPO alpha
EPO beta
Darbopoietin (aranesp) `

181
Q

What is the condition where you have osteoclat resorption of calcified bone leading to replacement with fibrous tissue?

A

Osteitis fibrosa

182
Q

What is the most important consequence of chronic kidney disease?

A

Cardiovascular disease - GFR directly predicts risk of CVS event (reduced below 60 is where it starts!)

183
Q

What is the active from of vit D

A

1,25-(OH_2 dihydroxycholecalciferol

184
Q

What should ou always check if there is hypercalcaemia/

A

PTH - is it suppressed?

185
Q

If PTH is suppressed in hypercalacaemia what should you suspect?

A

MALIGNANCY

186
Q

What should you suspect if PTH is not suppressed in hypercalcaemia?

A

primary hyperparathyroidism - the high calcium should normally suppress the parathyroid gland production of PTH so this is an abnormal response showing something wrong with the regulatory system.

187
Q

What is a rare cause of hypercalcaemia without PTH suppression?

A

Familial hypocalciuric hypercalcaemia

188
Q

in which receptor is there a mutation in Familial hypocalciuric hypercalcaemia

A

the calcium sensing receptor on parathyroid gland - CaSR

189
Q

What is the order of the layers of the adrenal gland from outside to in?

A

Outside = zona glomerularis
Zona fasciculata
Zona reticularis
Medulla

190
Q

What do the medulla, zona fasciculata and Zona glomerulosa of the adrenal produce

A 
medulla = adrenaline
fasciculata = cortisol 
glomerulosa = aldosterone
191
Q

What are the 3 classic lab findings for addisons?

A

Low Na+
Low Glucose
High K+

++ ADDisons

192
Q

What is the name of the combination of primary hypotthyroidism and addisons?

A

Schmidt’s syndrome (old)

now polyglandular autoimmune syndrome

193
Q

what test should you do to confirm addisons disease

A

Synacthen test

194
Q

what are the 3 important differentials for adrenal mass with hypertension

A

Cushings
Conns
Phaeochromocytoma

195
Q

what is a phaeochromocytoma

A

tumour in the adrenal medulla causing increased production of catecholamines like adrenaline

196
Q

what is the urgent treatment of a phaeo?

A

ALPHA BLOCKADE with phenoxybenzamine to stop arrythmias from pulses of adrenaline and death

197
Q

conn’s syndrome signs and symtpms

A

Hypertension
low potassium
High aldosterone, low renin

198
Q

treatment of conn’s

A

aldosterone antagonist

K+ SPARING diuretics e.g. spironolactone

199
Q

cushings DISEASE means

A

there is a PITUITARY tumour making too much ACTH

200
Q

causes of cushing’s syndrome

A
  • iatrogenic steroids
  • pituitary adenoma
  • adrenal tumour
  • Tumour secreting ectopic ACTH
201
Q

What are you looking for with a high dose dexamethasone suppression test?

A

Want to see a pituitaary response from the 2mg every 6h for 2 days –> get a drop in the ACTH of 50% then it must be pituitary, if not then the ACTH must be from somewhere else

202
Q

What are the 3 most common causes of Hypothyroidism?

A
  1. Hashimoto’s (autoimmune)
  2. Atrophy of the thyroid
  3. Post Grave’s (surgery etc)
203
Q

how do you manage hypothyroidism?

A

investigate the cause - look for anti thyroid peroxidase antibodies

  • check for other autoimmune conditions e.g Addisons (early morning cortisol) and Coeliac screen
  • Do an ECG - CVS risk
  • Give T4 (levothyroxine)
204
Q

Do you give T3 or T4 to treat hypothyroidism?

A

T4 - no evidence of more benefit of T3

205
Q

what are the top 3 causes of hyperthyroidism

A
  1. graves disease
    2, toxic multinodular goitre
  2. single toxic adenoma
    also subacute thyroiditis and postpartum thyroiditis
206
Q

Which causes of hyperthyroidism have a high uptake on a technetium scan?

A

Grave’s, toxic multinodular goitre ad single toxic adenoma

207
Q

What should you avoid when treating patients with Grave’s eye disease

A

Dont treat with radioactive iodine…. the autoantibodies to thyroid receptor also in the eyes and Tx can damage them

208
Q

How do you screen for medullary thyroid carcinoma

A

Calcitonin or CEA

209
Q

What is thyroglobulin a marker for

A

Thyroid cancer - used to screen for recurrance of a cancer post-surgery and Thyroxine

My Year 5 Pathology (5 decks)

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