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Chem Path Flashcards

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1
Q

Formula for anion gap

A

(Na + K) - (Cl + HCO3)

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2
Q

Normal anion gap

A

14-18

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3
Q

Causes of raised anion gap

A

K etoacidosis
U raemia
L actic acidosis
T oxins

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4
Q

What is the difference between osmolality and osmolarity?

A

Osmolality - measured (mmol/kg)

Osmolarity - calculated (mmol/L)

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5
Q

Osmolarity formula?

A

2(Na+K) + urea + glucose

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6
Q

Raised osmolar gap means?

A

Exogenous solutes in plasma ie raised anion gap due to toxins rather than K, U or L

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7
Q

In hyponatraemic pts who are hypovolaemic what does it mean if urinary sodium is <20?

A

NON renal cause

  • diarrhoea
  • vomiting
  • sweating
  • burns
  • 3rd spacing eg ascites
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8
Q

In hyponatraemic pts who are hypovolaemic what does it mean if urinary sodium is >20?

A

Renal cause

  • diuretics
  • salt losing enteropathy
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9
Q

When does central pontine myelinolysis present?

A

2-6 days after correcting hyponatraemia too quickly

Increase in Na makes water move out of cells disrupting BBB and allowing entry of cytotoxic cells

  • quadriplegia
  • dysarthria
  • seizures
  • coma
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10
Q

SIADH diagnosed by:

A

Paired plasma and urine osmolality:

Plasma osmolality LOW
Urine osmolality HIGH

+ raised urinary sodium >20

In absence of heart, thyroid or adrenal disease (diag of exclusion)

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11
Q

Treatment for SIADH

A

1 fluid restrict

2 demeclocycline (decreases tubular response to ADH)

3 tolvaptan (V2 antag)

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12
Q

Causes of nephrogenic DI

A

Inherited receptor defect

Lithium

Hypokalaemia

Hylercalcaemia

Chronic renal failure

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13
Q

Treatment for DI

A

Fluid replacement
5% dextrose
0.9% NaCl

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14
Q

Stimuli for aldosterone secretion:

A

1 Ang II

2 raised serum K+

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15
Q

Causes of HYPOkalaemia

A

-GI loss (d and v)

  • Renal loss
    - conn’s (hyperaldosteronism)
    - cushing’s (xs cortisol can act of MR)
    - increased sodium delivery to DCT
    - Bartter syn
    - frusemide
    • type 1 and 2 renal tubular acidosis
      - type 1 cannot excrete H so K not exchanged and reabsorbed)
      - type 2 leak of HCO3
  • Redistribution into cells
    - alkalosis
    - insulin
    - beta agonists
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16
Q

Symptoms of HYPOkalaemia

A

Weakness

Arrhythmias

Polyuria and polydipsia (causes nephrogenic DI)

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17
Q

Treatment for HYPOkalaemia

A

Mod 3-3.5 Oral sandoK

Sev. <3
IV potassium chloride

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18
Q

Causes of HYPERkalaemia

A

Increased intake

  • oral
  • blood transfusion

Transcellular

  • acidosis
  • lack of insulin
  • tissue damage (rhabdo)

Decreased excretion

  • renal failure (low GFR so not excreted)
  • ACEi
  • ARBs
  • addisons
  • spironolactone (MR antag)
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19
Q

Treatment of HYPERkalaemia

A

“Small P big T widened QRS”

10ml 10% calcium gluconate

50ml 20% dextrose + insulin

Nebulised salbutamol

*calcium gluconate does NOT reduce potassium but stabilised cardiomyocyte membrane

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20
Q

AST:ALT. 2:1

A

Alcoholic hepatitis

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21
Q

AST:ALT. 1:1

A

Viral hepatitis

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22
Q

AST:ALT. 1:1

+raised gamma GT

A

NAFLD

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23
Q

Best marker of liver function?

A

Prothrombin time

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24
Q

Isolated raised gamma GT

A

Alcohol binge

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25
Q

Raised AST and ALT over 1000

A

?paracetamol toxicity

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26
Q

Half life of albumin?

A

20 days

If albumin LOW suggests chronic disease

Low in

  • liver disease (not produced)
  • renal disease (lost across epithelium)
  • sepsis (3rd spacing)
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27
Q

Aldosterone acts on?

A

Mineralocorticoid receptor

(Inbits Nedd4 to increase expression of Na channels at apical membrane and Na/K ATPase at basolateral

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28
Q

Physiological raised ALP?

A

Pregnancy (3rd T, produced by placenta)

Childhood (growth spurt)

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29
Q

Pathological raised ALP?

A

> 5x ULN
Bone - Pagets, osteomalacia

Liver- cholestasis, cirrhosis

<5xULN
Bone-tumour, fracture, osteomyelitis
Liver- hepatitis

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30
Q

Raised amylase

A

Acute pancreatitis (>10xULN)

Mumps

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31
Q

Creatine kinase is a marker of?

A

Muscle damage

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32
Q

CK in skeletal muscle?

In cardiac muscle?

In brain?

A

MM

MB (1 and 2)

BB

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33
Q

CK raised physiologically in?

A

Afro C

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34
Q

Ck raised pathologically in?

A

Duchenne muscular dystrophy

MI

Statin related myopathy

Rhabdomyolysis

(Excessive exercise)

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35
Q

ALP produced by what cells?

A

Liver
Bone
Gut
Placenta

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36
Q

Troponin is?

A

Not an enzyme - biomarker of cardiac injury

Troponin I better than T

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37
Q

When do you measure troponin?

When is it most sensitive?

How long does it stay elevated for?

A

0 (baseline), 6 and 12 hours

Most sensitive 12
- 24 hours

Elevated for 3-10 days therefore Ck-MB better for re-infarction

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38
Q

Diagnostic criteria for acute MI?

A

Rise in Troponin or Ck-MB and one of:

  • ischaemic Sx
  • pathological Q waves on ECG
  • ST changes on eCG
  • coronary artery intervention
  • post mortem pathology
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39
Q

What is the pattern of ck-MB rise in MI?

A

Increases 6-12 hours post MI

Peak at 24h

Return to normal by 48 hours

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40
Q

What is the calcium status of most patients with renal stones?

A

NORMOcalcaemic

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41
Q

Causes of stones:

A

1 hyperoxaluria

2 hypercalciuria

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42
Q

Prevention of stones:

A
  • avoid dehydration
  • reduce oxalate intake
  • maintain calcium intake
  • thiazide diuretics remove calcium from urine
  • alkalinise urine (citrate)
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43
Q

Most common stone?

A

Calcium -mixed 45%

Then calcium oxalate 35%

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44
Q

Radiolucent stones?

A

Uric acid

Cysteine

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45
Q

Struvite stones aka Staghorn are associated with?

A

Klebsiella and proteus infection (urea splitting organisms)

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46
Q

Rate limiting step of lipoprotein metabolism in liver?

A

HMG coA reducatase

Converts mevalonic acid to cholesterol
Inhibited by statins

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47
Q

Main cholesterol carrier?

A

LDL (70%)

Transports cholesterol from liver to periphery

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48
Q

Lipoproteins in order of density?

A 
Chylomicron (LEAST)
FFA
VLDL
IDL
LDL
HDL (MOST)
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49
Q

Cholesterol converted to bile acids by?

A

7alpha hydroxylase

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50
Q

Cholesterol converted to cholesterol ester by?

A

ACAT

51
Q

HDL converted to VLDL by?

A

CETP

Cholesterol ester transfer protein

52
Q

BMI classes?

A

<18 underweight
18-24 normal
25-30 overweight
30+ obese

53
Q

Statins?

A

HMG coA reductase inhibitors
Can reduce cholesterol 50% by reducing endogenous synthesis in liver

s/e statin related myopathy (raised ck)

+GI disturbance
+rash
+insomnia

54
Q

Ezetimide?

A

Cholesterol absorption blocker

55
Q

Fibrates?

A

Increase lipoprotein lipase, apo A1 and apoA5

Decrease VLDL secretion

s/e
Myositis
Gallstones

56
Q

Bile acid sequestrants?

A

E.g. Colestyramine

Prevent reabsorption via enterohepatic circulation

S/e constipation
Reduced Vit ADEK absorption

57
Q

Anti - PCSK9 mab ?

A

Lowers LDL levels by preventing degradation of LDL R (so more LDL taken up from blood by liver)

58
Q

Vitamin A?

  • name
  • deficiency
  • excess
A

Retinol

Colour blindness, dry skin, Bitot’s spots (keratin)

Hepatitis
Teratogenic

59
Q

Vitamin D?

  • name
  • deficiency
  • excess
A

Active - calcitriol
Synth in skin - cholecalciferol (D3)
Plan - ergocalciferol (D2)

Osteomalacia/Ricketts

Hypercalcaemia

60
Q

Vitamin E?

  • name
  • deficiency
A

Tocopherol

Neuropathy (ataxia, areflexia)

61
Q

Vitamin K?

  • name
  • deficiency
  • test
A

Phytomenadione

Defective clotting (low 2,7,9,10 and protein C and S)
Bruising
Haemorrhagic disease of newborn

Test = prothrombin time

62
Q

Vitamin B1?

  • name
  • deficiency
  • excess
  • test
A

Thiamine

Beri Beri 
    Wet - oedema and heart failure
     Dry - Neuro Sx
Neuropathy
Wernicke's
     1confusion
      2ataxia
        3 opthalmoplegia
(Progression to korsakoffs if +confabulation and amnesia which would be irreversible)
GIVE PABRINEX

Test = RBC transketolase

63
Q

Vitamin B2?

  • name
  • deficiency
  • test
A

Riboflavin

Glossitis and dry mucous membranes

Test = RBC glutathione reductase

64
Q

Vitamin B3?

  • name
  • deficiency
A

Niacin

3 Ds of pellagra

  • dementia
  • diarrhoea
  • dermatitis (casal’s necklace)
65
Q

Vitamin B6?

  • name
  • deficiency
A

Pyridoxine

Dermatitis, sideroblasric anaemia, neuropathy (isoniazid)

Test = RBC AST activation

66
Q

Vitamin B12?

  • name
  • deficiency
A

Cobalamin

Pernicious anaemia
Subacute combined degen of cord

67
Q

Vitamin C?

  • name
  • deficiency
A

Ascorbate

Scurvy - bleeding gums, poor wound healing

Excess vit C assoc renal stones

68
Q

Folate deficiency?

A

Megaloblastic anaemia
And neural tube defect

*folate = vitamin B9

69
Q

Commonest type of thyroid cancer?

A

Papillary

70
Q

Thyroid cancer that produces calcitonin?

A

Medullary (assoc Men2)

71
Q

Thyroid cancer assoc chronic hashimotos?

A

Lymphoma (MALT)

72
Q

Formula for hydrogen ion conc.

A

H+ = k x CO2/HCO3

Where k = 180

73
Q

Is caeruloplasmin high or low in wilson’s?

A

Low

74
Q

Thyroid cancer with worst prognosis?

A

Anaplastic

75
Q

What are the purines?

A

Adenosine, guanine, inosine

76
Q

Purines –> ? –> ? –> ?

A

Purines –> hypo xanthine –> xanthine –> urate

  • catalysed by xanthine oxidase
  • in animals urate converted to allantoin (highly soluble) but not in humans
77
Q

Functional excretion of uric acid?

A

10%

78
Q

Purine synthesis pathway?

A

Salvage pathway

Rate limiting step = PAT

*HPRT transfers hypoxanthine and guanine back to inosinic acid

79
Q

Enzyme deficiency in Lesch Nyan syndrom?

A

HPRT

80
Q

Features of Lesch Nyan?

A

X linked

Normal at birth
Developmental delay at 6mo
Hyperuricaemia –> gout
SELF MUTILATION

81
Q

Features of gout?

A

Monosodium urate crystals
NEEDLE SHAPED
NEGATIVELY BIREFRINGENT

Acute - podagra
(swollen v painful 1st mtp (big toe))

Chronic - tophaceous

82
Q

Gout management?

A

Acute:

  • NSAIDs
  • colchicine

Chronic:

  • hydration
  • allopurinol
  • probenecid (increased renal excretion urate)
83
Q

How does allopurinol work?

A

Inhibits xanthine oxidase

84
Q

S/e of allopurinol?

A

Increases toxicity of azathioprine

85
Q

Pseudogout crystals?

A

BRICK SHAPED

POSITIVELY BIREFRINGENT

86
Q

Where does pseudogout typically affect?

A

Knee

87
Q

Treatment of pseudogout?

A

Self limiting 1-3 weeks

88
Q

Why does aspirin worsen gout?

A

Competes directly with urate for renal excretion

89
Q

Why does ETOH cause gout?

A

Activates salvage pathway leading to hyperuricaemia and decreases renal urate excretion

90
Q

When does newborn screening programme take place?

A

Days 5-9

91
Q

Band keratopathy?

A

In eye secondary to chronic hypercalcaemia

92
Q

HONK?

A

Hyperglycaemia + hypersomolality but NO ketones

*associated with T2DM where insulin present therefore no ketones

93
Q

Metformin?

A

Insulin sensitizer

*least weight gain

94
Q

Sulphonylurea?

A

E.g. Gliclazide

Increased insulin secretion

95
Q

Pioglitazone?

A

PPARa agonist

Insulin sensitizer

96
Q

GLP-1 analogues?

A

Incretins eg exenatide

97
Q

Gliptins

A

DPP4 inhibitors

98
Q

Normal GFR?

A

120 ml/min

*7.2 L/hr

99
Q

Clearance?

A

Vol of plasma that can be completely cleared of a marker substance per unit time

  • not bound to plasma proteins
  • freely filtered
  • not secreted or reabsorbed by tubule
100
Q

Gold standard for GFR?

A

Inulin

101
Q

Clinical measure used rarely eg pre chemo when accuracy needed?

A

51Cr EDTA

102
Q

Most common clinical measure of GFR?

A

Creatinine

But actively secreted by tubular cells

103
Q

Equations for eGFR?

A

Cockcroft Gault

MDRD

cKD Epidemiology Collaboration 2009

104
Q

New alternative marker of

GFR?

A

Cystatin C

*but not offered by all labs

105
Q

Top causes of AKI?

A

1 renal hypoperfusion
2 drugs
3 contrast
4 sepsis

106
Q

Stages of chronic kidney disease?

A 
1 GFR 90+
2 60-90
3 30-60
4 15-30
5 <15 or on dialysis (ESKD)
107
Q

Top causes of CKD?

A

1 diabetes

2 atherosclerotic renal disease

3 HTN

108
Q

Complications of CKD?

A

Metabolic acidosis

Hyperkalaemia

Anaemia of chronic disease (low EPO production when GFR<30)

Uraemia

Vascular calcification (high phosphate beings calcium and deposits)

Renal bone disease

109
Q

How does CKD affect vitamin D?

A

Osteomalacia (reduced Vit D activation)

*reduced Vit D and high retained phosphate cause secondary hyperparathyroidism

110
Q

What is osteitis fibrosia?

A

Osteoclastic resorption of bone and replacement by fibrous tissue

111
Q

Cortisol produced from?

A

Zona fasciculata of adrenal cortex

*hypothalamus (CRH) -> pituitary (ACTH) -> cortisol in circadian rhythm (high am, low Pm)

112
Q

Aldosterone from?

A

Zona glomerulosa (most peripheral adrenal cortex)

113
Q

Order of hormones lost in panhypopituitarism?

A 
LH/FSH
GH
TSH
ACTH
prolactin (last)
114
Q

Hyperprolactinaemia treatment?

A

DA agonists

Bromocriptime, cabergoline

S/e psychotic sx

115
Q

Type 1 crigler najjar?

A

Complete UDPGT deficiency

*unconjugated BR jaundice from birth -> kernicterus

116
Q

Type 2 crigler Najjar?

A

Partial UDPGT def

117
Q

Haem is a?

A

Tetrapyrole with Fe2+ core

118
Q

What cells do porphyrias affect?

A

Erythroid and liver

119
Q

ALA synthase deficiency

A

NOT a porphyria

Causes x linked sideroblastic anaemia

120
Q

PBG synthase def

A

Plumboporphyria

121
Q

HMB synthase (aka PBG deaminase) def.

A

Acute intermittent porphyria

122
Q

Diagnosing AIP?

A

Raised urinary ALA and PBG

  • PBG oxidised to prophobilin = port wine urine
  • neurovisceral sx ONLY as no build up of porphyrinogen
123
Q

“Black liver”

A

Dubin Johnson

124
Q

Treatment for AIP?

A

IV dextrose
Haem arginate

*haem is negative feedback to switch off ALA synthesis

Chem Path (2 decks)

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