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Pathology > Chemical Pathology- Part 2 (p85-100- Adrenals, calcium, enzymes, nutrition, metabolic disorders, sugar, paeds + renal) > Flashcards

Chemical Pathology- Part 2 (p85-100- Adrenals, calcium, enzymes, nutrition, metabolic disorders, sugar, paeds + renal) Flashcards

1
Q

What are the common causes of Cushing’s syndrome?

A

Pituitary tumour- Cushing’s disease 85%
Adrenal tumour 10%
Ectopic ACTH producing tumour 5%
Iatrogenic steroid use

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2
Q

Common symptoms and signs of Cushing’s?

A 
Moon face
Buffalo hump
Striae
Acne
HTN
Diabetes
Muscle weakness- proximal myopathy
Hirsutism
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3
Q

What are the investigations to diagnose Cushing’s?

A

Low dose dexamethasone- 0.5mg- will fail to suppress cortisol in all causes of Cushing’s
High dose dexamethasone 2mg- will suppress pituitary cushing’s

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4
Q

How do you treat Cushing’s?

A

Treat underlying disease- e.g. surgical removal of lesion

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5
Q

What causes Addison’s?

A 
Autoimmune 
TB
Tumour mets
Adrenal
Haemorrhage
Amyloidosis
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6
Q

What are the symptoms and signs of Addison’s?

A 
Increased K+
Decreased Na+ + Glucose
Postural hypotension
Skin pigmentation
Lethargy
Depression
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7
Q

What investigations are used to diagnose Addison’s?

A

SynACTHen test

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8
Q

How do you treat Addison’s?

A

Hormone replacement- hydrocortisone/fludrocortison if primary lesion

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9
Q

What causes Conn’s?

A

Adrenal tumour

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10
Q

What are the symptoms and signs of Conn’s?

A

Uncontrollable HTN
Raised Na+
Decreased K+

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11
Q

What investigations are used to diagnose Conn’s?

A

Aldosterone:Renin ratio high

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12
Q

How do you treat Conn’s?

A

Aldosterone antagonists/potassium sparing diuretics- spironolactone, eplerenone, amiloride

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13
Q

What causes phaeo?

A

Adrenal medulla tumour leading to increased adrenaline

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14
Q

What are the symptoms and signs of phaeo?

A

Hypertension
Arrhythmias
Death if untreated

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15
Q

What investigations are used to diagnose phaeo?

A

Plasma and 24h urinary metadrenaline measurement/catecholamines + VMA (vanillylmandelic acid)

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16
Q

How do you treat phaeo?

A

Alpha blockade
Beta blockade
Surgery when blood pressure is well controlled

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17
Q

What is phenytoin used to treat?

A

Seizures

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18
Q

What is digoxin used to treat?

A

Arrhythmias

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19
Q

What is lithium used to treat?

A

Relapse of mania in BPAD

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20
Q

What are the signs of phenytoin toxicity?

A

Ataxia and nystagmus

Treated with omission or reduction of dose

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21
Q

What are the signs of digoxin toxicity and how is it treated?

A

Arrhythmias
Heart block
Confusion
Xanthopia (seeing yellow)

Treated with digibind aka digoxin immune Fab

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22
Q

What are the signs of lithium toxicity?

A 
Tremor (early)
Lethargy
Fits
Arrhythmia
Renal failure- treated with haemodialysis
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23
Q

What are the signs of gentamicin toxicity?

A

Tinnitus
Deafness
Nystagmus
Renal failure

Treated with omission or reduction of dose

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24
Q

What are the signs of theophyline toxicity?

A

Arrhythmia
Anxiety
Tremor
Convulsions

Treated with omission or reduction of dose

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25
Q

Normal plasma range of calcium?

A

2.2-2.6mmol/l

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26
Q

How does calcium exist in the blood in terms of bound/free etc?

A

45% ionised (free- biologically active)

50% bound to albumin, therefore affected by albumin level- use corrected calcium

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27
Q

What does Parathyroid Hormone (PTH) do?

A

Increased tubular 1a hydroxylation of vit D (25(OH)D) to form calcitriol
Mobilises calcium and PO4 from bone
Increased renal calcium reabsorption
Increased renal phosphate excretion

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28
Q

What does calcitriol (1,25 (OH)2D) do?

A

Increased calcium and phosphate absorption from the gut

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29
Q

What causes PTH release?

A

Decreased plasma Ca

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30
Q

What is the primary defect in 1’ hyperparathyroidism?

A

Increase of PTH (80% parathyroid adenoma)

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31
Q

What is the primary defect in 2’ hyperparathyroidism?

A

Renal osteodystrophy

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32
Q

What is the primary defect in 3’ hyperparathyroidism?

A

Autonomous PTH secretion post renal transplant

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33
Q

What is the primary defect in hypoparathyroidism?

A

Low levels of PTH
1’- DiGeorge syndrome
2’- Post-thyroid surgery

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34
Q

What is the primary defect in Rickets/osteomalacia?

A

Vit D deficiency

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35
Q

What is the primary defect in osteoporosis?

A

Bone loss

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36
Q

What would you see in 1’ hyperparathyroidism in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Increased Ca
Decreased PO4
Increased/Normal PTH
Increased/Normal ALP
Normal Vit D
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37
Q

What would you see in 2’ hyperparathyroidism in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Decreased/Normal Ca
Increased PO4
Increased PTH
Increased ALP
Normal Vit D
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38
Q

What would you see in 3’ hyperparathyroidism in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Increased Ca
Decreased PO4
Increased PTH
Increased/Normal ALP
Normal Vit D
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39
Q

What would you see in hypoparathyroidism in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Decreased Ca
Increased PO4
Decreased PTH
Decreased/Normal ALP
Normal Vit D
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40
Q

What would you see in Rickets/Osteomalacia in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Decreased Ca
Decreased PO4
Increased PTH
Increased ALP
Decreased Vit D
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41
Q

What would you see in Paget’s in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Normal Ca
Normal PO4
Normal PTH
Increased ALP
Normal Vit D
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42
Q

What would you see in osteoporosis in terms of Ca, PO4, PTH, ALP + Vit D?

A 
Normal Ca
Normal PO4
Normal PTH
Normal ALP
Normal Vit D
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43
Q

What are the causes of hypocalcaemia with increased phosphate?

A

CKD
Hypoparathyroidism (inc post-thyroid surgery)
Pseudohypoparathyroidism
Hypomagnesaemia

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44
Q

What are the causes of hypocalcaemia with normal or decreased phosphate?

A

Osteomalacia
Acute pancreatitis
Overhydration
Respiratory alkalosis

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45
Q

Symptoms of hypocalcaemia?

A

Perioral paraesthesia
Carpopedal spasm
Neuromuscular excitability- Chvostek’s + Trousseau’s

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46
Q

What is Chvostek’s sign?

A

Abnormal reaction due to stimulation of facial nerve due to existing nerve hyperexcitability in hypocalcaemia

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47
Q

What is Trousseau’s sign?

A

Carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes in hypocalcaemia

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48
Q

What is the treatment of mild and severe hypocalcaemia?

A

Mild- give calcium

Severe- 10% calcium gluconate IV

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49
Q

Causes of hypercalcaemia?

A

Dehydration
Primary or tertiary hyperparathyroidism
With raised ALP and phosphate- Bone mets, thyrotoxicosis + sarcoidosis
With normal ALP and raised phosphate- myeloma, excess vit D, sarcoid, milk alkali syndrome

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50
Q

Symptoms of hypercalcaemia?

A 
Stones (renal)
Bones (Pain)
Groans (psych)
Moans (abdo pain)
Polyuria
Muscle weakness
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51
Q

How do you treat hypercalcaemia?

A

Correct dehydration
Bisphosphonates
Correct cause e.g. chemo for cancer

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52
Q

What are the RFs for renal stones?

A

Dehydration
Abnormal urine PH (meat intake, renal tubular acidosis)
Increased excretion of stone constituents
Urine infection
Anatomical abnormalities

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53
Q

What are the common constituents of renal stones?

A 
Calcium- mixed 45%
Calcium oxalate 35%
Calcium phosphate 1%
Triple phosphate "Struvite" 10%
Uric acid 5%
Cysteine 1-2%
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54
Q

Which types of renal stones are radiolucent?

A

Uric acid

Cysteine

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55
Q

Which renal stones have a ‘staghorn’ appearance

A

Triple phosphate “Struvite”

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56
Q

What marker would be 10x upper limit of normal serum levels in acute pancreatitis?

A

Amylase

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57
Q

What is Creatine Kinase a marker of?

A

Muscle damage

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58
Q

Which creatine kinase is a marker of skeletal muscle damage and which is a marker of cardiac muscle damage?

A

CK-MM = skeletal muscle

CK-MB (1+2)= cardiac muscle

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59
Q

What causes raised CK levels physiologically?

A

Race- Afro-Caribbean

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60
Q

What causes raised CK levels pathologically?

A

DMD (>10x ULN)
MI (>10x ULN)
Statin myopathy
Rhabdomyolysis

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61
Q

Where is alkaline phosphatase high in concentrations?

A

Liver
Bone
Intestine
Placenta

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62
Q

What are the physiological causes of raised ALP?

A

Pregnancy (3rd trimester)

Childhood during growth spurt

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63
Q

What are the pathological causes of raised ALP (Bone + Liver)?

A 
>5x ULN-
Bone- Pagets, Osteomalacia
Liver- Cholestasis, Cirrhosis
<5x ULN-
Bone- tumours, fractures, osteomyelitis
Liver- infiltrative disease + hepatitis
64
Q

What is the biomarker of myocardial injury?

A

Troponin I/T

65
Q

When do you test Troponin?

A

6h and 12h post onset of chest pain

66
Q

How long does Troponin remain elevated for?

67
Q

What is one international unit?

A

The quantity of enzyme that catalyses 1uMol of substrate in a minute- measure of MASS or CONCENTRATION

68
Q

What does PCSK9 do?

A

Binds LDLR and promotes its degradation leading to raised LDL
Loss of function mutation leads to low LDL- novel LDL-therapy is Anti-PCSK9 MAb

69
Q

Which vitamins are fat soluble?

70
Q

Which vitamins are water soluble?

A

B1 (thiamine), B2 (riboflavin), B6 (pyroxidine), B12 (cobalamin), C, Folate, B3 (Niacin)

71
Q

What does Vit A deficiency lead to?

A

Colour blindness

72
Q

What does Vit D deficiency lead to?

A

Osteomalacia/Rickets

73
Q

What does Vit E deficiency lead to?

A

Anaemia/neuropathy

?Malignancy/IHD

74
Q

What does vit K deficiency lead to?

A

Defective clotting

75
Q

What does excess vit A lead to?

A

Exfoliation

Hepatitis

76
Q

What does excess vit D lead to?

A

Hypercalcaemia

77
Q

What does vit B1 (thiamine) deficiency lead to?

A

Beri-Beri
Neuropathy
Wernicke syndrome

78
Q

How do you test vit K?

79
Q

What does B2 (riboflavin) deficiency lead to?

80
Q

What does B6 (pyroxidine) deficiency lead to?

A

Dermatitis/anaemia

81
Q

What does B6 excess lead to?

A

Neuropathy

82
Q

How do you test B2 (riboflavin)?

A

RBC glutathione reductase

83
Q

How do you test B6 (pyroxidine)?

A

RBC AST activation

84
Q

What does B12 deficiency lead to?

A

Pernicious anaemia

85
Q

How do you test B12?

86
Q

What does vit C deficiency lead to?

87
Q

What does excess vit C lead to?

A

Renal stones

88
Q

What does folate deficiency lead to?

A

Megaloblastic anaemia

Neural tube defect

89
Q

What does B3 (niacin) deficiency lead to?

A

Pellagra- 3Ds (Dementia, dermatitis, diarrhoea)

90
Q

What does iron deficiency lead to?

A

Hypochromic anaemia

91
Q

What does iron excess lead to?

A

Haemochromatosis

92
Q

What does iodine deficiency lead to?

A

Goitre

Hypothyroid

93
Q

What does zinc deficiency lead to?

A

Dermatitis

94
Q

What does copper deficiency lead to?

95
Q

How do you test copper?

A

Cu

Caeroplasmin

96
Q

What is the Guthrie blood spot test and what does it test for?

A

Heel prick in neonates to screen for serious conditions, mainly metabolic e.g. CF, phenylketonuria, congenital hypothyroidism, medium chain acylcoA dehydrogenase deficiency

97
Q

What causes phenylketonuria?

A

Phenylalanine hydroxylase deficiency

98
Q

How do you screen for phenylketonuria?

A

Phenylalanine levels

99
Q

What happens in cystic fibrosis?

A

Mutation in CFTR- viscous secretions -> ductal blockages

100
Q

How do you screen for cystic fibrosis?

A

Immune reactive trypsin

If positive -> DNA mutation detection

101
Q

What happens in medium chain acylcoA dehydrogenase deficiency?

A

Fatty acid oxidation disorder

102
Q

How do you screen for medium chain acylcoA dehydrogenase deficiency?

A

Acylcarnitine levels by tandem mass spectrometry

103
Q

What is the definition of specificity?

A

The probability in % that someone without the disease will correctly test negative
TN/FP+TN

104
Q

What is the definition of sensitivity?

A

Probability that someone with the disease tests correctly positive
TP/TP+FN

105
Q

What is the definition of PPV?

A

Probability that someone who tests positive actually has the disease
TP/TP+FP

106
Q

What is the definition of NPV?

A

Probability that someone who tests negative actually doesn’t have the disease
TN/TN+FN

107
Q

What are the 5 different groups of metabolic conditions?

A 
1- Accumulation of toxins
2- Reduced energy stores
3- Large molecule synthesis
4- Defects in large molecule metabolism 
5- Mitochondrial
108
Q

Give examples of metabolic conditions with accumulation of toxins?

A

Organic acidaemias
Urea cycle disorders
Aminoacidopathies (e.g. PKU + maple syrup urine disease)

109
Q

Give examples of metabolic conditions with reduced energy stores?

A

Glycogen storage disorders (Von Gierke’s)
Galactossaemia
Fatty acid oxidation disorders (MCADD)

110
Q

Give examples of metabolic conditions with large molecule synthesis problems?

A

Peroxisomal disorders

Glycosylation disorders

111
Q

Give examples of metabolic conditions with defects in large molecule metabolism?

A

Lysosomal disorders e.g. Tay Sachs disease

112
Q

Give examples of metabolic mitochondrial conditions?

A

MELAS
Kearn’s
Sayre
POEMS

113
Q

What are the key features of organic acidaemias?

A

High urea + ketones
Metabolic acidosis
Funny smells

114
Q

How do you treat organic acidaemias?

A

Low protein diet, acylcarnitine + haemofiltration

115
Q

What are the key features of urea cycle disorders?

A

High ammonia leading to encephalopathy + developmental delay
Resp alkalosis
Vomiting
?Diarrhoea

116
Q

How do you treat urea cycle disorders?

A

Low protein diet- stops urea formation

117
Q

What are the key features of aminoacidopathies?

A 
High phenylalanine
Blue eyes
Fair hair/skin
Retardation
MSUD- sweaty feet
118
Q

What are the key features of glycogen storage disorders?

A

Hypoglycaemia + lactic acidosis
Hepatomegaly
Developmental delay
Hepatoblastoma risk

119
Q

How do you treat glycogen storage disorders?

A

Regular CHO

120
Q

Key features of galactossaemia?

A

Increased Gal-1 phosphate levels cause cataracts
Hypoglycaemia
Neonatal jaundice

121
Q

How do you treat galactossaemia?

A

Treat with low lactose/galactose

122
Q

Key features of fatty acid oxidation disorders?

A

Hypoglycaemia
Cardiomyopathy
Rhabdomyolysis
Low ketones

123
Q

How do you treat fatty acid oxidation disorders?

A

Regular carbs

124
Q

What are the key features of peroxisomal disorders?

A 
Poor feeds
Seizures
Retinopathy
Hepatomegaly
Mixed hyperbiliribinaemia
125
Q

How do you screen for glycosylation disorders?

A

Measure serum transferrins

126
Q

What are the key features of lysosomal disorders?

A

Very slow progress
Neuroregression
Hepatomegaly
Cardiomyopathy

127
Q

How do you test for lysosomal disorders?

A

Test urine mucooligopolysaccharides + WBC enzyme levels

128
Q

How is DM diagnosed?

A

Typical symptoms plus one of fasting glucose >7, OGTT >11.1 or random glucose>11.1, or without symptoms but with 2 of the above tests
NICE also recommends you use HbA1C>48

129
Q

What is the definition of impaired glucose tolerance?

A

Random or OGTT >7.8 but <11.1

130
Q

What is the definition of impaired fasting glucose?

A

Fasting glucose >6.1 but <7

131
Q

In which type of DM are DKA more common?

132
Q

In which type of DM are hyperosmolar hyperglycaemic state (HHS) more common?

133
Q

What are the HHS criteria?

A

pH >7.3
Osmolarity >320mOsm
Blood Glucose > 30mM
Develops over few dats

134
Q

What are the DKA criteria?

A

pH<7.3
Plasma glucose >11mM
Blood ketones >3mM
DKA- rapid

135
Q

What are causes of hyperinsulinaemic hypoglycaemia?

A

Iatrogenic insulin
Sulfonylurea excess
Insulinoma

136
Q

What are causes of hypoinsulinaemic hypoglycaemia?

A

+ve ketones- alcohol binge, no food, pituitary insufficiency, Addison’s, liver failure
-ve ketones- Non-pancreatic neoplasms- fibrosarcomata, fibromata

137
Q

What would you see in blood tests for non-islet tumour hypoglycaemia?

A

Low glucose, insulin, C-peptide, FFA and ketones

138
Q

What causes non-islet tumour hypoglycaemia?

A

Tumour causes paraneoplastic syndrome secreting big IGF-2 which binds to IGF-1 and insulin receptors

139
Q

What common problems originate from low birth weight?

A 
Respiratory distress syndrome
Retinopathy of prematurity
Intraventricular haemorrhage
Patent ductus arteriosus
Necrotising enterocolitis (inflammation of bowel wall)- necrosis and perforation
140
Q

Why does renal function differ in babies compared to adults?

A

Functional maturity only at 2yo
Low GFR for SA
Less reabsorption due to short proximal tubule
Reduced concentrating ability due to short loops of Henle + DCTs
Persistent sodium loss due to distal tubule being aldosterone insensitive

141
Q

Why is there high insensible water loss in babies compared to adults?

A

High SA:BW ratio
Skin blood flow is increased
Metabolic/respiratory rate is higher than adults
Transepidermal fluid loss (skin not the best barrier)

However hypernatraemia common in first 2w of life

142
Q

What would you suspect with jaundice within first 24h of life?

A

Acute haemolysis or sepsis

143
Q

What would you suspect with jaundice after 2wks of life?

A

Hepatobiliary failure

144
Q

What is normal GFR?

145
Q

What is renal clearance defined as?

A

Volume of plasma that can be completely cleared of a marker substance in a unit of time

146
Q

What is the gold standard measure of GFR?

147
Q

What is the problem with the use of inulin?

A

It requires steady state infusion and it is difficult to assay so reserved for research

148
Q

Which measure is used in clinical practice to measure renal function?

A

Creatinine- an endogenous marker

149
Q

What is the problem with the use of creatinine?

A

Very variable between individuals and muscular ppl have high creatinine

150
Q

What is the definition of an AKI?

A

A rise in serum creatinine over 26.5 in 48h or to 1.5x baseline in 48h
Can also be defined as urine output of less than 0.5ml/kg/hr

151
Q

What are the different causes of AKI?

A

Pre-renal- reduced renal perfusion with no structural abnormality
Renal- vascular, glomerular, tubular, interstitial
Post-renal- characterised by obstruction to urinary flow

152
Q

What emergency indications are there for dialysis?

A 
Pulmonary oedema
Refractory hyperkalaemia
Metabolic acidosis
Uraemic encephalopathy
Drug toxicity e.g. lithium
153
Q

5 stages of CKD?

A 
1- kidney damage with GFR>90
2- mild decrease in GFR 60-89
3- Moderate decrease in GFR 30-59
4- Severe decrease in GFR 15-29
5- End stage <15 or dialysis
154
Q

Commonest causes of CKD?

A 
Diabetes
Atherosclerotic renal disease
HTN
Chronic glomerulonephritis
Infective or obstructive uropathy
PKD
155
Q

What are the 4 main consequences of CKD?

A
  1. Progressive loss of homeostatic function- acidosis + hyperkalaemia
  2. Progressive failure of hormonal function- anaemia (loss of EPO synthesis) + Renal bone disease (2’ hyperparathyroidism due to low vit D)
  3. CVD- vascular calcification + atherosclerosis and uraemic cardiomyopathy
  4. Uraemia and death

Pathology (13 decks)

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