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Arjun's Copy- Owen's Path > Chemical Pathology > Flashcards

Chemical Pathology Flashcards

1
Q

What is normal concentration of H+

A

35-45nmol/L in ECF
pH= inverse log concentration of H+

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2
Q

How is H+ buffered

A

Bicarbonate is a weak acid which mops up H+ in the short term- long term the kidney needs to excrete H+ and regenerate bicarbonate ions

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3
Q

How is H+ buffered in RBC

A

Using haemoglobin

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4
Q

Main buffering equation

A

H+ + HCO3-= H2CO3 = H2O + CO2

carbonic acid
remember carbonic anhydrase enzyme converts H2O and CO2 into carbonic acid

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5
Q

What principles causes a metabolic acidosis and examples

A

Increased H+ production- DKA
Decreased H+ excretion- renal tubular acidosis
Loss of bicarb- intestinal fistula, diarrhoea

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6
Q

What do lungs do in metabolic acidosis

A

Hyperventilate to shift equation

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7
Q

What will see in compensated metabolic acidosis

A

Drop in CO2 with a compensated H+

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8
Q

How does body compensate for respiratory alkalosis

A

Will try to increase regeneration of bicarb- harder and slower to compensate metabolically so short term will not see increase in bicarb

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9
Q

What causes metabolic alkalosis

A

Increased H+ excretion (e.g. vomiting)
Can be potassium excretion too
Ingestion of bicarb

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10
Q

How is metabolic alkalosis compensated for

A

Hypoventilate

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11
Q

What causes respiratory alkalosis

A

Hyperventiation- panic attack, salicylates stimulate the brainstem early

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12
Q

What causes a loss of bicarb

A

Diarrhoea
High output stoma
Pancreatic fistula

RTA 2 - can’t reabs bicarb

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13
Q

What causes an increase in H+ production

A

DKA
Lactate
Ethylene glycol
Aspirin OD
Metformin
Uraemia

MUDPILES/KULT

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14
Q

What causes a reduction in H+excretion

A

Addisons (remember aldosterone causes Na+/H+ exchnager so loss of H+, so addison’s in opposite)
Renal failure- renal tubular acidosis

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15
Q

What causes a metabolic alkalosis

A

Hypokalaemia
H+ loss from vomiting
Bicarbonate ingestion

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16
Q

What do you get in an aspirin overdose

A

Can get mixed respiratory alkalosis and metabolic acidosis
alkalosis as stimulates resp centre
Increases excretion of bicarb

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17
Q

What are causes of addisons

A

TB
Autoimmune
Metastases
Adrenal haemorrhage
Amyloidosis

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18
Q

What causes adrenal haemorrhages

A

Meningococcal infections- waterhouse friederichsen syndrome

side note: most common cause of hyperaldosteronism is BL adrenal hyperplasia not conn’s

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19
Q

Blood findings of addisons

A

Low sodium
High K
Low glucose (key as lack glucocorticoid!)

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20
Q

Signs on examination of addisons

A

Skin pigmentation
Postural drop in BP

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21
Q

Test for addisons

A

Short synacthen test
Measure cortisol and ACTH then administer ACTH
Check the cortisol and 30 and 60 mins

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22
Q

Managmeent of addisons

A

Hydrocortisone/fludrocortisone if primary addisons

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23
Q

Presentation of conns

A

Uncontrollable HTN
High Na
Low K

most common cause of hyperaldosteronism is BL adrenal hyperplasia not conn’s

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24
Q

Investigation for conns

A

Plasma aldosterone:renin ratio will be higher

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25
Q

Managment for conns

A

Spironolactone-
Surgery if indicated

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26
Q

Presentation of phaeos

A

Severe transient hypertensionin young person
Arrythmias

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27
Q

Treatment of phaeos

A

Alpha blockade
Beta blockade
Surgery when BP controlled

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28
Q

Investigations for phaeos

A

Plasma and urinary 24 hour metanephrines/catecholamines/Vanillylmandelic acid (VMA)
Metanephrines are breakdown product
VMA in final synthesis step

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29
Q

How are inherited metabolic disorders screened for in the UK

A

Guthrie blood spot test on heel at 6 days old

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30
Q

What metabolic diseases are screened for in guthrie blood spot test

A

Congenital hypothyroidism
Cystic fibrosis (IRT)
Thalassaemias (some places) and haemoglobinopathies (SCD!)
Metabolic disorders
- isovalaeric acidaemia
- maple syrup disease (MSUD)
- PKU
- homocysteinuria
- MCADD
- glutaric aciduria type 1

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31
Q

What is the defect of phenylketonuria

A

Phenylanine hydroxylase deficiency which converts phenylalanine to tyrosine

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32
Q

What is screened for in phenylketonuria

A

Phenylalanine in the blood

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33
Q

What 2 metbaolites other than phenylalanine are raised in phenylketonuria and where

A

Phenylpyruvate in the blood
Phenylacetic acid in the urine

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34
Q

How is phenylketonuria treated

A

Phenylalanine replacement and amino acid supplements
Must be started in first 6 weeks of life

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35
Q

What is screened for in congenital hypothyroidism

A

TSH levels

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36
Q

What is screened for in CF

A

Immune reactive trypsin- must be above 99.5th centil 3 times
If positive then do genetics

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37
Q

What is MCAD and the pathophysiology

A

Medium chain acylCoA dehyodrogenase deficiency
Involved in fatty acid breakdown for glucose sparing metabolism

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38
Q

What is screened for in MCAD

A

Acylcartinine by tandem Mass spectometry

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39
Q

Triad for phenylketonuria

A

Mental retardation
Blonde hair
Blue eyes

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40
Q

Triad for homocysteinuria

A

Lens dislocation
Mental retardation
Thromboembolism

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41
Q

What do urea cycle disorders present with

A

Resp alkalosis
Vomiting (not diarrhoea)
Neuro encephalopathy
Dietary avoidance of things-e.g. proteins

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42
Q

How do you treat hyperammonaemia

A

Low protein diet

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43
Q

What is blood finding of urea cycle disorder

A

High ammonia as urea not being formed
Resp alkalosis

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44
Q

What are organic acidurias

A

A group of inherited metabolic disorders where acidic metabolites accrue in the blood/urine

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45
Q

What causes cheesy or sweaty smelling urine

A

Isovalaeric acidaemia

dont confuse with MSUD - sweet urine smell + sweaty feet

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46
Q

How do organic acidurias present

A

Depends on if neonate or later on
Neonates
- Unusual odour
- Truncal hypotonia
- Limb hypertonia
- Hyperammonaemia with metabolic acidosis high AG

Chronic intermitten form
- recurrent episodes of ketoacidosis, cerebral abnormalities
- Reye syndrome

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47
Q

What is Reye syndrome

A

Vomiting
Lethargy
Increased confusion
Resp arrest

liver and brain affected

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48
Q

What are triggers for Reye syndrome

A

Salicylates
Anti-emetics
Valproate

viral infections (eg VZV)
cuase unknown but ppl think it’s viral infection + aspirin

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49
Q

What is done in screen for Reye syndrome

A

Ammonia
Amino acids in blood and urine
Urine organic acids
Glucose and lactate
Blood spot carnitine

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50
Q

What is blood finding of MCAD

A

Hypoketotic hypoglycaemia as shows cant break down fats

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51
Q

Clinical associations of MCAD

A

Hepatomegaly
Cardiomyopathy

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52
Q

How is MCAD treated

A

Regular carbohydrates

never in fasting state

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53
Q

What is galactosaemia

A

A disorder of galactose metabolism where Gal-1-put is mutated leading to elevated levels of Gal-1-phosphate which causes kidney and liver disease

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54
Q

What is main pathological finding in galactossaemia

A

High neonatel conjugated bilirubin

metabolites interfere with BR conjugation for some reason high conj BR
enzyme missing in galactossaemia is GAL-1-PUT

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55
Q

Presentation of galactossaemia

A

Hypoglycaemia
Jaundice
Severe vomiting
Cataracts
Recurrent E coli infections

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56
Q

How to treat galactossaemia

A

Low galactose diet

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57
Q

What is Von gerkes disease

A

Glycogen storage disorder where cant break down glycogen so liver accumulates glycogen

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58
Q

Blood findings of von gierkes disease

A

Hypoglycaemia
Lactic acidosis
Neutropenia

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59
Q

Examination finding of von gierkes

A

Hepatomegaly
Nephromegaly

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60
Q

How are mitochondrial disorders diagnosed

A

Muscle biopsy

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61
Q

Which is predominant transporter of cholesterol in fasted state

A

LDL

lipoprotein with most cholesterol - jsut think - it’s the one that takes cholesterol to perioheral tissues
VLDL has most TGs, as once loses some TGs becomes LDL

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62
Q

Where does cholesterol come from in GI tract

A

Diet
Bile

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63
Q

Where are bile acids absorbed

A

Terminal ileum

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64
Q

Where is cholesterol absorbed

A

Jejunum

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65
Q

What is major transporter of triglycerides in fasting state

A

VLDL

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66
Q

Genes involved in FH

A

Dominant mutations of LDLR, APOB, PCSK9
Rarely get autosomal recessive-LDLRAP1

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67
Q

What are causes of primary hypercholesterolaemia

A

FH
Polygenic hypercholesterolaemia
Familial hyper alpha lipoproteinaemia
Phytosterolaemia

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68
Q

What is phenotype of familial hyper alpha lipoproteinaemia

A

Deficiency of CETP which results in high HDL- beneficial

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69
Q

Mutations seen in phytosterolaemia

A

ABC G5 and G8
These are proteins which prevent cholesterol absorption in the jejunum
If mutated get

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70
Q

What is function of PCSK9

A

Binds to LDLR and promotes degradation
Gain of function mutations cause FH
Loss of function are protective against CVD

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71
Q

What causes primary hypertriglyceridaemia

A

Familial type 1
Familial type V
Familial type IV

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72
Q

What causes familail type I hypertriglyceridaemia

A

Lipoprotein lipase or apoC II deficiency

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73
Q

What causes familail type IV hypertriglyceridaemia

A

increased synthesis of TG

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74
Q

What causes familail type V hypertriglyceridaemia

A

apoA V deficiency

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75
Q

Causes of primary mixed hyperlipidaemias

A

Familial combined hyperlipidaemia
Familial dys-beta-lipidaemia Type III
Familial hepatic lipase deficiency

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76
Q

What causes Familial dys-beta-lipidaemia Type III

A

Aberrant Apo E/2

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77
Q

What disease is famial dys-beta-lipidaemia assoicated with a risk of

A

Alzheimers

remember ApoE4 causes AD, apoE2 protects

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78
Q

Pathognomic sign of Familial dys-beta-lipidaemia Type III

A

Yellow palmar crease (palmar striae)

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79
Q

Secondary causes of hyperlipidaemia

A

Exogenous sex hormones
Hypothyroidism
Prengnacy
Nephrotic syndrome
Obstructive liver disease

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80
Q

What are causes of hypolipidaemia

A

Abeta-lipoproteinaemia
HypoBeta-lipoproteinaemia
Tangier disease
Hypo-alpha lipoproteinaemia

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81
Q

Pathophysiology of Abeta-lipoproteinaemia

A

MTP deficiency

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82
Q

Pathophysiology of HypoBeta-lipoproteinaemia

A

Truncated apoB protein

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83
Q

Pathophysiology of Tangier disease

A

HDL deficiency

remember pic of tonsils

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84
Q

Pathophysiology of Hypo-alpha lipoproteinaemia

A

ApoA-I mutations

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85
Q

Best drug for reducing TG

A

Fibrates

(work by increasing LPL activity - lower TGs, also increase HLD)

must check notes for summary page on lipid drugs!

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86
Q

Treatment for reducing high lipoprotein a

A

Nicotinic acid

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87
Q

MOA of statin

A

HMG-CoA reductase inhibitor
Reduces liver cholesterol synthetic function

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88
Q

Treatment for obesity

A

First line hypocaloric conservative
Medical- orlistat
Bariatric surgery, BMI>35

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89
Q

What other drug has been trialled for obesity but was disconitnued and why

A

Rimonabant- cannabinoid antagonist
Increased risk of suicide

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90
Q

What are 4 fat soluble vitamins and where stored

A

ADEK
Adipose

+ liver

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91
Q

Where are water soluble vitamins stored

A

Theyre not
In blood and pass through to urine

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92
Q

What is name for vit B1

A

Thiamine

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93
Q

What is name for vit B2

A

Riboflavin

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94
Q

What is name for Vit B6

A

Pyridoxine

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95
Q

What is name for vit B12

A

Cobalamine

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96
Q

What is deficiency of vit B1

A

Beri Beri
Wernickes
Neuropathy

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97
Q

Test for vit B1

A

RBC transketolase

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98
Q

Deficiency of Vit B2

A

Glossitis
Corneal ulceration

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99
Q

Test for B2

A

RBC glutathione reductase

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100
Q

Test for vit B6

A

RBC AST activation

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101
Q

Name for Vit C

A

Ascorbate

ascorbic acid

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102
Q

Vit C deficiency

A

Scurvy- bleeding gums, teeth can fall out, joint pain, low mood

corkscrew hairs

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103
Q

B6 deficiency

A

Skin changes
Sideroblastic anaemia

neuropathy also (isoniazid). Also excess causes neuopathy too!

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104
Q

B6 excess

A

Neuropathy

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105
Q

Vit C excess

A

Renal stones

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106
Q

What is B3

A

Niacin

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107
Q

Niacin deficiency

A

Pellagra- 3ds
Diarrhoea
Dementia
Dermatitis

casal’s necklace rash!

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108
Q

Test for B12

A

Serum B12

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109
Q

Test for folate

A

RBC folate

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110
Q

Test for Vit C

A

Plasma vit C

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111
Q

Tests for iron

A

FBC
Serum Fe
Ferritin

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112
Q

Iodine deficiency

A

Goitre
Hypothyroidism

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113
Q

Name for vit A
- deficiency
- excess
- test

A

Retinol
night blindness/Colour blindess
Hepatitis and exfoliation
Serum level

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114
Q

Name for vit D
- deficiency
- excess
- test

A

Cholecalciferol
- rickets or osteomalacia
- hypercalcaemia
- serum

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115
Q

Name for vitamin E
- deficiency
- test

A

Tocopherol
- anaemia, neuropathy, IHD risk later in life
- serum level

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116
Q

Name for vitamin K
- deficiency
- test

A

Phytomenadione
- defective clotting
- PTT

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117
Q

Zinc deficiency

A

Dermatitis

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118
Q

Copper deficiency
- excess
- test

A

Anaemia- as body absorbs less iron and osteoporosis
Wilsons
Cu and caeruplasmin

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119
Q

Fluoride deficiency
- excess

A

Dental caries
- flurosis white and borwn speckles on your teeth

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120
Q

What is best way to determine obesity in a clinical setting

A

Waist hip ratio- good for predicting adiposity and CHD risk
BMI affected by things such as race and muscle mass

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121
Q

What is cut off BMI for obesity

A

30
Minus 2.5 for south asia

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122
Q

What is marasmus

A

Deficiency in all macronutrients (i.e. protein + calorie)
- shrivelled
- retarded growth
- mscle wasting
- no subcut fat

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123
Q

What is kwashiorkor

A

Lack of protein where become oedematous

but normal/slightly reduced calorie intake

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124
Q

When do babies reach functional maturity of GFR

A

2 years
- babies born prior to 36 weeks wont have a full complement of nephrons

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125
Q

How do babies compare to adults in terms of total body water

A

Adults are 60%
Neonates 75%
Even higher in preterm (85%)
This is why babies lose weight in the first week of life

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126
Q

Why do neonates lose so much water

A

High surface are to body weight
Increased skin blood flow
Metabolic respiratory rate is higher than adults
Transepidermal fluid loss as skin isnt properly keratinised yet

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127
Q

How does CAH present in neonates

A

Addisonian crisis
Hypoglycaemia

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128
Q

What metabolite is raised in CAH

A

17-OH-progesterone

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129
Q

How is calcium transported in the blood

A

50% free
40% bound to albumin
10% to phosphate

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130
Q

How does PTH gland respond to hypocalcaemia

A

Increases calcium reabsorption in the kidney
Increases tubular hydroxylation of Vitamin D
Mobilises calcium from bone

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131
Q

How does PTH affect phosphate

A

Increases excretion of phosphate in kidney

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132
Q

What is difference between Vit D2 and D3

A

D2 is a plant vitamin
D3 is an animal synthesised
Both active

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133
Q

What is the stored and measured form of vitamin D

A

25-hydroxy-vitamin D

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134
Q

Actions of calcitriol

A

Intestinal calcium and phosphate absorption and same form kidney
Bone osteblast activity
Other actions- immune gene control therefore get deficiency associations with cancers and autoimmune disease

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135
Q

Risk factors for Vitamin D deficiency

A

Lack of sunlight
Dark skin
Diet
Malabsorption

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136
Q

What do you get in osteomalacia

A

Bone and muscle pain
Looser zones

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137
Q

What are looser zones

A

Pseudo fractures

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138
Q

Blood findings of Vit D deficiency

A

Low Ca and Po
Raised PTH and ALP
Low Vit D

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139
Q

Presentation of rickets

A

Bowed legs
Costochondral swelling
Widened epiphyseal areas wrists
Myopathy

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140
Q

Causes of osteomalacia

A

Renal failure
Anticonvulstants can cause vit D
Lack of sunlight
Chappatis (phytic acid high levels) - so less vit D absorbed?

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141
Q

Why get high ALP in osteomalacia

A

PTH gets raised which causes in excess bone resorption

so osteoblasts activated to fix resorbed areas releasing ALP

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142
Q

Classic fractures seen in osteoporosis

A

Colles fracture
Neck of femur
Vertebra

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143
Q

How is osteoporosis diagnosed

A

Using DEXA scan of wrist, lumbar spine and neck of femur
T score less than -2.5
Osteopenia between -1 and -2.5

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144
Q

What is T score vs Z score

A

T= healthy person comparison
Z= age matched control

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145
Q

What is the Z score used for

A

To idnetify bone loss in younger patinets

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146
Q

Risk factors for osteoporosis

A

Childhood illness (as never reached peak BMD)
Low Vit D
Early menopause
Long term steroids/ cushnigs, hyperprolactinaemia, thyrotoxicosis
Smoking
Alcohol

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147
Q

Treatment for osteoporosis

A

Lifestyle
- smoking and alcohol
- weight bearing alcohol
Drugs
- Vit D
- alendronate
- PTH analogue (toliperitide)
- oestrogen
- SERM (raloxifene)

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148
Q

What is alendronate
- side effect

A

Bisphophonate
- side effect= gastric irritation and so is low compliance

osteonecrosis of the jaw

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149
Q

What is example of PTH analogue

A

Teriparatide

150
Q

What should PTH be in hypercalcaemia

A

Zero

151
Q

Questions when get hypercalcaemia

A

Is it an anomaly- repeat test
Check PTH
If suppressed most likely cancer- then sarcoid etc
If high then hyperparathyroidism

152
Q

Causes of hypercalcaemia

A

Hyperparathyroidism- most common in young healthy and community
Cancer- most common in old and ill, in secondary care
Vit D excess
Sarcoid
Milk alkali syndrome

153
Q

Most common cause of hypercalcaemia

A

Primary parathyroidism

154
Q

Causes of primary hyperparathyroidism in order of likelihood

A

Single adenoma
Hyperplasia
Multiple adenomas- association with MEN1
Carcinoma

155
Q

Which bone most commonly affected in primary hyperparathyroidism

A

Wrist- get colles fracture

156
Q

What causes Familial hypocalcuric/benign Hypercalcaemia

A

Mutation in Calcium sensing receptor which means doesnt excrete PTH as early as should
Have mild hypercalcaemia naturally

157
Q

3 types of malignant hypercalcaemia

A

PTHrP from Sq cell lung cancer
Bone metastases
Haematological malignancy

158
Q

How does myeloma cause hypercalcaemia

A

Cytokines produced not infiltration

i.e. increases osteoclast activity but blasts not affected hence no rise in ALP

159
Q

What can causes excess vitamin D

A

Sunbeds
Too many tablets

160
Q

Treatment of hypercalcaemia

A

Fluids- normal saline as much as can give 4L daily
Bisphosphonates- if cause known to be cancer
Treat cause

161
Q

When is only time can give bisphosophonates in hypercalcaemia

A

If cancer is known to be cause

162
Q

Signs and symptoms of hypocalcaemia

A

Chvostek- tap face
Trousseau- BP cuff
Hyperrreflexia
Stridor - as can cause laryngospasm so breathing difficulty!
Convulsions

163
Q

ECG finding of hypocalcaemia

A

Prolonged QT

164
Q

Non PTH driven causes of hypocalcaemia

A

Vit D deficiency
CKD
PTH resistance

165
Q

PTH driven causes of hypocalcaemia

A

Post surgical (eg thyroidectomy)
Radiation
Mg deficiency
Auto-immune hypoparathyroidism

166
Q

What causes secondary hyperparathyroidism

A

CKD
Vit D deficiency

167
Q

Tertiary hyperparathyroidism causes

A

Prolonged secondary- mainly from dialysis
Renal transplant

168
Q

Symptoms of pagets disease

A

Focal pain
Warmth
Deformity
Fracture

169
Q

Complications of pagets

A

HF (high output)
Increased risk of malignancy
sensorineural hearing loss

170
Q

Treatment of pagets

A

Bisphosphonates

171
Q

Investigations for pagets

A

ALP
Nuclear scan/XR

172
Q

What causes renal osteodystrophy

A

Secondary hyperparathyroidism (from CKD)
Aluminium retained from CKD

173
Q

How does evolocumab affect prognosis in patients with known cardiovascular disease

A

Reduces incidence of events but not mortality
BUT….
Absolute risk reduction very small and very expensive to do so

174
Q

Who should evolocumab only be used in

A

Statin intolerant
Uncontrolled lipids like FH

175
Q

What is the legacy effect

A

Benefits persist from early intervention in glucose control
If have tight control later in disease course in those with established CVD disease can increase mortality

176
Q

What are the important physiological effects of SGLT2i

A

Reduce glucose, weight, waist circumfrence and BP

177
Q

What endocrine condition can be seen alongside addisons

A

Primary Hypothyroidism (Schmidt’s syndrome)
Due to concurrent autoimmune conditions

vitiligo, T1DM etc.

178
Q

Example of alpha blockade

A

Phenoxybenzamine

179
Q

1st line investigation for cushings

A

24 hour urinary cortisol
Overnight dexamethasone suppression test (LDDST)

180
Q

Presentation of cushings

A

Moon face
Buffalo hump
Striae
Acne
HTN
DM
Proximal myopathy
Hirsutism

181
Q

What is only aetiology which causes cushings disease

A

Pituitary tumours

182
Q

Causes of cushings

A

ACTH dependant- pituitary tumour, ectopic ACTH production
ACTH independent- adrenal adenoma, adrenal nodular hyperplasia, iatrogenic steroids

183
Q

Which tumours can cause cushings

A

Small cell lung cancer
Carcinoid tumour

adrenal tumour

184
Q

Most common cause of cusings syndrome

A

Iatrogenic steroids

185
Q

Most common electrolte abnormality

A

Hyponatraemia

186
Q

how is water balance controlled

A

ADH increasing aquaporin insertion in collecting duct via V2

187
Q

Where are V1 receptors for vasopressin

A

Vascular smooth muscle increasing vascular constriction
Only at high concentrations of vasopressin

188
Q

2 main stimuli for ADH release

A

Serum osmolality- hypothalamic osmoreceptors-> drives thirst
Blood pressure- baroreceptors in carotid and aorta

189
Q

First thing assess when patient has hyponatraemia

A

Volume statuts

190
Q

What is most useful clinical sign of hypovolaemia

A

Low urine Na+

191
Q

Which drugs make interpreting urinary sodium difficult

A

Diuretics

192
Q

Hypovolaemic cause of hyponatraemia

A

Diarrhoea
Vomiting
Diruretics
Salt losing nephropathy

193
Q

Euvolaemiac causes of hypontraemia

A

SIADH
Addisons
Hypothyroidism

194
Q

Causes of hypervolaemiac hyponatraemia

A

Liver, renal and cardiac failure

nephrotic syndrome

195
Q

What causes hypervolaemia in cirrhosis

A

Excess NO which is a vasodilator as should be filtered by liver

196
Q

Causes of SIADH

A

Lung pathology
CNS pathology
Drugs- SSRIs, opiates, TCA, PPIs, carbamezapine
Tumours
Surgery

197
Q

Investigations for euvolaemiac hyponatraemia

A

TFTs, short synacthen, plasma and urine osmolality

198
Q

Plasma and urine osmolality in SIADH

A

Low plasma
High urine

199
Q

How to diagnose SIADH

A

Rule out hypovolaemia, hypothyroidism and addisons
Reduced plasma osmolality
Urine osmolality over 100

200
Q

How to manage a hypovolaemic hyponatraemic patient

A

Volume replacement with 0.9% saline

201
Q

How to treat hypervolaemic hyponatraemia

A

Fluid restriction
Treat underlying cause

202
Q

How to treat euvolaemic hyponatraemia

A

Fluid restriction
Treat underlying cause

side note on CPM-
Serum Na must NOT be corrected > 8-10 mmol/L in the first 24 hours
Risk of osmotic demyelination (central pontine myelionlysis)

203
Q

What can result from severe hyponatraemia

A

Reduced GCS
Seizures

204
Q

How to treat severe hyponatraemia

A

Seek expert help only with hypertonic 3% saline
Only when reduced GCS and seizures

205
Q

If fluid restriction isnt useful in treating hyponatraemia what can give (e.g. SIADH)

A

Demeclocycline- reduces responsiveness of collecting duct to ADH
Tolvaptan- V2 antagonist

206
Q

What causes hypernatraemia

A

Unreplaced water loss
- GI and sweat losses
- diabetes insipidus
Poor intake of water seen in elderly and children

207
Q

What investigations for patients with suspected diabetes insipidus

A

Serum glucose, potassium and calcium (to exclude DM, hypokalaemia and hyperkalaemia as all cause excess water loss)
Plasma and urinary osmolality
Fluid deprviation test

208
Q

Treatment for hypernatraemia

A

Fluid with 5% dextrose to correct water deficit
0.9% saline to replace ECF volume loss
Sodium mesurements every 5 hours

2 key parts - 5% dextrose (as glucose eaten up so baso water) and 0.9% NaCl

209
Q

How can DM affect serum sodium

A

Very variable
Draws water out of cells causing hyponatraemia
Osmotic diuresis causing loss of water and hypernatraemia

210
Q

Which electrolyte imbalance can lead to depression

A

Hypercalcaemia

211
Q

Difference between smiths and colles fracture

A

Smiths- fallen on flexors of hands
Colles- fall with hands out on extensors

212
Q

Complications of hypercalcaemia

A

Renal stones
Pancreatitis
Peptic ulcer disease
Skeletal changes/fractures
Osteitis fibrosa cystica

213
Q

Sign on examination of hypercalcaemia

A

Band keratopathy- corneal degeneration

214
Q

What is late complication of hypercalcemia

A

Osteitis fibrosa cystica- bone remodelling and weakening

215
Q

Interesting feature of sarcoid hypercalcaemia

A

Is seasonal- is increased in summer

216
Q

Factors which contribute to whether clearance = eGFR

A

Not bound to serum proteins
Freely filtered and not secreted or reabsorbed by tubular cells

217
Q

What is gold standard for eGFR

A

Ready state infusion of Inulin but mainly used in research

218
Q

What is normal GFR rate and the normal age related decline rate

A

120ml/hr
1ml/hr/ year as age

219
Q

What posioning can lead to calcium oxalate stones

A

Ethylene glycol

220
Q

Grade 1-3 AKI creatinine

A

Stage 1- increase in 26 or by 1.5-1.9 from reference creatinine
Stage 2- increase in 2.0 to 2.9
Stage 3 increase in over 3.0 or > 354

221
Q

Causes of pre-renal AKI

A

Reduced circulating fluid perfusion or specific to kidney ie renal artery stenosis

222
Q

Which drugs predispose to pre renal AKI

A

NSAIDS
Calcineurin inhibitiros
Diuretics

223
Q

How do NSAIDS and calcinruin inhibitors cause pre renal AKI

A

Reduce afferent arteriole pressure

less afferent arteriole vasodilation

224
Q

Causes of renal AKI

A

Vascular disease- vasculitides
Acute glomerulonephritis
Tubular injuries
Infiltration- lymphoma, myeloma, amyloidosis
Thrombotic glomerulonephritis

anatomy of kindey tissue- tubular, interstitial, vascular, glomerular injuries

225
Q

What causes direct tubular injury (i.e. ATN)

A

Ischaemia
Endogenous toxins- light chain in myeloma, myoglobin
Exogenous- aminoglycosides, aciclovir, contrast

226
Q

What is most common cause of acute renal failure

A

Acute tubular necrosis

227
Q

Causes of post renal AKI

A

Blocked catheter
BPH
Stones
Bladder/prostate cancers

228
Q

Effects of prolonged obstructive uropathy

A

Glomerula ischaemia
Interstitial scarring
Tubular damage

229
Q

What are used to measure severity of AKI

A

Urine output or creatinine

230
Q

CKD stages

A
  1. GFR over 90
  2. GFR 60-89
  3. 30-59
  4. 15-29
  5. less than 15 or dialysis
231
Q

Most common causes of CKD

A

DM
Glomerulonephritis
HTN/atherosclerosis
Reflux nephropathy
PCKD

232
Q

Causes of hyperkalaemia in CKD

A

Spironolactone
ACEi
Eating foods like chocolate, dried fruits and tomatoes

233
Q

Problem of hyperkalaemia in CKD

A

Tachyarrythmias which can become VT

234
Q

Anaemia in CKD

A

Normochromic normocytic anaemia
Seen in GFR less than 30

as EPO made by kidneys

235
Q

What is used to treat CKD anaemia

A

EPO stimulating agents like darbapoetin

236
Q

Cardiac complications of CKD

A

Uraemiac cardiomyopathy with 3 phases
LVH->LV dilation->LV failure

237
Q

Vascular complications of CKD

A

Calcified vessels which leads to increased CVD risk

238
Q

Preferred sample for post mortem blood analysis

A

Post mortem femoral vein as allows for screening and quantitation

239
Q

How to calculate anion gap

A

Na+K-Cl-bicarb

ie gap of anions to not neutralise cations

240
Q

What causes itching in liver disease

A

MUST BE OBSTRUCTIVE JAUNDICE
Caused by bile salts

241
Q

What is Km (michaelis-menten)

A

Substrate concentration at which reaction velocity is at 50% of maximum (Vmax50)

242
Q

Where is ALP found and what causes it to be raised

A

Liver- Cholestatic disease
Bone- fracture, pagets, osteomalacia, rickets, cancer, hyperparathyroidism, renal osteodystrophy
Placenta- pregnancy in last trimester, germ-cell tumour
Intestine- none

243
Q

Where is AST versus ALT more prevalent

A

AST- heart
ALT- liver
ALT mores specific for liver disease

244
Q

Where are AST and ALT found

A

Liver
Heart
Muscle
Kidney
Pancreas

245
Q

Where is GGT found and what can increase itt

A

Hepatobiliary
Pancreas
Kidney
Diseases of these
Certain

246
Q

What drugs can induce GGT

A

Alcohol
Rifampicin
Barbiturates

247
Q

Where is LDH found and what raises it

A

WBC- lymphoma
RBC- haemolysis
Placenta- seminoma
Skeletal muscle- myositis
Liver- any injury
Heart- any cell death

248
Q

Where is amylase found

A

Pancreas- bowel obstruction, perf duodenal ulcer, bowel obstruction
Salivary gland- stones, infection like mumps

249
Q

What is macro-amylase

A

Amylase bound to immunoglobulin which can cause confusion

250
Q

Where is CK found and what raises it

A

Muscle- myositis, strenuous exercise, myopathy, rhabdomyolysis
Cardaic- any injury
higher in afrocarribeans

251
Q

When does troponin I begin to rise post injury

A

2 hours

  • Measure at 6 hours and then at 12 hours post onset of chest pain (100% Se and 98% Sp at 12-24 hours)  troponin only rises after 4hrs from infarct (don’t expect a raised trop in 30mins) - think lecture says 2hrs post infarct
252
Q

How is troponin measured post MI

A

Measured then measure again hour later
Look for over 50% rise

253
Q

In heart failure what cardiac marker is measured

A

NT Pro-BNP
NOT BNP as half life too short

254
Q

Management of hypoglycaemia in adults if alert and oriented

A

For rapid acting- juice and sweets
For longer acting sanwich

255
Q

Management of hypoglycaemia if drowsy and confused but swallow intact

A

Buccal glucose- hypostop or glucogel

256
Q

Management of hypoglycaemia if unconscious or concerned not able to swallow

A

IV access and 20% glucose through

257
Q

What use if hypoglycaemia patient deteriorating, treatment refractory, insulin induced or difficult IV access

A

IM glucagon 1mg

258
Q

Response of body to hypoglycaemia

A
  1. Suppress insulin
  2. Increased glucagon
  3. Sympathetic activation
  4. Cortisol, ACTH and GH all released

key insulin drops first - most sensitive

259
Q

What are counter regulation responses to hypoglycaemia

A

Increased glucose
Low insulin and c-peptide
Beta oxidation increases free fatty acids and ketone production

260
Q

Venous versus capillary blood glucose measurements in hypoglycaemia

A

Venous collected with fluoride oxalate preservative whereas CGB point of care analyser
Venous is gold standard as better precision with low glucose

261
Q

Causes of hypoglycaemia in non diabetic

A

Fasting
Very unwell
Hyperinsulinism
Post gastric bypass
Drugs- eta blocker, salicylates, alcohol
Extremely low BMI
Factitious

262
Q

Causes of hypoglycaemia in diabetic

A

Medication
Missed meal/ low carb
Excessive alcohol
Strenuous exercise
Co-existing autoimmune conditions

263
Q

How can hypoglycaemia be classified

A

Hypoinsulinaemic
Hyperinsulinaemia- then can be with low or high C-peptide

264
Q

Hypoglycaemia with high insulin and low c peptide

A

Factitious insulin

remember c-peptide is 1:1 ratio with insulin

265
Q

Main differentials for hyperinsulinaemic hypoglycaemia with high c peptide

A

Islet cell tumour- insulinoma
Sulphonylurea toxicity
Differentiate by doing urinary/serum drug screen

266
Q

What presents with hypoglycaemia, low insulin and low cpeptide, low FFA and ketones

A

Paraneoplastic syndrome where produce big IGF2 which binds to IGF-1 receptor and insulin receptor

267
Q

Which tumours do you get non-islet cell tumour hypoglycaemia in

A

Mesenchymal- mesothelioma and fibroblastoma
Occsaionally carcinomas
Production of big IGF2

268
Q

What is autoimmune insulin syndrome

A

Where get abs directed against insulin typically triggered by drugs or infections
Very common in japan

269
Q

What can cause hypoglycaemia after eating a meal

A

Post gastric bypass
Hereditary fructose intolerance
Early DM

270
Q

What are definitions of DM

A

Fasting glucose over 7mm
Glucose tolerance test over 11
HbA1c over 48mmol

271
Q

How can non functioning pituitary adenoma cause hyperprolactin

A

They can press on stalk which prevents dopamine travelling to APH

272
Q

What is main difference between blood gas in acute vesus chronic resp acidosis

A

Acute- increased CO2 leading to increase in H+ and bicarb (this IECOPD - less gas exchange)
Chronic- H+ may return to normal however bicarb will remain high with Co2 - i.e. it compensates (this is COPD)

273
Q

Why does hypokalaemia cause metabolic alkalosis

A

To retain potassium the kidney retains more sodium at expense of H+

274
Q

What are the 3 main mitochondrial disorders

A

Presents at birth
- Barth (cardiomyopathy, neutropenia and myopathy)

Presents 5-15
- MELAS ( mitochondrial encephalopathy, lctic acids and stroke like episodes)

Presents 12-30
- Kearns- Sayre (Chronic progressive external opthalmoplegia, retinopathy, deafness, ataxia)

275
Q

Presentation of osteopenia of prematurity

A

Cupping of long bones
Easy fractures
Extremely high ALP

276
Q

How is osteopenia of prematurity treated

A

With calcium and phosophate supplements

277
Q

What are the different types of vitamin D

A

Vitamin D2- ergocalciferol the plant one
Vitamin D3- cholecalciferol
Calcitriol

278
Q

What is corrected calcium

A

Accounts for that bound to albumin
Corrected calcium= serum calcium+0.02*(40-serum albumin)

279
Q

Describe the synthesis of Vitamin D

A

In the skin 7 dehydrocholesterol is converted to cholecalciferol (Vitamin D3)
Liver converts to 25 hydroxycholecalciferol
Kidney converts to 1,25-dihydroxycalciferol (calcitriol)

280
Q

Other than cancer what can cause non-PTH driven hypercalcaemia

A

Sarcoidosis (non-renal 1α hydroxylation)
Thyrotoxicosis (thyroxine -> bone resorption)
Hypoadrenalism (renal Ca2+ transport)
Thiazide diuretics (renal Ca2+ transport)
Excess vitamin D (eg sunbeds…)

281
Q

Qujestions when get hypocalcaemia

A

Is it a genuine result- repeat and adjust for albumin
What is PTH?

282
Q

High TSH
Low T4
Low glucose
Hyponatraemia
Hyperkalaemia

A

Schmidt syndrome- as hypothyroidism and addisons

283
Q

How do pre renal akis respond to fluids

A

Restorative
BUT
If prolonged leads to ischaemia which causes ATN which does not respond

284
Q

What are problems of acidosis from CKD

A

Failure to excrete protons
- muscle degradation
- osteopenia
- cardiac dysfunction

285
Q

How is acidosis from CKD treated

A

Oral sodium bicarb

286
Q

How much does hair grow in a month

A

1cm according to hair analysis

287
Q

Describe RAAS system

A

Renin converts angtionensin from liver to angiotensin 1 peripherally
Angiotensin 1 converted in lung by ACE to angiotensin II which acts on adrenal

more renin release - when less blood to JGA (hypotension), when less NA+ delivery to kidneys, when SNS stim JGA e.g. fight or flight response)

288
Q

How does aldosterone increase K secretion

A

Increases number of open Na channels on luminal membrane
Increased Na reabsorption makes lumen electronegative and creates electrical gradient
K secreted into lumen

289
Q

Causes of hyperkalaemia

A

Renal injury
Drugs- ACEi, ARBs, spironolactone, NSAIDS
Low aldosterone- T4 renal tubular acidosis, addisons
Release from cells in acidosis and rhabdomyolysis

Inhibition of prostaglandin synthesis by NSAIDs can lead to reduced renal blood flow and glomerular filtration rate (GFR), affecting kidney function
PGs also stimulate renin release from JGA (so stopping them causes less aldosterone)

290
Q

ECG change of hyperkalaemia

A

Peaked T waves

291
Q

Management of hyperkalaemia

A

10ml 10% calcium gluconate
50ml 50% dextrose with 10 units of insulin
Nebulised salbutamol
Treat cause

292
Q

Causes of hypokalaemia

A

GI loss
Renal loss- excess cortisol and aldosterone (Conn’s), loop diuretics and thiazides, T1 and T2 renal tubular acidosis, Barter syndrome and gieltman syndrome
Redistrubtion to cells- insulin, salbutamol, alkalosis

293
Q

What is difference of where barter and gieltman syndrome affect

A

Both cause hypokalaemia
Barter- loop of henle triple transporter (Na+K+Cl- , thick ascending limb)
Gieltman- DCT (Na+ Cl- co-transp not working)

more Na+ delivery to DCT so more Xchange for K+ so more K+ in urine so hypoK+

294
Q

Presentation of hypokalaemia

A

Muscle weakness
Cardiac arryhmia
Polyuria and polydipsia

can cause nephrogenic DI
ECG - In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

295
Q

How is hypokalaemia treated

A

3-3.5
- oral potassium chloride tablets ( 2 sandok tablets)
- recheck levels

less than 3
- IV KCl max 10mmol/hour as irritant to veins

296
Q

What is lesch-nyan disease

A

Get a deficiency in the enzyme HPGRT which leads to primary hyperuricaemia

297
Q

Presentation of lesch-nyan disease

A

Developmenal delay at 6 months
Choreiform movements around 1 year
Self mutilation (bite lips and fingers)
Severe UMN disease
Mental retardation

298
Q

Management of gout

A

NSAIDS
Colchicine
(Do not modift urate concentration)

299
Q

How to manage hyperuricaemia

A

Drink lots of water
Allopurinol

i.e. gout Rx in non-acute setting

300
Q

Which patients is pseudogout normally seen in

A

Osteoarthritis

301
Q

What are the hormones produced by the anterior pituitary

A

ACTH-> affected by CRH
TSH-> affected by TRH
LH > affected by LHRH
FSH-> affected by LHRH
GH -> affected by GHRH
Prolactin- affected by TRH and negatively from dopamine

302
Q

How does combined pituitary testing work

A

Triple test
Must check heart beforehand and no epilepsy - key CIs
Gain IV access for administration of IV 20% dextrose if needed
Fast overnight and give insulin (Blood glucose must be <2.2), TRH and LHRH in combined syringe
Measure glucose, cortisol, TSH, thyroxine and prolactin every 30 mins

303
Q

In pituitary failure which hormone replacement is needed most urgently

A

Hydrocortisone

304
Q

Treatment of prolactinoma

A

Dopamine agonist- cabergoline or bromocriptine
Surgery if needed

305
Q

What is the test for acromegaly

A

Glucose tolerance test
Can also measure IGF-1

306
Q

Management of acromegaly

A

Surgery if needed
Octreotide- somatostain analogue
Cabergoline- dopamine agonist

307
Q

What class of drug is octerotide

A

Somatostain analagoue which reduces GHRH released

308
Q

What is a porphyria

A

Deficiency in enzymes of haem biosynthesis pathway

309
Q

What is inheritance of hereditary coproporphyria and variegate porphyria

A

Autosomal dominant

310
Q

What is the most common acute porphyria

A

AIP

311
Q

What is the most common porphyria

A

Porphyria cutanea tarda

312
Q

How do the non-acute porphyrias present

A

Skin lesions only- blistering, pigmentation, erosions
EPP- happens immediately after sun exposure - but no blistering

313
Q

What is the only porphyria which presents in children

A

Erythopoietic protoporpyria

‘proto’ so children

314
Q

What is pathophysiology of porphyria cutanea

A

Uroporphyrinogen III decarboxylase deficiency (UROD)
Normally precipitated by liver diseases and alcohol use

315
Q

Investigation for erythopoietic protoporphyria

A

RBC protoporphyrin levels

remember EPP is cutaneous but NON-blistering

316
Q

In acute porphyria most useful sample to send is

A

Urine

317
Q

Causes of raised anion gap metabolic acidosis

A

MUDPLIES
Metformin
Uraemia
DKA
Paraldehyde
Iron
Lactate
Ethanol
Salicylate

318
Q

In mixed resp and metabolic acidosis in a COPD patient what could be causing the metabolic acidosis

A

Uraemia
DM leading to ketones
Renal tubular acidosis

319
Q

What are blood findings of tertiary hyperparathyroidism

A

High calcium
High PTH
High phosphate

high PO43- if due to CKD and kidneys can’t excrete

320
Q

What are blood and urine findings of diabetes insipidus

A

Hypernatraemia
Very low urinary osmolality

321
Q

What are blood and urine findings of primary/secondary polydipsia

A

Hyponatraemia
Low urinary osmolality

322
Q

What are urinary and plasma findings which suggest diabetes insipidus

A

Plasma osmolality:urine osmolality ratio over 2
Urine very dilute despite concentrated plasma

323
Q

Treatment for cranial diabetes insipidus

A

Desmopressin

324
Q

Treatment for nephrogenic diabetes insipidus

A

Thiazide diuretics

325
Q

How does cranial diabetes insipidus react in water deprivation test

A

Urine osmolality responds to desmopressin by increasing over 600

326
Q

How does nephrogenic diabetes insipidus react in water deprivation test

A

Urine osmolality to remain constant even after desmopressin

327
Q

What are the 5 thyroid cancers in order of prevalence and invasiveness

A

Papillary
Follicular
Medullary
Anaplastic
Lymphoma

328
Q

Thyroid cancer with psammoma bodies and orphan eyes on histology

A

Papillary

329
Q

Which thyroid cancer produces calcitonin

A

Medullary

330
Q

How is bilirubin conjugated

A

After breakdown from haem group forming unconjugated bilirubin get addition of glucuronyl group

331
Q

How to interpret AST:ALT ratio

A

If above 1 then fibrosis
If above 2 very severe alcoholic disease

332
Q

What do AST, ALT, ALP and GGT all stand for

A

Aspartate transaminase
Alanine transferase
Alkaline phosphatase
Gamma glutamyl transferase

333
Q

If reject liver biopsy what can offer

A

Fibroscan which measures elasticity

334
Q

Diagnostic test for gilberts

A

Fasting unconjugated bilirubin

335
Q

Which antibiotic is best known for causing drug induced cholestasis

A

Augmentin- Co-amox

336
Q

How to tell if liver disease acute

A

Preserved albumin synthetic liver function

337
Q

What causes ALT of over 1000 in MI

A

Ishcaemic liver (rare as liver has such a rich blood supply)

also viral hepatitis
also toxins/drugs (paracetamol overdose)

338
Q

Results of low dose dexamethasone test

A

Normal would be a low cortisol
High shows cushings of any cause

339
Q

After low dose dexamethasone test/ 24 hour urinary cortisol what is next done investigation

A

Inferior petrosal sinus sampling
Used to be high dose dexamethasone test

340
Q

How to interpret results of high dose dexamethasone test

A

If cortisol suppressed then suggests cushings disease
If remains high then either ectopic ACTH or adrenal cushings
If ACTH high then ectopic, if low then adrenal

341
Q

Order of most common causes of non-iatrogenic cushings

A

Cushings disease 85%
Adrenal adenoma/hyperplasia 10%
Ectopic ACTH 5%

342
Q

Causes of hyperthyoidism

A

Primary in order of prevalence
- Graves
- Toxic multinodular goitre
- Adenoma
Dequervains
Post partum thyroiditis
Molar pregnancy
struma ovarii from teratoma

343
Q

Management options for hyperthyroidism

A

Carbimazole or propylthiouracil
Radio-iodine
Thyroidectomy

Isotopes: iodine- 123 for nuclear imaging, iodine 131 for treatment!

344
Q

Dense firm thyroid

A

Riedels thyroiditis

345
Q

Causes of hypothyroid

A

Iodine deficiency
Hashimotos
Dequervains
Drugs- lithium, amiodarone
Riedels thyroiditis
Post thyroidectomy

346
Q

What is cancer marker for papillary and follicular thyroid cancer

A

Thyroglobulin

remember papillary spreads via LNs, follicular via haematogenous so reaches distant sites

347
Q

Histology of anaplastic thyroid cancer

A

Undifferentiated follicular, large pleomorphic giant cells,
spindle cells with sarcomatous appearance

348
Q

Histology of medullary thyroid cancer

A

Amyloid sheets as calcitonin broken down into it
Dark cell sheets

from parafollicular cells

349
Q

Pathophysiology of CAH

A

Less alpha 21 hydroxylase which means no progression down pathway to cortisol and aldosterone
Get excess of progesterone

350
Q

What does GH do

A

Increase glucose
Causes increase in insulin growth factor 1

351
Q

What inhibits GH release

A

Somatostain

352
Q

Blood findings of acromegaly

A

Hyperglycaemia
Prolactin

353
Q

Causes of hyperglycaemia

A

DM
Post stroke
Pancreatitis
Cushings
Acromegaly

354
Q

MOA of metformin

A

Increases sensitivity to insulin peripherally
Reduces hepatic gluconeogenesis

METformin can cause metabolic acidosis in overdose - lactic acidosis

355
Q

MOA of acarbose

A

Inhibits alpha glucosidase on brush border of small bowel

‘a’ carbohydrates i.e. less absorption

356
Q

MOA of gliptins

A

Inhibits dipeptidyl dipeptidase IV which increases incretin

357
Q

MOA of sulphonylureas

A

Increase insulin production from beta cells

358
Q

MOA of empaglifizon

A

SGLT2 inhibitor which increases excretion of glucose

359
Q

When can diagnose HHS

A

pH>7.3
Glucose over 30
Osmolarity over 320

360
Q

Treatment of HHS

A

0.9% saline
Insulin only if ketones over 1

361
Q

What does OGTT between 7.8 and 11.0 diagnose you with

A

Impaired glucose tolerance

362
Q

What does fasting glucose 6.1 to 6.9 diagnose you with

A

Impaired fasting glucose

363
Q

Where is bicarbonate reabsorbed

A

PCT

think of RTA 2

364
Q

Which gives positive urine dipstick for blood other than erythrocytes

A

Myoglobin and haemoglobin

365
Q

What is only drug that can increase bone density

A

Denosumab

366
Q

MOA of cholestyramine

A

Binds to bile acids to prevent cholesterol reabsorption

so less enterohepatic circulation of BAs so more cholesterol used up to produce BAs

367
Q

What are brown tumours

A

Aggregations of osteoclasts caused by hyperparathyroidism

osteitis fibrosa cystica

368
Q

Histology of browns tumours

A

Multinucleate giant cells

369
Q

How to calculate osmolar gap

A

2Na + glucose + urea

370
Q

What trnasports cholesterol to liver

A

HDL

371
Q

Treatment of prolactinoma

A

Surgery
Dopamine agonist- cabergoline or bromocriptine

Arjun's Copy- Owen's Path (8 decks)

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