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Chemical pathology Flashcards

1
Q

How is urate made?

A

Purines –> intermediaries (via Xanthine Oxidase) –> Urate

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2
Q

What are the pathways in producing purines?

A

De novo synthesis and (PAT) recycling/salvage pathways (HPRT or HGPRT)

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3
Q

What are the key enzymes involved?

A

PAT (rate limiting step), HGPRT

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4
Q

What is Lesch-Nyhan syndrome? What are the Sx/Ix?

A

X-linked complete deficiency of HGPRT enzyme –> ↓ purine recycling –> ↑ de novo pathway –> ↑ urate (hyperuricaemia) Hyperuricaemia, Development delay, Choreiform movements

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5
Q

Tx of Gout?

A

Acute gout (↓ inflammation): NSAID, Colcichine, Glucocorticoids Chronic gout: (treat ↑ urate): Drink water, Allopurinol (inhibits XO, C/I Azathioprine as blocks its metabolism so ↑ effect), Probenecid (uricosuric –> ↑ renal excretion)

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6
Q

Ix for Gout?

A

Bloods: raised urate, tap effusion + view under polarised light (2 filters to look for birefringence)

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7
Q

Gout vs Pseudogout

A

GOUT: monosodium urate crystals, needle-shaped, negative birefringence, perpendicular to axis of red compensator PSEUDOGOUT: calcium pyrophosphate crystals, rhomboid shaped, positive birefringence, parallel to axis of red compensator

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8
Q

Types of lipoproteins (largest to smallest) + function

A

Chylomicrons (largest) VLDL - main carriers of TG LDL - main carriers of cholesterol HDL (smallest)

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9
Q

Main enzyme involved in cholesterol synthesis

A

HMG-CoA reductase –> ↑ cholesterol synthesis This enzyme is downregulated by dietary cholesterol

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10
Q

Function of LDLs and HDLs

A

LDL: Transport cholesterol from Liver –> tissues HDL: Transport cholesterol from Tissues –> Liver

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11
Q

Function of CETP (cholesterylester transfer protein)

A

Converts cholesterol esters from HDL –> VLDL and TG from VLDL –> HDL

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12
Q

Absorption of cholesterol

A

Cholesterol (in diet) –> GI epithelium –> hydrolysed into bile acids (re-cycles) OR esterifised into Cholesterol ester Cholesterol ester + TG + ApoB –> VLDL –> LDL –> binds to LDL receptor –> LDL particle is endocytosed into cells

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13
Q

Absorption of triglycerides

A

TG –> Chylomicrons –> hydrolysed into Free Fatty Acids –> taken up by Liver and Aidpose tissue FFA re-synthesised into TG

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14
Q

Types of dyslipidaemia

A

Hypercholesteralaemia Hypertriglycidaemia Mixed hyperlipiademia Hypolipidaemia

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15
Q

Types of primary hypercholesterolaemia

A

Familial hypercholesterolaemia Type II (autosomal dominant mutation in LDL-R, ↑ risk of CVD) Polygenic hypercholesterolaemia (many loci) Familial hyper-a-lipoproteinaemia (CETP deficiency –> ↑ HDL –> longevity) Phytosterolaemia (↑ plant sterols)

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16
Q

Signs of hypercholesterolaemia

A

Arcus, Atheroma, Tendon xanthoma, Eruptive xanthoma

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17
Q

Types of primary hypertriglyceridaemia

A

Familial Type I: deficiency of Lipoprotein lipase or ApoC II deficiency (↑ chylomicrons) Familial Types IV: unknown –> ↑ synthesis of TG (↑ VLDL) Familial Types V: ApoA V deficiency (↑ VLDL and ↑ Chylomicrons)

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18
Q

DDx types of primary hypertriglyceridaemia

A

Overnight fridge test

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19
Q

Types of primary mixed hyperlipidaemia

A

Familial combined hyperlipidaemia Familial hepatic lipase deficiency Familial dys-B-lipoproteinaemia (type III)

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20
Q

Causes of secondary hyperlipidaemia

A

Pregnancy, Hypothyroidism, Diabetes, Obesity, Primary biliary cirrhosis, Alcohol

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21
Q

Types of hypolipidaemia

A

AB-lipoproteinaemia Hypo-B-lipoporteinaemia Tangier disease Hypo-a-lipoproteinaemia

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22
Q

Components of atherosclerosis

A

Necrotic core containing foam cells (full of cholesterol) and cholesterol cystals (foam cells die) with a thin fibrous cap

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23
Q

Pathophysiological of atherosclerosis

A

LDL crosses endothelium –> oxidased and phagocytosed by Macrophages –> esterified to become Foam cells –> die and release lipids –> Necrotic core

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24
Q

Types of lipid regulating drugs

A

Statins –> ↓ LDL, ↑ HDL, ↓ TG Fibrates (Gemfibrozil) –> ↓ TG Ezetimibe –> ↓ cholesterol absorption Resin –> binds to bile acids –> ↓ re-absorption

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25
Q

Tx of Obesity

A

Hypocaloric diet, Exercise, Orlistat (stearrhoea), GLP-1 analogue (exenatide), Bariatric surgery (Gastric banding, Roux-en-Y gastric bypass = stomach to Jejenum, Bilippancreatic diversion)

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26
Q

Causes of metabolic acidosis (3) + examples + compensation

A

↑ H+ production: e.g. DKA ↓ H+ excretion: e.g. renal failure Bicarbonate loss: e.g. gastro-intestinal fistula COMPENSATE: Hyperventilation (↑ RR)

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27
Q

Causes of respiratory acidosis (3) + examples + compensation

A

↓ venilation (e.g. Opiate overdose –> respiratory depression) ↓ perfusion Impaired gas exchange (e.g. COPD) COMPENSATION: long term renal compensation (↑ H+ excretion, ↑ Bicarb regeneration)

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28
Q

Causes of metabolic alkalosis (3) + examples

A

Loss of H+ HypoK Ingest Bicarb NO COMPENSATION: would compensate by ↑ CO2 but this would involve stopping breathing, resp centres stop this

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29
Q

Causes of respiratory alkalosis (3) + examples

A

Hyperventilation (voluntary, anxiety, artificial ventilation - CPAP, stimulation by drugs) COMPENSATION: long term renal compensation (↓ H+ excretion, ↓ Bicarb regeneration)

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30
Q

How do kidneys compensate for acidosis?

A

↑ renal excretion of H+ and ↑ bicarb regeneration

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31
Q

Explain switch in stimulus for COPD

A

Impaired gas exchange (e.g. COPD) –> Respiratory acidosis —– Eventually, brainstem ignores —– With exertion, COPD becomes breathless due to hypoxia (as hypercapnia is ignored) Renal compensation (Bicarb reabsorption, Excrete H+ ions)

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32
Q

List Dx in newborn screening program (9)

A

Cystic fibrosis (immunoreactive trypsinogen) Hypothyroidism (TSH) Sickle cell PKU (Phenylalanine levels) MCADD (acylcarnitine levels by tandem mass spec) Maple syrup urine disease Isovaleric aciduria Glutaric aciduria Homocystinuria

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33
Q

PKU enzyme deficiency, Sx and Tx

A

PKU = Phenylalanine hydroxylase deficiency Asymptomatic, Moderate-Severe LD if untreated Alternative meals for PKU

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34
Q

Define sensitivity, specificity, NPV, PPV

A

Sensitivity = true positive / total disease present Specificity = true negative / total disease absent NPV = true negative / total negative results PPV = true positive / total positive results

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35
Q

Cystic fibrosis - Ix, mutation

A

Gutherie test: ↑ immunoreactive trypsinogen Sweat test: Cl- > 60 Genetic testing: autosomal recessive, delta(F508) is most common

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36
Q

MCADD - Pathogenesis, Ix

A

Fatty acid oxidation defect –> cannot liberate acetyl CoA from fat –> dies of hypoglycaemia Ix: Hypoketotic hypoglycaemia (cannot make ketones as cannot breakdown fat), Hepatomegaly, Cardiomyopathy

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37
Q

Red flag for urea cycle disorder

A

↑ Hyperammnoaemia + ↑ Glutamine (excess ammonia added to glutamate to make glutamine)

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38
Q

Tx for hyperammonaemia

A

Remove ammonia (sodium benzoate, dialysis), ↓ ammonia production (low protein diet)

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39
Q

Red flag for organic aciduria

A

Hyperammonaemia + Metabolic acidosis + High anion gap

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40
Q

Isovaleric acidaemia - Aet, Sx, Ix

A

Aetiology: deficiency of isovaleryl CoA-dehydrogenase –> ↑ isovaleryl CoA, ↓ Leucine Sx: Funny smelling urine (maple syrup urine disease), ↑ hyperammonaemia, myoclonic jerks, ketoacidotic coma Ix: serum ammnoia, serum amino acids, urine organic acids, glucose, lactate, blood spot carnitine profile

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41
Q

Galactosaemia - Aet, Sx, Ix

A

Aetiology: Gal-1-PUT deficiency Sx: Conjugated ↑ BR, Hypoglycaemia, Hepatomegaly Ix: urine reducing substances - ↑ galactose Tx: galactose free diet

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42
Q

Red flag for mitochondrial disorders

A

Multiple organ systems affected, ↑ CK, ↑ Lactate

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43
Q

Examples of mitochondrial disorders

A

Barth, MELAS, Kearns-Sayre disease

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44
Q

Peroxisomal disorders - Sx, Ix

A

Aetiology: defective metabolism of very-long chain FA Sx: Seizures, hypotonia, dysmorphic signs (large fontnaelle), calcified stippling (x-ray) Ix: Very long-chain FA profile

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45
Q

Lysosomal stroage disease

A

Aetiology: autosomal recessive –> ↑ stroage of material in cells Sx: Organomegaly, Dysmorphia Ix: Urine mucopolysaccharides Treatment: BM transplant, exogenous enzyme

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46
Q

Differences in neonatal renal function c.w. adults

A

Function maturity reached by 2 years old ↓ GFR (relative to SA) Shorter PCT –> ↓ reabsorption Short LoH –> ↓ concentrating ability DCT relatively aldosterone insensitive

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47
Q

Fluid differences in neonates c.w. adults

A

↑ water loss due to ↑ SA:V ratio, ↑ skin blood flow, ↑ trans-epidermal fluid loss All babies lose 10% BW in first weight of life

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48
Q

Electrolyte differences in neonates c.w. adults

A

↑ requirements: ↑ fluid (6x), ↑ Na+ (3.5x), ↑ K+ (2x) Hypernatraemia is common in first 2 weeks of life (after 2 weeks –> ↑ Na+ indicates dehydration)

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49
Q

Neonatal causes of fluid overload

A

Bronchopulmonary dysplasia Necrotising enterocolitis

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50
Q

Neonatal causes of Hypernatraemia

A

Normal in first 2 weeks of life IVH Sodium bicarbonate when treating acidosis

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51
Q

Neonatal causes of Hyponatraemia

A

CAH Caffeine/Theophylline (when treating apnoea)

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52
Q

Osteopenia of prematurity

A

Inability to get enough Calcium ex utero, Ca (last to go), ↓ PO4, ↑↑ ALP, Tx with Ca supplements

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53
Q

Transient hyperphosphataemia of infancy

A

↑↑ ALP in absence of liver or bone disease, returns to normal within weeks-months

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54
Q

Pathological neonatal jaundice

A

Jaundice < 24 hours (haemolysis, jaundice) Jaundice > 14 days (hepatobiliary failure) Conjugated hyperBR at any stage of infancy

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55
Q

Define porphyria

A

Deficiency of haem biosynthesis pathway –> build-up of haem precursors

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56
Q

Rate limiting step in Haem biosynthesis pathway

A

ALA synthase

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57
Q

Classify porphyria based on presentation/onset

A

Acute –> Neuro-visceral symptoms +/- Cutaneous symptoms Chronic –> Cutaneous symptoms (blistering or non-blistering)

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58
Q

Mechanisms of symptoms of porphyria

A

5-ALA is neurotoxic Porphyrinogen (precursors) oxidised by UV light in skin –> cutaneous skin lesion

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59
Q

Porphyrinogens vs Porphyrins

A

Porphyrinogen: colourless, unstable (readily oxided to porphyrin) Porphyrin: coloured, water soluble –> urine, insoluble –> faeces

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60
Q

Acute porphyrias (4) + enzymes involved

A

ALA dehydratase = Plumboporphyria –> PBG synthase deficiency = ALA dehydratase deficiency — Neurocutaneous lesions Acute intermittent porphyria –> HMB synthase deficiency — Neurocutaneous lesions — Intermittent symptoms (triggered by CYP450 inducers) — Tx: IV Haem arginate Hereditary coproporphyria –> Coproporphyrinogen oxidase deficiency — Neurocutaneous lesions + Skin lesions Variegate porphyria –> Protoporphyrinogen oxidase deficiency — Neurocutaneous lesions + Skin lesions

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61
Q

Porphyrias - neurovisceral symptoms + Ix

A

Psychosis, Abdo pain, Motor neuropathy, Constipation, Hyponatraemia (due to ↓ renin), Bulbar palsy, Coma Ix: Urinary PBG

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62
Q

Porphyrias - cutaneous symptoms + Ix

A

Blistering (vesicles, skin crusting) or Non-blistering (photosensitive rash, burning, itching, oedema) Ix: Urine and Faecal and Plasma porphyrins + Red cell protoporphyrins

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63
Q

Chronic porphyrias (4) + enzyme involved

A

Congenital erythropoietic porphyria –> Uroporphyrinogen III synthase — Blistering Porphyria cutanea tarda –> Uroporphyrinogen decarboxylase — Blistering Erythropoietic protoporphyria –> Ferrochetolase — Non-blistering

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64
Q

Most common porphyria

A

Porphyria cutanea tarda –> Uroporphyrinogen decarboxylase

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65
Q

Most common porphyria in children

A

Erythropoietic protoporphyria –> Ferrochetolase

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66
Q

ALA synthase deficiency

A

X-linked sideroblastic anaemia (it does NOT cause porphyria)

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67
Q

Thyroid physiology (iodide to T4)

A

Iodine absorbed in GIT (blocked by perchlorate) and converted to Iodide In Thyroid gland, TPO converts iodide to iodine – thyroglobulin within colloid Iodine –> mono- –> di- –> T3 –> T4 In periphery, T4 converted to T3 TSH acts to ↑ iodine uptake into thyroid, ∑ conversion, ∑ movement of T4 into basememnt mebrane, ∑ excretion of T4 into blood

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68
Q

Causes of Hypothyroidism

A

Primary - Hashimoto’s thyroiditis (autoimmune, anti-TPO antibodies, anti-TG antibodies, plasma cell infiltration) - Primary atrophy hypothyroidism: difficuse lymphocytic infiltration + atrophy (small thyroid), no antibodies - Iodine deficiency (common worldwide) - Post thyroidectomy - Drugs (Lithium, amiodarone, anti-thyroid drugs) Secondary - pituitary adenoma

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69
Q

Ix + Tx of Hypothyroidism

A

↓ T4, ↑ TSH in primary hypothyroidism T4 (titrated until normal TSH)

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70
Q

Subclinical hypothyroidism - Ix

A

T4, ↑ TSH, asymptomatic (incidental) May progress to Primary hypothyroidism, esp if anti-TPO antibody +ve Only treat if ↑ cholesterol levels

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71
Q

Thyroid function in pregnancy

A

↑ hCG (similar to TSH), ↑ T4, ↑ Thyroglobulin, ↑ Thyroid-binding globulin

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72
Q

Most important test for Thyroid disease

A

TSH

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73
Q

Sick euthyroid syndrome

A

Sick (e.g. sepsis) –> ↓ T4/T3, ↑/ TSH –> with aim of ↓ BMR

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74
Q

Causes of Hyperthyroidism + Ix

A

↑ uptake - Grave’s disease (diffuse enlargement, exothalphmos, pre-tibial myxoedema, thyroid acropathy) - Toxic multi-nodular goitre - Single toxic adenoma ↓ uptake - Subacute de Quervains thyroiditis (initial hyperthyroid, then hypothyroid) - Post-partum thyroiditis Ix: Technetium scan

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75
Q

Tx of Hyperthyroidism

A

Thionamides (Carbimazole, propylthiouracil) Radioactive iodine (release radiation to destroy thyroid gland, S/E thyroid storm - Tx: β blocker) Potassium perchlorate: ↓ iodine absorption in GI tract β blockers

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76
Q

Tx of thyroid carcinoma

A

Surgery Radioactive iodine T4 –> suppresses TSH so tumour does not growth

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77
Q

Marker of recurrence of thyroid cancer

A

Thyroglobulin

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78
Q

5 types of thyroid neoplasia

A

Papillary (most common) - Psammoma bodies Follicular Medullary - from parafollicular C cells, MEN2, produces Calcitonin Lymphoma - MALT origin Anaplastic

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79
Q

Normal range of calcium

A

2.2 - 2.6 mmol / L

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80
Q

Why do you use corrected Calcium

A

If ↓ albumin –> ↓ total Ca2+ ∴ look at corrected Ca2+

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81
Q

Vitamin D synthesis pathway

A

Cholesterol –> D3 (from skin or diet) –> 25-hydroxylase produces 25-OH D3 (in Liver, inactive form) –> 1α-hydroxylase produces 1,25 (OH)2 Vitamin D3 (in Kidney, active form, enzyme controlled by PTH)

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82
Q

Rate limiting step in Vit D synthesis

A

1 α hydroxylase (controlled by PTH)

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83
Q

Vitamin D2

A

Ergocalciferol (in plants) Tip = “ER” = 2

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84
Q

Vitamin D3

A

Cholecalciferol (in mammals) Tip: “CHO” = 3

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85
Q

Effects of 1, 25 Vitamin D (2)

A

↑ intestinal Ca2+ absorption and ↑ intestinal PO4 absorption

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86
Q

Effects of PTH (3)

A

↑ 1α-hydroxylase –> ↑ Vitamin D –> ↑ intestinal Ca2+ absorption and ↑ intestinal PO4 absorption ↑ renal absorption of Ca2+ + ↓ renal PO4 resorption (phosphate trashing hormone) Activates osteoclasts –> consume bone to release Ca2+ ∴ Osteoblasts repair bone –> ↑ ALP

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87
Q

Vitamin D deficiency vs Osteoporosis

A

Vitamin D deficiency: defective bone mineralisation (↓ Vit D, ↓ Ca2+, ↑ PTH) - secondary hyperparathyroidism Osteoporosis: loss of bone mass, normal bone mineralisation (NORMAL biochemistry)

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88
Q

Causes of Vitamin D deficiency

A

Dietary deficiency, Lack of sunlight, Renal failure

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89
Q

Pathophysiology of Vitamin D deficiency

A

↓ Vit D –> ↓ Ca2+ –> ↑ PTH –> ↑ bone resorption by osteoclasts –> ↓ bone mineralisation = Osteomalacia

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90
Q

Types of Vitamin D deficiency (age) + Sx

A

Vitamin D deficiency in children = Rickets (bowed legs, widened epiphyses) Vitamin D deficiency in Adults = Osteomalacia (Looser’s zone = pseudofracture, ↑ risk of fractures)

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91
Q

Tx of Vitamin D deficiency

A

Vitamin D, adjust dose to Ca2+ levels

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92
Q

Causes of Osteoporosis

A

Excess breakdown: Cushing’s syndrome, Hyperthyroidism Deficient production: oestrogen deficiency, Old age Dietary

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93
Q

Sx of Osteoporosis

A

Asympatomic UNTIL fracture

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94
Q

Dx of Osteoporosis

A

DEXA scan Osteoporosis = T score < -2.5 Osteopenia = T score -1 & -2.5 -1 < Normal < 1

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95
Q

DEXA Z score vs T score

A

T score = SD from young healthy population (determine fracture risk) Z score = SD from mean age-matched controls (identify accelerated bone loss) Tip: Z is at the end of the alphabet so it is the old people who are leftover in society

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96
Q

Tx for Osteoporosis

A

Vitamin D / Ca2+ Bisphosphonates (Alendronate) - creates special C-N bond not found in nature, not biodegradable, GI S/E Teriparatide (PTH derivative) Strontium - anabolic (many S/E) SERMs (Raloxifene) Denosumab - binds to RANK ligand –> ↓ maturation of osteoclasts –> ↓ bone resorption

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97
Q

Symptoms of Hypercalcaemia

A

Stones - renal stones Bones - bone pain Abdo Moans - constipation, pancreatitis Psychic Groans - depression Thrones - polyuria/polydipsia Band keratopathy (deposition in front of eye)

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98
Q

Classify causes of Hypercalcaemia

A

PTH driven (↑ or inappropriate normal PTH) or non-PTH driven (↓ PTH - appropriately supressed)

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99
Q

Treatment of Hypercalcaemia

A

Fluids ++++++ (1L/1hr then 1L/8 hour –> overal 3-6L/24hr) +/- Furosemide (if elderly, to ↓ risk of pulmonary oedema) If malignancy –> Bisphosphonates (otherwise avoid as it makes diagnosis harder later!) Treat underlying cause

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100
Q

Symptoms of Hypocalaemia

A

CATs go numb (neuronal excitability) - Convulsions - Arrhythmias - Tetany (Trosseau’s sign/BP cuff, Chvostek’s sign/Facial tetany) - Parasthesia

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101
Q

Classify causes of Hypocalcaemia

A

↑ PTH (non-PTH driven i.e. secondary hyperparathyroidism, appropriate response to ↓ Ca2+) or ↓ PTH (lack of PTH-driven)

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102
Q

Tx of hypocalcaemia

A

Calcium, Vitamin D (usually activated form, unless Vit D deficiency)

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103
Q

DDx ↑ Ca2+, ↑/ PTH

A

Primary hyperparathyoidism (parathyroid adenoma) Familial benign hypercalcaemia (mutation in Ca sensing receptor - CaSR - higher set point for PTH release, benign)

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104
Q

DDx ↑ Ca2+, ↓ PTH

A

= Secondary hypoparathyroidism - Malignancy —- Hypercalcaemia of Malignancy (small cell lung cancer releases PTHrP) — Bone mets (invades bone –> releases Ca2+) — Multiple myeloma (cytokines –> release Ca2+) - Sarcoidosis (ectopic 1α-hydroxylation) - Vitamin D excess Tip: DDx by giving steroids (if normalised, the cause is sarcoidosis)

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105
Q

DDx ↓ Ca2+, ↑ PTH

A

Secondary hyperparathyroidism (LOWEST CALCIUM) - Vitamin D deficiency (↓ Vit D –> ↓ Ca2+ –> ↑ PTH) - Chronic Kidney Disease (failure of 1α-hydroxylation) - may progress to tertiary hyperPTH - Pseudohypothyroidism = PTH resistance (↓ Ca2+, ↑ PTH, skeletal abnormalities - abnormal 4th metacarpal)

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106
Q

DDx ↓ Ca2+, ↓ PTH

A

Primary hypoparathyroidism - Surgery = post-thyroidectomy - Autoimmune (rare) - Congenital absence (e.g. DiGeorge syndrome) - Mg2+ deficiency (required for PTH synthesis)

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107
Q

↑ Ca2+, ↓ PO4, ↑ PTH, ↑/ ALP, Vitamin D

A

Primary hyperPTH (or Tertiary hyperPTH)

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108
Q

↑ Ca2+, ↓ PO4, PTH, ↑/ ALP, Vitamin D

A

Primary hyperPTH (or Tertiary hyperPTH)

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109
Q

↓ Ca2+, ↑ PO4, ↑ PTH, ↑ ALP, Vitamin D

A

Secondary hyperPTH (Vitamin D deficiency, CKD, Pseudohypoparathyroidism)

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110
Q

Ca2+, ↑ PO4, ↑ PTH, ↑ ALP, Vitamin D

A

Secondary hyperPTH (Vitamin D deficiency, CKD, Pseudohypoparathyroidism)

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111
Q

↓ Ca2+, ↓ PO4, ↑ PTH, ↑ ALP, ↓ Vitamin D

A

Vitamin D deficiency

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112
Q

↓ Ca2+, ↑ PO4, ↓ PTH, ALP, Vitamin D

A

Primary hypoparathyroidism

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113
Q

, Ca2+, PO4, PTH, ↑ ALP, Vitamin D

A

Paget’s disease

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114
Q

, Ca2+, PO4, PTH, ALP, Vitamin D

A

Osteoporosis

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115
Q

Primary hyperparathyroidism (↑ PTH)

A

Parathyroid adenoma –> ↑ PTH –> ↑ Ca2+ –> no negative feedback Bloods: ↑ Ca, ↑ PTH

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116
Q

Secondary hyperparathyroidism (↑ PTH)

A

Vitamin D deficiency –> ↓ Ca2+ –> secondary ↑ PTH Bloods: ↓ Ca, ↑ PTH

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117
Q

Tertiary hyperparathyroidism (↑ PTH)

A

CKD –> ↓ 1α-hydroxylase –> ↓ Vitamin D –> ↓ Ca2+ –> secondary ↑ PTH Long-standing CKD, ↑ PTH –> parathyroid hyperplasia After renal transplant, parathyroid hyperplasia becomes autonomous (no -ve feedback) –> ↑ PTH, ↑ Ca2+ Bloods: ↑ Ca, ↑ PTH (same as Primary hyperPTH) Clue lies in the history

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118
Q

Primary hypoparathyroidism (↓ PTH)

A

Causes: Surgical, Autoimmune, Congenital agenesis (DiGeorge) Bloods: ↓ Ca2+, ↓ PTH

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119
Q

Secondary hypoparathyroidism (↓ PTH)

A

Suppressed by ↑ Ca Bloods: ↑ Ca2+, ↓ PTH

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120
Q

Pseudohypoparathyroidism

A

PTH resistance, skeletal abnormalities Bloods: ↓ Ca2+, ↑ PTH

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121
Q

Pseudopseudohypoparathyroidism

A

Clinical abnormalities of pseudohypoparathyroidism NORMAL biochemistry

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122
Q

Paget’s disease

A

↑ bone turnover / remodelling –> ↑ ALP Focal bone pain, bone warmth, fracture, bone scan: hot bone Bloods: Ca, PO4, ↑ ↑ ALP Tx: Bisphosphonates

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123
Q

Which deaths need to be reported to Coroner (3)

A

Violent, Unnatural/Sudden or Cause of death is unknown

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124
Q

Forensic samples

A

Ante-mortem blood - drugs before death PM blood (most important) - drugs at time (some may be broken down) Urine Stomach contents (drugs not yet absorbed) Vitreous humour (similar conc to blood) Hair (tape recording of drug use with time) Liver (drugs) Bile (opiates concentrate here) Items found near person

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125
Q

Drugs with respiratory depressant effects (3)

A

Alcohol, Opiates, BDZ

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126
Q

Duration of substance still undetectable (blood, urine, hair)

A

Blood < 12 hr, Urine 2-3 days, Hair 1cm/month (only specimen which gives long-term drug history)

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127
Q

Actions for ADH/Vasopressin + receptors

A

V2 - acts on collecting tubules to ↑ AQP2 –> ↑ water reabsorption –> ↓ Na+ V1 - vasoconstriction (smooth muscle)

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128
Q

Stimuli for ADH secretion

A

↑ serum osmolality - medicated by hypothalamic osmoreceptors ↓ BP (or ↓ blood volume) - mediated by baroreceptors

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129
Q

True hyponatraemia vs False

A

True hypontraemia has LOW osmolality

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130
Q

Classification of hyponatraemia

A

Hypovolaemic / Euvolaemic / Hypervolaemic

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131
Q

Sx of hyponatraemia

A

N&V, Confusion, Seizures, Coma, Death

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132
Q

Clinical features of Hypovolaemia

A

↓ BP, ↑ HR, Dry mucous membranes, ↓ skin turgor, ↓ urine output ↓ urine Na+ (most important / most sensitive) - Na+ retained by kidneys to maintain BP

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133
Q

Clinical features of Hypervolaemia

A

Pulmonary oedema, Peripheral oedema, ↑ JVP

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134
Q

Causes of Hypovolaemic hyponatraemia

A

Diarrhoea Vomiting Diuretics Due to: hypovolaemia –> ↑ ADH secretion –> ↑ water retention (only partially compensates for volume loss) –> ↓ Na+ (overall ↓ Na+)

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135
Q

Ix of Hypovolaemic hyponatraemia

A

Clinically hypovolaemic ↓ urine Na+

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136
Q

Tx of Hypovolaemic hyponatraemia

A

Fluids (0.9% saline)

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137
Q

Causes of Euvolaemic hyponatraemia

A

Hypothyroidism (–> ↓ cardiac contracility –> ↓ BP –> ↑↑ ADH) Addison’s (–> ↓ cortisol –> ↓ BP –> ↑ ADH) SIADH (–> ↑↑ ADH) Due to: excess ADH –> ↑ water retention –> ↓ Na+ (excess ↑ water retention –> ↑ ANP –> lose Na+ and water in urine so volume normalises - so no oedema)

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138
Q

SIADH - causes

A

CNS pathology - ANY Lung pathology - ANY Tumours - ANY Drugs Surgery

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139
Q

SIADH - Ix

A

↓ plasma osmolality (hyponatraemia) ↑ urine osmolality (↑ ADH –> ↑ water retention –> urine concentrates)

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140
Q

Ix of Euvolaemic hyponatraemia

A

TFTs, synACTHen test, plasma osmolality, urine osmolality

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141
Q

Tx of Euvolaemic hyponatraemia

A

Fluid restriction Treat underlying cause If SIADH –> Demeclocycline (↑ ADH resistance) + Tolvaptin (V2 receptor antagonist) + Furosemide

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142
Q

Causes of Hypervolaemic hyponatraemia

A

Tip FAILURES - Cardiac failure (↓ CO –> ↓ BP) - Liver failure (↑ NO as less broken down –> vasodilation –> ↓ BP) - Nephrotic syndrome (lose albumin –> ↓ oncotic pressure –> fluid enters tissues –> ↓ BP) Due to: ↓ BP –> ↑ ADH –> ↑ water retention –> ↑ fluid volume –> oedema

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143
Q

Ix of Hypervolaemic hyponatraemia

A

Clincially fluid overloaded

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144
Q

Tx of Hypervolaemic hyponatraemia

A

Fluid restriction Treat underlying cause

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145
Q

Tx of severe hyponatraemia

A

Hypertonic saline (2.7%) - under specialist guidance Only indicated if ↓ GCS or Seizures

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146
Q

Rate of correcting hyponatraemia

A

1 mmol/L per hour OR < 10 mmol/L per 24 hours (monitor 4 hourly)

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147
Q

Dangers of correcting hyponatraemia too quickly

A

Central pontine myelinolysis (paralysis, dysarthria, seizures, coma, death)

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148
Q

Sx of hypernatraemia

A

Thirst, Confusion, Seizures, Ataxia, Coma

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149
Q

Classification of hypernatraemia

A

Hypovolaemic / Euvolaemic Tip: 3 Ds of Hypernatraemia (Diarrhoea, Diabetes mellitus, Diabetes insipidus)

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150
Q

Causes of hypovolaemic hypernatraemia

A

GI losses - Diarrhoea Skin losses Renal losses - Diabetes mellitus (osmotic diuresis)

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151
Q

Causes of euvolaemic hypernatraemia

A

Inability to access water (children, elderly) Diabetes insipidus

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152
Q

Types of diabetes insipidus

A

Central DI: no ADH release - due to Hypophysitis (inflammation) or Pituitary adenoma (less common) Nephrogenic DI: ADH resistance - due to: Hypercalcaemia, Hypokalaemia, Lithium

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153
Q

DDx types of diabetes insipidus

A

Measure urine osmolality (& plasma osmolality) Fluid deprived: normal will ↑ urine osmolality, rest remain same Give DDAVP: only central DI will ↑ urine osmolality, nephrogenic DI will remain same

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154
Q

Tx of hyperntraemia

A

Fluid replacement (5% dextrose if euvolaemic, 0.9% saline if hypovolaemic)

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155
Q

Dangers of correcting hypernatraemia too quickly

A

Cerebral oedema

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156
Q

NONE

A

NONE

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157
Q

RAAS

A

Angiotensinogen (Liver) –> A-I by Renin –> AT-II by ACE (in Lung) –> Aldosterone (by Adrenaline) Aldosterone –> Na+/H2O re-absorption and K+ excretion

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158
Q

Stimuli for Aldosterone release

A

Angiotensin II ↑ K+

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159
Q

Causes of Hyperkalaemia (8)

A

↓ GFR (Renal failure) - most common cause ↓ Renin (NSAIDs, Type 4 renal tubular acidosis) ACE inhibitors ARBs Addison’s disease (↓ aldosterone) MR antagonists (Spironolactone = K+ sparing diuretic) Acidosis (K+ moves out of cells as H+ moves into cells, to compensate for acidosis) Rhabdomyolysis (damage to muscle cells –> release of K+)

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160
Q

ECG findings of Hyperkalaemia

A

Tented T waves, Absent p waves, Widened QRS, Bradycardia Eventually –> VF

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161
Q

Management of Hyperkalaemia

A

K+ > 6.5 or ECG changes - 10ml 10% Calcium gluconate (stabilise myocardium) - 100ml 20% Dextrose + 10 units Insulin (drives K+ into cells) - Nebulised salbutamol (drive K+ into cells) - Treat underlying cause K+ 5.3 - 6.5 –> consider haemolysed sample

162
Q

Causes of Hypokalaemia (12)

A

(1) GI loss - Diarrhoea - Vomiting (2) Renal loss ——> ↑ urinary [K+] - Hyperaldosteronism (↑ aldosterone) - Cushing’s syndrome (excess cortisol –> binds to MR –> aldosterone-like effect) - Osmotic diuresis - ↑ Na+ delivery to distal nephron —– Lack of Na+ reabsorption in LoH (Na/K/Cl channel) ———- Bartter syndrome ———- Loop diuretics (e.g. Furosemide) —– Lack of Na+ reabsorption in DCT (Na/Cl- channel) ———- Gitelman syndrome ———- Thiazide diuretics (e.g. Bendroflumethiazide) (3) Restriction into cells - Alkalosis - Insulin - β agonists

163
Q

Clinical features of Hypokalaemia

A

Muscle weakness Arrhythmia Polyuria/Polydipsia (nephrogenic DI)

164
Q

Ix + Cause of ↓ K+ and ↑ BP

A

Ix = aldosterone : renin ratio (↑ in Primary hyperaldosteronism = Conn’s syndrome) normally, expect ↓ renin (suppressed)

165
Q

Tx of Hypokalaemia

A

Serum K 3.0 - 3.5 –> check K+ +/- oral KCl Serum K < 3.0 –> IV KCl (max rate 10 mmol/hr) Treat underling cause

166
Q

Henderson-Hasselback equilirium

A

H + HCO3 CO2 + H2O

167
Q

Osmolality equation

A

Osmolarity = 2(Na+K) + Urea + Glucose (NR 275-295)

168
Q

Anion gap equation

A

Anion gap = Na + K - Cl - Bicarb (NR = 14-18)

169
Q

Osmolar gap

A

Osmolality (measured) - Osmolarity (calculated) NR < 10 Elevated osmolar gap = presence of abnormal/extra solute (ethylene glycol, ethanol, methanol, mannitol)

170
Q

Causes of ↑ anion gap (excess anions) (5)

A

Ketones, Methanol, Ethanol, Lactate, Metformin overdose

171
Q

Osmolality vs Osmolarity

A

osmolality = total number of particles in a solution (units = mmol/kg) osmolarity = 2(Na+K)+U+G, units = mmol/L

172
Q

Alkalosis is associated with what electrolyte abnormality

A

Hypocalaemia

173
Q

Hyperglycacemia Hyperosmolar State (HHS) - Aetiology, Ix, Tx = Hyperglycaemia Hyperosmolar Non-ketotic Coma (HONKC)

A

More common in T2DM Long-term uncontrolled diabetes (undiagnosed) –> ↑ ↑ blood glucose –> ↑ symptomatic (polyria, polydipsia, glycosuria) –> ↑ water loss –> VERY DEHYDRATED Overall: ↑ ↑ blood glucose, ↑↑ Na+ (i.e. ↑ osmolality) Hypernatraemia –> coma Tx: normal saline (↓ Na+ slowly to avoid cerebral oedema)

174
Q

Metformin overdose causes …

A

Lactic acidosis (Metformin blocks lactate –> glucose)

175
Q

Defintion of Diabetes

A

Fasting PLASMA glucose > 7.0 mmol/L (must be plasma glucose, plasma is excreted from blood by centrifuging and removing red cells) or OGTT 2hr > 11.1 mmol/L or HbA1c > 48 mmol/mol (>6.5%) - NR is < 42 mmol/mol

176
Q

Defintion of impaired glucose tolerance

A

Fasting PLASMA glucose < 7.0 mmol/L OGTT 2hr > 7.8-11.1 mmol/L

177
Q

7 classes of Diabetes drugs

A

Metformin Sulphonylurea SGLT2 inhibitor α-glucosidase inhibitor Thiazolidinediones GLP-1 analogues Gliptins (DPPG-4 inhibitor)

178
Q

Mechanism of Metformin

A

MOA: ↓ insulin resistance

179
Q

Example of Sulphonylurea + Mechanism

A

Example: Glibencamide MOA: ↑ insulin secretion (insulin secretagogue) S/E: Hypoglycaemia

180
Q

Example of SGLT2 inhibitor + Mechanism

A

Example: Empaglifozin MOA: SGLT2 inhibitor –> urinary glucose re-absorption –> ↑ urinary glucose (glycosuria)

181
Q

Example of α-glucosidase inhibitor + Mechanism

A

Example: Acarbose MOA: delays gut transit –> prolongs absorption of sugars –> gives pancreas more time to produce sufficient insulin S/E: Flatus

182
Q

Example of Thiazolidinediones + Mechanism

A

Example: Pioglitazone MOA: PPAR-γ receptor agonist (on Fat cells) –> ↓ peripheral insulin resistance

183
Q

Example of GLP-1 analogues + Mechanism

A

Example: Exenatide, Liraglutide MOA: ↑ insulin, ↓ glucagon, ↑ satiety

184
Q

Example of Gliptins + Mechanism

A

Example: Sitagliptin, Linagliptin MOA: ↑ half-life of endogenous GLP-1

185
Q

Layers of the adrenal (4) + hormones

A

Zona glomerulosa –> Aldosterone Zona fasciculata –> Cortisol Zona reticularis –> Sex steroids Medulla –> Catecholamines

186
Q

Adrenal vasculature

A

L adrenal vein –> L renal vein R adrenal vein –> IVC Arteries on outside (picks up aldosterone –> cortisol –> sex steroids –> adrenaline –> central vein)

187
Q

Macroscopic appearance of adrenals

A

Golden-yellow outer cortex Inner red-grey medulla Mercedes-Benz sign

188
Q

Causes of adrenal atrophy

A

Addison’s disease, TB, Chronic cortisteroid use

189
Q

Causes of adrenal enlargement

A

Cushing’s syndrome or Idiopathic adrenal hyperplasia

190
Q

Schmidt’s syndrome

A

Schmidt’s syndrome = Addison’s disease + Primary hypothyroidism

191
Q

Primary hypothyroidism - Ix

A

↓ T4, ↑ TSH

192
Q

Addison’s disease - Causes, Dx

A

Addison’s disease = ↓ cortisol, ↓ aldosterone –> ↓ Na, ↑ K, ↓ glucose Causes - Autoimmune - TB Ix: Short synACTHen test - Normal: ↑ Cortisol - Addisons: ↓ Cortisol

193
Q

Phaeochromocytoma - Ix, Tx, RF, Staining, rule of 10s, location

A

Phaeochromocytoma = adrenal medullary tumour secreting catecholaemines Ix: ↑ 24 hr urinary catecholaemines Tx: α blockade (phenolamine), then β-blockade, then surgery RF: MEN2(A/B), VHL, NF1 Chromaffin staining: dichromate fixative turns brown with catecholaemines 10% bilateral, 10% extra-adrenal (paraganglia - carotid bodies, aortic bodies, bladder wall), 10% in children, 10% malignant

194
Q

Primary hyperaldosteronism - Causes, Sx, Ix

A

Conn’s syndrome (2/3) Bilateral adrenal hyperplasia (1/3)

195
Q

Bilateral adrenal hyperplasia - causes

A

Cushing’s syndrome or Idiopathic adrenal hyperplasia

196
Q

Conn’s syndrome - Sx, Ix

A

Conn’s syndrome = tumour of zona glomerulosa –> produces Aldosterone ↑ Aldosterone –> ↑ Na+, ↓ K+, Hypertension (in a young individual), ↓ Renin Hypertension + Hyperkalaemia –> CONN’S

197
Q

Benign adrenal mass - Epi

A

10% general population have incidental non-functioning adrenal mass

198
Q

Cushing’s syndrome - causes

A

Exogenous steroids - most common Pituitary adenoma (Cushing’s disease) - 85% Ectopic ACTH (lung cancer) Adrenal adenoma (zona fasciculata)

199
Q

Cushing’s syndrome - Ix

A

Diurnal cortisol (9am cortisol, midnight cortisol) - Normal: ↑ 9am cortisol, ↓ midnight cortisol (if asleep) - unreliable if awake - Cushing’s: ↑ 9am cortisol, ↑ midnight cortisol (if asleep) - only reliable in well individuals (no stress) Low-dose dexamethasone supression test - Normal: LOW cortisol - Cushing’s: Cortisol remains HIGH ——- If remains high –> Inferior Petrosal Sinus Sampling (IPSS) ——- If we remove pitutiary, guessing would be correct 85% of time ——- If MRI pituitary, 10% will have small pitutiary incidentoma ACTH - Adrenal adenoma :↓ ACTH - Exogenous steroids :↓ ACTH - Pituitary adenoma: ↑ ACTH - Ectopic ACTH (lung cancer):↑ ACTH High dose dexamethasone suppression test - 80% of Pituitary adenoma will supress (but so will 20% of ectopic ACTH)

200
Q

How to DDx Cushing’s syndrome

A

Inferior Petrosal Sinus Sampling (IPSS) - confirms pitutiary origin of pathology (i.e. Cushing’s disease) - only done to exclude pituitary-cause of ACTH

201
Q

High dose dexamethsone suppression test - results

A

80% of Cushing’s disease (pituitary-dependent) will supress BUT 20% of ectopic ACTH (lung cancer) will also suppress ∴ now do IPSS

202
Q

Obese with Cushing’s syndrome Ix

A

↑ 9am cortisol ↓ midnight cortisol (if asleep) Low dose dexamethasone supression test: ↓ cortisol If midnight cortisol incorrectly performed when awake –> ↑ midnight cortisol Sent for MRI (10% have benign pituitary incidentoma) –> pituitary removed –> now hypopit….

203
Q

Stain for amyloid

A

Congo Red (apple green birefringence)

204
Q

DDx Rosette (histology)

A
  • Adrenal neuroblastoma - Pancreatic neuroendocrine tumour - Medulloblastoma (CNS)
205
Q

Should you aggressively manage BP and lipids?

A

Aggressive management of BP and lipids –> ↑ survival

206
Q

Options for statin intolerant patients

A

Ecetemibe Plasma exchange Evolocumab (PCSK9 monoclonal antibody –> ↓ LDL receptor recycling –> ↑ LDL receptors –> ↓ circulating LDLs)

207
Q

Benefits of Evolucumab

A

↓ LDL cholesterol ↓ non-fatal MI BUT no effect on cardiovascular death

208
Q

Does good glucose control prevent complications

A

YES - but benefits only seen after 15 years in newly diagnosed T2DM ∴ should start good glucose control ASAP

209
Q

How long do benefits of good glucose control last?

A

Despite stopping intense control, benefits last 10-30 years = Legacy effects

210
Q

Should you intensely controly BMs in long-standing diabetics

A

Sudden tight control in long-standing diabetic patients (with knacked coronary arteries) will prevent some complications (nephropathy) BUT will ↑ mortality

211
Q

Which drugs should be used in long-standing sub-optimal T2DM

A

SGLT2 inhibitor (empagliflozin) or GLP-1 analogue (liraglutide)

212
Q

Step-up management of T2DM

A

(1) Metformin If not reach HbA1c target within 3 months –> (2) + 2nd agent If long-standing sub-optimally controlled T2DM –> add SGLT2 inhibitor (Empagliflozin)

213
Q

Management of Hypoglycaemia

A

Alert + Orientated –> oral carbohydrate (rapid + long acting) Drowsy/Confused + Swallow intact –> Gel glucose (sublingual) Unconscious OR concerns about swallow –> IV 50ml 50% glucose +/- 1mg Glucagon (takes 20min to work)

214
Q

Whipple’s triad

A

Low glucose < 4 mmol/L Symptoms of Hypoglycaemia - Adrenergic: Tremor, Palpitation, Sweating, Anxeity - Neurological: Confusion, Seizures - Asymptomatic (if recurrent –> impaired awareness) Relieved with glucose administration

215
Q

Response to hypoglycacemia (in order of timing)

A

In order of timing: ↓ Insulin, ↑ glucagon, ↑ adrenaline, ↑ cortisol ↑ glycogenolysis, ↑ gluconeogenesis, ↑ liposis –> ↑ Glucose, ↑ FFA (–> ketones)

216
Q

C-peptide (formation, marker, feedback)

A

β-cells produce pro-insulin –> C-peptide and Insulin (equimolar amounts) C-peptide is marker of insulin production (longer half life) If ↑ insulin –> ↓ production –> ↓ C-peptide (-ve feedback)

217
Q

DDx ↓ insulin, ↓ C-peptide

A

Hypoinsulinaemic hypoglycaemia - i.e. endogenous insulin production is switched off in response to hypo (something else causes hypo) - Fasting / Starvation - Strenuous exercise - Addison’s - Liver failure - Anorexia nervosa (limited endogenous glycogen stores)

218
Q

↓ Glucose, ↓ insulin, ↓ C-peptide, ↓ FFA, ↓ Ketones

A

Non-islet cell tumour hypoglycaemia - Paraneoplastic tumour secretes Big IGF-2 which has same effect as insulin - ↓ suppresses endogenous insulin production –> ↓ insulin, ↓ C-peptide

219
Q

Hypoglycaemia + ↓ Ketones

A

Fatty acid oxidation defect (e.g. MCADD) Normally, hypoglycaemia –> ↓ insulin, ↑ glucagon –> ↑ glucose, ↑ FFA –> ketones (but this doesn’t happen)

220
Q

Exampes of ketone bodies

A

3-hydroxybutyrate, Acetoacetate, Acetone (pear-drop smeall in DKA)

221
Q

DDx ↑ insulin, ↑ C-peptide

A

Hyperinsulinaemic hypoglycaemia - i.e. endogenous insulin drives hypo - Insulinoma - Sulphonylurea (↑ insulin effect) - Islet cell hyperplasia - Familial hypoglycaemia (glucokinase activating mutation)

222
Q

Dx insulinoma

A

Must exclude sulphonylurea abuse - Ix Sulphonylurea drug screen - in order to diagnose insulinoma

223
Q

DDx ↑ insulin, ↓ C-peptide

A

Exogenous insulin

224
Q

Autoimmune hypoglycaemia

A

Anti-insulin receptor Ab and Anti-insulin Ab

225
Q

Post-prandial hypoglycaemia

A

Food intake –> hypoglycaemia (in insulin sensitive individuals)

226
Q

Portal triad

A

Hepatic artery, Hepatic vein, Bile duct

227
Q

Hepatic lobule flow

A

Blood flows from portal triad –> Sinusoids (endothelium is discontinuous with Space of Disse where metabolism occurs) –> central vein Bile flows in opposite direction

228
Q

Zones of Liver (differences of metabolism)

A

Zone 1 (around portal triad, best O2), Zone 2, Zone 3 (least O1, most metabolically active cells)

229
Q

Van den Bergh reaction

A

Direct reaction measures conjugated BR Adding methanol –> measure total BR Indirectly measure unconjugated BR

230
Q

BR cycle

A

BR in bile –> Bowel –> converted to sterobilinogen –> re-absorbed as Urobilinogen –> Urine

231
Q

Gilbert’s syndrome

A

Autosomal recessive –> ↓ activity of UDPGT enzyme

232
Q

Hepatitis A

A

Faecal-oral transmission (contaminated water), Acute IgM reponse, Then IgG response (can only get Hepatitis A once)

233
Q

Hepatitis B

A

HbSAg = +ve indicates active infection (acute or chronic) anti-HBs = +ve indicates vaccination or previous exposure/cleared anti-HBc = previous exposure/cleared IgM anti-Hbc = +ve acute infection IgG anti-Hbc = +ve indicates chronic infection eAg +ve = highly infectious eAb +ve = not very infectious

234
Q

Histological features of Alcohol hepatitis

A

Fatty change Mallory Denk bodies (damaged hepatocyte intermediate filaments) Megamitochondria Inflammation (PMN neutrophils) Fibrosis (collagen-staining)

235
Q

Histological features of NASH

A

Same as Alcoholic hepaitis Clues in the history - alcohol

236
Q

Liver failure results in

A

↓ synthetic function –> ↓ clotting, ↓ albumin ↓ clearance of BR and ammonia –> encephalopathy

237
Q

Macroscopic changes of Alcoholic liver disease

A

Pale (fatty), Nodular (regenerating hepatocytes), Fibrous cuffs around nodules

238
Q

Types of shunting

A

Intrahepatic shunting - Fibrosis blocks normal flow of blood ∴ intra-hepatic shunting bypasses hepatocytes –> central vein (toxins enter systemic circulation) Extrahepatic shutning - Caput medusae - Oesophgeal varices - Ascites - Splenomegaly Tx: β-blockers, spleno-renal shunt (bypass liver + toxins enter systemic circulation)

239
Q

Courvoisier’s law

A

Jaundice + palpable gallbladder = Pancreatic cancer Gallstones –> non-palpable, shrunken, small, fibrotic gallbladder

240
Q

Define GFR + NR

A

Glomeruar filtration rate = flow from glomerulus to Bowman’s capsule NR > 90 ml/min

241
Q

Ideal marker for GFR

A

Not bound to serum proteins Freely filtered Not secreted or absorbed IF ALL TRUE –> Clearance = GFR

242
Q

Define clearance

A

Clearance = [urine] x V / [plasma] = volume of plasma which is completed cleared of a substance in a unit of time

243
Q

Markers of GFR (5)

A

Inulin Cr-EDTA Blood urea Serum creatinine Cystatin C

244
Q

Gold standard marker for GFR

A

Inulin BUT not used clinically (difficult measuring inulin concentration), only used in Research

245
Q

Exogenous marker of GFR used clinically

A

Cr-EDTA (single injection GFR measurement, measure radioactivity in plasma samples) BUT only used prior to chemotherapy (requires accurate GFR measurement)

246
Q

Endogenous markers of GFR

A

Blood urea (highly dependent on nutritional state ∴ limited clinical value) Creatinine - geneartion depends on muscle mass, age, sex and ethnicity, actively secreted by tubular cells and non-linear relationship with GFR Cystatin C - difficult to acquire this assay (only used if eGFR 45-59 and normal albumin-to-Creatinine ratio), influenced by thyroid dysfunction

247
Q

Equation to estimate GFR using Creatinine

A

CKD-EPI –> used to calculate eGFR

248
Q

How to quantify proteinuria

A

Urine Protein:Creatinine Ratio (PCR) 24 hour urine collection no longer used

249
Q

Urine dipstick: haematuria

A

-ve reliably excludes haematuria +ve suggests blood OR myoglobinuria (rhabdomyolysis)

250
Q

Urine dipstick: protein

A

Sensitive for albumin (poor sensitivity for Bence Jones proteins)

251
Q

Urine dipstick: leucocyte esterase

A

-ve result is clinically significant

252
Q

Urine dipstick: nitrite

A

Detects bacteria (esp Gram -ve) -ve result does NOT exclude UTI (not all bacteria produce nitrites)

253
Q

Urine microscopy

A

Looks for Crystals (stones) RBC (stones, UTI) WBC (UTI, glomerulonephritis) Casts (glomerulonephritis) Bacteria (UTI)

254
Q

Calcium oxalate crystals suggest

A

Anti-freeze poisoning Ethylene glycol is metabolised to calcium oxalate –> precipitates as crystals in renal tubules/ureters

255
Q

1st line Ix for renal stones

A

CT KUB

256
Q

Staghorn calculi - cause, component

A

Due to recurrent UTI with urease-producing bacteria (proteus, klebsiella, pseudomonas, Enterobacter) Composed of magnesium ammonium phosphate

257
Q

Use of USS KUB

A

Hydronephrosis suggests AKI Small, shrunken kidneys suggest CKD

258
Q

Use of DMSA scan

A

Look for anatomical defects

259
Q

Use of renal biopsy

A

Gold standard for diagnosis

260
Q

Define AKI

A

↑ serum Creatinine (↑ 0.3mg/dl) ↓ urine volume (<0.5ml/kg/hr)

261
Q

AKI vs CKD

A

AKI: acute ↓ GFR, reversible, Tx aims to reverse disease process CKD: long standing ↓ GFR, irreversible, Tx aims to prevent worsening disease + prevent complications of CKD

262
Q

DDx AKI vs CKD

A

Renal biopsy (AKI will likely show acute tubular necrosis)

263
Q

Types of AKI

A

Pre-renal, Intrinsic, Post-renal

264
Q

Causes of pre-renal failure

A

Acute blood loss Hypotension Oedematous states (ascites, pleural effusion) Renal artery stenosis Drugs (NSAIDs, Calcineurin inhibitors, ACEi, ARBs, Diuretics)

265
Q

ACEi and renal artery stenosis

A

Kidney compensates for renal artery stenosis by constricting/dilating other renal arteries/arterioles to maintain GFR ACE inhibitor disrupts these compensatory mechanisms –> acute AKI

266
Q

Causes of post-renal failure

A

Intra-renal obstruction Ureteric obstruction Prostatic / Urethral obstruction Blocked urinary catheter

267
Q

USS to DDx likely location of post-renal failure

A

If single kidney has dilated calyces, obstructive uropathy –> issue in ureter If both kidneys affected, problem in bladder or lower down

268
Q

Causes of Intrinsic AKI

A

Vascular disease (e.g. vasculitis) Glomerular disease (e.g. glomerulonephritis) Tubular disease - Ichaemic (most common) - prolonged pre-renal AKI –> acute tubular necrosis - Endogenous toxins (rhabdomyolysis –> myoglobinuria, Ig in multiple myeloma) - Exogenous toxins (contrast, nephrotoxic drugs) Interstitial disease (e.g. analgesic nephropathy)

269
Q

Mechanisms of renal injury

A

Inflammation (glomerulonephritis, vascultisi) Protein deposition OR infiltration (amyloidosis, lymphoma, myeloma)

270
Q

Nephrotoxic drugs

A

Aminoglycosides (gentamicin, amikasin), aciclovir

271
Q

Signs of ATN

A

Epithelial cell casts in urine

272
Q

Causes of CKD

A

Diabetes Atherosclerosis Hypertension Chronic glomerulonephritis Obstructive uropathy Polycystic kidney disease

273
Q

Normal kidney function

A

Homeostatic function (excretion of water-soluble waste, water balance, electrolyte balance, acid-base) Hormonal funcion (EPO, RAS, Vitamin D)

274
Q

Consequences of CKD

A

Failure of acid base homeostasis –> Metabolic acidosis, Hyperkalaemia (failure to excrete H+ ions, K+ leaves cells to swap for H+ to maintain elec neutrality) —– Tx: oral sodium bicarbonate Failure of hormonal function –> Anaemia, Renal bone disease —– Tx: EPO —– Tx: Phosphate bindiners, activated Vitamin D, Cinacalcet (suppresses PTH), Dialysis ↑ risk of CVD - Vascular calcification - different to traditional lipid-rich atheromas - Uraemic cardiomyopathy (LV hypertrophy, dilatation, dysfunction) Uraemia

275
Q

Major cause of hyperkalaemia in CKD

A

Dietary intake (milk, chocolate, dried fruit, tomatoes)

276
Q

Types of renal bone disease

A

Osteitis fibrosa - due to HyperPTH –> resorption of calcified bone (replaced by fibrosis tissue) Osteomalacia - due to Vitamin D deficiency –> demineralisation of bone osteoid Adyanmic bone disease - complication of Tx of HyperPTH, supression of PTH –> LOW bone turnover and LOW osteoid

277
Q

Types of renal replacement therapy

A

Haemodialysis - through fistula, in hospital Peritoneal dialysis - at home, less effective Transplantation - pelvic kidney

278
Q

Contraindications for renal transplant

A

Untreated malignancy Untreated HIV infection Active infection Life expectancy < 2 years

279
Q

Indications for dialysis as an emergency

A

Pulmonary oedema Refractory hyperkalaemia Metabolic acidosis Uraemic encephalopathy Drug toxicity (e.g. Lithium)

280
Q

Smith’s fracture

A

Smith’s fracture = Reverse of Colles’s fracture (i.e. fracture if forward, not backwards) Fallen on hand inflexed (land on back of hand)

281
Q

DDx haematuria

A

Renal stones - painful haematuria Glomerulonephritis - painless haematuria, autoimmune Subacute bacterial endocarditis - microscopic haematuria

282
Q

Ix for renal stones

A

Abdo X-ray: detects Calcium renal stones (radio-opaque), quick, misses non-calcified renal stones (uric acid, gout = radiolucent) OR Abdo USS: detects ALL renal stones, need to book

283
Q

Ix of choice if found renal stones

A

Calcium (N.B. PTH is un-interpretable without Ca)

284
Q

Complications of hypercalcaemia

A

Renal stones (calcium), Pancreatitis, Osteitis fibrosa et cystica (↑ osteoclast activation –> osteolytic lesions –> fractures)

285
Q

Which organism causes UTI in Calcium renal stones

A

Proteus maribilius

286
Q

Risk factors for renal calcium stones

A

Dehydration, Hypercalacemia, Hyperparathyroidism, Hypercalciuria

287
Q

Tx of renal stones

A

Watchful waiting (most stones pass), Lithotrypsy (USS waves), Cystopscopy (look and pull), Lithotomy (open and remove)

288
Q

Parathyroidectomy - Ix to open or not?

A

Technicium scan + USS results concordant –> do not need to open neck If NOT concordant –> surgical open neck to visual all 4 parathyroids + remove largest parathyroid

289
Q

CXR of Sarcoidosis

A

Bilateral hilar lympadenopathy

290
Q

Histology of Sarcoidosis

A

Non-caseating granuloma

291
Q

Histology of TB

A

Caseating granuloma

292
Q

DDx of non-caseating granuloma

A

Sarcoidosis, Crohn’s disease, PBC

293
Q

ECG territories + arteries

A

II, III, aVF = RCA I, aVL, V5, V6 = LCA V1-V4 = LAD

294
Q

Anterior pitutary hormones (6) + their hypothalmic control

A

GHRH –> GH TRH –> TSH & Prolactin LHRH –> FSH/LH CRH –> ACTH N.B. Prolactin is controlled by TRH (+ve) and Dopamine (-ve)

295
Q

Define macroadenoma and microadenoma

A

MRI pituitary macroadenoma > 1cm (visual field defects) and microadenoma < 1cm (10% general population)

296
Q

Ix for Macroadenoma

A

MRI + visual field assessment

297
Q

Causes of ↑ prolactin

A

Prolactinoma, DA antagonists (anti-psychotics), Pregnancy

298
Q

Components of combined pitutiary function test (CPFT)

A

Tip: it’s gonna get LIT —- LHRH –> stimulates LH/FSH —- Insulin –> induce hypoglycaemia –> stimulates ACTH and GH —- TRH –> stimulates TSH and Prolactin Assess function of anterior pituitary

299
Q

Contraindications to pituitary function test (3)

A

IHD, Epilepsy, untreated hypothyroidism (impairs GH and cortisol response)

300
Q

Interpreting pitutiary function test

A

Direction of change (rise, fall) is important - rather than absolute numbers Glucose < 2.2mM required for test to be valid (adequate hypoglycaemia) Prolactin > 6000 suggests Prolactinoma

301
Q

Treatment for Pituitary failure

A

Hormone replacement - Hydrocortisone (most urgent) - Thyroxine - Oestrogen replacement - GH replacement N.B. Do not need to give Fludrocortisone (aldosterone replacement) as Pituitary does NOT control Aldosterone (RAS does!)

302
Q

Treatment for prolactinoma

A

Dopamine agonists (Cabergoline, Bromocriptine) +/- Surgery

303
Q

Non-functioning pitutiary adenoma

A

Non-functioning adenoma compresses stalk –> pituitary failure Prevent DA reaching pitutiary ∴ ↓ negative inhibition to produce prolactin –> hyperprolactinaemia

304
Q

Acromegaly - Ix

A

GH: ↑ IGF-1: ↑ OGTT: - normal: ↓ GH - Acromegaly: ↑ GH (unknown why)

305
Q

Stimulate GH relase

A

Exercise, Insulin (gold standard)

306
Q

Acromegaly - Tx

A

Pituitary surgery Pituitary radiotherapy Cabergoline Octerotide

307
Q

Should you use prednisolone vs hydrocortisone

A

Prednisolone mimics circadian rhythm of cortisol release more closely than hydrocortisone (rapidly metabolised, needs multiple doses)

308
Q

Does pituitary failure cause hypotension?

A

NO - pitutiary failure causes ↓ GH, ↓ Prolactin, ↓ TSH, ↓ FSH/LH, ↓ ACTH (–> ↓ Cortisol) Cortisol does not control BP Addison’s disease –> ↓ cortisol + ↓ aldosterone (–> ↓ BP) Aldosterone controls BP Pituitary does NOT control aldosterone (RAS does!)

309
Q

Posterior pituitary hormones

A

ADH/Vasopressin, Oxytocin

310
Q

Use of enzymes

A

Identify disease, detect tissue injury, markers of therapeutic response, enzymes to measure other substances

311
Q

Release of enzymes following tissue injury (location)

A

Small amount of intracellular enzymes normally reponse (normal cell turnover) Tissue injury –> release of cytosolic enzymes, then sub-cellular enzymes

312
Q

Define iso-enzyme

A

Different forms of the same enzyme

313
Q

Which tissues produce ALP

A

Liver, Bone, Placenta, Intestine

314
Q

DDx iso-forms of ALP

A

Electrophoresis or bone-specific assay of ALP

315
Q

Physiological causes of ↑ ALP

A

Pregnancy, growth spurt

316
Q

Pathological causes of ↑ ALP (from bone)

A

Paget’s (highest ALP), Osteomalacia, Tumours, Fractures, Osteomyelitis

317
Q

Pathological causes of ↑ ALP (from liver)

A

Cholestasis (highest ALP), Cirrhosis, Infiltrative disease of liver, Hepatitis

318
Q

Enzyme markers in acute pancreatitis

A

↑ Amylase, ↑ Lipase (more specific)

319
Q

Causes of ↑ amylase

A

Acute pancreatitis, Salivary gland pathology (Mumps), acute abdomen states

320
Q

3 isoforms of creatine kinase

A

Forms dimers, 3 isoforms — CK-MM = Muscle (95%) — CK-MB = Cardiac (5%) — CK-BB = Brain (1%) N.B: mesauring CK measures all 3 isoforms (individual isoforms are NOT routinely measured)

321
Q

Causes of ↑ CK

A

Muscle damage (falls, injection) Myopathy —– Statin-related myopathy (onset within weeks of starting statin, spectrum from myalgia to rhabdomyolysis –> AKI) —– Ducheene muscular dystrophy —– Polymyositis / Dermatomyosistis MI (non-specific marker) Ethnicity (Afro-Carribean)

322
Q

Cardiac biomarkers for MI

A

(1) Myoglobin - rapid rise and fall (non-specific as found in all muscle fibres, found in cytoplasm) (2) Cardiac troponin (2nd to rise, found within contractile apparatus) (3) CK-MB (found in nucleus and mitochondria)

323
Q

Current marker of choice for MI

A

Cardiac troponin (NOT an enzyme)

324
Q

When to measure cardiac troponin

A

Measure at 6 hours and 12 hours AFTER onset of chest pain Lack of troponin rise excludes MI (98% specifcity and 100% sensitivity at 12 hours) Cardiac troponin rises 4-6 hours post MI, peaks at 12 hours and remains elevated for 10 days

325
Q

Diagnostic criteria for MI

A

Rise and fall or Troponin OR rise and fall or CK-MB + 1 of following (ischaemic symptoms, pathological Q waves, ECG ischaemic changes, coronary artery intervention)

326
Q

Biomarkers in heart failure

A

Atrial natriuretic peptide (secreted by atria) Brain natriuretic peptide (secreted by ventricles)

327
Q

What do enzyme assays measure

A

Enzyme activity (NOT enzyme mass)

328
Q

Define the unit of enzyme activity

A

1 international unit = quantity of enzyme required to catalyse the reaction of 1umol of substrate per minute (at a given tmperature and pH) Unit = U/L

329
Q

Specific liver enzyme marker

A

GGT

330
Q

Vitamin and Mineral markers

A

Vitamin A: serum Vitamin A (rare) Vitamin D: 25(OH)D3 = inactive form Vitamin E: serum Vitamin E (rare) Vitamin K: INR Vitamin B1: RBC transketolase (rare) Vitamin B2: Serum Vitamin B2 (rare) Vitamin B6: RBC AST activation (rare) Vitamin B12: Serum B12 Vitamin C: Serum Vitamin C (rare) Folate: RBC folate Niacin: no test available

331
Q

Fat soluble vitamins

A

Vitamin A, D, E, K

332
Q

Vitamin A deficiency

A

Colour blindness

333
Q

Vitamin A excess

A

Exfoliation hepatitis

334
Q

Vitamin D deficiency

A

Osteomalacia/Rickets

335
Q

Vitamin D excess

A

Hypercalcaemia (and secondary hypoparathyroidism)

336
Q

Vitamin E deficiency

A

Anaemia, Neuropathy

337
Q

Vitamin K deficiency

A

Prolonged PT –> bleeding

338
Q

Types of Vitamin B1 deficiency (thiamine)

A

Wet Beri Beri and Dry Beri Beri

339
Q

Wet Beri-Beri

A

Heart failure, Oedema

340
Q

Dry Beri-Beri

A

Wernicke’s encephalopathy (Ataxia, Confusion, Eye signs - opthalmoplagia)

341
Q

Vitamin B2 deficiency (riboflavin)

A

Glossitis

342
Q

Vitamin B6 deficiency (pyridoxine)

A

Dermatitis, Anaemia

343
Q

Vitamin B6 excess

A

Neuropathy

344
Q

Vitamin B12 deficiency (cobalamin)

A

Due to: Pernicious anaemia Peripheral neuropathy

345
Q

Vitamin C deficiency (ascorbate)

A

Scurvy

346
Q

Vitamin C excess

A

Renal stones

347
Q

Folate deficiency

A

Megaloblastic anaemia, Neural tube defects

348
Q

Niacin deficiency

A

Pellegra (Dermatitis, Diarrhoea, Dementia, Death)

349
Q

Iron deficiency

A

Microcytic anaemia

350
Q

Iron excess

A

Due to haemochromatosis Bronze diabetes, Infertility (iron deposition)

351
Q

Iodine deficiency

A

Hypothyroidism, Goitre

352
Q

Zinc deficiency

A

Dermatitis

353
Q

Copper deficiency

A

Anaemia

354
Q

Copper excess

A

Due to Wilson’s disease Kayser-Flyscher rings, deposition in basal ganglia

355
Q

Fluoride deficiency

A

Dental caries (tooth decay)

356
Q

Fluoride excess

A

Flourosis (teeth staining)

357
Q

Hunger hormone

A

Ghrelin

358
Q

Satiety hormones

A

PYY, Leptin

359
Q

Defintion of obesity

A

Based on BMI (>25), Waist:hip ratio, Waist circumference

360
Q

Types of protein

A

Indispensable proteins (only available from diet) “Conditoinally” indispensable proteins (required for certain parts of lifespan e.g. fetus) Dispensable proteins = human body can only produce 5 amino acids

361
Q

Assessment of protein

A

Assessment of muscle bulk

362
Q

Types of fat

A

Saturated (bad), Monounsaturated, Polyunsaturated (best), Trans-monosaturates (worst), Cis-monosaturates

363
Q

Types of carbohydrates

A

Oligosaccharides (simple), Polysaccharides (complex), non-starch carbohydrates (fibre)

364
Q

Metabolic syndrome pentad

A

Diabetes, ↑ waist circumference, insulin resistance, ↓ HDL levels, hypertension

365
Q

Types of Malnutrition

A

Marasmus: due to low calorie intake –> severe muscle wasting, no subcutaneous fat Kwashiorkor: due to lack of protein –> oedematous, hepatomegaly, lethargic

366
Q

Ix to decide whether to start statin therapy

A

Total plasma cholesterol, plasma LDL

367
Q

6 liver functions

A

Intermediary metabolism (glycolysis, glycogen storage, gluconeogenesis) Protein synthesis (clotting factors, albumin) Xenobiotic metabolism (detoxification of drugs) Hormone metabolism (Vitamin D, steroid hormone, peptide hormone catabolism/recycling amino acids) Bile synthesis Reticulo-endothelial (Kupffer cells clear infection, Erythropoesis in thalassaemia)

368
Q

Process of xenobiotic metabolism

A

(1) Chemical modification (redox, acetylation/de-acetylation, CYP450) (2) Conjugation (glucoronate, sulphate) (3) Excretion in bile

369
Q

LFTs

A

ALT, AST, ALP, GGT

370
Q

Markers of liver’s synthetic function

A

Albumin, PT

371
Q

AST > ALT

A

Alcoholic hepatitis (alcoholicS)

372
Q

ALT > AST

A

ViraL hepatitis

373
Q

↑ GGT

A

Chronic alcohol use, bile duct disease, liver mets, drugs

374
Q

↑ ALP

A

Obstructive jaundice (gallstones, pancreatic cancer), Bile duct damage, viral hepatitis, alcoholic liver disease

375
Q

Albumin half life

A

Long half life (20 days) ∴ ↓ albumin indicates long-term change

376
Q

Causes of ↓ albumin

A

↓ production (chronic liver disease, malnutrition) Loss (in gut, in kidney) Sepsis (3rd spacing sepsis, albumin enters tissue spaces –> oedema)

377
Q

Clotting half life

A

T1/2 = hours ∴ acute marker of liver function

378
Q

↑ AFP

A

Hepatocellular carcinoma (hepatic damage, pregnancy, testicular cancer)

379
Q

If ↑ ALP, next Ix

A

USS If ducts dilated –> gallstones, cancer If ducts not dilated –> drugs, PBC, PSC, pregnancy

380
Q

Why pale stools, dark urine

A

No BR enters gut –> no sterco/urobilinogen –> pale stools Conjugated BR backpressure into systemic circulation –> water soluble so enters urine –> dark urine (only conjugated BR is water soluble)

381
Q

Isolated ALT + asymptomatic

A

Fatty liver

382
Q

↑ serum bile acids

A

Cholestasis of pregnancy, PBC, PSC

383
Q

Drug-induced cholestasis

A

Augmentin, Co-amoxiclav

384
Q

Causes of ALT > 1000

A

Toxins (paracetamol) Viruses (viral hepatitis, EBV, CMV) Ischaemia

385
Q

Isolated ↑ unconjugated BR, normal LFTs

A

Gilbert’s syndrome

386
Q

NR of Na

A

135 - 145

387
Q

NR of K

A

3.5 - 5.3

388
Q

NR of Hb

A

M 13.5 - 18.0, F 11.5 - 16.0

389
Q

NR of WBC

A

4-11

390
Q

NR of Plt

A

150-400

391
Q

NR of Urea

A

2-7

392
Q

NR of Creatinine

A

55-120

393
Q

NR of osmolality

A

275-295

394
Q

MEN1 (3Ps)

A

Pituitary, Pancreatic, Parathyroid

395
Q

MEN2A (2Ps, 1M)

A

Parathyroid, Phaeo, Medullary thyroid

396
Q

MEN2B (1P, 2Ms)

A

Phaeo, Medullary thyroid, Mucocutaneous neurmas (& Marfanoid)

397
Q

ALP stands for

A

Alkaline phosphatase (ALP)

398
Q

ALT stands for

A

Alanine aminotransferase (ALT)

399
Q

AST stands for

A

Aspartate aminotransferase (AST)

400
Q

GGT stands for

A

Gamma glutamyl transferase (GGT)

RW Pathology (9 decks)

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