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Path Laz (condensed) > Chem Path > Flashcards

Chem Path Flashcards

1
Q

What are the three main purines?

A

Adenosine

Guanine

Inosine

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2
Q

Which joint is most commonly affected by gout and why might this be?

A

1st metatarsophalangeal joint – found at the periphery of the body so is likely to be cooler (lower temperatures reduce the concentration at which urate precipitates out of solution)

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3
Q

Describe how the kidneys handle urate.

A

The proximal convoluted tubule reabsorbs and secretes urate

NOTE: the reason urate is reabsorbed is probably because it is an important anti-oxidant that protects us from oxidative stress

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4
Q

Roughly what proportion of filtered urate will be found in the urine? What term is used to describe this?

A

10%

This is fractional excretion of uric acid (FEUA)

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5
Q

What inborn error of purine metabolism is characterised by HPRT deficiency?

A

Lesch-Nyhan syndrome - x-linked recessive

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6
Q

Outline the clinical features of Lesch-Nyhan syndrome

A

Normal at birth

Developmental delay at 6 months

Hyperuricaemia

Choreiform movements at 1 year

Spasticity and mental retardation

Self-mutilation present in 85% (e.g. biting lips very hard)

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7
Q

What are the two types of gout?

A

Acute (podagra)

Chronic (tophaceous)

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8
Q

Describe how the birefringence/crystals differ between gout and pseudogout.

A

Gout – monosodium urate crystals – needle-shaped and negatively birefringent

Pseudogout – calcium pyrophosphate crystals – rhomboid-shaped and positively birefringent

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9
Q

List three drug classes that are used in the acute management of gout.

A

NSAIDs

Colchicine

Glucocorticoids

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10
Q

Describe the management of gout after the acute phase is over.

A

Encourage fluid intake

Reverse factors that may increase the concentration of uric acid (e.g. stopping diuretics)

Allopurinol – reduces synthesis of urate by inhibiting xanthine oxidase

Probenecid – increases renal excretion of urate (increases FEUA)

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11
Q

Which drug is contraindicated with allopurinol?

A

Azathioprine

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12
Q

What underlying condition is pseudogout often associated with?

A

Osteoarthritis

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13
Q

List some clinical features of familial hypercholesterolaemia.

A

Xanthelasma

Corneal arcus

Tendon xanthomata

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14
Q

List some causes of secondary hyperlipidaemia.

A

Pregnancy

Hypothyroidism

Obesity

Nephrotic syndrome

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15
Q

List some lipid-lowering drugs and their effect on lipid levels.

A

Statins – reduce LDLs, increase HDLs, slight increase in triglycerides

Fibrates – lower triglycerides, little effects on LDL/HDL

Ezetimibe – reduces cholesterol absorption (blocks NPC1L1)

Colestyramine – resin that binds to bile acids and reduces their absorption

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16
Q

List some novel forms of lipid-lowering drugs

A

Lomitapide – MTP blocker

REGN727 – anti-PCSK9 monoclonal antibody

Mipomersen – anti-sense ApoB oligonucleotide

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17
Q

List three types of bariatric surgery.

A

Gastric banding

Roux-en-Y gastric bypass

Biliopancreatic diversion

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18
Q

List some beneficial effects of bariatric surgery.

A

Reduced diabetes risk

Reduced serum triglycerides

Increased HDLs

Reduced fatty liver

Reduced blood pressure

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19
Q

Which investigations are performed if a pre-hepatic cause of jaundice is suspected?

A

FBC

Blood film

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20
Q

What is the most common cause of paediatric jaundice?

A

Neonates have immature livers that cannot conjugate bilirubin fast enough resulting in a UNconjugated hyperbilirubinaemia

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21
Q

What is the inheritance pattern of Gilbert’s syndrome?

A

Autosomal recessive

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22
Q

Which drug can reduce bilirubin levels in Gilbert’s syndrome?

A

Phenobarbital

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23
Q

Outline the pathophysiology of Gilbert’s syndrome.

A

UDP glucuronyl transferase activity is reduced to 30% of normal

Unconjugated bilirubin is tightly albumin bound and does not enter the urine

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24
Q

What can worsen bilirubin levels in Gilbert’s syndrome?

A

Fasting

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25
Q

What is the significance of absent urobilinogen in the urine?

A

The absence of urobilinogen in the urine is suggestive of biliary obstruction

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26
Q

What is the most representative marker of liver function?

A

Prothrombin time (normal = 12-14 seconds)

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27
Q

What is another good marker of liver synthetic function

A

Albumin

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28
Q

Outline how hepatitis A serology changes over time.

A

As viral titres start to drop following initial infection, there will be a rise in IgM antibodies (during this time you will be unwell with jaundice)

After a few weeks, you will start to produce IgG antibodies (leading to cure and ongoing protection from Hep A)

NOTE: hepatitis A does NOT recur

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29
Q

Name the vaccine for hepatitis A.

A

Havrix (contains some antigens)

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30
Q

Outline the features of hepatitis B serology in acute infection.

A

Initial rise in HBeAg and HBsAg

Eventually you will develop HBeAb and HBsAb resulting in a decline in HBeAg and HBsAg

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31
Q

Outline the features of hepatitis B serology in someone who has been vaccinated.

A

They will have HBsAb but no other antibodies

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32
Q

Describe the histology of hepatitis.

A

Hepatocytes will become fatty and swell (balloon cells), containing a lot of Mallory hyaline

There will also be a lot of neutrophil polymorphs

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33
Q

What are the defining and associated histological features of alcoholic hepatitis?

A

Defining: liver cell damage, inflammation, fibrosis

Associated: fatty change, megamitochondria

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34
Q

List a differential diagnosis for fatty liver disease.

A

NASH (most common cause of liver disease in the Western world)

Alcoholic hepatitis

Malnourishment (Kwashiorkor)

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35
Q

Outline the treatment of alcoholic hepatitis.

A

Supportive

Stop alcohol

Nutrition (vitamins especially thiamine)

Occasionally steroids (controversial but may have useful anti-inflammatory effects)

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36
Q

Vitamin B1 deficiency

A

Beri Beri

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37
Q

Vitamin B3 deficiency

A

Pellagra

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38
Q

List some features of chronic alcoholic liver disease.

A

Palmar erythema

Spider naevi

Gynaecomastia (due to failure of liver to break down oestradiol)

Dupuytren’s contracture

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39
Q

Where does pancreatic cancer tend to metastasise to?

A

Liver

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40
Q

What is phenylketonuria caused by?

A

Phenylalanine hydroxylase deficiency

This enzyme is responsible for converting phenylalanine to tyrosine

Deficiency results in an accumulation of phenylalanine which is toxic

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41
Q

What is the main consequence of untreated PKU?

A

Low IQ

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42
Q

How is PKU investigated?

A

Blood phenylalanine level

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43
Q

Describe the treatment of PKU.

A

Monitor the diet and ensure that the patient is having enough phenylalanine (but not too much)

This must be started within the first 6 weeks of life

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44
Q

What is congenital hypothyroidism usually caused by?

A

Thyroid dysgenesis or agenesis

NOTE: diagnosis is based on high TSH

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45
Q

Describe the pathophysiology of MCAD deficiency.

A

Without MCAD, you will not produce acetyl-CoA from fatty acids, which is necessary in the TCA cycle to produce ketones (which spares glucose)

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46
Q

Outline the treatment of MCAD deficiency.

A

Avoid hypoglycaemia

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47
Q

What are the clinical features of homocystinuria?

A

Lens dislocation

Mental retardation

Thromboembolism

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48
Q

What is the screening test for cystic fibrosis?

A

High serum immune reactive trypsinogen

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49
Q

What do all urea cycle disorders result in?

A

High ammonia

NOTE: this is toxic

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50
Q

What is the mode of inheritance of all of these urea cycle defects?

A

Autosomal recessive

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51
Q

What is the treatment of urea cycle disorders?

A

Remove ammonia (using sodium benzoate, sodium phenylacetate or dialysis) Reduce ammonia production (low protein diet)

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52
Q

List the key features of urea cycle disorders.

A

Vomiting without diarrhoea

Respiratory alkalosis

Hyperammonaemia

Encephalopathy

Avoidance or change in diet

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53
Q

What tends to cause hyperammonaemia with metabolic acidosis and a high anion gap?

A

Organic acidurias

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54
Q

Describe the presenting features of organic acidurias in neonates.

A

Unusual odour

Lethargy

Feeding problems

Truncal hypotonia/limb hypertonia

Myoclonic jerks

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55
Q

Describe the chronic intermittent form of organic acidurias.

A

Recurrent episodes of ketoacidotic coma

Cerebral abnormalities

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56
Q

What is Reye syndrome?

A

Rapidly progressive encephalopathy that can be triggered by aspirin use in children (also triggered by antiemetics and valproate)

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57
Q

Describe the features of Reye syndrome.

A

Vomiting

Lethargy

Increased confusion

Seizures

Decerebration

Respiratory arrest

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58
Q

What would constitute the metabolic screen for Reye syndrome?

A

Plasma ammonia

Plasma/urine amino acid

Urine organic acids

Plasma glucose and lactate

Blood spot carnitine profile (stays abnormal in remission)

NOTE: the top 4 need to be measured during an acute episode because the abnormal metabolites will disappear after a few days

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59
Q

What do defects in mitochondrial fatty acid beta oxidation cause?

A

Hypoketotic hypoglycaemia

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60
Q

Describe the presentation of galactosaemia.

A

Vomiting

Diarrhoea

Conjugated hyperbilirubinaemia

Hepatomegaly

Hypoglycaemia

Sepsis (galactose-1-phosphate inhibits the immune response)

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61
Q

What is a long-term complication of galactosaemia if it is not detected in the neonatal period?

A

Bilateral cataracts

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62
Q

What are the clinical features of Glycogen storage disease type I?

A

Hepatomegaly

Nephromegaly

Hypoglycaemia

Lactic acidosis

Neutropaenia

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63
Q

What is the characteristic appearance of mitochondrial myopathy on a muscle biopsy?

A

Ragged red fibres

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64
Q

List some common problems in LBW babies.

A

Respiratory distress syndrome

Retinopathy of prematurity

Intraventricular haemorrhage

Patent ductus arteriosus

Necrotising enterocolitis

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65
Q

What is necrotising enterocolitis?

A

Inflammation of the bowel wall progressing to necrosis and perforation

Characterised by bloody stools, abdominal distension and intramural air (pneumatosis intestinalis)

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66
Q

Why does glycosuria occur at a lower plasma glucose level in neonates?

A

Short proximal tubule means that they have a lower ability to reabsorb glucose

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67
Q

How are the daily fluid and electrolyte requirements different in neonates compared to adults?

A

Sodium, potassium and water requirements are higher

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68
Q

Drugs can cause electrolyte disturbances in neonates. Give examples of drugs that can do this and briefly describe the mechanism.

A

Bicarbonate for acidosis (contains high Na+)

Antibiotics (usually sodium salts)

Caffeine/theophylline (for apnoea) – increases renal Na+ loss

Indomethacin (for PDA) – causes oliguria

NOTE: growth can also cause electrolyte disturbance

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69
Q

What is hypernatraemia usually caused by in neonates?

A

Dehydration

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70
Q

What is hyponatraemia usually caused by in neonates?

A

Congenital adrenal hyperplasia

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71
Q

Outline the pathophysiology of congenital adrenal hyperplasia.

A

Most commonly caused by 21-hydroxylase deficiency

Leads to reduce cortisol and aldosterone production and shunting of 17-OH progesterone and 17-OH pregnenelone which goes towards androgen synthesis

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72
Q

Outline the clinical features of congenital adrenal hyperplasia.

A

Hyponatraemia/hyperkalaemia

Hypoglycaemia

Ambiguous genitalia in female neonates

Growth acceleration

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73
Q

What is the issue with free bilirubin?

A

It can cross the blood-brain barrier leading to kernicterus

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74
Q

List some causes of neonatal jaundice.

A

G6PD Deficiency

Haemolytic anaemia (ABO, rhesus)

Crigler-Najjar syndrome

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75
Q

List some causes of prolonged jaundice (neonatal)

A

Prenatal infection/sepsis

Hypothyroidism

Breast milk jaundice

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76
Q

List the main biochemical features of osteopaenia of prematurity.

A

Calcium is usually normal

Phosphate < 1 mmol/L

ALP > 1200 U/L (10 x adult ULN)

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77
Q

How is osteopaenia of prematurity treated?

A

Phosphate/calcium supplements

1-alpha calcidol

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78
Q

List some presenting features of rickets.

A

Frontal bossing

Bowed legs

Muscular hypotonia

Tetany/hypocalcaemic seizure

Hypocalcaemic cardiomyopathy

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79
Q

What is porphyria?

A

Disorders caused by deficiencies in enzymes of the haem synthesis pathway

This leads to the accumulation of toxic haem precursors

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80
Q

What is the most common type of porphyria?

A

Porphyria cutanea tarda

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81
Q

What is the most common type of porphyria in children?

A

Erythropoietic protoporphyria

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82
Q

What does ALA synthase deficiency cause?

A

X-linked sideroblastic anaemia

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83
Q

Outline the clinical features of acute intermittent porphyria.

A

Rise in PBG and ALA

Autosomal dominant

Neurovisceral attacks

· Abdominal pain

· Tachycardia and hypertension

· Constipation, urinary incontinence

· Hyponatraemia and seizures

· Sensory loss/muscle weakness

· Arrhythmias/cardiac arrest

IMPORTANT: there are NO skin symptoms (because no porphyrinogens are produced)

NOTE: 90% will be asymptomatic

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84
Q

List some precipitating factors for acute intermittent porphyria.

A

ALA synthase inhibitors (e.g. steroids, ethanol, anticonvulsants (CYP450 inducers))

Stress (infection, surgery)

Reduced caloric intake

Endocrine factors

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85
Q

Describe how acute intermittent porphyria is diagnosed.

A

Increased urinary PBG (and ALA)

PBG gets oxidised to porphobilin

Decreased HMB synthase activity in erythrocytes

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86
Q

How is acute intermittent porphyria managed?

A

Avoid attacks (adequate nutrition, avoid precipitant drug, prompt treatment of other illnesses)

IV carbohydrate (inhibits ALA synthase)

IV haem arginate (switches off haem synthesis through negative feedback)

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87
Q

Which drug can trigger porphyria cutanea tarda?

A

Hexachlorobenzene

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88
Q

What haematological condition are erythropoietic protoporphyria and congenital erythropoietic porphyria associated with?

A

Myelodysplastic syndromes

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89
Q

During acute porphyria, what is the most useful sample to send?

A

Urine

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90
Q

Which enzyme converts iodide to iodine?

A

Thyroid peroxidase

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91
Q

How is thyroxine produced?

A

Iodination of tyrosine residues in thyroglobulin generates MIT and DIT which leads to the formation of T3 and T4

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92
Q

What does thyroxine bind to in the blood?

A

Thyroxine binding globulin (TBG)

Thyroxine-binding prealbumin (TBPA)

Albumin

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93
Q

List some causes of hypothyroidism.

A

Hashimoto’s thyroiditis (autoimmune)

Atrophic thyroid gland

Post-Graves’ disease (after treatment)

Post-thyroiditis

Drugs (e.g. amiodarone, lithium)

Iodine deficiency

Pituitary disease

Peripheral thyroid hormone resistance

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94
Q

Outline the investigation findings that may be seen in hypothyroidism.

A

High TSH

Low T4

Thyroid peroxidase antibodies

Look out for other autoimmune conditions

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95
Q

Why is it important to do an ECG in patients with suspected hypothyroidism?

A

If someone with hypothyroidism has underlying cardiovascular disease, giving them thyroxine may induce ischaemia

NOTE: so you would start on a low dose of thyroxine and ten escalate

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96
Q

What are some risks of overtreatment with thyroxine?

A

Osteopaenia

Atrial fibrillation

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97
Q

What is subclinical hypothyroidism?

A

Normal T4 with high TSH, associated with hypercholesterolaemia

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98
Q

Outline how thyroid function changes in pregnancy.

A

hCG has a similar structure to TSH so high hCG levels can cause hyperthyroidism

Free T4 levels rise slightly

TBG level increase dramatically

NOTE: hCG level drops later on in pregnancy

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99
Q

How is neonatal hypothyroidism diagnosed?

A

Guthrie test

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100
Q

What are the TFT findings in sick euthyroid?

A

Low T4 and T3

Normal/high TSH

NOTE: these patients do not have symptoms of hypothyroidism

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101
Q

What are the three main causes of hyperthyroidism?

A

Graves’ disease

Toxic multinodular goitre

Single toxic adenoma

Others: subacute thyroiditis, post-partum thyroiditis

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102
Q

List some features of Graves’ disease.

A

Diffuse goitre

Thyroid-associated ophthalmopathy

Pretibial myxoedema

Thyroid acropachy

NOTE: radioiodine can make Graves’ eye disease worse

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103
Q

What is the mechanism of action of thionamides?

A

Prevents the conversion of iodide to iodine by thyroid peroxidase

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104
Q

Outline the management of hyperthyroidism.

A

Beta-blocker

ECG

Bone mineral density

Radioiodine

Thionamides

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105
Q

What is a rare but important side-effect of thionamides?

A

Agranulocytosis

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106
Q

Which drug can be given to hyperthyroid patients prior to surgery to block uptake of iodide?

A

Potassium perchlorate

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107
Q

What are the two most common forms of thyroid cancer?

A

Papillary thyroid cancer

Follicular thyroid cancer

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108
Q

How is thyroid cancer treated?

A

Total thyroidectomy

NOTE: radioiodine treatment may also be given

NOTE: high dose thyroxine may be given to suppress TSH levels to prevent TSH from stimulating any remaining cells

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109
Q

Which cells do medullary thyroid cancer arise from?

A

Calcitonin-producing C cells

NOTE: it is part of MEN2

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110
Q

Name two tumour markers used for medullary thyroid cancer?

A

Calcitonin

CEA

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111
Q

What are the consequences of high and low plasma calcium for nerve conduction?

A

High calcium – failure of depolarisation

Low calcium – trigger happy neurological system leading to epilepsy

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112
Q

What are the three forms in which calcium is present in the plasma?

A

Free (ionised) – 50% - biologically active

Protein-bound – 40% - bound to albumin

Complexed – 10% - citrate/phosphate

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113
Q

State the equation for corrected calcium.

A

Corrected calcium = serum calcium + (0.02 x (40 – serum albumin in g/L))

NOTE: if your albumin level is constant, the total serum calcium will be roughly double the concentration of free calcium

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114
Q

What are the main effects of PTH?

A

Liberation of calcium from the bone (increased bone breakdown) and kidneys (increased calcium resorption)

Stimulates 1a-hydroxylase activity resulting in increased activated vitamin D

Stimulates renal phosphate excretion

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115
Q

What is the rate-limiting step in vitamin D activation?

A

1a-hydroxylase

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116
Q

How can sarcoidosis lead to hypercalcaemia?

A

Lung cells of sarcoid tissue express 1a-hydroxylase

117
Q

What are the main roles of vitamin D?

A

Increased intestinal calcium absorption

Increased intestinal phosphate absorption

Critical for bone formation

118
Q

What is ALP?

A

By-product of osteoblast activity

119
Q

What disease states does vitamin D deficiency cause?

A

Osteomalacia

Rickets

120
Q

List some risk factors for vitamin D deficiency.

A

Lack of sunlight

Dark skin

Dietary

Malabsorption

121
Q

Outline some clinical features of osteomalacia.

A

Bone and muscle pain

Increased fracture risk

Looser’s zones

122
Q

Outline the biochemical changes in osteomalacia.

A

Low calcium

Low phosphate

High ALP

123
Q

List some clinical features of rickets.

A

Bowed legs

Costochondral swelling

Widened epiphyses of the wrists

Myopathy

124
Q

Outline the pathophysiology of osteomalacia.

A

Vitamin D deficiency leads to secondary hyperparathyroidism which stimulates the liberation of calcium from the bone (leading to demineralisation of the bone)

125
Q

Which group of drugs is associated with vitamin D deficiency?

A

Anticonvulsants – promote the breakdown of vitamin D

126
Q

List some causes of osteoporosis.

A

Age-related decline in bone mass

Early menopause

Sedentary lifestyle

Alcohol

Low BMI

Thyrotoxicosis

Hyperprolactinaemia

Cushing’s syndrome

Prolonged recurrent illness

127
Q

List some drugs that may be used in the treatment of osteoporosis.

A

Vitamin D

Bisphosphonates

Teriparatide (PTH derivative)

Strontium (anabolic and anti-resorptive)

HRT

SERMs (e.g. raloxifene)

128
Q

List some symptoms of hypercalcaemia.

A

Polyuria/polydipsia

Constipation

Confusion, seizures, coma

129
Q

What are the main causes of primary hyperparathyroidism?

A

Parathyroid adenoma

Parathyroid hyperplasia (associated with MEN1)

Parathyroid carcinoma

130
Q

What are the three types of hypercalcaemia of malignancy?

A

Humoral hypercalcaemia of malignancy (e.g. small cell lung cancer) caused by PTHrP release

Bone metastases (e.g. breast cancer) caused by local bone osteolysis

Haematological malignancy (e.g. myeloma) caused by cytokines

131
Q

List some other non-PTH driven causes of hypercalcaemia.

A

Sarcoidosis

Thyrotoxicosis (increases bone resorption)

Hypoadrenalism (renal Ca2+ transport)

Thiazide diuretics (renal Ca2+ transport)

Excess vitamin D (e.g. sun beds)

132
Q

Outline the management of hypercalcaemia.

A

Fluids, fluids and more fluids

Bisphosphonates (stops cancer from eating bone)

Treat the underlying cause

133
Q

Where can a sample be taken from for drug concentration measurement?

A

Femoral vein blood

134
Q

When is vitreous humour used as a sample?

A

Used to measure glucose (may be elevated in DKA)

135
Q

Describe the consequences of amphetamine overdose.

A

Causes hyperthermia to rhabdomyolysis to renal failure

Also has a direct toxic effect on the heart

136
Q

What is the underlying pathogenesis of hyponatraemia?

A

Increased extracellular water

137
Q

What are the two main stimuli for ADH release?

A

Increased serum osmolality (via hypothalamic osmoreceptors)

Blood volume/pressure (via baroreceptors)

138
Q

What is the most reliable clinical sign of hypovolaemia?

A

Low urine sodium (suggests that you are trying to retain fluid)

NOTE: this may be high in patients on diuretics

139
Q

List some causes of hyponatraemia:

A

a. Hypovolaemic

Diarrhoea

Vomiting

Diuretics

Salt-losing nephropathy

b. Euvolaemic

Adrenal insufficiency

Hypothyroidism

SIADH

c. Hypervolaemic

Cirrhosis

Cardiac failure

Nephrotic syndrome

140
Q

List some causes of SIADH.

A

CNS pathology

Lung pathology

Drugs (SSRIs, TCAs, opiates, PPIs, carbamazepine)

Tumours

Surgery

141
Q

List the main investigative feature of SIADH.

A

Low plasma osmolality

High urine osmolality

142
Q

Which tests would you do for euvolaemic hyponatraemia?

A

TFTs

Short synacthen test

Plasma and urine osmolality

143
Q

What is the main danger of rapidly correcting hyponatraemia?

A

Can cause central pontine myelinolysis (osmotic demyelination)

This can lead to quadriplegia, dysarthria, dysphagia, seizures, coma and death

144
Q

Name and describe the mechanism of action of two drugs used to treat SIADH if fluid restriction is insufficient.

A

Demeclocycline – reduces the responsiveness of collecting duct cells to ADH

· NOTE: monitor U&E because it can be nephrotoxic

Tolvaptan – V2 receptor antagonist

Alternative: fluid restriction + salt tablets + diuretics

145
Q

List some investigations that are used in suspected diabetes insipidus.

A

Plasma glucose (rule out DM)

Plasma K+ (rule out hypokalaemia)

Plasma Ca2+ (rule out hypercalcaemia)

Plasma and urine osmolality

Water deprivation test

146
Q

How is hypernatraemia treated?

A

Fluid replacement – use dextrose because this will replace the fluid without adding to the salt

NOTE: if someone is hypovolaemic with hypernatraemia, they may initially be given 0.9% saline to treat the hypovolaemia before switching to dextrose to treat the hypernatraemia

147
Q

How often should serial Na+ measurements be taken in someone being treated for hypernatraemia?

A

4-6 hours

148
Q

What are the two main hormones involved in the regulation of potassium?

A

Angiotensin II

Aldosterone

149
Q

What does aldosterone do?

A

Aldosterone stimulates sodium reabsorption and potassium excretion in the principal cells of the cortical collecting tubule

NOTE: water will also be drawn in with the sodium so aldosterone should not greatly affect sodium concentration

150
Q

List some causes of hyperkalaemia.

A

Reduced GFR (renal failure)

Reduced renin activity (renal tubular acidosis type 4, NSAIDs)

ACE inhibitors/ARBs

Addison’s disease

Aldosterone antagonists

Potassium release from cells (rhabdomyolysis, acidosis)

151
Q

Explain how acidosis leads to hyperkalaemia.

A

When plasma H+ concentration is high, the cells try to take in more H+ from the plasma

To maintain electrochemical neutrality, K+ must leave the cell when H+ enters

This leads to hyperkalaemia

152
Q

Outline the management of hyperkalaemia.

A

10 mL 10% calcium gluconate

50 mL 50% dextrose + 10 U insulin

Nebulised salbutamol

Treat the cause

153
Q

What are the clinical features of hypokalaemia?

A

Muscle weakness

Arrhythmia

Polyuria and polydipsia (due to DI)

154
Q

What screening test should be done in a patient with hypokalaemia and hypertension?

A

Aldosterone: renin ratio (primary hyperaldosteronism will show high aldosterone and low renin)

155
Q

Outline the management of hypokalaemia:

A

a. 3-3.5 mmol/L

Oral potassium chloride (2 x SandoK TDS for 48 hours)

Re-check serum K+ concentration

b. < 3 mmol/L

IV potassium chloride infusion

Maximum rate: 10 mmol/hr

NOTE: rates > 20 mmol/hr irritate the superficial veins

TREAT THE CAUSE

156
Q

State the equation for osmolality

A

Osmolality = 2(Na + K) + urea + glucose

157
Q

List some causes of high anion gap.

A

Ketosis

Lactic acidosis

Methanol

Ethylene glycol poisoning

158
Q

How does an increase in plasma pH affect serum calcium levels?

A

As pH increases, plasma proteins start to stick to calcium more than usual

Total plasma calcium levels will remain normal but there will be less free ionised calcium (active form)

This leads to tetany (which can make patients hyperventilate even more)

159
Q

What is the danger of giving lots of fluids to someone with hyperglycaemic hyperosmolar state?

A

It can cause cerebral oedema, so 0.9% saline should be used to achieve a slower reduction in plasma sodium

160
Q

What is a major consequence of metformin overdose?

A

Lactic acidosis

161
Q

How are the results of an oral glucose tolerance test (75 g glucose) interpreted?

A

Impaired glucose tolerance = 7.8 – 11.1 mM at 2 hours

Diabetes = > 11.1 mM at 2 hours

162
Q

What is the difference between pink puffers and blue bloaters in COPD?

A

Pink puffers – very breathless, because they are still sensitive to CO2 which rises due to poor lung function in COPD

Blue bloaters – the brain stops responding to rising CO2 so you are not breathless and the CO2 will continue to rise

163
Q

What are the five layers of the adrenal gland?

A

Capsule

Glomerulosa

Fasciculata

Reticularis

Medulla

164
Q

What can cause adrenal glands to appear wasted?

A

Addison’s disease

Long-term steroid use

165
Q

What can cause adrenal glands to become hyperplastic?

A

Cushing’s disease

Ectopic ACTH

166
Q

What is the term used to describe the co-existence of primary hypothyroidism and Addison’s disease?

A

Schmidt syndrome

167
Q

What is the differential diagnosis for hypertension with an adrenal mass?

A

Phaeochromocytoma

Conn’s syndrome

Cushing’s syndrome

168
Q

What is a useful investigation for diagnosing phaeochromocytoma?

A

Urine catecholamines

169
Q

What are the disastrous consequences of phaeochromocytoma?

A

Severe hypertension

Arrhythmia

Death

170
Q

Outline the treatment of phaeochromocytoma.

A

Urgent alpha blockade (with phenoxybenzamine or phentolamine or doxazocin)

Some fluids may be given before alpha blockade as it can cause a dramatic drop in blood pressure

A beta-blocker should be given after the alpha-blocker to prevent reflex tachycardia

Patients should receive high-dose alpha and beta-blockade before surgery as the action of surgery can cause the release of catecholamines from the adrenals

171
Q

Name three genetic syndromes associated with phaeochromocytomas.

A

MEN2

Von Hippel Lindau syndrome

Neurofibromatosis type I

172
Q

Describe the levels of aldosterone and renin in Conn’s syndrome.

A

High aldosterone

Low renin

173
Q

What is pseudo-Cushing’s syndrome?

A

Obesity can change your metabolism of cortisol to produce a clinical syndrome that looks like Cushing’s syndrome

174
Q

What proportion of endogenous Cushing’s syndrome is caused by Cushing’s disease?

A

85%

175
Q

What is the optimal medical therapy for people with coronary heart disease?

A

Intensive lifestyle modification

Aspirin

High-dose statin (atorvastatin 40-80 mg OD)

Optimal blood glucose control

Thiazides

Assessment for probably T2DM

176
Q

Describe how SGLT2 inhibitors (Empagliflozin) can reduce blood glucose.

A

Increases urinary excretion of glucose causing a reduction in blood glucose and blood pressure

NOTE: this can also be used in heart failure because of its diuretic effect

177
Q

What are the effects of SGLT2 inhibitors on incidence of cardiovascular events and mortality?

A

Reduces the incidence of cardiovascular events

Reduces mortality

Reduced the incidence of renal failure

178
Q

How long is it likely to take for IM glucagon to cause an increase in blood glucose?

A

15-20 mins

179
Q

Which group of patients may not respond to IM glucagon?

A

Starving

Anorexic

Hepatic failure

These patients will have poor liver glycogen stores that can be accessed by glucagon

180
Q

List some non-diabetic medications that can cause hypoglycaemia.

A

Beta-blockers

Salicylates

Alcohol

181
Q

How could co-morbidities in a diabetic patient lead to increased risk of hypoglycaemia?

A

Renal/liver failure could lead to impaired drug clearance

Concurrent Addison’s disease could result in hypoglycaemia (polyglandular autoimmune syndrome)

182
Q

List some physiologically explicable causes of neonatal hypoglycaemia.

A

Prematurity

IUGR

Inadequate glycogen/fat stores

NOTE: this should improve with feeding

183
Q

List some tests that may be useful in the investigation of neonatal hypoglycaemia.

A

Insulin/C-peptide

FFA

Ketone bodies

Lactate

Hepatomegaly

184
Q

Name an alternative endogenous marker of GFR.

A

Cystatin C

185
Q

Aside from blood, what else can cause a urine dipstick to be positive for blood?

A

Myoglobinuria (from rhabdomyolysis)

186
Q

What is specific gravity?

A

A measure of urine concentration

187
Q

List some causes of pre-renal AKI.

A

True volume depletion

Hypotension

Oedematous state

Selective renal ischaemia (e.g. renal artery stenosis)

Drugs affecting renal blood flow

188
Q

List some drugs that affect renal blood flow.

A

ACE inhibitors – reduce efferent arteriolar constriction

NSAIDs – decreased afferent arteriolar constriction

Calcineurin inhibitors – decrease afferent arteriolar constriction

Diuretics – affect tubular function and decrease preload

189
Q

What is a consequence of prolonged pre-renal insult?

A

Acute tubular necrosis (ATN)

190
Q

What might be seen on urine microscopy in a patient with ATN?

A

Epithelial cell casts

191
Q

What can cause direct tubular injury?

A

Ischaemia (MOST COMMON)

Endogenous toxins (e.g. myoglobin, immunoglobulin)

Exogenous toxins (e.g. aminoglycosides, amphotericin, aciclovir)

192
Q

Which diseases can cause AKI due to infiltration/abnormal protein deposition?

A

Amyloidosis (associated with nephrotic syndrome)

Lymphoma

Myeloma

193
Q

What are the four processes of acute wound healing?

A

Haemostasis

Inflammation

Proliferation

Remodelling

194
Q

List some causes of CKD.

A

Diabetes mellitus

Hypertension

Chronic glomerulonephritis

Atherosclerotic renal disease

Infective or obstructive uropathy

Polycystic kidney disease

195
Q

Outline the consequences of CKD.

A

Progressive failure of homeostatic function (acidosis, hyperkalaemia)

Progressive failure of hormonal function (anaemia, renal bone disease)

Cardiovascular disease (vascular calcification, uraemic cardiomyopathy)

Uraemia and death

196
Q

What are the consequences of renal acidosis?

A

Muscle and protein degradation

Osteopaenia due to mobilisation of bone calcium

Cardiac dysfunction

197
Q

How is renal acidosis treated?

A

Oral sodium bicarbonate

198
Q

Which medications can cause hyperkalaemia?

A

ACE inhibitors

Spironolactone

Potassium-sparing diuretics

199
Q

How is anaemia of chronic renal disease treated?

A

Erythropoietin alfa (Eprex)

Erythropoietin beta (NeoRecormon)

Darbopoietin (Aranesp)

NOTE: if CKD is not responding to erythropoiesis stimulating agents, consider iron deficiency, malignancy, B12 deficiency etc.

200
Q

List some types of renal bone disease.

A

Osteititis fibrosa cystica

Osteomalacia

Adynamic bone disease

Mixed osteodystrophy

201
Q

What is osteitis fibrosa cystica?

A

Caused by osteoclastic resorption of calcified bone and replacement by fibrous tissue (feature of hyperparathyroidism)

202
Q

What is adynamic bone disease?

A

Overtreatment leading to excessive suppression of PTH result in low bone turnover and reduced osteoid

203
Q

Outline the treatment of renal bone disease.

A

Phosphate control – dietary, phosphate binders

Vitamin D activators – 1-alpha calcidol, paricalcitol

Direct PTH suppression – cinacalcet (works by increasing the sensitivity of the calcium sensing receptor)

204
Q

Describe the effect of hypokalaemia on the myocardium.

A

Increases myocardial irritability

205
Q

Describe the cardiac consequences of plasma potassium being too high or too low.

A

Too Low – ventricular fibrillation

Too High – asystole (ultimate stable rhythm)

206
Q

What is the difference between a Colles’ fracture and a Smith’s fracture?

A

Colles’ – fracture caused by falling on an outstretched hand. The radial head will be displaced backwards (away from the palm)

Smith’s – fracture caused by falling on a flexed wrist. The radial head will be displaced forwards (towards the palm)

207
Q

What is a Pott’s fracture?

A

Ankle fracture involving the tibia and fibula

208
Q

What would you expect to see on the urine dipstick of someone with subacute bacterial endocarditis?

A

Microscopic haematuria

209
Q

What is a key difference between calcium stones and urate stones?

A

Calcium stones are radio-opaque

Urate stones are radiolucent

210
Q

List some complications of hypercalcaemia.

A

Renal stones

Pancreatitis

Peptic ulcer disease

Skeletal changes (osteitis fibrosa cystica)

211
Q

List some risk factors for hypercalcaemia.

A

Family history

Dehydration

Hyperparathyroidism

212
Q

Which bacterium has a predilection to infect urinary tract stones?

A

Proteus mirabilis

213
Q

What are some management options for urinary tract stones?

A

Lithotripsy

Cystoscopy

Lithotomy

214
Q

What feature may you see on an X-ray of the hands in a patient with primary hyperparathyroidism?

A

Cystic changes in the radial aspect

215
Q

What is a characteristic histological feature of long-standing undiagnosed hyperparathyroidism?

A

Brown tumours – they are multinucleated giant cells in the bone. The giant cells are activated osteoclasts

216
Q

What is the mainstay of treatment of sarcoidosis?

A

Steroids

217
Q

What is the histological hallmark of sarcoidosis?

A

Non-caseating granulomas

218
Q

List some causes of metabolic alkalosis.

A

H+ loss (e.g. vomiting)

Hypokalaemia

Ingestion of bicarbonate

219
Q

Outline the relationship between hypokalaemia and alkalosis.

A

Low K+ leads to a shift of H+ into cells

This causes alkalosis

Similarly, low H+ will result in a shift of K+ into cells

220
Q

How can ectopic ACTH be distinguished from other causes of Cushing’s syndrome?

A

Ectopic ACTH cannot be suppressed by high-dose dexamethasone suppression test

221
Q

Which cause of Cushing’s syndrome is most commonly associated with hypokalaemia?

A

Ectopic ACTH

222
Q

What is the only definitive way of distinguishing acute renal failure from chronic renal failure?

A

Renal biopsy

223
Q

What does slow-onset upper motor neurone lesions in a cancer patient suggest?

A

Brain metastases

224
Q

Why doesn’t hypopituitarism cause low blood pressure?

A

The adrenals are still able to produce aldosterone

225
Q

Which hypothalamic hormones affect prolactin release?

A

Dopamine – negative

TRH – positive

NOTE: hypothyroidism causes hyperprolactinaemia

226
Q

How might pituitary failure present in women?

A

Amenorrhoea and galactorrhoea

227
Q

What physical manifestation might a macroadenoma of the pituitary gland (> 1 cm) cause?

A

Bitemporal hemianopia

228
Q

What blood glucose concentration is normally required to stimulate the pituitary gland?

A

< 2.2 mM

229
Q

How frequently should hormone levels in the blood be measured in combined pituitary function test?

A

Every 30 mins for 60 mins – LH, FSH, TSH, prolactin

Every 30 mins for 120 mins – glucose, GH, cortisol

230
Q

List the order of hormone replacement in someone with panhypopituitarism.

A

HYDROCORTISONE

Thyroxine

Oestrogen

GH

231
Q

How should a patient with a prolactinoma be treated?

A

Dopamine agonists (e.g. cabergoline)

This reduces the size of the tumour and can avoid surgery

232
Q

Name two tests that may be used to investigate suspected acromegaly.

A

Oral glucose tolerance test

IGF-1 levels

NOTE: the normal ranges for IGF-1 are not fully resolved and they vary with age

233
Q

In which tissues is ALP present in high concentration?

A

Liver

Bone

Intestines

Placenta

234
Q

What is an increase in bone ALP caused by?

A

Increased osteoblast activity

235
Q

List some physiological causes of high ALP.

A

Pregnancy – 3rd trimester (from placenta)

Childhood – growth spurt

236
Q

List some causes of very high ALP (> 5 x upper limit of normal).

A

Bone – Paget’s disease, osteomalacia

Liver – cholestasis, cirrhosis

237
Q

List some causes of moderately raised ALP (< 5 x upper limit of normal).

A

Bone – tumours, fractures, osteomyelitis

Liver – infiltrative disease, hepatitis

238
Q

What are the three forms of creatine kinase?

A

CK-MM = skeletal muscle

CK-BB = brain

CK-MB = cardiac muscle

239
Q

List some risk factors for statin-related myopathy

A

Polypharmacy (particularly fibrates and ciclosporin and other drugs metabolised by CYP3A4)

High dose

Genetic predisposition

Previous history of myopathy

Vitamin D deficiency

240
Q

List some other causes of high CK.

A

Muscle damage

Myopathy (e.g. Duchenne muscular dystrophy)

MI

Severe exercise

Physiological (Afro-Caribbeans)

241
Q

Describe how troponin levels change with time following an MI.

A

Rise at 4-6 hours post-MI

Peaks at 12-24 hours

Remains elevated for 3-10 days

So, troponins should be measured at 6 hours and 12 hours after the onset of chest pain in a suspected MI

242
Q

Vitamin A deficiency

A

Colour blindness

243
Q

Vitamin D deficiency

A

Osteomalacia/ rickets

244
Q

Vitamin E deficiency

A

Anaemia, neuropathy

245
Q

Vitamin K deficiency

A

Defective clotting

246
Q

Vitamin B1 deficency

A

Beri Beri

Neuropathy

Wernicke’s

247
Q

Vitamin B2 deficiency

A

Glossitis

248
Q

Vitamin B6 deficiency

A

Dermatitis, anaemia

249
Q

Folate deficiency

A

Megaloblastic anemia

250
Q

Vitamin A excess

A

Exfoliation, hepatitis

251
Q

Vitamin D excess

A

hypercalcaemia

252
Q

Vitamin B6 excess

A

neuropathy

253
Q

Vitamin C excess

A

Renal stones

254
Q

What are the main features of pellagra?

A

Dementia

Diarrhoea

Dermatitis

255
Q

What are the effects of leptin, ghrelin and PYY?

A

Leptin – anti-hunger hormone

Ghrelin – hunger hormone

PYY – satiety hormone produced by the intestines

256
Q

What are the roles of Kupffer cells?

A

Clearance of infection and lipopolysaccharide (LPS)

Antigen presentation

Immune modulation (e.g. cytokine production)

257
Q

Where is ALT and AST found?

A

Within the cytoplasm of hepatocytes

258
Q

Other than the liver, where else is ALT and AST found?

A

Muscle, kidney, bone, pancreas

259
Q

Describe the rise in ALT and AST seen in alcoholic liver disease.

A

AST: ALT > 2:1 in alcoholic liver disease

260
Q

Describe typical ALT and AST levels in cirrhosis.

A

May be raised

May be normal in long-standing chronic liver disease

261
Q

List some causes of raised GGT.

A

Alcohol abuse

Bile duct disease (e.g. gallstones)

Hepatic metastases

262
Q

List some causes of low albumin.

A

Low production (e.g. chronic liver disease, malnutrition)

Increased loss (e.g. gut, kidney)

Sepsis (3rd spacing – endothelium becomes leaky and albumin leaks into the tissues)

263
Q

What causes a high alpha-fetoprotein?

A

Hepatocellular carcinoma

Pregnancy

Testicular cancer

264
Q

List some causes of increased urobilinogen in the urine.

A

Haemolysis

Hepatitis

Sepsis

265
Q

List some other investigations that may be used as part of a liver panel.

A

Coeliac serology

Hepatitis serology

Alpha-1 antitrypsin

Caeruloplasmin

Immunoglobulins

Ferritin

266
Q

Name a dye test used to assess liver function.

A

Indocyanine green/bromsulphalein – measures excretory capacity of the liver and hepatic blood flow

267
Q

Name a breath test used to assess liver function

A

Aminopyrine/galactose (carbon 14) – measures residual functioning of liver cell mass

268
Q

What is an important cause of jaundice with LFT changes consistent with biliary obstruction?

A

Drug-induced cholestasis

NOTE: biliary USS will be normal. It usually resolves over 3 weeks

269
Q

What is the most common cause of drug-induced cholestasis?

A

Co-amoxiclav

270
Q

State three causes of ALT > 1000.

A

Toxins (paracetamol)

Viruses

Ischaemia (e.g. post-resuscitation)

271
Q

How often should patients with cirrhosis be followed up to check for hepatocellular carcinoma?

A

Every 6 months

272
Q

Describe how the AST and ALT levels differ in alcohol liver disease and viral hepatitis.

A

AST: ALT < 1 = viral hepatitis

AST: ALT > 2 = alcoholic liver disease

273
Q

What happens to vitamin D levels in primary hyperparathyroidism?

A

Decreases – because PTH activates 1-alpha hydroxylase leading to more conversion of vitamin D to the activated form

NOTE: assays for vitamin D levels will actually measure 25-OH vitamin D levels

274
Q

State the indications for dialysis.

A

Hyperkalaemia

Acidosis

Pulmonary oedema

Uraemia (pericarditis, encephalopathy)

275
Q

Which markers are increased in Paget’s disease of the bone?

A

ALP and osteocalcin

NOTE: activity of osteoclasts and osteoblasts is increased

276
Q

What is a characteristic morphological feature of Paget’s disease

A

Bowed tibia

277
Q

How is Paget’s disease of the bone treated?

A

Bisphosphonates (only if painful)

278
Q

What is the difference between the Z-score and T-score with regards to DEXA scans?

A

Z-score: number of standard deviations from the bone mineral density of an age and gender-matched individual

T-score: number of standard deviations from the bone mineral density of a healthy young person

279
Q

Which diseases tend to cause low bone density and fractures in the spine?

A

Cushing’s syndrome

Hyperthyroidism

Post-menopausal

280
Q

Which part of the body tends to get fractured due to low bone mineral density caused by primary hyperparathyroidism?

A

Wrist (radius)

281
Q

Age 0 most likely meningitis organism

A

Escherichia coli

Group B Streptococcus

Listeria monocytogenes

282
Q

Age 6 most likely meningitis organism

A

Haemophilus influenzae

Neisseria meningitidis

Streptococcus pneumoniae

283
Q

Age 18-25 most likely meningitis organism

A

Neisseria meningitidis

Streptococcus pneumoniae

Haemophilus influenzae

284
Q

Age 60+ most likely meningitis organism

A

Streptococcus pneumoniae

Listeria monocytogenes

285
Q

Mycoplasma pneumoniae is difficult to culture. What is a different laboratory feature that can help identify this organism?

A

Cold agglutinins

286
Q

List some signs of infective endocarditis.

A

Roth spots

Splinter haemorrhages

Janeway lesions

Osler’s nodes

Clubbing

Microscopic haematuria

Splenomegaly

287
Q

Describe the appearance of pseudogout crystals under polarised light microscopy.

A

Positively birefringent rhomboid-shaped crystals

288
Q

What type of deafness could Paget’s disease cause?

A

BOTH

Conductive – Paget’s disease of the ossicles will cause conductive deafness

Sensorineural – Paget’s disease of the skull can compress the 7th cranial nerve causing sensorineural deafness

Path Laz (condensed) (5 decks)

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