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Year 5 Pathology > Chemical Pathology > Flashcards

Chemical Pathology Flashcards

1
Q

Primary hyperparathyroidism caused by hyperplasia is associated with which gene

A

MEN1 (multiple endocrine neoplasia type 1)

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2
Q

Is primary hyperparathyroidism more common in men or women?

A

Women

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3
Q

The commonest cause of hypercalcaemia is

A

Primary hyperparathyroidism

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4
Q

Blood results in primary hyperparathyroidism
PTH
Calcium
Phosphate

A

PTH inappropriately normal or high
Calcium high
Phosphate low

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5
Q

Congenital absence of parathyroids is known as

A

DiGeorge syndrome

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6
Q

Causes of low calcium due to low PTH

A

Surgical including post thyroidectomy
Auto-immune hypoparathyroidism
DiGeorge syndrome (congenital absence of parathyroids)
Mg Deficiency

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7
Q

Formula for osmolality

A

Osmolality= cations+anions+urea+glucose
So

Osmolality= Na+K+Cl+HCO3+urea+glucose
since anions=cations this can be reduced to

Osmolality 2(Na+K) + Urea+ Glucose

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8
Q

Formula for anion gap

A

Na + K - Cl - Bicarb

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9
Q

Normal anion gap=

A

Approximately 18mM

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10
Q

…+… injected is known as speedball

A

Cocaine

Heroin

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11
Q

Acute dangers of cocaine:

A

Cardiac dysrhythmias, MI, Acute heart failure

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12
Q

Fatal dose of methadone in a healthy adult:

A

60ml

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13
Q

Fatal dose of methadone in a child

A

5ml

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14
Q

Benzodiazepine antidote

A

flumazenil

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15
Q

Problems with interpreting post-mortem blood toxicology

A

PM redistribution of drugs
Degradation of drugs post mortem e.g. cocaine
Individual variation in response (tolerance)
Site dependence

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16
Q

Why use hair for post mortem toxicology?

A

Blood/serum, drugs typically can be detected for no more than 12 hours

Urine, drugs typically detected for 2-3 days

Hair is the only specimen can give information about long term drug use

Drugs are incorporated into hair from the blood stream during the growth phase

Hair growth approx 1cm/month – “tape-recording of drug use”

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17
Q

Problems with hair analysis for post mortem toxicology

A 
Environmental Contamination
Absorbed from sweat or sebum coating hair
Passive inhalation
Cosmetic treatment
Shampoo washing
Perming, dyeing, bleaching
Hair colour
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18
Q

Most common causes of death after heroin use

A

Respiratory depression

Aspiration pneumonitis

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19
Q

Applications of hair analysis (toxicology)

A

Applications of hair analysis
• Child custody cases
• Investigating spiked drinks defences
• Drug naïve deaths
• Monitoring drug use prior to return of driving license – Germany, Italy
• Investigation of drug use in exhumed/putrefied bodies
• Employment, pre-employment screening - USA

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20
Q

Causes of metabolic acidosis

A
  1. Increased H+ production e.g. diabetic ketoacidosis
  2. Decreased H+ excretion e.g. Renal tubular acidosis
  3. Bicarbonate loss e.g. intestinal fistula
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21
Q

Types of renal tubular acidosis. Brief pathogenesis

A

Type 1 is distal: due to failure of alpha cells in collecting ducts to secrete H+ into urine. Due to autoimmune e.g. RA, drugs e.g. lithium, genetics and hypercacliuric conditions e.g. hyperPTH

Type 2 is proximal: caused by decrease in bicarbonate reabsorption. Caused by genetics, amyloidosis, multiple myeloma, HAART (HIV meds), basically anything that causes deposits in kidneys.

Type 3: combo of 1 and 2. Not used.

Type 4: Caused by hypoaldosteronism or resistance to aldosterone e.g. CAH, primary hypoaldosteronism, NSAIDs, ACEi, Aldosterone blockers, sarcoidosis.

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22
Q

Causes of metabolic alkalosis

A

Ingestion of bicarb
Reduced H+ excretion e.g. pyloric stenosis
Hypokalaemia

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23
Q

Management of hypovolaemia hyponatraemia due to diuretics

A

Stop diuretic

0.9% NaCl

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24
Q

Causes of euvolaemic hyponatraemia

A

SIADH
Hypothyroidism
Adrenal insufficiency

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25
Q

Causes of hypovolaemic hyponatraemia

A

Diuretics
Diarrhoea
Vomiting
Salt losing nephropathy

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26
Q

Causes of hypervolaemic hyponatraemia

A

Cirrhosis
Cardiac failure
Nephrotic syndrome

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27
Q

Features of SIADH

A

No hypovolaemia
High urine osmolality (over 100)
Low plasma osmolality

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28
Q

Causes of SIADH

A

CNS pathology
Lung pathology
Drugs (SSRI, TCA, opiates, PPIs, carbamazepine)
Tumours (most likely small cell lung cancers)

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29
Q

Investigations in suspected diabetes insipidus

A

Serum glucose (exclude diabetes mellitus)
Serum potassium (exclude hypokalaemia)
Serum calcium (exclude hypercalcaemia)
Plasma & urine osmolality (high plasma osmolality, and low urine osmolality)
Water deprivation test

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30
Q

Key features of ECG in hyperkalaemia

A

Peaked/tented T waves
Absent p waves
Broad complexes

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31
Q

Management of hyperkalaemia

A

10 ml 10% calcium gluconate
50 ml 50% dextrose + 10 units of insulin
Nebulised salbutamol
Treat the underlying cause

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32
Q

Features of primary hyperaldosteronism

A

Hypertension (resistant to treatment)
Low potassium
High sodium
High aldosterone, low renin (negative feedback)

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33
Q

Causes of hyperkalaemia

A

Renal impairment
Drugs (e.g. spironolactone, ACEi, A2RBs)
Adrenal insufficiency (Addison’s disease)
Rhabdomyloysis
Acidosis (hydrogen moves into cells, potassium leaves cells)
Type 4 renal tubular acidosis (rare)

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34
Q

Drive for potassium secretion in distal nephron

A

Na reabsorption through ENaC (epithelial sodium channels) leads to tubular lumen negative electrical potential, driving potassium secretion.

Happens in the principal cells of the collecting tubule.

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35
Q

How does aldosterone increase potassium secretion?

A

Aldosterone increases transcription of genes for:
Epithelial sodium channels in collecting tubule (lumen side)
Basolateral sodium/potassium pumps in collecting tubule

So Na absorption is increased

Na reabsorption through ENaC (epithelial sodium channels) leads to tubular lumen negative electrical potential, driving potassium secretion.

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36
Q

Stimuli for aldosterone secretion

A

Angiotensin II

Potassium

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37
Q

Causes of hypokalaemia

A

GI loss: D+V
Renal loss: Loop and thiazide diuretics, Barrter syndrome, Gitelman syndrome, excess aldosterone, excess cortisol
Redistribution into cells

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38
Q

What is Barrter syndrome

A

A rare inherited defect in the thick ascending limb of the loop of Henle.Causes low potassium levels. Caused by mutations in genes for multiple proteins leading to a similar outcome

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39
Q

What is Gitelman syndrome

A

Defect in Na/Cl co-transporters in distal tubule. Leads to hypokalaemia

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40
Q

Clinical features of hypokalaemia

A

Muscle weakness
Cardiac arrhythmia
Polyuria and polydipsia (nephrogenic DI, hypokalaemia makes you resistant to ADH)

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41
Q

Management of hypokalaemia

A

Serum potassium 3.0-3.5 mmol/L:
Oral potassium chloride (two SandoK tablets tds for 48 hrs)
Recheck serum potassium

Serum potassium 20 mmol per hour are highly irritating to peripheral veins

Treat the underlying cause e.g. give spironolactone for Conn’s

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42
Q

Glucagon is not effective in patients with…

A

Liver failure

They have no glycogen stores

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43
Q 
Treatment for hypoglycaemia (acute) if:
Alert and orientated
Drowsy/confused but swallow intact
Unconconcious/ concerns about swallow
Deteriorating / refractory /insulin induced /difficult IV access
A

Rapid acting oral carbohydrates e.g. Lucozade

Buccal glucose e.g. hypostop

IV access: 50ml 50% glucose (Do not do this in real life!)

Consider IM/SC 1mg glucagon

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44
Q

Which patients (with diabetes) most commonly experience no symptoms with hypoglycaemia

A

Patients on B-blockers

Patients who have recurrent hypoglycaemia

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45
Q

First response to hypoglycaemia (substance released/suppressed). Followed by…

A

Suppression of insulin
THEN

Release of glucagon
Release of adrenaline
Release of cortisol

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46
Q

End product of glycogen breakdown in muscle

A

Glucose-6 phosphate

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47
Q

C-peptide is

A

The cleavage product of pro-insulin (along with insulin).

Secreted in equimolar amounts to insulin

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48
Q

Half life of c-peptide

Half-life of insulin

A

4-6 minutes

30 minutes

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49
Q

The 3 ketone bodies

A

Acetone (pear drop smell in pts with DKA and is volatile), beta hydro and acetoacetate

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50
Q

Inherited metabolic disorders leading to hypoketotic hyooglycaemia in neonates

A

FAOD : no ketones produced
GSD type 1 ( gluconeogentic disorder)
Medium chain acyl coA dehydrogenase def.
Carnitine disorders

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51
Q

Beckwith Weidemann syndrome is…

A

An overgrowth disorder usually present at birth. Characterised by certain features including:
neonatal hypoglycaemia (islet cell hyperplasia)
macgroglossia
Macrosomia
Midline abdominal wall defects
Hepatoblastoma
Ear creases or ear pits

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52
Q

Mechanism of action of sulphonylureas

A

Bind to Sur 1 subunit of potassium channel (on insulin secreting cell) and cause it to close. Membrane depolarisation leads to insulin release

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53
Q

MEN1 is associated with tumours of the…

A

Pituitary
Parathyroid
Pancreas

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54
Q

How does Non-islet cell tumour cause hypoglycaemia

A

Tumour secretes “big IGF-2” which binds to IGF-1 receptors and insulin receptors. Produces downstream effects of insulin

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55
Q

Quinine causes hypoglycaemia by…

A

Stimulating insulin secretion

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56
Q

`Rate limiting step in haem biosynthesis

A

Creation of 5-Aminolaevulinic Acid (ALA) from succinyl-CoA and glycine.
Enzyme: ALA synthase

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57
Q

5-Aminolaevulinic Acid (ALA) created from glycine and CoA by ALA synthase. Next step in the haem biosynthesis pathway is…

A

ALA enters the cytoplasm and porphobilinogen formed from ALA by PBG synthase.

58
Q

Principal sites of haem biosynthesis

A

Erythroid cells

Hepatocytes

59
Q

Differences between porphyrins and porphyrinogens

A

Porphyrinogens are raised in porphyria
Colourless compounds
Unstable and readily oxidised to the corresponding porphyrin by the time urine /faeces reaches lab

Porphyrins are highly coloured (detected in urine or faeces)
Porphyrins near start of the pathway are water soluble – urine (uro-)
Porphyrins near end less soluble – faeces (copro-)

60
Q

Deficiency in ALA synthase causes…

A

Sideroblastic aneamia (inability to incorporate iron into haemoglobin, form sideroblasts)

Presents acutely with neurovisceral attacks:
skin paleness, fatigue, dizziness, and enlarged spleen and liver. Heart disease, liver damage, and kidney failure can result from iron buildup in these organs

NOT A PORPHYRIA

61
Q

PBG synthase deficiency causes…

A

Acute porphyria. Specifically ALA dehydratase/plumboporphyria

Extremely rare form of porphyria
Build-up of ALA, but not PBG

Diagnostic implications – with a porphyria the Uroporphyrinogen in the urine is measured. However with this deficiency, there is no Uroporphyrinogen produced and therefore cannot be detected.

62
Q

HMB synthase deficiency causes

A

Acute intermittent porphyria.

Neurovisceral attacks:
Abdo pain and vomiting
Tachycardia and hypertension
Constipation, urinary incontinence
Hyponatraemia +/- seizures (thought to be due to SIADH)
Psychological symptoms
Sensory loss / muscle weakness
Arrythmias / cardiac arrest

No skin symptoms: No production of porphyrinogens

63
Q

Mode of inheritence of acute intermittent porphyria

A

Autosomal dominant

64
Q

Neurotoxic haem precursor

A

5-Aminolaevulinic Acid (ALA)

65
Q

Precipitating factors for acute intermittent porphyria

A 
ALA synthase inducers
Barbiturates, steroids, ethanol, anticonvulsants
Stress
Infection, surgery
Reduced caloric intake
Endocrine factors
More common in women and premenstrual
Just started OCP (classic examination)
66
Q

Treatment of acute intermittent porphyria

A

Avoid attacks
Adequate nutritional intake (high carb diet)
Precipitant drugs
Prompt treatment infection/illness

iv carbohydrate
iv haem arginate
Suppresses pathway from the top

67
Q

Signs/symptoms of acute intermittent porphyria

A 
Neurovisceral attacks
Abdo pain and vomiting
Tachycardia and hypertension
Constipation, urinary incontinence
Hyponatraemia +/- seizures (thought to be due to SIADH)
Psychological symptoms
Sensory loss / muscle weakness
Arrythmias / cardiac arrest
68
Q

Acute porphyrias that cause skin lesions

A

Hereditary coproporphyria

Variegate porphyria

69
Q

Signs and symptoms of hereditary coproporphyria

A 
Neurovisceral attacks:
Constipation and urinary incontinence 
Abdo pain and vomiting 
Tachycardia and hypertension 
Arrhythmia/ cardiac arrest 
Seizures 
Psychological symptoms 
Sensory loss/ muscle weakness

Skin:
Blistering
Skin fragility

70
Q

Mode of inheritence of coproporphyria

A

Autosomal dominant

71
Q

Consequence of coproporphyrinogen deficiency

A

Acute porphyria: specifically hereditary coproporphyria

Neurovisceral attacks and skin symptoms

72
Q

Consequence of protoporphyrinogen deficiency

A

Acute porphyria: Specifically variegate porphyria

73
Q

Main type of acute porphyria

A

Acute intermittent porphyria

74
Q

Mode of inheritance of variegate porphyria

A

Autosomal dominant

75
Q

Signs symptoms of variegate porphyria

A 
Neurovisceral attacks 
Abdo pain and vomiting 
Constipation and urinary incontinence 
Seizures 
Sensory loss and muscle weakness 
Psychological symptoms 
Tachycardia and Hypertension 
Arrhythmias/cardiac arrest

Skin symptoms
Photosensitivity
Skin fragility
Blistering

76
Q

How do we use urine and stool testing to differentiate the acute porphyrias

A

In plumboporphyria tere will be no porphobilinogen produced and no uroporphyrinogen produced (so no porphyrins in stool or urine)

In AIP, VP, and HCP PBG is raised but:
Porphyrins raised in HCP or VP, but not AIP

77
Q

Consequence of uroporphyrinogen III synthase deficiency

.

A

Congenital erythropoietic porphyria. A non-acute porphyria

78
Q

Consequence of uroporphyrinogen decarboxylase deficiency

A

Porphyria cutanea tarda. A non-acute porphyria

79
Q

Consequence of ferrochetolase deficiency

A

Erthropoietic porphyria. A non-acute porphyria.

80
Q

Signs and symptoms of porphyria cutanea tarda

A

Formation of vesicles on sun-exposed areas of skin crusting, superficial scarring, pigmentation

81
Q

Biochemical features of porphyria cutanea tarda

A

Urinary and plasma uroporphyrins increased.

Ferritin increased

82
Q

Precipitants of porphyria cutanea tarda

A

Alcohol
Oestrogen
Hepatic compromise (e.g. hepatitis infection)

83
Q

Features of erythropoetic porphyria

A

Photosensitivity only, no blisters
Only erythroid cells affected, therefore need to measure RBC protoporphyrin
Caused by ferrochetolase deficiency. Raised RBC protoporphyrin is the result.

84
Q

Features of congenital erythropoietic porphyria

A

Deficiency of uroporphyrinogen III synthase
Raised HMB

Skin features:
Formation of vesicles that can rupture
Photosensitivity

Haemolytic anaemia
Porphyrins additionally accumulate in the bone and teeth, resulting in erythrodontia (red discolouration of teeth)

Very acute attacks:
Vomiting and constipation can follow attacks

85
Q

Reactions catalysed by ALT and AST

A

The transfer of the alpha-amino groups of alanine and aspartate, respectively, to the alpha-keto group of ketoglutarate, which results in the formation of pyruvate and oxaloacetate.

86
Q

Reaction catalysed by gamma GT

A

Gamma-glutamyl transpeptidase (GGT) catalyzes the transfer of the gamma-glutamyl group from gamma-glutamyl peptides such as glutathione to other peptides and to L-amino acids

87
Q

Gamma GT is elevated in…

A

Chronic alcohol use
Bile duct disease
Hepatic metastases

88
Q

ALP markedly rises in…

A 
Obstructive jaundice or bile duct damage
Bone disease (especially metastatic and pregnancy)
89
Q

Causes of low albumin

A

low production (chronic liver disease, malnutrition)
loss (eg gut, kidney)
sepsis (“3rd spacing”)

90
Q

Alpha-feto protein raised in…

A

HCC
Hepatic damage/regeneration
Pregnancy
Testicular cancer

91
Q

Bilirubin is conjugated with

A

Glucuronic acid

92
Q

In pre-hepatic jaundice bilirubin is (conjugated/unconjugated)

A

Unconjugated

93
Q

In hepatic jaundice bilirubin is (conjugated/unconjugated)

A

Both

94
Q

In post hepatic jaundice bilirubin is…

A

Conjugated

95
Q

Post-hepatic causes of jaundice

A

Bile duct obstruction

Drugs

96
Q

Hepatic causes of jaundice

A

Genetic (e.g. Gilbert’s)
Hepatitis
Drug reaction

97
Q

Pre-hepatic causes of jaundice

A

Haemolysis

98
Q

Bilirubin in urine is (conjugated/unconjugated)

A

Conjugated (but should not be present)

99
Q

Urobilinogen in urine is raised in…

A

haemolysis, hepatitis, sepsis

100
Q

What is Courvoisier’s Sign

A

In the presence of a painless palpable gallbladder, jaundice is unlikely to be caused by gall stones

101
Q

Mode of inheritance of Gilbert’s syndrome

A

Autosomal recessive

102
Q

Effect of vitamin A

a) excess
b) deficiency

A

a) Colour blindness

b) Exfoliation and hepatitis

103
Q

Effect of vitamin A

a) deficiency
b) excess

A

Rickets/osteomalacia

Hypercalcaemia

104
Q

Effect of vitamin E (tocopherol)

a) Deficiency
b) Excess

A

a) Anaemia and neuropathy. Possibly malignancy/IHD

b) None

105
Q

Effect of vitamin K (phytomenadione)

a) deficiency
b) Excess

A

Defective clotting

None

106
Q

Effect of vitamin B1 (thiamine)

a) Deficiency
b) Excess

A

Beri-beri, Neuropathy and Wernicke syndrome

None

107
Q

Effect of vitamin B2 (riboflavin)

a) Deficiency
b) Excess

A

Glossitis

None

108
Q

Effect of vitamin B6 (pyridoxine)

a) Deficiency
b) Excess

A

Dermatitis and anaemia

Neuropathy

109
Q

Effect of vitamin B12

a) Deficiency
b) Excess

A 
Perninicious anaemia (macrocytic anaemia) 
None
110
Q

List tests for vitamin B enzymes

A

B1 (thiamine): RBC transketolase
B2 (riboflavin): RBC glutathione reductase
B6 (pyridoxine): RBC AST activation
B12 (cobalamin): serum B12

111
Q

Effect of vitamin C (ascorbate)

a) Deficiency
b) Excess

A

Scurvy

Renal stones

112
Q

Effect of folate

a) Deficiency
b) Excess

A

a)Megaloblastic anaemia
Neural tube defects in foetus

b) None

113
Q

Effect of niacin

a) Deficiency
b) Excess

A

a) Pellagra

b) None

114
Q

Excess fluoride causes…

A

Fluorosis: characterised by mottling of the teeth and if severe calcification of the ligaments

115
Q

Effect of copper

a) Deficiency
b) Excess

A

Anaemia

Wilson’s

116
Q

Effect of zinc

a) Deficiency
b) Excess

A

Dermatitis

None

117
Q

Ideal diet contains 50%….

A

carbohydrate

118
Q

Definition of overweight and obese according to BMI

A

25-30 kg/m2 overweight
>30 kg/m2 obese
>40 kg/m2 morbidly obese

119
Q

Metabolic syndrome is…

A

Metabolic syndrome is a clustering of at least three of five of the following medical conditions:
abdominal (central) obesity,
elevated blood pressure,
elevated fasting plasma glucose,
high serum triglycerides,
low high-density lipoprotein (HDL) levels.

120
Q

Marasmus is…

A

Marasmus is a form of severe malnutrition characterized by energy deficiency.
It occurs before the age of 1
Marasmus is commonly represented by a shrunken (growth retardation), wasted appearance, loss of muscle mass and subcutaneous fat mass.

121
Q

Kwashiorkor is

A

A form of severe protein–energy malnutrition characterized by oedema, irritability, ulcerating dermatoses, and an enlarged liver with fatty infiltrates.

Sufficient calorie intake, but with insufficient protein consumption, distinguishes it from marasmus.

Kwashiorkor cases occur in areas of famine or poor food supply

122
Q

Key features of kwashiorkor

A 
Oedematous
Scaling/ulcerated 
Lethargic
Large liver, s/c fat
Protein deficient
123
Q

Emergency treatment of hypercalcaemia

A 
Ca2+ >3.0 mmol/L &/or unwell
(Dehydrated, confused, drowsy, coma, seizures, renal failure)
IV access (venflon/central line)
Catheter
Rehydrate:	0.9% saline (can be litres++)
Initiate calciuresis:
				0.9% saline
				Frusemide
IV pamidronate 30 - 60 mg if cause is cancer (hold off)
124
Q

Non emergency treatment of hypercalcaemia

A

Keep well hydrated
Avoid thiazides
Surgery

125
Q

What are brown tumours?

A

The brown tumor is a bone lesion that arises in settings of excess osteoclast activity, such as hyperparathyroidism. It is not a true neoplasm

Brown tumours consist of fibrous tissue, woven bone and supporting vasculature, but no matrix.

The osteoclasts consume the trabecular bone that osteoblasts lay down and this front of reparative bone deposition followed by additional resorption can expand beyond the usual shape of the bone, involving the periosteum thus causing bone pain.

The characteristic brown coloration results from hemosiderin deposition into the osteolytic cysts.

Hemosiderin deposition is not a distinctive feature of brown tumors; it may also be seen in giant cell tumors of the bone

126
Q

Brown tumours are seen in which condition

A

Hyperparathyroidism

127
Q

In sarcoidosis PTH is…

A

suppressed to undetectable levels

128
Q

Treatment of sarcoidosis

A

Steroids

129
Q

Cause of hypercalcaemia in sarcoidosis…

A

Systemic disease where macrophages express 1 alpha hydroxylase (which activates vitamin D)

So calcium is higher in summer

130
Q

Cause of seasonal hypercalcaemia…

A

Sarcoidosis

131
Q

Gold-standard measure of GFR

A

Inulin clearance

132
Q

Urine microscopy:

Urine is examined to look for:

A 
Crystals
Red blood cells
White blood cells 
Casts
Bacteria
133
Q

About 80% of kidney stones are partially or entirely formed of…

A

Calcium oxalate

134
Q

Causes of pre-renal AKI

A 
True volume depletion
Hypotension
Oedematous states
Selective renal ischaemia
Drugs affecting glomerular blood flow
135
Q

Causes of post renal AKI

A 
Ureteric obstruction (bilateral)
Prostatic / Urethral obstruction
Blocked urinary catheter
136
Q

Commonest causes of CKD

A 
Diabetes
Atherosclerotic renal disease
Hypertension
Chronic Glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease
137
Q

Consequences of CKD

A 
1]Progressive failure of homeostatic function
	-Acidosis
	-Hyperkalaemia
2]Progressive failure of hormonal function
	-Anaemia
	-Renal Bone Disease
3]Cardiovascular disease
	-Vascular calcification
	-Uraemic cardiomyopathy
4]Uraemia and Death
138
Q

Consequences of renal acidosis

A
  • Muscle and protein degradation
  • Osteopenia due to mobilization of bone calcium
  • Cardiac dysfunction
139
Q

Features of hyperkalaemia ECG

A

Tall peaked t wave
Prolonged pr interval
Widened flattened p waves (eventually disappear)
Widened QRS (with tall T wave)

140
Q

Treatment of CKD bone disease

A 
Phosphate control
	-Dietary
	-Phosphate binders
Vit D receptor activators
	-1alpha calcidol
	-Paricalcitol
Direct PTH suppression
	-Cinacalcet
141
Q

3 phases of uraemic cardiomyopathy

A

LV hypertrophy
LV dilatation
LV dysfunction

Year 5 Pathology (7 decks)

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