Chem Path Qs Flashcards

1
Q

Combined Pituitary Function Tests involves what:

A

Insulin tolerance test - this should increase cortisol (>170nmol/l) and GH (>6mcg/l)
TRH test - Stimulates TSH and prolactin, the 30m sample should be greater than the 60m sample, otherwise primary hypothalamic disease is indicated.
GnRH test - LH > 10U/l and FHS > 2U/l (early hypopirtuitarism).

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2
Q

Non functioning pituitary adenoma casuses:

A

Panhypopituitarism and raised prolacting. Adenoma presses on stalk and causes pituitary failure. Dopamine can reach pituitary and suppress prolactin.

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3
Q

Acromegaly - Cause and Treatment

A

Excess GH from the pituitary. Treat with ocreotide or ianreotide (somatostatin analogues).

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4
Q

Osteoporosis
Low/High Turnover?
Main Causes?
Risks (nutrition/social, endocrine, immobile and iatrogenic)

A

High turnover from increase resorption
Low turnover from decrease resorption.
90% due to insufficient Ca intake or menopause.
Nutritional/Social - age, female, smoking, xs alcohol, vit d/ca deficiency, immobility, malabsorption.
Endocrine - thyroid, PTH, menopause, cushings, DM
Inatrogenic - steroids, heparin (long-term).

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5
Q

Osteomalacia
Definition
Two causes
Symptoms

A

Defective bone mineralisation
Cause by deficiency in Vit D or phosphate.
Bone pain/tenderness, fracture, proximal weakness, bone deformity.
FRACTURES IN LOOSER’S ZONE

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6
Q

Hyperparathyroidism

Urine and Serum changes?

A

Excess PTH leads to increase Ca and PO excretion in unripe. Hypercalcaemia, hypophosphataemia.
INAPPROPRIATELY NORMAL PTH level relative to Ca

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7
Q

Hyperparathyroidism

Skeletal Changes?

A

Osteitis fibrosa cystica (replacement of bone with fibrous tissue)

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8
Q

Hyperparathyroidism

Skeletal Changes?

A

Osteitis fibrosa cystica

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9
Q

Primary Hyperparathyroidism

Causes?

A

Parathyriod adenoma (85-90%) - chief cell hyperplasia

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10
Q

Secondary Hyperparathyroidism

Cause?

A

Chronic renal deficiency, vit D deficiency, malabsorption.

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11
Q

Renal Ostendystrophy

Bone Changes?

A
Comprises all skeletal changes of chronic renal disease. 
Osteitis fibrosa cystica
Osteomalacia
Osteosclerosis
Growth retardation
Osteoporosis
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12
Q

Renal Osteodystrophy

Serum Changes?

A
hyperphospataemia
hypo calcaemia as a results of decrease vit d
Secondary hyperparathyroidism
Metabolic acidosis
Al deposit.
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13
Q

Paget’s - Definition and Sx

A
Disorder of bone turnover.
Pain, microfracturers, nerve compression, skull changes. 
Onset > 40y
M=F
Rare in asian and africans
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14
Q

Commonest electrolyte abnormality in hospitalised patients?

A

Hyponatraemia

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15
Q

ADH/Vasopressin
Target?
Effect?
Controls?

A

Acts on V2 receptors
Results in aquaporin insertion in DCT
At high concentration bind V1 receptors on smooth muscle causing contraction.
Results in water retention.

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16
Q

ADH/Vasopressin
Target?
Effect?
Controls?

A

Acts on V2 receptors
Results in aquaporin insertion in DCT
At high concentration bind V1 receptors on smooth muscle causing contraction.
Results in water retention and DECREASE Na

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17
Q

What are the two main stimuli for ADH?

A
Serum osmolality (via hypothalmic osmoreceptors, also stimulates thirst)
Blood volume (barroreceptors in carotids, atria, aorta).
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18
Q

What is the first step in the assessment of a patient with hyponatraemia?

A

Check volume status

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19
Q

What are the clinical signs of hypovolaemia? (6)

A

Tachycardia, postural hypotension, dry mucous membranes, reduced skin turgor, confusion, reduce urine output.

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20
Q

What are the clinical signs or hypervolaemia? (3)

A

Raised JVP, bibasal crackles, peripheral oedema.

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21
Q

What are the causes of hypovolaemic hyponatraemia? (3)

A

Renal causes of volume depletion (diuretics)
Extra-renal causes of volume depletion (diarrhoea, vomiting).
Salt loosing nephropathy.

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22
Q

What are the causes of hypervolaemic hyponatraemia? (3)

A

Cirrhosis
Cardiac Failure
Nephrotic Syndrome

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23
Q

What are the causes of euvolaemic hyponatramia? (3)

A

Hypothyroidism
Adrenal insufficiency
SIADH

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24
Q

SIADH Causes? (4)

A

Malignancy - small cell lung, prostate, pancreas, lymphoma
CNS disorder - meningoencephalitis, haemorrhage, abscess
Chest disease - TB, pneumonia, abscess
Drugs - opitates, SSRIs, TCA, carbemazepine

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25
Q

SIADH Lab Criteria?

Urine Osmolality?

A

Reduced plasma osmolaity
Inappropriately high urine osmolality (>100) and increase renal sodium excretion. Normal renal, adrenal, thyroid and cardiac function.

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26
Q

What Ix in a patient in euvolaemic hyponatraemia? (3)

A

TFTs, Short Synacthen Test, Plasma and urine osmolality

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27
Q

How would you manage a hypovolaemic patient with low Na?

A

Volume replacement with 0.9% saline

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28
Q

How would you manage a hypervolaemic patient with low Na?

A

Fluid restriction and treat cause.

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29
Q

How would you manage a euvolaemic patient with low Na?

A

Fluid restriction and treat cause.

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30
Q

Symptoms of Severe hyponatraemia?

A

Reduced GCS, seizures

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31
Q

At what rate can you correct hyponatraemia?

A

Less that 12mmol/l in the first 24h

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32
Q

What is the risk of correcting Na too quickly>

A
Osmotic demyelination (central pontine myelionlysis) leading to?
quadriplegia, pseudobulbar palsy, seizures, coma, death.
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33
Q

What is the risk of correcting Na too quickly>

A
Osmotic demyelination (central pontine myelionlysis) leading to?
quadriplegia, pseudobulbar palsy, seizures, coma, death.
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34
Q

What drugs can be used to treat SIADH? (2)

A

Demeclocycline - reduces responsiveness of collecting tube cells to ADH (SE nephrotoxic)
Tolvaptal (V2 receptor antagonist)

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35
Q

Hyponatraemia is mostly due to?

A

Increase extra cellular water

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36
Q

What are the main causes of hypernatraemia?

A

Unreplaced water loss - GI losses, sweat losses, renal losses (osmotic diuresis, reduced ADH release aka DI)
Patient cannot control water intake (elderly/children)

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37
Q

What Ix for at patient in suspected DI?

A
Serum glucose (exclude DM)
Serum K (exclude hypokalaemia)
Serum Ca (exclude hypercalcaemia)
Plasma and urine osmolality
Water deprivation test
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38
Q

How do you treat raised Na?

A

Fluid replacement, treat cause.

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39
Q

What are the effects of DM on serum Na?

A

Variable. Hyperglycaemia draws water out of cells leading to hyponatraemia.
Osmotic diuresis in diabeteres leads to loss of water and hypernatraemia.

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40
Q

What are the effects of DM on serum Na?

A

Variable. Hyperglycaemia draws water out of cells leading to hyponatraemia.
Osmotic diuresis in diabeteres leads to loss of water and hypernatraemia.

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41
Q

Causes of Nephrogeic DI (3)

A

Inherited
Lithium
Chronic renal failure

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42
Q

Causes of Cranial DI (3)

A

Head trauma
Tumour
Surgery

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43
Q

Which hormones regulate K (renal)

A

Angiotensin 2 and Aldosterone. Angiotensin 2 causes aldosterone release from adrenal. which leads to Na reabsorption and K loss.
K can directly stimulate the adrenal leading to aldosterone secretion.

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44
Q

What are the main causes of hyperkalaemia due to decrease excretion?

A
CRF (leading to decreased GFR)
Renal tubular acidosis (diabetic nephropathy)
NSAIDS
ACE/ARB
Addisons
Aldosterone antagonists (Spiro)
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45
Q

What causes hyperkalaemia due to transcellular movement?

A

Rhabdo
Acidosis
Insulin shortage

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46
Q

What is the main ECG change assoc with raised K?

A

Peaked T waves

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47
Q

How would you manage raised K?

A

10ml 10% Ca gluconate
50ml 50% dextrose + 10 units of insulin
Neb salbutamol
Treat cause

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48
Q

How would you manage raised K?

A

R10ml 10% Ca gluconate
50ml 50% dextrose + 10 units of insulin
Neb salbutamol
Treat cause

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49
Q

Causes of hypokalaemia?

A
Renal loss (hyperaldoseronism, excess cortisol, osmotic diuresis)
GI loss
Redistribution into cells (insulin, beta agonists, alkalosis)
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50
Q

What are the clinical features of hypokalaemia?

A

Muscle weakness
arrhythmia
polyuria and polydipsia (neprogenic DI)

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51
Q

Which diuretics causes K loss?

A

Loop (equivalent to Bartters synd)

Thiazide (equivalent to Gitelman syndrome)

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52
Q

What Ix would you do in a patient with hypokalaemia and hypertension?

A

Aldosterone:Renin ratio to assess primary hyperaldoseronism.

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53
Q

How do you manage a serum potassium between 3 and 5?

A

Oral potassium chloride (two SandoK tablets tds for 48h) and recheck

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54
Q

How do you manage a serum potassium less that 3?

A

IV KCl max rate 10mmol/h (higher rates irritate peripheral veins).

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55
Q

How do you manage a serum potassium less that 3?

A

IV KCl max rate 10mmol/h (higher rates irritate peripheral veins).

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56
Q

Drugs that cause hypoglycaemia?

A

Sulphonylureas
Insulin
Beta blocker, salicylate, alcohol.

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57
Q

Causes of hypoglycaemia which suppressed insulin and C-peptide?

A

Normal response to hypoglycaemia

Exercise, fasting, critical illness, endrocrine deficiency, liver failure, Anorexia

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58
Q

Neonate hypoglycaemia with decrease insulin, c-peptide and ketons and FFAs present?

A

Premature, IUGR, Co-morbidity

If no ketones suggest a metabolic disorder.

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59
Q

Insulinoma - symptoms and lab results

A

Fitting, weight gain, increased appetite, personality change.
Raised insulin, raised c-peptide, negative sulphonylurea screen (required for dx of insulinoma).
Assoc with MEN1

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60
Q

Non-islet cell tumour hypoglycaemia

A

Decrease insulin, c-peptide, FFAs and Ketones. Tumours that secrete big-IGF2 which binds insulin receptors (paraneoplastic syndrome)

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61
Q

Non-islet cell tumour hypoglycaemia

A

Decrease insulin, c-peptide, FFAs and Ketones. Tumours that secrete big-IGF2 which binds insulin receptors (paraneoplastic syndrome)

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62
Q

Metabolic Acidosis Causes (4)

A

DKA (increase H ion production)
Renal Tubular Acidosis (Decreased H ion excretion)
Intenstinal fistula (bicarb loss)
Lactate build up

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63
Q

Resp Acidosis Causes (3)

A

Decreased ventilation
Poor lung perfusion (PE)
Impaired gas exchange (pneumonia, COPD)

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64
Q

Metabolic Alkalosis Causes (3)

A

Pyloric stenosis (H ion loss)
Hypokalaemia
Ingestion of bicarobonate

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65
Q

Res Alkalosis Causes (2)

A

Panic/hyperventilation

Artificial ventilation

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66
Q

Useful in staging extracaspular spread of prostate CA

A

Acid phosphatase

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67
Q

Hashimotos Thyroditis is associated with

A

autoimmune hepatitis

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68
Q

SCID is often caused by a deficiency in?

A

Adenosine deaminase

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69
Q

Which cardiac marker is a good indication of reinfarction?

A

CKMB

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70
Q

A 44-year-old woman known to have multi-focal ER and PR negative breast cancer that is inoperable is admitted with sudden onset of nausea, vomiting, polyuria and delirium. She also has reduced muscle strength and her husband describes her marked personality change and increased thirst over the previous few days as well as increasing back and hip pain not well relieved with her oral morphine preparation. Pelvic radiology reveals Osteolytic lesions. Which of the above do you think would be raised given her presenting symptoms?

A

Calcium

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71
Q

McArdle’s Glycogen Storage Disease (type V) Stiffness after exercise. Is a deficiency in which enzyme?

A

Mycophosphorylase

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72
Q

Farby’s Disease. X-linked disorder of glycolipid metabolism due to deficiency in?
Symptoms?

A

Galactosidase A.

Recurrent febrile illness, painful parasthesiae in hands and feet. Red papules in pelvic region. Protinuria.

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73
Q

Thiamine Deficiency Sx?

A

Nystagmus and board based gate. Associated with Alcoholics.

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74
Q

Vitamine D Def Sx?

A

Bone pain, knock-kneed (gunu varus), bow legged, waddling gate.

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75
Q

Wilsons Disease is a deficiency in?

A

Caeruloplasmin

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76
Q

Riboflavin (vit B2) deficiency Sx?

A

Cheilosis (chapping and fissure of lips), a sore red tongue, scaly skin rashes on scrotum, vulva and philtrum.
Riboflavin is absorbed in the terminal ileum.

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77
Q

Folic Acide Def Sx?

A

Anaemia, weightloss

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78
Q

Thiamine (B1) Deficiency Sx?

A

Nystagmus and board based gate. Associated with Alcoholics.

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79
Q

Folic Acide Def Sx?

A

Anaemia, weightloss

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80
Q

Atrophic gastritis can lead to deficiency in?

A

Lack of intrinsic factor produced by the parietal cells leads to b12 deficiency and a megaloblastic anaemia.

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81
Q

Vitamin C (ascorbic acid) def?

A

Required for the synthesis of collagen.
Early -Malaise, lethargy
Middle (1-3m) -SOB, bone pain
Other - Bruising, gum bleeding, poor wound healing and emotional changes.

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82
Q

Vitamin A deficiency?

A

Difficulty seeing in dim light.

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83
Q

A 35 yr old woman presents with pain in her neck which radiates to her upper neck, jaw and throat. The pain is worse on swallowing. She has a Hx of an upper respiratory tract infection two weeks ago. On Ix she has a free T4 of 30pmol/l, free T3 of 11pmol/l and a TSH level of 0.1mU/l. On technetium scanning of the thyroid there is low iodine uptake.

A

Subacute granulomatous thyroditis

84
Q

Thyroid Canacer associated with calcitonin and MEN1?

A

Medullary

85
Q

32 year old female presented with weight loss and anxiety. The thyroid gland was enlarged, firm, fleshy and pale, infiltrated by lymphocytes. Askanazy cells were noted

A

Hashimoto’s thyroditis

86
Q

Metformin effect of TSH?

A

suppression

87
Q

Askanazy cells (aka Hurthle cells) are found in? (3)

A

Benign adenoma, hashimoto’s thyroditis, toxic multinodular goitre. Are of follicular cell origin.

88
Q

Drugs contraindicated in porphyria?

A

Alcohol, NSAID (diclofenac), Co-trimoxazole.

89
Q

Treatment for acute intermittent porphyria?

A

Haem arginate

90
Q

Autosomal dominantly inherited porphyria with neurovisceral manifestations only, resulting from porphobilinogen deaminase deficiency.

A

Acute intermittent porphyria

91
Q

Neurotoxic product(s) of heme breakdown producing neurovisceral damage in certain porphyrias

A

5-aminolevulinic acid

92
Q

Autosomal dominantly inherited (or spontaneous mutation) porphyria with cutaneous manifestations only, resulting from uroporphyrinogen decarboxylase deficiency

A

Porphyria cutanea tarda

93
Q

Enzyme that catalyses the rate-limiting step of heme breakdown

A

ALA synthase

94
Q

Product(s) of heme breakdown resulting in photosensitivity (i.e. cutaneous) damage in certain porphyrias

A

Activated porphyrinsand oxygen free radicals.

95
Q

Porphyria definition?

A

Deficiency in enzymes of haem biosynthesis pathway

96
Q

Enzyme affected in acute intermittent porphyria?

A

HMB synthase

97
Q

Enzyme affected in Porphyria cutanea tarda

A

Uroporphyrinogen decarboxylase

98
Q

Enzyme affected in Congenital erythopoietic porphyria

A

Uroporphyrinogen III synthase

99
Q

ALA synthase deficiency gives?

A

X-linked sideroblastic anaemia

100
Q

Acute Intermitted Porphyria
Inheritance?
Symptoms?

A

Autosomal dominanat.
Neurovisceral attached. Abdo pain, vomiting. Tachycardia, hypertension, constipation, urinary incontinence, seizures, psychological symptoms. NO SKIN SYMPTOMS

101
Q

Acute Intermittent Porphyria
Enzyme activity level?
Precipitating Factors?

A

Usually 50% of normal 90% of people have no symptoms.
ALA synthase inducers - barbituates, steroids, ethanol, anticonvulsants
Stress - infection surgery

102
Q

Acute Intermittent Porphyria diagnosis? Treatment?

A

Raised urinary PBG and ALA

Avoid precipitators, IV carbohydrate, IV haem arginate

103
Q

Hereditary Coprophorphyria (HCP)

A

Autosomal dominant
Acute neurovisceral attacks
Skin lesions - blistering, skin fragility
Coprophorphyrinogen oxidase deficiency

104
Q

Variegate Porphyria (VP)

A

Autosomal dominant
Acute attacks
Skin lesions
Protoporphyrinogen oxidase deficiency

105
Q

Phorphyria cutanea Tarda

A

Inherited or acquired.
Uroporphyrinogen decarboxylase deficiency
Vesicle in sun-exposed skin, crusting, scarring, pigmentation.
Urinary and plasma uroporphyrin increased

106
Q

Erythropoietic protoporphyria

A

Photosensitivity, burning, itching, oedema following sun exposure. NOT Acute.
Only RBCs affected. May need phlebotomy for haemochromotosis.

107
Q

A 67-year-old man was started on bendroflumethiazide for hypertension 2 weeks ago. On examination he has dry mucous membranes and decreased skin turgor. His past medical history is otherwise unremarkable.
Na 129, K 3.5, Ur 8, Cr 100

A

Thiazide induced hypovlaemic hyponatraemia, Treat with 0.9% saline

108
Q

A 57-year-old woman is admitted with increasing breathlessness worse on lying flat. Her past medical history includes a Non-STEMI and hyperlipidaemia. She is on ramipril, bisoprolol, aspirin and simvastatin. On examination she has elevated JVP, bibasal crackles and bilateral leg oedema.
Na 128, K 4.5, Ur 8, Cr 100

A

Cardiac failure leading to hypervolaemic hyponatraemia. Treat underlying cause and fluid restriction.

109
Q

A 55-year-old man presents with jaundice. He has a past history of excessive alcohol intake. On examination he has multiple spider naevi, shifting dullness and splenomegaly.
Na 122, K 3.5, Ur 2, Cr 80

A

Hyervolemic hyponatramia secondary to alcoholic liver disease. Fluid restriction and treat underlying cause.

110
Q

A 40-year-old woman presents with fatigue, weight gain, dry skin and cold intolerance. On examination she looks pale.
Na 130, K 4.2, Ur 5, Cr 65

A

Euvolaemic hyponatraemia secondary to hypothyrodism. Treat cause. Thyroxine replacement.

111
Q

A 45-yeard-old woman presents with dizziness and nausea. On examination she looks tanned and has postural hypotension.
Na 128, K 5.5, Ur 9, Cr 110

A

Addisions disease. Euvolemic hyponatraemia. Treat with hydrocortisone and fludrocortisone. Dx with short synacthen test.

112
Q

A 62-year-old man presents with chest pain, cough and weight loss. On examination he looks cachectic. He has a 30 pack year smoking history.
Na 125, K 3.5, Ur 7, Cr 85

A

SIADH 2nd to malignanacy. Dx plasma and urine osmolality. Treat underlying cause.

113
Q

Causes of SIADH

A

CNS or Lung Pathology.
Drugs - SSRIs, TCA, opiates, PPIs, Carbemazepine
Malignancy

114
Q

Causes of SIADH

A

CNS or Lung Pathology.
Drugs - SSRIs, TCA, opiates, PPIs, Carbemazepine
Malignancy

115
Q

A 20-year-old man presents with polyuria and polydipsia. On examination he has bitemporal hemianopia.
Na 150, K 4, Ur 5, Cr 70

A

Cranial DI. ADH insufficiency leading to water loss in collecting duct.

116
Q

DI investigations?

A

Serum glucose, K, Ca, plasma and urine osmolality, Water deprivation test.

117
Q

When is a death reported to a coroner? (3)

A

Violent
Unnatural/sudden
Cause unknown

118
Q

Schmidt Syndrom

A

Addisions (autoimmune adrenal isufficiency) with AI hypothyroidism and/or DM. Is part of polyendocrine syndrome.
In exam hypothyroidism with disturbed electrolytes.

119
Q

Test for Addisions?

A

Short Synacthen Test.
Measure ACTH and cortisol at the start of the test.
Administer 250mcg of ACTH
Check cortisol at 30 and 60. Cortisol doesn’t rise.

120
Q

32, with hypertension and an adrenal mass. Three possible Ddx?

A

Cons (Aldosterone secreting tumour)
Phaeochromocytoma (adrenaline secreting tumour in medulla)
Cushing’s Syndrome (crotisol secreting tumour)

121
Q

Phaeochromocytoma
Investigation?
Treatment?

A

Hypertension, high urinary catecholamines.
Alpha block with phenoxybenzamine
Add beta block
Surgery

122
Q

Hypertensive 33 year old
Na 147, K 2.8, U 4, Glucose 4
Raised aldosterone, suppressed renin

A
Cons syndrome (primary hyperaldosteronism)
Causes HTN which in turn suppresses renin at the JGA
123
Q

Hypertensive 33 year old
Na 147, K 2.8, U 4, Glucose 4
Raised aldosterone, suppressed renin

A
Cons syndrome (primary hyperaldosteronism)
Causes HTN which in turn suppresses renin at the JGA
124
Q

32 year old obsess woman with DM, HTN and bruising. Na 146, K 2.9, U 4, Glucose 14. Aldosterone low, Renin Low

A

Cushing’s Syndrome. Investigation 9am cortisol and midnight cortisol.
Low Dose Dexamethasone suppression test. Dex wont suppress cortisol in Cushing’s SYNDROME!

125
Q

Causes of Cushing’s

A

Iatrogenic
Pituitary dependent 85%
Adrenal Adenoma 10%
Ectopic ACTH 5%

126
Q

Pituitary Dependent Cushing’s Disease Investigation?

A

Low dose Dex suppression test won’t suppress cortisol

How dose Dex suppression test WILL suppress cortisol if pituitary dependent.

127
Q

Serum Calcium is in 3 forms?

A

Free 50%
Protein bound 40% (albumin)
Complexed 10% (citrate/phosphate)

128
Q

Three effects of PTH

A

Increased Vit D which causes increase Ca absorption in intestine
Increase renal Ca resorption
Increase bone resorption

129
Q

Four effects of PTH

A

Increased Vit D which causes increase Ca absorption in intestine
Increase renal Ca resorption
Increase bone resorption
Stimulate renal phosphate wasting

130
Q

Vitamine D (1,25 (OH)2 cholecalciferol) functions?

A

Intestinal Ca absorption
Intestinal PO4 absorption
Deficiency associated with ai disease, cancer and metabolic syndrome

131
Q

Hypercalcaemia symptoms

A

Polyuria, polydipsia
Constipation
Neuro - confusion, seizures, coma

132
Q

Primary Hyperparathyroid
Serum Ca, PO and PTH?
Cause?

A

Raised Ca with inappropriately normal or raised PTH (i.e. not suppressed), decreased phospate
Parathyroid adenoma/hyperplasia/carcinoma
Hyperplasia associated with MEN1
F>M

133
Q

Familial Hypocalciuric hypercalcaemia

A

Calcuium sensing receptor mutation increased the set point for PHT release causing a mild hypercalcaemia. Benign

134
Q

Hypercalcaemia in malignancy (3)

A
Humoral hypercalcaemia of malignancy (small cell lung Ca and PTHrP)
Bone mets (local bone osteolysis)
Haem malignancy (myeloma)
135
Q

Non-PTH drive hypercalcaemia

A
Sarcoidosis
Thyrotoxicosis
Hypoadrenalism
Thiaide diruetic
Excess vit D (sunbeds)
136
Q

Non-PTH drive hypercalcaemia

A
Sarcoidosis
Thyrotoxicosis
Hypoadrenalism
Thiazide diuretic
Excess vit D (sunbeds)
137
Q

Hypercalcaemia acute treatment

A

Fluids, bisphosphonates, treat underlying cause

138
Q

Symptoms of hypocalcaemia

A

Neuro-muscular excitability (Trousseau’s and Chvosteks signs), hyperreflexia, laryngeal spasm, convulsions, choked disc (retina)

139
Q

Non-PTH causes of hypocalcaemia (3)

A
Vit D deficiency
Chronic kidney disease
PTH resistance (pseudohypoparathyroidism)
140
Q

PTH related causes of hypocalcaemia (4)

A

Surgical (post thyroidectomy)
Autoimmune hypoparathyroidism
Congenital absence of parathyroid (DiGeorge)
Mg deficiency (required for PTH regulation)

141
Q

Dexa Scan Results
Osteoporosis?
Osteopenia?

A

Osteoporosis T-score

142
Q

Risks for osteoporosis?

A

Sedentary, EtOH, Smoking, low BMI, malnutrition
Endocrine - hyperprolatin, thyrtoxicosis, cushings
steroids
prolonged illness

143
Q

Treatment for osteoporosis

A

Lifestyle modification (exercise, stop drink/smoke)
Vitamin D/Ca
Bisphosphonates (decrease bone respiration)
Strontium
Oestrogen (HRT)

144
Q

Treatment for osteoporosis

A

Lifestyle modification (exercise, stop drink/smoke)
Vitamin D/Ca
Bisphosphonates (decrease bone respiration)
Strontium
Oestrogen (HRT)

145
Q

Risk Factors for Renal Stones?

A

Dehydration
Abnormal urine pH -high meat intake, renal tubular acidosis.
UTI
Anatomical abnormalities

146
Q

Renal stone compositions?

A

Calcium 80%
Struvite (stage head) 10%
Uric acid 5%

147
Q

Struvite stones pathogenesis?

A

Mg and Ca phosphate stones. Form during UTI from urea splitting organisms like Klebsiella or proteus
Give stag horn calculi

148
Q

Lesch Nyham Syndrome

A

HGPRT deficiency which is required for purine metabolism. Leads to increase urate.
Normal at birth, developmental delay by 6/12
Choreiform movements (1y)
Spasticity and mental retardation. Self-mutilation.
Hyperuricaemia

149
Q

Clinical features of gout?

A

Exquisit pain, hot, red, swollen joint.

1st MTP 50%

150
Q

Mx Acute Gout?

A

NSAIDs
Colchicine
Glucocorticoids
Do NOT modify plasma urate conc.

151
Q

Mx hyperuricaemia

A
Not in an acute attack
Drink water
Reverse lifestyle factors
Reduce synthesis with allopurinol
Increase renal excretion with probenecid
152
Q

Mx hyperuricaemia

A
Not in an acute attack
Drink water
Reverse lifestyle factors
Reduce synthesis with allopurinol
Increase renal excretion with probenecid
153
Q

SEs of Allopurinol?

A

Makes Azathioprine more toxic to bone marrow

Allopurinol makes the azathioprine intermediary mercaptopurine last longer which interferes with purine metabolism.

154
Q

Dx of Gout?

A

Negatively birefringent crystals, needle shaped.

155
Q

Pseudogout?

A

Occurs in OA patients, last 1-3 weeks, PYROPHOSPHATE crystals. Positively birefringent.

156
Q

Immune Cells of the Liver?

A

Kupffer Cells. Clear infection and LPS.
Antigen presenting and immune modulating.
Break down RBCs?

157
Q

Serum markers of Liver Damage?

A

ALT, AST, ALP, GGT

158
Q

Serum markers of Liver Function

A

Albumin, Pro-thrombin Time, Bilirubin

159
Q

Liver Enzyme that rises more in alcohol and cirrhosis

A

AST - in cytoplasm of hepatocyte, elevate when hepatocyte dies. Also present in other organs (muscle, kidney, brain, pancreas)

160
Q

GGT
Locations?
Raises in?

A

Found in hepatocytes and epithelium of small bile ducts. Also found in liver, kidney, pancreas, spleen, heart, brain and seminal vesicles.
Elevated in chronic alchohol abuse, bile duct disease and hepatic metastasis.

161
Q

ALP
Sources?
Raised in?

A

Liver and also bone, small intestine, kidney, WBCs and placenta.
Markedly elevated in obstructive jaundice or bile duct damage.

162
Q

Reasons for low albumin? (3)

A

Low production - liver disease, malnutrition
Loss - kidney or gut pathology
Sepsis - 3rd spacing

163
Q

Albumin function and half life

A

Half life 20d

contributes to oncotic pressure, binds steroids, drugs, bilirubin, Ca

164
Q

Measure of extrinsic pathway function

A

PT - 2, 5, 7, 10. Affected by Warfarin?

165
Q

Alpha Feto Protein

A

Fetal transport/immune regulation protein. No know function in adults.
Used to diagnose hepatocellular carcinoma
Also raised in hepatic damage, regeneration, pregnancy and testicular cancer.

166
Q

Gilberts Ix?

A

Fasting and non-fasting bilirubin. Raised fasting unconjugated bilirubin.

167
Q

38 y/0 female presents with itch, jaundice, dark urine. Treated for UTI 5/7 ago.
Bil +, ALT & AST +, ALP +++, GGT +
No bile duct obstruction on USS

A

Dx - drug induced cholestasis 2nd to augmentin.

168
Q

Physiological causes of raised ALP?

A

Pregnancy and childhood (growth spurt)

169
Q

Pathological causes of raised ALP?

A

> 5x normal - bone disease (pagers), cholestasis, cirrhosis

170
Q

Pathological causes of raised ALP?

A

> 5x normal - bone disease (pagers), cholestasis, cirrhosis

171
Q

Three forms of CK

A

CK-MM muscle
CK-MB cardiac muscle
CK-BB brain

172
Q

Statin Related Myopathy
What is it?
Risks?

A
Spectrum of myalgia to rhabdo
Risks
Polypharmacy - fibrates, cyclosporin
High dose
Genetic
Previous Hx of statin myopathy
173
Q

Causes of Raised CK?

A
Muscle damage 
Myopathy (Duchennes >10x)
MI (>10x)
Severe exercise (5x)
Physiological - afro-caribbean (
174
Q

Troponin time course post MI

A

Rises 4-6h post
Peaks at 12-24h (100% sensitive, 98% specific at 12-24h)
Remains elevated for 3-10d
Measure at 6 and 12h post onset of chest pain

175
Q

Diagnostic criteria for acute MI

A

One of the following
(1) Typical rise and fall of troponin or rapid rise and fall of CK-MB with at least one of:
ischemic symptoms, pathological Q waves, ECG changes of schema, coronary artery intervention.
(2) Pathological findings of an acute MI

176
Q

One inter nation unite of enzyme activity is?

A

Quantity of enzyme that catalyses the reaction of one micro mol of substrate per minute. Temperature and pH dependent.

177
Q

Fat soluble vitamins?

A

A (Retinol): Def - colour blindness, Exc - exfoliant hepatitis
D (Cholecalciferol) Def - osteomalacia, Exc - hypercalcaemia
E (Tocopherol) - anaemia/neuopathy
K (Phytomenadion) - defective clotting

178
Q

Fat soluble vitamins? def/excess

A

A (Retinol): Def - colour blindness, Exc - exfoliant hepatitis
D (Cholecalciferol) Def - osteomalacia, Exc - hypercalcaemia
E (Tocopherol) - anaemia/neuropathy
K (Phytomenadion) - defective clotting

179
Q

Thiamin (B1) def/excess

A

Deficiency - beri beri, neuropathy, wernicke syndrome

180
Q

Pyridoxine (B6) def/excess

A

Def - dermatitis/anaemia

Excess - neuropathy

181
Q

Ascorbate © def/excess?

A

Deficiency - scurvy

Excess - renal stones

182
Q

Pellagra

A

Niacin (B3) deficiency.

Symptoms - photosensitivity, aggression, red tongue, red skin lesions.

183
Q

Marasmus

A

Severe deficiency of protein, carbs and fat

Shrivelled, growth retarded, muscle wasting, no s/c fat.

184
Q

Kwashiorkor

A

Protein deficient
Odematous, scaling/ulcerataed
lethargic
large liver, s/c fat

185
Q

Normal GFR?

A

120ml/min

186
Q

Gold standard measurement of GFR?

A

Inulin clearance. GFR = (urin conc of inulin x volume cleared)/plasma conc of inulin

187
Q

Gold standard measurement of GFR?

A

Inulin clearance. GFR = (urin conc of inulin x volume cleared)/plasma conc of inulin
To difficult to be clinically useful

188
Q

Disadvantages of Cratinine as a marker of GFR?

A

Variable resorption by tubular cells.
Influenced by intake of fat
Related to muscle mass
Lower in black population

189
Q

Cockcroft Gault

A

Estimates creatinine clearance (not GFR directly) can overestimate GFR when

190
Q

MDRD

A

Estimates GFR based on age, sex, serum creat and ethnicity. May underestimate GFR if above average weight and young.

191
Q

CKD-EPI

A

Similar to MDRD to calculate eGFR, current recommended equation.

192
Q

Causes of pre-renal AKI

A
Volume depletion
Hypotension
Odematous states
Selective renal ischemia
Drugs affecting GFR (NSAID, calcineurin inhibitors, ACEi/ARB)
193
Q

Causes of pre-renal AKI

A
Volume depletion
Hypotension
Odematous states
Selective renal ischemia
Drugs affecting GFR (NSAID, calcineurin inhibitors, ACEi/ARB)
194
Q

AKI/RTA

A

AKI is dependent on circulating volume, RTA is structural damage to kidney.

195
Q

Obstructive uropathy causes?

A
Ureteric obstruction
Intra-renal obstruction
Prostatic
Blocked urinary catheter
Immediate relief restores GFR with no structural damage. Prolonged obstruction can cause structural damage (glomerular schema, scarring).
196
Q

Stages of CKD?

A
1 - kidney damage normal GFR > 90
2 -Mild GFR 60-89
3 - Moderate GFR 30-59
4 - Severe 15-29
5 - End-stage
197
Q

Common causes of CKD (6)

A
Diabetes
Astherosclerotic renal disease
HTN
Chronic glomerulonephritis
Infective/Obstructive uropathy
PCKD
198
Q

Renal Acidosis

A

Failure of renal excretion of protons in CKD
Results in: muscle and portein degradation, osteopenia, cardiac dysfunction
Treat with oral sodium bicarb

199
Q

Consequences of CKD

A
Acidosis and Hyperkalaemia
Anaemia - decline in EPO cells
Renal bone disease
Cardiovascular disease due to vascular calcification/uraemic cardiomyopathy. 
Uraemia and death
200
Q

Stages of uraemia cardiomyopathy?

A

LV hypertrophy
LV dilation
LV dysfunction

201
Q

Antibodies raised in Coeliac Disease?

A

AntiTTG and Anti emdomysial

202
Q

Antibodies raised in Coeliac Disease?

A

AntiTTG and Anti emdomysial

203
Q

Ix for herediatary shereocytosis?

A

Osmotic fragility

204
Q

Antibody in primary billary cirrhosis

A

Anti mitochodrial

205
Q

Ix for Paroxysmal nocturnal haemoglobinuria?

A

Ham’s test

206
Q

Anti GAD is raised in

A

T1DM