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DPD > Haem&Endo > Flashcards

Haem&Endo Flashcards

1
Q

What are the two main components of a full blood count and what are the names of the conditions in which they get deranged?

A

Hb – anaemia or polycythaemia

Platelets – thrombocytopaenia or thrombocytosis

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2
Q

List two causes of polycythaemia

A

Primary polycythaemia (polycythaemia rubra vera)

Secondary polycythaemia (secondary to chronic hypoxia in COPD patients, a tumour that is producing ectopic EPO)

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3
Q

What are the three mechanisms of thrombocytopaenia? State a cause for each

A

Reduced production of platelets (e.g. bone marrow infiltration, leukaemia, lymphoma, drugs (e.g. chemotherapy))

Destruction of platelets (e.g. consumption of platelets in DIC)

Pooling of platelets (e.g. pooling within the spleen in patients with chronic liver disease and portal hypertension)

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4
Q

Broadly speaking, what can cause a high WCC?

A

Infection

Malignancy

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5
Q

List two main causes of microcytic anaemia

A

Iron deficiency anaemia

Beta thalassemia heterozygosity

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6
Q

What are the two main mechanisms of iron deficiency anaemia

A

Blood loss

Dietary deficiency

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7
Q

List some causes of normocytic anaemia

A

Anaemia of chronic disease

Infection

Malignancy

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8
Q

Describe the ferritin level in anaemia of chronic disease

A

Normal/high – because ferritin is an inflammatory marker, that is raised in inflammatory conditions (e.g. rheumatoid arthritis)

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9
Q

Describe the relationship between MCV and Hb in beta thalassemia heterozygosity

A

The MCV is very low and out of proportion to the degree of anaemia

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10
Q

List 5 causes of macrocytic anaemia. State some clinical clues that can be found on history, examination and investigation.

A

Alcoholism – history + raised GGT
Myelodysplasia – pancytopaenia + bone marrow biopsy
Hypothyroidism – history + TFTs (low T4 + high TSH)
Liver disease – history + exam
Folate/B12 deficiency – history (e.g. small bowel disease)

NOTE: mnemonic – alcoholics may have liver failure

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11
Q

List the main symptoms of polycythaemia.

A 
Headache
Pruritus after a hot bath
Blurred vision
Tinnitus
Thrombosis (DVT/stroke)
Gangrene
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12
Q

What are the three main complications of sickle cell anaemia

A

Acute painful crisis

Sequestration crisis

Gallstones/chronic cholecystitis

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13
Q

Describe the management of acute painful crisis

A

Analgesia

Oxygen (hypoxia can cause sickling)

IV fluids (dehydration can cause sickling)

Antibiotics

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14
Q

How is stroke treated in sickle cell patients?

A

Exchange blood transfusion to remove the sickled cells

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15
Q

Where can blood cells pool in sequestration crisis and what symptoms does this cause?

A

Lungs – SOB, cough, fever

Spleen – exacerbation of anaemia

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16
Q

How do you treat splenic sequestration crisis?

A

Splenectomy

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17
Q

Why do patients with sickle cell anaemia suffer from chronic cholecystitis?

A

Increased breakdown of Hb leads to increased risk of forming pigment stones

This can lead to chronic cholecystitis

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18
Q

How is chronic cholecystitis treated in sickle cell patients?

A

Cholecystectomy

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19
Q

What are the four main features of multiple myeloma? List important findings on presentation/investigation

A

Calcium – polyuria, polydipsia, constipation

Renan impairment – high urea and creatinine

Anaemia – SOB, lethargy, FBC

Bone – fracture, pain, DEXA scan

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20
Q

What are two other important complications of multiple myeloma?

A

Increased risk of infection

Cord compression

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21
Q

Why are multiple myeloma patients more likely to suffer from infections?

A

Multiple myeloma leads to increased production of one type of immunoglobulin

This leads to reduced production of other immunoglobulins, which increases risk of infection

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22
Q

What can cord compression due to multiple myeloma lead to?

A

Spastic paraparesis – partial paralysis of the lower limb

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23
Q

Describe the ALP in multiple myeloma. Why is this the case?

A

ALP is normal/low in multiple myeloma

Multiple myeloma suppresses the osteoblasts, which are responsible for producing ALP

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24
Q

List the two main causes of anaemia with HIGH reticulocytosis

A

Haemorrhage

Haemolysis

NOTE: reticulocytosis occurs when there is an increased demand for red blood cells

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25
Q

List three causes of anaemia with LOW reticulocytes

A

Parvovirus B19

Aplastic crisis in sickle cell patients

Blood transplant

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26
Q

List the three main diagnostic criteria for diabetes mellitus

A

Fasting blood glucose > 7 mmol/L

Random blood glucose > 11.1 mmol/L

HbA1c > 6.5% or > 48 mmol/mol

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27
Q

Why was the diagnostic cut-off for fasting blood glucose set at > 7 mmol/L?

A

Epidemiological studies showed that the rate of incidence of retinopathy significantly increased in patients with fasting blood glucose > 7 mmol/L

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28
Q

What is impaired glucose tolerance (IGT)?

A

A blood glucose of 7.8-11.1 mmol/L measured 2 hours after an oral glucose tolerance test (OGTT), in which 75 g of glucose is administered orally

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29
Q

Other than type 1 and type 2 diabetes mellitus, what else can cause diabetes?

A

Pancreatic insufficiency

NOTE: complete pancreatic insufficiency is difficult to treat because the lack of glucagon and pancreatic polypeptide is difficult to manage

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30
Q

What is the first drug that is given to patients with type 2 diabetes mellitus?

A

Metformin

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31
Q

At what point do you add more medications for diabetics on metformin?

A

If the patient fails to achieve the target HbA1c despite metformin

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32
Q

Which commonly used medication for type 2 diabetes can cause hypoglycaemia?

A

Sulfonylureas

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33
Q

If the patient is overweight or you want to avoid hypoglycaemia, which diabetic medication might you consider using?

A

GLP-1 agonists

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34
Q 
Briefly describe the mechanism of action of:
Metformin
Sulfonyureas
DPP-IV inhibitors
GLP-1 agonists
A

Metformin
Decreases insulin resistance

Sulfonylureas
Stimulates insulin release

DPP-IV inhibitors
Reduces GLP-1 breakdown

GLP-1 agonists
Incretin that stimulates glucose-stimulated insulin release. Also inhibits glucagon release, reduces appetite and may cause some weight los

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35
Q

What is one of the first signs of diabetic nephropathy?

A

Increase in albumin: creatinine ratio

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36
Q

When might you put a patient on an insulin sliding scale

A

If a diabetic patient is not eating or really unwell

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37
Q

Sliding scales are not indicated in patients with sepsis. What medication would you initially try

A

Daily long-acting insulin is preferred

NOTE: if the patient is ill and not eating very much, the long-acting insulin along may be sufficient to meet their insulin demands at the time

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38
Q

What is the main difficulty with insulin sliding scales?

A

It requires constant monitoring of blood glucose and constant adjustment of the insulin delivery rate

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39
Q

In what context is a sliding scale most useful?

A

Surgery – a patient might have to be NBM for a long time

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40
Q

List some symptoms of Graves’ disease.

A

Weight loss

Increased appetite

Irritability

Palpitations

Irregular periods

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41
Q

Describe the TFT results in a patient with Graves’ disease?

A

High T4/T3

Low TSH

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42
Q

What would a high TSH with high T4/T3 suggest?

A

Secondary hyperthyroidism

43
Q

After performing TFTs and putting together a clinical picture of primary hyperthyroidism, what test would you do next?

A

TSH receptor stimulating antibodies

44
Q

Other than stimulating the TSH receptors, what else do TSH receptor stimulating antibodies do?

A

They stimulate adipocytes and fibroblasts at the back of the eye to produce glycosaminoglycans (GAGs), which are hydrophilic and cause proptosis

They are also responsible for the skin changes in pretibial myxedema

45
Q

What are TPO antibodies a marker of?

A

Autoimmunity

They are present in about 5% of the general population

46
Q

What will radioiodine uptake scans of Graves’ disease patients show?

A

Diffuse increased uptake

47
Q

What needs to happen for the thyroid gland to be able to take up iodine?

A

The TSH receptor must be stimulated for there to be iodine uptake

48
Q

Describe and explain the iodine uptake in thyroiditis

A

NO iodine uptake because TSH is suppressed in thyroiditis

49
Q

Describe and explain the iodine uptake in toxic nodular goitre

A

The scan will show a single hot nodule that is autonomous and no longer controlled by TSH

There will not be much uptake from the rest of the gland, because high T4/T3 suppresses TSH levels, which, therefore, will not stimulate iodine uptake in the rest of the thyroid gland that is functioning normally

50
Q

List some risk factors for thyroid cancer

A

Radiation

Family history

Rapid enlargement/compression

Lymphadenopathy

51
Q

What percentage of the general population has thyroid nodules?

A

60-70%

52
Q

Where do most thyroid cancers metastasise to? Which type of thyroid cancer has a propensity to metastasise to this location?

A

Lungs

These tend to be mostly follicular thyroid cancer

53
Q

List two investigations that may be used in the diagnosis of thyroid cancer

A

Ultrasound scan

Fine needle aspiration cytology

Uptake scan (thyroid cancers are cold)

54
Q

List four types of thyroid cancer

A

Papillary

Follicular

Medullary

Anaplastic

55
Q

Which type of thyroid cancer has the worst prognosis?

A

Anaplastic

56
Q

List two treatments that are used after surgery in patients with thyroid cancer

A

Thyroxine – replace the function of the lost thyroid gland

Radioiodine – in high-risk patients

57
Q

List the signs of a prolactinoma

A

Amenorrhoea

Galactorrhoea

Bitemporal hemianopia

Sexual dysfunction

58
Q

Which type of prolactinoma can compress the pituitary stalk?

A

Macroprolactinoma

59
Q

What is the first-line treatment for prolactinoma?

A

Dopamine agonists (e.g. cabergoline, bromocriptine)

60
Q

Roughly how long are prolactinoma patients kept on this treatment?

A

4 years – then they can gradually be weaned off and some may be able to stop it entirely

61
Q

Describe the symptoms of acromegaly

A

Headaches

Sweating

Obstructive sleep apnoea (poor sleep, snoring)

Carpal tunnel syndrome (tingling fingers)

62
Q

What causes obstructive sleep apnoea?

A

Excessive soft tissue obstructing the upper airways during sleep

63
Q

What is the first test you do in the investigation of acromegaly?

A

IGF-1 levels

64
Q

What is the test you do to diagnose acromegaly after IGF-1 levels?

A

Oral Glucose Tolerance Test

Failure of suppression of GH after oral intake of glucose suggests acromegaly

65
Q

How do you test pituitary function?

A

Insulin tolerance test

Insulin causes hypoglycaemia, which should lead to an increase in the production of GH

66
Q

What is a dexamethasone suppression test used for?

A

Test for Cushing’s syndrome

In normal people, dexamethasone will suppress ACTH and hence suppress cortisol

In people with Cushing’s syndrome, the cortisol level will remain high

67
Q

What is a short synacthen test used for?

A

Test for adrenal insufficiency

In normal people, synacthen will stimulate the adrenals to produce cortisol so cortisol levels will rise considerably following the administration of cortisol

In people with adrenal insufficiency, cortisol levels will not rise considerably after the administration of synacthen

68
Q

What are the three distinguishing symptoms of Cushing’s syndrome?

A

Proximal myopathy

Easy bruising

Striae > 1 cm wide

69
Q

List some disease states that are caused by Cushing’s syndrome

A

Hypertension

Diabetes mellitus

Osteoporosis

70
Q

What are striae?

A

Capillaries that become visible due to stretching and thinning of the skin

71
Q

Broadly speaking, how can the causes of amenorrhoea/oligomenorrhoea be divided?

A

Pregnancy

Hypothalamus

Pituitary

Thyroid

Ovaries

72
Q

List two hypothalamic causes of amenorrhoea

A

Excessive exercise

Low BMI

73
Q

Why does low BMI lead to amenorrhoea?

A

Low BMI will mean that leptin levels are low

Leptin has a permissive effect over the hypothalamo-pitutiary-gonadal axis

74
Q

What is the main pituitary cause of amenorrhoea?

A

Prolactinoma

75
Q

What derangements of thyroid function can cause amenorrhoea?

A

Hypothyroidism

Hyperthyroidism

76
Q

List two ovarian causes of amenorrhoea

A

PCOS -> excess androgens

Ovarian failure -> low oestradiol + high FSH/LH

77
Q

What are the three main signs of hypokalaemia?

A

Weakness

Arrhythmia

Polyuria

78
Q

List the three main causes of hypokalaemia

A

Vomiting

Diuretics

Primary hyperaldosteronism

79
Q

Describe how hypokalaemia leads to polyuria

A

Hypokalaemia causes nephrogenic diabetes insipidus, which leads to polyuria

80
Q

List two examples of primary hyperaldosteronism

A

Conn’s syndrome

Bilateral adrenal hyperplasia

81
Q

What can be measured to assist with a diagnosis of primary hyperaldosteronism?

A

Aldosterone: renin ratio

82
Q

Why is hypernatraemia very rare?

A

Normally, if our serum Na+ is high, we would drink some water to dilute it

83
Q

List two conditions that can cause hypernatraemia

A

Diabetes insipidus

Dementia (forgetting to drink water

84
Q

State the formula for calculation of urine osmolality

A

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

85
Q

List causes for hypernatraemia with:
High urine osmolality
Low urine osmolality

A

High urine osmolality
Dehydration
Hyperosmolar hyperglycaemic state (HHS)
NOTE: urine osmolality is high in HHS because of glycosuria

Low urine osmolality
Diabetes insipidus

86
Q

Describe the actions of PTH

A

Increase resorption of calcium in the bones

Increased reabsorption of calcium in the kidneys

Increased excretion of phosphate in the kidneys

87
Q

Describe biochemical features of primary hyperparathyroidism

A

High Ca2+

Low phosphate

88
Q

Describe the calcium, phosphate and PTH levels in hypercalcaemia of malignancy

A

High Ca2+

Normal phosphate

Low PTH

89
Q

Name the two hormones that control serum calcium concentration

A

PTH

Calcitriol (Vitamin D)

90
Q

Describe the biochemical features of hypoparathyroidism

A

Low Ca2+

High phosphate

Low PTH

91
Q

Describe the biochemical features of renal failure

A

Low Ca2+

High phosphate

High PTH

92
Q

Explain the biochemical features of renal failure

A

The kidneys are not able to reabsorb calcium and they are not able to activate vitamin D leading to hypocalcaemia

The kidneys are also unable to excrete phosphate leading to hyperphosphataemia

The hypocalcaemia leads to a secondary hyperparathyroidism

93
Q

Describe the biochemical features of vitamin D deficiency

A

Low Ca2+

Low phosphate

High PTH

94
Q

List causes for each of the following types of AKI:
Pre-renal
Intrinsic renal
Post-renal

A

Pre-renal
Hypovolaemia
Sepsis
Heart failure

Intrinsic renal
Drugs
Glomerulonephritis

Post-renal
Obstruction (e.g. stones)

95
Q

What can be found in the urine of a patient with glomerulonephritis?

A

Active urine sediment: blood and protein

96
Q

Which investigation does every AKI patient need?

A

Ultrasound scan – check for signs of obstruction

97
Q

What anatomical deformity does renal artery stenosis lead to?

A

Asymmetrical kidneys

98
Q

How is renal artery stenosis investigated?

A

Magnetic resonance angiography (MRA)

99
Q

Which drug class is contraindicated in bilateral renal artery stenosis and why?

A

ACE inhibitors

It can cause a massive drop in GFR

100
Q

Why does hyperventilation cause tingling in the hands?

A

Hyperventilation leads to hypocalcaemia, which causes neuromuscular excitation -> tingling

101
Q

Describe the pattern of arthritis in rheumatoid arthritis

A

Symmetrical polyarthritis

102
Q

List the five types of psoriatic arthritis

A

Asymmetrical oligoarthritis (more common and affects distal joints)

Symmetrical polyarthritis (look like rheumatoid arthritis)

Large joints (e.g. swollen knee)

Arthritis mutilans (telescoping of the fingers)

Psoriatic spondyloarthritis (axial skeleton involvement e.g. sacroiliitis)

103
Q

Describe the appearance of a BCC

A

Pearl-like lesion with a rolled edge and telangiectasia

DPD (4 decks)

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