Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DPD interactive cases > Haematology and Endocrinology > Flashcards

Haematology and Endocrinology 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Broadly speaking, what can cause a high WCC?

A

Infection

Malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List two main causes of microcytic anaemia.

A

Iron deficiency anaemia

Beta thalassemia heterozygosity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the two main mechanisms of iron deficiency anaemia?

A

Blood loss

Dietary deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List some causes of normocytic anaemia.

A

Anaemia of chronic disease
Infection
Malignancy
Inflammation (RhA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List 5 causes of macrocytic anaemia.

Mnemonic – alcoholics may have liver failure

A 
Alcoholism
Myelodysplasia
Hypothyroidism
Liver disease 
Folate/B12 deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

For each of the 5 causes, 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, ?gastrectomy)
Alcoholics May Have Liver Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List the main symptoms of polycythaemia.

A 
Headache 
Pruritus after a hot bath
Blurred vision 
Tinnitus
Thrombosis (DVT/stroke)
Gangrene
Choreiform movement (dancelike)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the three main complications of sickle cell anaemia.

A

Acute painful crisis
Sequestration crisis
Gallstones/chronic cholecystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the management of acute painful crisis.

A

Analgesia
Oxygen (hypoxia can cause sickling)
IV fluids (dehydration can cause sickling)
Antibiotics - if underlying infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is stroke treated in sickle cell patients?

A

Exchange blood transfusion to remove the sickled cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Lungs – SOB, cough, fever

Spleen – exacerbation of anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you treat splenic sequestration crisis?

A

Splenectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is chronic cholecystitis secondary to SCA treated?

A

Cholecystectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the four main features of multiple myeloma?

A

Calcium (high)
Renal impairment
Anaemia
Bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

For each of the four main features, list important findings on presentation/investigation.

A

Calcium – polyuria, polydipsia, constipation (leads to ADH resistent so Nephrogenic DI develops)
Renal impairment – high urea and creatinine
Anaemia – SOB, lethargy, FBC
Bone – fracture, pain, DEXA scan for OP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are two other important complications of multiple myeloma?

A

Increased risk of infection

Cord compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
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 (immune paresis), which increases risk of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What can cord compression due to multiple myeloma lead to?

A

Spastic paraparesis – partial paralysis of the lower limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are reticulocytes?

A

Immature red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List three causes of anaemia with LOW reticulocytes.

A

Parvovirus B19
Aplastic crisis in sickle cell patients
Blood transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Other than type 1 and type 2 diabetes mellitus, what else can cause diabetes? Why is this difficult to treat?

A

Pancreatic insufficiency - complete lack of enzymes - ‘Type 3’
NOTE: complete pancreatic insufficiency is difficult to treat because the lack of glucagon and pancreatic polypeptide is difficult to manage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

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

A

Metformin (reduces insulin resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

At what point do you add more medications for diabetics on metformin? What is the pathway?

A

If the patient fails to achieve the target HbA1c despite metformin - add Sulfonylurea or GLP1 agonist, then if still high, add DPP4 inhibitor
Eventually consider insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A

Sulfonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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

A

GLP-1 agonists (incretin effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Mechanism of action of Metformin

A

Decreases insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Mechanism of action of Sulfonylureas

A

Stimulates insulin release (insulin secretalogue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Mechanism of action of DDP-IV inhibitors

A

Reduces GLP-1 breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Mechanism of action of GLP-1 agonists

A

Incretin that stimulates glucose-stimulated insulin release

Also inhibits glucagon release, reduces appetite and may cause some weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is one of the first signs of diabetic nephropathy?

A

Increase in albumin: creatinine ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When might you put a patient on an insulin sliding scale? What is it?

A

If a diabetic patient is not eating or really unwell
(IV infusion at rate determined by blood glucose) - give basal (glargine) and bolus insulin + fluids (could include dextrose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When are insulin sliding scales not indicated?

What medication would you initially try? Why?

A

Sepsis
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
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.
Associated with increased mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

In what context is a sliding scale most useful?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

List some symptoms of Graves’ disease.

A 
Weight loss 
Increased appetite (DDx infx, inflx)
Irritability 
Palpitations 
Irregular periods

Tremor
Proptosis
Smooth Goitre
Pretibial Myxoedema (skin changes) - specific

47
Q

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

A 
High T4/T3
Low TSH (<0.05)
48
Q

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

A

Secondary hyperthyroidism

49
Q

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

A

TSH receptor stimulating antibodies

50
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

51
Q

What are TPO antibodies a marker of?

A

Autoimmunity

They are present in about 5% of the general population

52
Q

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

A

Diffuse increased uptake

53
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

54
Q

Describe and explain the iodine uptake in thyroiditis.

A

NO iodine uptake because TSH is suppressed in thyroiditis

55
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

56
Q

List some risk factors for thyroid cancer.

A

Radiation
Family history
Rapid enlargement/compression
Lymphadenopathy

57
Q

What percentage of the general population has thyroid nodules?

A

60-70%

58
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

59
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)

60
Q

List four types of thyroid cancer.

A

Papillary
Follicular
Medullary (FHx)
Anaplastic

61
Q

Which type of thyroid cancer has the worst prognosis?

A

Anaplastic

62
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

63
Q

List the signs of a prolactinoma.

A

Amenorrhoea
Galactorrhoea
Bitemporal hemianopia
Sexual dysfunction, irregular periods

64
Q

Which type of prolactinoma can compress the pituitary stalk?

A

Macroprolactinoma

65
Q

What is the first-line treatment for prolactinoma?

A

Dopamine agonists (e.g. cabergoline, bromocriptine)Shrinks and normalises PRL

(TransSph if not responsive)

66
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

67
Q

Describe the symptoms of acromegaly.

A

Headaches
Sweating
Obstructive sleep apnoea (poor sleep, snoring)
Carpal tunnel syndrome (tingling fingers)

68
Q

What causes obstructive sleep apnoea?

A

Excessive soft tissue obstructing the upper airways during sleep

69
Q

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

A

IGF-1 levels

70
Q

What is the next test you do to diagnose acromegaly?

A 
Oral Glucose Tolerance Test 
Failure of suppression of GH after oral intake of glucose suggests acromegaly
NOT GHRH (distractor)
71
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
  • Dynamic pituitary function test (check pit. status post surgery)
72
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

73
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

74
Q

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

A

Proximal myopathy
Easy bruising, thin skin
Purple Striae > 1 cm wide

75
Q

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

A

Hypertension
Diabetes mellitus
Osteoporosis
(at young age)

76
Q

What are striae?

A

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

77
Q

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

A 
Pregnancy 
Hypothalamus
Pituitary
Thyroid
Ovaries
78
Q

List two hypothalamic causes of amenorrhoea.

A 
Excessive exercise (less oestrogen --> OP)
Low BMI
79
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 –> less leptin = less GnRH

80
Q

What is the main pituitary cause of amenorrhoea?

A

Prolactinoma

81
Q

What derangements of thyroid function can cause amenorrhoea?

A

Hypothyroidism

Hyperthyroidism

82
Q

List two ovarian causes of amenorrhoea.

A

PCOS -> excess androgens

Ovarian failure -> low oestradiol + high FSH/LH

83
Q

What are the three main signs of hypokalaemia?

A

Weakness
Arrhythmia
Polyuria

84
Q

List the three main causes of hypokalaemia.

A

Vomiting
Diuretics
Primary hyperaldosteronism

85
Q

Describe how hypokalaemia leads to polyuria.

A

Hypokalaemia causes ADH resistance –> nephrogenic diabetes insipidus, which leads to polyuria
Similar to hypercalcaemia

86
Q

List two examples of primary hyperaldosteronism.

A

Conn’s syndrome

Bilateral adrenal hyperplasia

87
Q

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

A

Aldosterone: renin ratio

88
Q

Why is hypernatraemia very rare?

A

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

89
Q

List two conditions that can cause hypernatraemia.

A

Diabetes insipidus

Dementia (forgetting to drink water)

90
Q

State the formula for calculation of urine osmolality.

A

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

91
Q

List causes for hypernatraemia with high urine osmolality

A

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

92
Q

List a cause for hypernatraemia with low urine osmolality

A

Diabetes insipidus

Lack of ADH –> less water absorption –> water loss in urine

93
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

94
Q

Describe biochemical features of primary hyperparathyroidism.

A

High Ca2+

Low phosphate

95
Q

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

A

High Ca2+
Normal phosphate
Low PTH

96
Q

Name the two hormones that control serum calcium concentration.

A

PTH

Calcitriol (Vitamin D)

97
Q

Describe the biochemical features of hypoparathyroidism.

A

Low Ca2+
High phosphate
Low PTH

98
Q

Describe the biochemical features of renal failure.

A

Low Ca2+
High phosphate
High PTH

99
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

100
Q

Describe the biochemical features of vitamin D deficiency.

A

Low Ca2+
Low phosphate
High PTH

101
Q

List causes for each of the following types of AKI:

A

Pre-renal: hypovolaemia, sepsis, heart failure

Intrinsic renal: drugs, glomerulonephritis
Post-renal: obstruction (e.g. stones) - nephrostomy to relieve obstruction

102
Q

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

A

Active urine sediment: blood and protein

103
Q

Which investigation does every AKI patient need?

A

Ultrasound scan – check for signs of obstruction

104
Q

What anatomical deformity does renal artery stenosis lead to?

A

Asymmetrical kidneys

105
Q

How is renal artery stenosis investigated?

A

Magnetic resonance angiography (MRA)

106
Q

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

A

ACE inhibitors

It can cause a massive drop in GFR

107
Q

Why does hyperventilation cause tingling in the hands?

A

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

108
Q

Describe the pattern of arthritis in rheumatoid arthritis.

A

Symmetrical polyarthritis

109
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)
110
Q

Describe the appearance of a BCC.

A

Pearl-like lesion with a rolled edge and telangiectasia

111
Q

Complications of diabetes

A

Microvascular - Retinopathy, Nephropathy, Neuropathy

Macrovascular: MI/Stroke/PVD

Metabolic: DKA/HHS/Hypoglycaemia

112
Q

Explain Retinopathy and Nephropathy

A

Retinopathy - Backgroud, pre-proliferative (soft exudates/cotton wool spots), proliferative

Nephropathy: raised urine ACR (albumin:creatinine ration), decreased renal function
(Send dip to lab to detect microalbuminuria, cannot get ratio from urinalysis)

113
Q

What should you note in Grave’s?

A

TPO Ab is a marker of AI (5% of normal population), not cause of disease; so do not need to check

114
Q

Psoriatic Arthritis Symptoms

A 
Swollen fingers and toes
Tender, painful or swollen joints
Red Scaly Skin patches known as Plaques 
Reduced Range of motion of the joints 
Morning stiffness
Lower back, upper back and neck pain
General fatigue
Nail changes

DPD interactive cases (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions