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DPD interactive cases > Haematology and Endocrinology > Flashcards

Haematology and Endocrinology Flashcards

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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
Inflammation (RhA)

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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.

Mnemonic – alcoholics may have liver failure

A 
Alcoholism
Myelodysplasia
Hypothyroidism
Liver disease 
Folate/B12 deficiency
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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

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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)
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13
Q

What are the three main complications of sickle cell anaemia.

A

Acute painful crisis
Sequestration crisis
Gallstones/chronic cholecystitis

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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

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15
Q

How is stroke treated in sickle cell patients?

A

Exchange blood transfusion to remove the sickled cells

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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

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17
Q

How do you treat splenic sequestration crisis?

A

Splenectomy

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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

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19
Q

How is chronic cholecystitis secondary to SCA treated?

A

Cholecystectomy

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20
Q

What are the four main features of multiple myeloma?

A

Calcium (high)
Renal impairment
Anaemia
Bone

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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

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22
Q

What are two other important complications of multiple myeloma?

A

Increased risk of infection

Cord compression

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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

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24
Q

What can cord compression due to multiple myeloma lead to?

A

Spastic paraparesis – partial paralysis of the lower limbs

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25
Describe the ALP in multiple myeloma. Why is this the case?
ALP is normal/low in multiple myeloma | Multiple myeloma suppresses the osteoblasts, which are responsible for producing ALP
26
What are reticulocytes?
Immature red blood cells
27
List the two main causes of anaemia with HIGH reticulocytosis.
Haemorrhage Haemolysis NOTE: reticulocytosis occurs when there is an increased demand for red blood cells
28
List three causes of anaemia with LOW reticulocytes.
Parvovirus B19 Aplastic crisis in sickle cell patients Blood transfusion
29
List the three main diagnostic criteria for diabetes mellitus.
Fasting blood glucose > 7 mmol/L Random blood glucose > 11.1 mmol/L HbA1c > 6.5% or > 48 mmol/mol
30
Why was the diagnostic cut-off for fasting blood glucose set at > 7 mmol/L?
Epidemiological studies showed that the rate of incidence of retinopathy significantly increased in patients with fasting blood glucose > 7 mmol/L
31
What is impaired glucose tolerance (IGT)?
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
32
Other than type 1 and type 2 diabetes mellitus, what else can cause diabetes? Why is this difficult to treat?
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
33
What is the first drug that is given to patients with type 2 diabetes mellitus?
Metformin (reduces insulin resistance)
34
At what point do you add more medications for diabetics on metformin? What is the pathway?
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
35
Which commonly used medication for type 2 diabetes can cause hypoglycaemia?
Sulfonylureas
36
If the patient is overweight or you want to avoid hypoglycaemia, which diabetic medication might you consider using?
GLP-1 agonists (incretin effect)
37
Mechanism of action of Metformin
Decreases insulin resistance
38
Mechanism of action of Sulfonylureas
Stimulates insulin release (insulin secretalogue)
39
Mechanism of action of DDP-IV inhibitors
Reduces GLP-1 breakdown
40
Mechanism of action of GLP-1 agonists
Incretin that stimulates glucose-stimulated insulin release | Also inhibits glucagon release, reduces appetite and may cause some weight loss
41
What is one of the first signs of diabetic nephropathy?
Increase in albumin: creatinine ratio
42
When might you put a patient on an insulin sliding scale? What is it?
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)
43
When are insulin sliding scales not indicated? | What medication would you initially try? Why?
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
44
What is the main difficulty with insulin sliding scales?
It requires constant monitoring of blood glucose and constant adjustment of the insulin delivery rate. Associated with increased mortality
45
In what context is a sliding scale most useful?
Surgery – a patient might have to be NBM for a long time
46
List some symptoms of Graves’ disease.
``` Weight loss Increased appetite (DDx infx, inflx) Irritability Palpitations Irregular periods ``` Tremor Proptosis Smooth Goitre Pretibial Myxoedema (skin changes) - specific
47
Describe the TFT results in a patient with Graves’ disease?
``` High T4/T3 Low TSH (<0.05) ```
48
What would a high TSH with high T4/T3 suggest?
Secondary hyperthyroidism
49
After performing TFTs and putting together a clinical picture of primary hyperthyroidism, what test would you do next?
TSH receptor stimulating antibodies
50
Other than stimulating the TSH receptors, what else do TSH receptor stimulating antibodies do?
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
What are TPO antibodies a marker of?
Autoimmunity | They are present in about 5% of the general population
52
What will radioiodine uptake scans of Graves’ disease patients show?
Diffuse increased uptake
53
What needs to happen for the thyroid gland to be able to take up iodine?
The TSH receptor must be stimulated for there to be iodine uptake
54
Describe and explain the iodine uptake in thyroiditis.
NO iodine uptake because TSH is suppressed in thyroiditis
55
Describe and explain the iodine uptake in toxic nodular goitre.
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
List some risk factors for thyroid cancer.
Radiation Family history Rapid enlargement/compression Lymphadenopathy
57
What percentage of the general population has thyroid nodules?
60-70%
58
Where do most thyroid cancers metastasise to? Which type of thyroid cancer has a propensity to metastasise to this location?
Lungs | These tend to be mostly follicular thyroid cancer
59
List two investigations that may be used in the diagnosis of thyroid cancer.
Ultrasound scan Fine needle aspiration cytology Uptake scan (thyroid cancers are cold)
60
List four types of thyroid cancer.
Papillary Follicular Medullary (FHx) Anaplastic
61
Which type of thyroid cancer has the worst prognosis?
Anaplastic
62
List two treatments that are used after surgery in patients with thyroid cancer.
Thyroxine – replace the function of the lost thyroid gland | Radioiodine – in high-risk patients
63
List the signs of a prolactinoma.
Amenorrhoea Galactorrhoea Bitemporal hemianopia Sexual dysfunction, irregular periods
64
Which type of prolactinoma can compress the pituitary stalk?
Macroprolactinoma
65
What is the first-line treatment for prolactinoma?
Dopamine agonists (e.g. cabergoline, bromocriptine)Shrinks and normalises PRL (TransSph if not responsive)
66
Roughly how long are prolactinoma patients kept on this treatment?
4 years – then they can gradually be weaned off and some may be able to stop it entirely
67
Describe the symptoms of acromegaly.
Headaches Sweating Obstructive sleep apnoea (poor sleep, snoring) Carpal tunnel syndrome (tingling fingers)
68
What causes obstructive sleep apnoea?
Excessive soft tissue obstructing the upper airways during sleep
69
What is the first test you do in the investigation of acromegaly?
IGF-1 levels
70
What is the next test you do to diagnose acromegaly?
``` Oral Glucose Tolerance Test Failure of suppression of GH after oral intake of glucose suggests acromegaly NOT GHRH (distractor) ```
71
How do you test pituitary function?
- 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
What is a dexamethasone suppression test used for?
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
What is a short synacthen test used for?
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
What are the three distinguishing symptoms of Cushing’s syndrome?
Proximal myopathy Easy bruising, thin skin Purple Striae > 1 cm wide
75
List some disease states that are caused by Cushing’s syndrome.
Hypertension Diabetes mellitus Osteoporosis (at young age)
76
What are striae?
Capillaries that become visible due to stretching and thinning of the skin
77
Broadly speaking, how can the causes of amenorrhoea/oligomenorrhoea be divided?
``` Pregnancy Hypothalamus Pituitary Thyroid Ovaries ```
78
List two hypothalamic causes of amenorrhoea.
``` Excessive exercise (less oestrogen --> OP) Low BMI ```
79
Why does low BMI lead to amenorrhoea?
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
What is the main pituitary cause of amenorrhoea?
Prolactinoma
81
What derangements of thyroid function can cause amenorrhoea?
Hypothyroidism | Hyperthyroidism
82
List two ovarian causes of amenorrhoea.
PCOS -> excess androgens | Ovarian failure -> low oestradiol + high FSH/LH
83
What are the three main signs of hypokalaemia?
Weakness Arrhythmia Polyuria
84
List the three main causes of hypokalaemia.
Vomiting Diuretics Primary hyperaldosteronism
85
Describe how hypokalaemia leads to polyuria.
Hypokalaemia causes ADH resistance --> nephrogenic diabetes insipidus, which leads to polyuria Similar to hypercalcaemia
86
List two examples of primary hyperaldosteronism.
Conn’s syndrome | Bilateral adrenal hyperplasia
87
What can be measured to assist with a diagnosis of primary hyperaldosteronism?
Aldosterone: renin ratio
88
Why is hypernatraemia very rare?
Normally, if our serum Na+ is high, we would drink some water to dilute it
89
List two conditions that can cause hypernatraemia.
Diabetes insipidus | Dementia (forgetting to drink water)
90
State the formula for calculation of urine osmolality.
Osmolality = 2(Na+ + K+) + Ur + glucose
91
List causes for hypernatraemia with high urine osmolality
Dehydration Hyperosmolar hyperglycaemic state (HHS) NOTE: urine osmolality is high in HHS because of glycosuria
92
List a cause for hypernatraemia with low urine osmolality
Diabetes insipidus | Lack of ADH --> less water absorption --> water loss in urine
93
Describe the actions of PTH.
Increase resorption of calcium in the bones Increased reabsorption of calcium in the kidneys Increased excretion of phosphate in the kidneys
94
Describe biochemical features of primary hyperparathyroidism.
High Ca2+ | Low phosphate
95
Describe the calcium, phosphate and PTH levels in hypercalcaemia of malignancy.
High Ca2+ Normal phosphate Low PTH
96
Name the two hormones that control serum calcium concentration.
PTH | Calcitriol (Vitamin D)
97
Describe the biochemical features of hypoparathyroidism.
Low Ca2+ High phosphate Low PTH
98
Describe the biochemical features of renal failure.
Low Ca2+ High phosphate High PTH
99
Explain the biochemical features of renal failure.
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
Describe the biochemical features of vitamin D deficiency.
Low Ca2+ Low phosphate High PTH
101
List causes for each of the following types of AKI:
Pre-renal: hypovolaemia, sepsis, heart failure Intrinsic renal: drugs, glomerulonephritis Post-renal: obstruction (e.g. stones) - nephrostomy to relieve obstruction
102
What can be found in the urine of a patient with glomerulonephritis?
Active urine sediment: blood and protein
103
Which investigation does every AKI patient need?
Ultrasound scan – check for signs of obstruction
104
What anatomical deformity does renal artery stenosis lead to?
Asymmetrical kidneys
105
How is renal artery stenosis investigated?
Magnetic resonance angiography (MRA)
106
Which drug class is contraindicated in bilateral renal artery stenosis and why?
ACE inhibitors | It can cause a massive drop in GFR
107
Why does hyperventilation cause tingling in the hands?
Hyperventilation leads to hypocalcaemia, which causes neuromuscular excitation -> tingling
108
Describe the pattern of arthritis in rheumatoid arthritis.
Symmetrical polyarthritis
109
List the five types of psoriatic arthritis.
- 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
Describe the appearance of a BCC.
Pearl-like lesion with a rolled edge and telangiectasia
111
Complications of diabetes
Microvascular - Retinopathy, Nephropathy, Neuropathy Macrovascular: MI/Stroke/PVD Metabolic: DKA/HHS/Hypoglycaemia
112
Explain Retinopathy and Nephropathy
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
What should you note in Grave's?
TPO Ab is a marker of AI (5% of normal population), not cause of disease; so do not need to check
114
Psoriatic Arthritis Symptoms
``` 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 ```

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