Week 19 - Cases 1,2,3,4 and passmed Flashcards

1
Q

what are the causes of microcytic anaemia
- there are four
- MCV <80

A
  • iron deficiency anaemia
  • thalassaemia
  • sideroblastic anaemia
  • anaemia of chronic disease
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2
Q

what are the causes of normocytic anaemia
- there are 7
- MCV 80-100

A
  • acute blood loss
  • early iron deficiency anaemia
  • renal disease
  • haemolytic anaemia
  • malaria
  • sickle cell disease
  • aplastic anaemia
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3
Q

what are the causes of megaloblastic anaemia
- there are 2
- MCV >100

A
  • B12 deficiency
  • folate deficiency
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4
Q

what are the causes of non-megaloblastic macrocytic anaemia
- there are 2
- MCV >100

A
  • alcoholism
  • liver disease
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5
Q

what kind of cells are seen in iron deficiency anaemia

A

pencil cells

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6
Q

what may be seen on a blood film in B12/ folate deficiency

A

hyper segmented neutrophils

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7
Q

what are the causes of iron deficiency anaemia

A
  • dietary in origin, due to lack of red meat, or green vegetables in the diet
  • due to gastrointestinal blood loss and is a must not miss diagnosis
  • in females, due to loss during menstraton
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8
Q

if a patient has an iron deficiency anaemia, what would constitute red flag symptoms and require a 2 week wait referral to exclude cancer

A

Urgently refer (appointment within two weeks) people:

  • aged 40 and over with unexplained weight loss and abdominal pain
  • aged 50 and over with unexplained rectal bleeding
  • aged 60 and over with either:
    – iron deficiency anaemia
    – OR alteration in bowel habit
  • who have positively tested for occult blood in their faeces
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9
Q

what does ferroportin do

A

controls the release of iron from the intestinal enterocytes into the blood stream and the release of iron from the marrow macrophages for eryhtropoiesis

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10
Q

what does hepcidin do

A

in turn controls the levels of ferroportin in an inverse manner

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11
Q

what does an increase in hepcidin do

A

causes ferroportin to degrade, reducing ferroportin levels prevents iron release from GI tract enterocytes into the blood stream and also traps iron in the marrow macrophages, thus reducing total iron bio-availabiliy

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12
Q

therefore what happens when iron is plentiful and the transferrin saturation is high

A

less iron is absorbed and fewer red cells are produced in the bone marrow

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13
Q

what happens in inflammation when there are high levels of IL6

A

the same mechanism is activated, explaining the classical marrow iron findings of the normocytic, normochromic anaemia of chronic disease; with excess iron in the free and marrow particle marcophages but no iron in the eryhtroblasts

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14
Q

what does the lack of production in anaemia of chronic disease also explain

A

why sometimes this type of anaemia can be hypochromic and is not always normochromic and normocytic

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15
Q

what happens if there is a decrease in hepcidin

A

it promotes iron absorption from the gut and releasing iron rom the marrow macrophages to assist increased erythropoiesis

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16
Q

what happens does a low TFR situation inhibit in iron deficiency and what does this lead to

A

a low TFR situation inhibits hepcidin and ferroportin increases this promoting iron absorption and availabilityg

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17
Q

there are increased levels of what in haemolytic anaemia

A

increase in the levels of growth differentiation factor 15

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18
Q

how do high levels of GDF15 promote iron absorption

A

by inhibiting hepcidin and this explains why patients with chronic haemolysis can become iron overloaded without ingesting excess iron or by having blood transfusions

19
Q

what treatment would you give to a patient with iron deficiency anaemia secondary to heavy mentruation

A

oral iron treatment

20
Q

what are the four most common side effects of oral iron supplementation

A

diarrhoea
gastrointestinal discomfort
nausea
constipation

21
Q

chronic kidney disease is a risk factor for what

A

osteoporosis

22
Q

what are the side effects you should inform pregnant women about with paroxetine

A

Paroxetine use in pregnancy - can lead to increased risk of congenital malformations

23
Q

in cases of pregnancy of unknown location, a serum bHCG of what points towards a diagnosis of an ectopic pregnancy

A

In the case of pregnancy of unknown location, serum bHCG levels >1,500 points toward a diagnosis of an ectopic pregnancy§

24
Q

what is the pathway for oesophageal/gastric two week wait criteria

A

Urgent referral for endoscopy within two weeks. Urgently refer people:

of any age presenting with dysphagia (OG), or
aged 55 or over with weight loss, and
Upper abdominal pain, or
Reflux, or
Dyspepsia (OG)

25
Q

what is the treatment for microcytic, hypochromic anaemia

A

ferrous sulphate and refer urgently to the GI team

26
Q

what is glossitis

A

a red and inflamed tongue

27
Q

what does hyper-segmented neutrophils look like

A

neutrophils usually have 2-5 lobes and therefore anything over this is classed as hypersegmented

28
Q

how does megaloblastic anaemia cause macropcytic anaemia

A

from ineffective red blood cell production and intramedullary haemolysis

29
Q

what are the most common causes

A

folate deficiency and cobalamin deficiency

30
Q

a BMI of what is obese

A

a BMI of 30 or above is obese

31
Q

what are the 3 reasons for why eGFR as a single value has several limitations

A

It is based on serum creatinine and so may overestimate actual GFR in patients with low muscle mass (e.g., those with cachexia and amputees) and underestimate actual GFR in individuals taking creatine supplements (as creatinine is a metabolite of creatine) or trimethoprim (which inhibits secretion of creatinine).

It tends to underestimate normal or near-normal function, so slightly low values should not be over-interpreted.

In the elderly, who constitute the majority of those with low eGFR, there is controversy about categorising people as having chronic kidney disease on the basis of eGFR alone, particularly at stage 3A, since there is little evidence of adverse outcomes when eGFR is >45 mL/min/1.73 m2 unless there is also proteinuria.

32
Q

what is anaemia of chronic disease

A

microcytic hypochromic anaemia

33
Q

what is hepcidin

A

an iron-regulating peptide hormone made in the liver

34
Q

what is an accelerated progression of CKD defined as

A

A sustained decrease in GFR of 25% or more and a change in GFR category within 12 months or
A sustained decrease in GFR of 15 ml/min/1.73 m2 per year
Be aware that those patients are at increased risk of progression to end stage renal disease.

35
Q

what is CKD defined as

A

CKD is defined as abnormalities of kidney function or structure present for more than 3 months, with implications for health. This includes all people with markers of kidney damage and those with a glomerular filtration rate (GFR) of less than 60 ml/min/1.73m2 on at least 2 occasions separated by a period of at least 90 days (with or without markers of kidney damage).

36
Q

what is CKD classified based on

A

cause
GFR category
albuminruia category

37
Q

How can ACEI/ARBs delay disease progression?

A

By dilating the efferent arteriole

38
Q

what is HbH most often caused b¥

A

inherited deletion of three of the four alpha globin genes

39
Q

how can beta thalasseaemia major be ‘cured’

A

using a stem cell transplant

40
Q

A 65-year-old man known to have chronic kidney disease stage 3A secondary to diabetes was started on angiotensin converting enzyme inhibitor by his GP. Which percentage decline in eGFR from baseline would warrant stopping the treatment with ACE inhibitor?

A

We accept up to 25% decline in eGFR. This is due to the hemodynamic change at the level of the glomeruli because of efferent vasodilation and lowering of the intraglomerular pressure. More than 25% decline in eGFR from baseline should make you consider stopping the angiotensin converting enzyme inhibitor.

41
Q

A 58-year-old man is known to have chronic kidney disease stage 4. His calcium levels are low, but phosphate and PTH (parathormone hormone) levels are elevated. Which is the most likely diagnosis?

A

Secondary hyperparathyroidism

Secondary hyperparathyroidism occurs in patients with chronic kidney disease. Due to the drop in the glomerular filtration rate, phosphate levels increase which then activates FGF-23 and increases PTH levels. At the same time, failure to activate vitamin D will result in low calcium levels. Hence answer B is correct. For primary hyperparathyroidism, calcium levels are elevated, phosphate levels are low and PTH levels are elevated. Hence answer A is not correct. In hypoparathyroidism, calcium levels are low due to low PTH levels, which is not the case here. Tertiary hyperparathyroidism occurs after many years of having a secondary hyperparathyroidism. Those patients have been under continuous stimulation of PTH, and so they will form an autonomous focus on the parathyroid gland that will produce high calcium levels regardless of the low vitamin D levels. The results are similar to secondary hyperparathyroidism except for elevated calcium levels, which is not the case here.

42
Q

A 70-year-old man is known to have chronic kidney disease stage 3b. His haemoglobin level is 110g/l. T-sats 31% and ferritin of 250 ug/l. Which is the most appropriate management of his anaemia?

A

Regular monitoring
Based on the NICE guidelines, his haemoglobin levels, T-sats and ferritin levels are within acceptable range for a patient with chronic kidney disease. Regular monitoring is required to maintain those figures.

43
Q

A 65-year-old man with heart failure, known CKD and is non-diabetic, recently heard about the benefits of SGLT2i in preventing CKD progression. Given that he is non-diabetic, would you still consider treatment with SGLT2i for him?

A

Yes
Recent evidence has shown that SGLT2i delayed CKD progression in non-diabetics with heart failure and lowered the cardiovascular disease events

44
Q
A