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Semester 2 (3rd year) > Case 19: I feel tired > Flashcards

Case 19: I feel tired Flashcards

1
Q

where is erythropoietin produced

A

kidneys

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2
Q

erythropoietin is secreted in response to what

A

in response to hypoxia in blood
it is transported by the blood to bone marrow where it initates erythropoiesis (the formation of new RBCs)

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3
Q

erythropoietin stimulates what

A

RBC production in the red bone marrow

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4
Q

where does haematopoiesis take place

A

begins in the yolk sac in foetus
then liver temporarily
definitively it takes place in bone marrow and thymus

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5
Q

what 2 components make up haem

A

iron and protoporphyrin

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6
Q

where do we get most of our iron from

A

leafy green vegetables
red meat

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7
Q

where in the digestive tract is iron absorbed

A

duodenum

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8
Q

what does total iron binding capacity mean (TIBC)

A

how may transferrin molecules are in the blood

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9
Q

what does transferrin saturations % mean

A

how many transferrin molecules are bound to iron

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10
Q

what does ferritin mean

A

how much iron is in storage

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11
Q

when do urea and creatinine typically raise relative to eGFR

A

reduction of 50-60% eGFR

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12
Q

normal length of the kidneys

A

11cm longitudinal

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13
Q

what condition is common in those with chronic kidney disease

A

anaemia
this contributes to their non-specific symptoms such as fatigue and shortness of breath

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14
Q

what is a major cause of anaemia in CKD

A

definitely of erythropoietin

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15
Q

what to give if iron is normal but someone with CKD is anaemic

A

erythropoietin (epoetin) treatment with a target of Hb levels between 100-120

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16
Q

correcting low Hb in CKD carries what risks

A

hypertension
thrombosis

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17
Q

2 primary factors which can cause renal bone disease

A

high phosphate levels and failure to activate vitamin D

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18
Q

what are active and inactive vitamin D called

A

inactive= 25-hydroxyvitamen D
active= 1,25-dihydroxyvitamen D

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19
Q

the result of raised serum phosphate levels

A

promotes production of hormone fibroblast growth factor 23 (FGF23) from oesteocytes and stimulates PTH release and hyperplasia of the parathyroid glands

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20
Q

what do FGF23 and PTH do

A

promote tubular phosphate excretion therefore partly compensating for reduced glomerular filtration of phosphate

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21
Q

what does reduced active vitamin D do

A

impairs the intestinal absorption of calcium

raised levels of serum phosphate complex with calcium in the extra cellular space leads to calcium phosphate deposition

both reduced absorption and increased deposition of calcium causes hypocalcaemia

this also stimulates PTH production by parathyroid glands

therefore in many patients with CKD the compensatory responses initially maintain phosphate and calcium levels at the upper and lower ends of their respective normal ranges at the expense of elevated PTH level (secondary hyperparathyroidism)

this is associated with the gradual transfer of calcium and phosphate from the bone to other tissues leading to bone resorption (osteitis fibrosa cystica)

in severe cases this may result in bony pain and increased risk of fractures

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22
Q

presentation of acute myeloid leukaemia

A

tiredness and breathlessness
recurrent infections
abnormal bleeding (gum and nose)
weight loss

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23
Q

vitamin D deficiency presentation

A

fatigue
bone pain
muscle aches
low mood

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24
Q

microcytic anaemia values

A

MCV less than 80

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25
Q

normocytic anaemia values

A

MCV 80-100

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26
Q

macrocytic anaemia values

A

MCV>100

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27
Q

microcytic anaemias

A

iron deficiency
thalassemia
sideroblastic anaemia
anemia of chronic disease

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28
Q

normocytic anaemias

A

acute blood loss
early iron deficiency anaemia
renal disease
haemolytic anaemia
malaria
sickle cell disease
aplastic anaemia

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29
Q

macrocytic anaemias (megaloblastic)

A

B12 deficiency
folate deficiency

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30
Q

macrocytic anaemias (non-megaloblastic)

A

alcoholism
liver disease

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31
Q

which investigation could you do for B12/folate deficiency

A

blood film
may show hyper segmented neutrophils

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32
Q

what might a blood film show in iron deficiency anaemia

A

pencil cells

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33
Q

causes of iron deficiency anaemia

A

diet- lack of red meat/vegetables
GI blood loss
menstruation

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34
Q

causes of normochromic normocytic anaemias

A

acute blood loss
anaemia of chronic disease or secondary anaemia
anaemia or renal failure (deficiency of erythropoietin)

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35
Q

what is seen under microscope with normochromic normocytic anaemia

A

normal red cells- even size, even shape and area of central pallor (less than 33% of the red cell diameter)

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36
Q

which blood type is universal donor

A

O -ve

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37
Q

old hypothesis to remember is anaemia is microcytic or macrocytic

A

cell divisions in developing erythrocyte stop when normal mean cell haemoglobin concentration is reached and the nucleus is extruded

as the developing erythroblasts undergo cell devisions, they become smaller

anything that reduces the production of Hb inside the developing erythrocyte will tend to encourage more cell divisions than normal (iron deficiency, thalassemia) and the erythrocyte will become smaller- microcytic

anything that delays nuclear development (B12, folate deficiencies, chemotherapy) will tend to mean that fewer cell devisions will take place before the final MCH is attained and the red cells will be larger- macrocytic

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38
Q

beta thalassemia minor

A

mild to moderate hypochromic-microcytic anemia

one abnormal beta globin chain

reduced production of Hb but usually asymptomatic

diagnosis= raised HbA2

mild splenomegaly, bronze skin, hyperplasia of bone marrow

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39
Q

beta thalassemia major

A

aka cooley anaemia

two abnormal genes

HbF affected

detected before 2 years old (need blood transfusion before this or will die)

symptoms by 4-6 months- severe anaemia, growth retardation, abnormal facial structure, pathologic fractures, osteopenia, bone deformities, hepatosplenomegaly, jaundice

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40
Q

the genes of alpha thalassemia

A

1 gene deleted= clinical silent

2 genes deleted= alpha thalassemia trait (hypochromic microcytic)

3 genes deleted= Hb H disease

4 genes deleted= Barts hydrops fetalis

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41
Q

other causes of iron deficiency anaemia

A

physiological- rapid growth, menarche, pregnancy

neonatal- prematurity, low birth weight, blood loss (early cord clamping)

diet- cows mils is the commonest cause in UK toddlers

GIT- commonest cause is NSAIDs but in older males/post menopausal women colonic and gastric cancers must be investigated

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42
Q

diagnosis of iron deficiency anaemia on bloods

A

low Hb
low MCV
low MCH
can look at ferritin but this is affected by chronic inflammation

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43
Q

more specific symptoms of iron deficiency anaemia

A

tiredness and lethargy
headache especially with activity
craving for non-food items (pica)
sore/smooth tongue
brittle nails/hair loss
koilonychia
angular stomatitis

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44
Q

components of Hb

A

iron
b12
folic acid

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45
Q

sources of folate in diet

A

cereals
liver
yeast and yeast products (marmite, Vegemite, bovril)
dark leafy green vegetables (sprouts and spinach)
baked beans
oranges and orange juice

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46
Q

sources of B12 in diet

A

cereals
liver and kidney
fish (salmon and sardines especially)
dairy (yogurt)

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47
Q

nutritional causes of B12 deficiency

A

vegan
poor diet
pregnancy

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48
Q

malabsorption causes of B12 deficiency

A

gastric- surgery, pernicious anaemia

intestine- ileal resection, fish tapeworm, tropical sprue

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49
Q

which type of deficiency can excess alcohol cause

A

folate (thiamine)
not in alcoholics that drink beer however as beer is a good source of folate

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50
Q

specific signs of B12 deficiency

A

insidious onset

mild jaundice and anaemia

glossitis

angular cheilitis/stomatitis

neuropathy- peripheral, sub-acute degeneration of the cord (SADC), optic, dementia

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51
Q

specific signs of folate deficiency

A

same as B12 but more often sensory peripheral neuropathy only

deficiency in pre-conception is associated with increased incidence of NTDs in babies

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52
Q

causes of macrocytosis other than megaloblastic anaemia

A

alcohol
pregnancy
drugs- chemotherapy, anti-folate, anti-purines, anti-HIV
liver disease
raised reticulocyte
hypothyroidism
myelodysplasia, including acquired sideroblastic anaemia
aplastic anaemia and red cell aplasia
hypoxia
myeloma and other paraproteinaemias

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53
Q

what is haemolytic anaemia

A

anaemia due to the destruction rather than underproduction of red blood cells

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54
Q

investigations of haemolytic anaemia

A

RBC with reticulocytes (reticulocytes will go up)
bilirubin and lactic dehydrogenase (LDH) will increase

Coombs test (DAT)- for immune causes
EMA-binding
glucose-6-phosphate dehydrogenase level
haemoglobin identification (HPLC)

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55
Q

congenital haemolytic anaemias

A

congenial:
disorders of the RBC membrane (hereditary ellipocytosis, hereditary spherocytosis)
RBC enzyme deficiencies (G6PD, pyruvate kinase)
RBC haemoglobin disordes (thalassaemias, sickle cell)

acquired:
autoimmune haemolysis (AIHA)
microangiopathic haemolytic anaemia (HUS, TTP, DIC)
drugs, infections, toxins
copper deficiency (Wilsons)

56
Q

what is hereditary spherocytosis

A

an abnormality of the RBC membrane

commonest inherited red cell disorder in Northern Europeans

autosomal dominant

micro-spherocytes and polychromatic microcytes

57
Q

presentation of hereditary spherocytosis

A

often neonatal jaundice

chronic haemolysis

jaundice

gall stones

58
Q

management of hereditary spherocytosis

A

folic acid
splenectomy

59
Q

diagnosis of hereditary spherocytosis

A

family history in 75%

FBC

reticulocytes

blood film

EMA binding- proteins are missing in hereditary spherocytosis meaning the resulting fluorescence is weaker- THIS IS DIAGNOSTIC

60
Q

clinical findings of glucose-6-phosphate dehydrogenase deficiency

A

x linked

usually well between attacks

family history

history of neonatal jaundice

sudden onset of feeling unwell/lack energy, pale and yellow, backache, dark urine

61
Q

drugs and food to avoid with glucose-6-phosphate dehydrogenase deficiency

A

fava beans
broad beans

anti-malarials
aspirin in large doses
nitrofurantoin
vitamin K

62
Q

what is sickle cell disease

A

RBCs crescent shaped
beta globin variant
co-dominant
carriers HbAS normal
usually HbSS
auto-infarction of spleen with increased infection risk

63
Q

long term management of sickle cell disease

A

keep warm
keep hydrated
keep regular hours
eat well
take penicillin and folic acid
pneumococcal vaccine

64
Q

complications of sickle cell disease

A

stroke
infection/sepsis
acute chest syndrome (lungs lose their ability to breath in O2 often resulting in infection)
pulmonary hypertension

65
Q

stroke prevention in sickle cell disease

A

primary:
detect using transcranial doppler
start regular transfusions

secondary:
following stroke or finding evidence of previous strokes on MRI
start regular blood transfusions

for both consider stem cell transplant

66
Q

sickle cell disease and surgery

A

surgery is a problem as it increases risk of hypoxia- anaemia, dehydration, anaesthesia, blood loss

stress of surgery predisposes to sickle cell crisis- fever, post op hypoxia, post-op infection

these increase risk of painful crisis and acute chest syndrome

67
Q

other long term management of sickle cell

A

hydroxyurea
this switches on the foetal Hb gene (HbF)
if you get this level up to 50% it will prevent majority of painful crisis

68
Q

management of beta thalassemia major

A

long term blood transfusions and iron chelation (due to blood transfusions increasing iron) or stem cell transplantation

don’t start chelation too early- wait until ferritin is over 1000ug/L to avoid neurological an skeletal toxicity

69
Q

types of autoimmune haemolytic anaemias

A

warm and cold (depending upon the thermal range at which the antibody is active)

70
Q

diagnosis of autoimmune haemolytic anaemia

A

confirmed haemolysis as well as blood film

positive direct antiglobulin test (DAT/coombs test)

71
Q

DAT results for warm/cold autoimmune haemolytic anaemia

A

positive for IgG in warm
positive for compliment in cold

72
Q

secondary causes of warm autoimmune haemolytic anaemia

A

rheumatoid disease (SLE/lymphoma)
chronic lymphatic leukaemia
drugs- cephalosporins
ovarian teratoma

73
Q

secondary causes of cold autoimmune haemolytic anaemia

A

EBV infection
mycoplasma pneumonia
UC

74
Q

4 most common side effects of iron supplementation

A

GI discomfort
constipation
diarrhoea
nausea

75
Q

other side effects of iron supplementation

A

vomiting
tooth discolouration
iron overload
faeces discolouration

76
Q

hyper/hypo segmented neutrophils

A

neutrophils typically have 2-5 lobes

above/below this is hyper and hypo respectively

77
Q

what is pernicious anaemia

A

rare cause of vitamin B12 deficiency

autoimmune and prevents B12 absorption

affects people ages 60-80 of Northern European descent

there is a lack of gastric protein intrinsic factor which is required for B12 absorption

the immune system produces antibodies which blocks the protein intrinsic factor from carrying B12 across the mucosal lining to be absorbed

78
Q

what type of anaemia does megaloblastic anaemia cause

A

macrocytic anaemia from ineffective RBC production and intramedullary haemolysis

79
Q

most common causes of megaloblastic anaemia

A

folate (B9) deficiency
cobalamin (B12 deficiency)

80
Q

how is B12 deficiency treated

A

B12 injections every 2 months

81
Q

what is another symptom of B12 deficiency

A

pins and needles
in hands and feet?

82
Q

time frame of acute fatigue

A

one month or less

83
Q

time frame of chronic fatigue

A

over 6 months

84
Q

medications what can cause fatigue

A

benzodiazepines
antidepressants
muscle relaxants
first generation antihistamines
beta blockers
opioids

85
Q

what can cause proteinuria on urine dip

A

pregnancy
abnormally high BP
fever
CKD
after physical exercise
UTI
nephrotic/nephritic syndrome

86
Q

how to diagnose CKD based off of eGFR

A

the drop in eGFR must be consistent for more than 3 months therefore you need repeat bloods over months time

87
Q

why is using eGFR as a single value limiting

A

it is based on serum creatinine so may overestimate actual GFR in patients with low muscle mass (cachexia/amputees) and underestimate actual GFR in individuals taking creatinine supplements or trimethoprim (which inhibits secretion of creatinine)

it tends to underestimate normal or near-normal function, so slightly low values shouldn’t be over-interpreted

in the elderly (most of those who have low eGFR) there is controversy about categorising people as having CKD on basis of eGFR alone particularly at stage 3A since there is little evidence of adverse outcomes when eGFR is over 45 unless there is also proteinuria

88
Q

types of anaemia in those with poor kidney function

A

microcytic= GI bleed that can cause iron deficiency
normocytic= low erythropoietin
macrocytic= can be caused by poor nutrition in chronic renal failure resulting in B12 and folate deficiency

89
Q

how can hepcidin levels cause anaemia

A

hepcidin is an iron-regulating peptide hormone made in the liver- it controls the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte-recycling macrophages and from iron-storing hepatocytes

high levels block intestinal absorption and macrophage iron recycling, causing iron restricted erythropoiesis and anaemia

this is caused in part by inflammation involved in the pathogenesis of many kidney diseases

90
Q

what is an accelerated progression of CKD defined as

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 15ml/min per year

91
Q

what would you do for someone with progressive chronic renal dysfunction

A

refer to a renal specialist clinic

92
Q

what is the definition of CKD

A

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 snd those with GFR of less than 60 on at least 2 occasions separated by a period of at least 90 days (with or without markers of kidney damage)

93
Q

what GFR is considered normal/high

A

above 90

94
Q

what GFR is considered mildly decreased

A

60-89

95
Q

what GFR is considered mildly to moderately decreased

A

45-59

96
Q

what GFR is considered severely decreased

A

30-44

97
Q

what GFR is considered severely decreased

A

15-29

98
Q

what GFR is considered kidney failure

A

less than 15cm

99
Q

what is CKD classified on

A

cause
GFR category (G1-G5)
albuminuria category (A1-A3)

100
Q

what factors are taken into account in the kidney failure risk equation

A

sex
age
eGFR
urine albumin creatinine ratio

101
Q

why would you check urea and creatine in CKD

A

to assess for stability/progression of renal function

102
Q

why would you check urinalysis and quantification of proteinuria in CKD

A

to assess for stability/progression of renal function

103
Q

why would you check urinalysis and quantification of proteinuria in CKD

A

to look for haematuria and proteinuria

104
Q

why would you check electrolytes in CKD

A

to identify hyperkalaemia and acidosis

105
Q

why would you check calcium, phosphate, PTH and 25(OH)D in CKD

A

to assess for renal osteodystrophy

105
Q

why would you check albumin in CKD

A

low levels may indicate malnutrition, inflammation, nephrotic syndrome

106
Q

why would you check full blood count (plus Fe, ferritin, folate, B12) in CKD

A

to assess for anaemia

107
Q

why would you check lipids, glucose and HbA1c in CKD

A

to assess for cardiovascular risk

108
Q

why would you check renal ultrasound in CKD

A

if concerned about obstructive uropathy

109
Q

why would you check hepatitis and HIV serology in CKD

A

if dialysis/transplant planned

110
Q

ACEi are indicated in patients with what

A

HTN (under 55)
diabetes
proteinurea

111
Q

when would you give antiplatelet therapy to someone with diabetes

A

in someone with cardiovascular disease
give aspirin/clopidogrel

112
Q

what would give give to someone anaemic with T2D and CDK after replenishing iron stores

A

Aranesp (reengineered form of erythpropoietin

113
Q

why would you give bicarbonate

A

to correct acidosis
in CKD is delays progression, improves erythropoietin response, protects bones and controls hyperkalaemia

114
Q

why would you give calcium acetate

A

if giving vitamin D for secondary hyperparathyroidism, phosphate level absorption may increase

therefore, a calcium-containing phosphate binder will limit phosphate rise, improve calcium levels and thereby inhibit PTH

115
Q

which diabetes treatment is good for low eGFR

A

GLP-1 agonist (semaglutide, dulagutide)

116
Q

metformin and eGFR levels

A

metformin dose should be reviewed if eGFR below 45

should be stopped if eGFR below 30

117
Q

when would you give vitamin D (alfacalcidol)

A

to treat secondary hyperparathyroidism (by inhibiting PTH)

give a calcium containing phosphate binder too as phosphate levels may rise

this improves calcium levels therefore inhibiting PTH

118
Q

how are ACEi renoprotective

A

they dilate the efferent arteriole

this decreased intraglomerular pressure, prevents loss of protein and protects the kidneys long term

119
Q

how can ACEi/ARBs effect GFR

A

they lower intraglomerular pressure meaning GFR can drop (haemodynamic change inside glomeruli)

can have a 25% drop in GFR from baseline, any more than this would need to stop the medication

120
Q

indications to start urgent haemodialysis for CKD patients

A

fluid overload- intractable dependent oedema resistant to diuretics, pulmonary oedema, severe hypertension

hyperkalaemia- resistant to dietary control and medical intervention

uraemia- uraemic syndrome including anorexia, nausea, lethargy (this generally doesn’t happen until eGFR is less than 10

metabolic acidosis- chronic acidosis resistant to bicarbonate therapy

other- intractable anaemia despite erythropoietin and iron and hyperphosphatemia despite inhibitors

121
Q

which is the best dialysis modality

A

there is no strong evidence to suggest one modality over the other

122
Q

eligibility for renal transplant

A

all patients with end stage renal disease should be considered for transplantation

may are not suitable due to combination of comorbidity and advanced age (therefore conservative management)

no absolute age limit applies

123
Q

pros of haemodialysis

A

4 days a week dialysis free

can be done in centre or at home

124
Q

cons of haemodialysis

A

requires food and fluid restriction

increased risk of bleeding

tiredness post treatment

risk of catheter related infections

dialysis access at risk of stenosis and clots

risk of cardiac arrhythmias

risk of dialyser hypersensitivity

125
Q

pros of peritoneal dialysis

A

better haemodynamic stability

can start in less than 2 weeks

preserves residual kidney function

126
Q

cons of peritoneal dialysis

A

risk of encapsulating peritoneal sclerosis

causes constipation

risk of peritonitis

risk of ultrafiltration failure

127
Q

pros of renal transplant

A

significant survival advantage

no dietary or fluid restrictions

128
Q

cons of renal transplant

A

need for lifelong immunosuppression

risk of operations

risk of malignancy

129
Q

what operation is done before haemodialysis can commence

A

arteriovenous fistula must be made for dialysis access

130
Q

what happens in haemodialysis

A

there is diffusion of solutes from blood to dialysate across a semipermeable membrane down a concentration gradient

131
Q

what happens in haemofiltration

A

water and solutes and filtered across a porous semipermeable membrane by a pressure gradient

replacement fluid is added to the filtered blood before it is returned to the patient

132
Q

what happens in peritoneal dialysis

A

fluid is introduced into the abdominal cavity using a catheter

solutes diffuse from blood across the peritoneal membrane to peritoneal dialysis down a concentration gradient and the water diffuses via osmosis

133
Q

what happens in renal transplantation

A

blood supply of transplanted kidney is anastomosed to external iliac vessels and ureter to the bladder

transplanted kidney replaces all the functions of the failed kidney

134
Q

what are haemoglobinopathies

A

they are a group of recessively inherited genetic conditions affecting the Hb component of blood

Semester 2 (3rd year) (12 decks)

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