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3B GH > Haematology > Flashcards

Haematology Flashcards

1
Q

sx of anaemia

A 
fatigue
dyspnoea
lightheaded
palpitations
headache
tinnitus
anorexia
(angina if pre-existing coronary disease)
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2
Q

signs of anaemia

A

pallor (+ of conjunc)
tachycardia
flow murmurs (ejection systolic over apex)

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3
Q

causes of microcytic anaemia

A

iron def
thalassaemia
sideroblastic

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4
Q

causes of normocytic anaemia

A 
chronic disease
acute blood loss
bone marrow failure
renal failure (erythropoetin)
hypothyroid
haemolysis
pregnancy
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5
Q

in a patient with normocytic anaemia who also has low WCC an low platelets, what diagnosis would you suspect?

A

marrow failure

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6
Q

causes of high MCV (macrocytic) anaemia

A 
B12/folate def
alcohol excess/ liver disease
reticulocytosis (e.g. with haemolysis)
cytotoxics e.g. hydroxycarbamide
myeloma
marrow infiltration
hypothyroid
antifolate drugs e.g. phenytoin
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7
Q

causes of iron deficiency anaemia

A

blood loss - menorrhagia, GI
poor diet
malabsorption - coeliac
hookworm

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8
Q

signs of iron deficiency anaemia (now rare)

A

koilonychia (spoon nails)
atrophic glossitis
angular stomatitis

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9
Q

tests in iron deficiency

A 
FBC
haematinics
blood film
coeliac serology
gastroscopy + colonoscopy
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10
Q

Tx for iron deficiency anaemia

A

treat the cause
ferrous sulphate
(then IV iron)

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11
Q

Side effects of ferrous sulphate

A

nausea
abdo discomfort
constipation/ diarrhoea
black stools

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12
Q

pathophysiology behind anaemia of chronic disease

A
  1. poor use of iron in erythropoesis
  2. cytokines shorten RBC survival
  3. reduced EPO production + response to it
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13
Q

examples of causes of anaemia of chronic disease

A 
malignancy
RA
chronic infection
vasculitis
renal failure
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14
Q

Mx of anaemia of chronic disease

A

treat underlying cause

EPO

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15
Q

what is sideroblastic anaemia

A

ineffective erythropoesis and iron loading in marrow

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16
Q

what is haemosiderosis in sideroblastic anaemia

A

endocrine, liver and hear damage due to iron deposition

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17
Q

causes of sideroblastic anaemia

A 
congenital
idiopathic
chemo
anti-TB drugs
irradiation
alcohol excess
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18
Q

what test results would you see in sideroblastic anaemia

A 
low Hb
low MCV
high ferritin
hypochromic blood film
sideroblasts in marrow biopsy
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19
Q

Tx of sideroblastic anaemia

A

remove cause
tranfusion
pyridoxine

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20
Q

tests in macrocytic anaemia

A

FBC, haematinics, LFT, TFT
blood film
bone marrow biopsy

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21
Q

in what foods is folate found?

A

liver
green veg
nuts
yeast

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22
Q

maternal folate deficiency causes what problem in fetus

A

neural tube defects

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23
Q

causes of folate deficiency

A
  1. poor diet e.g. elderly, poverty, alcoholics
  2. increased demand e.g. preg, increased cell turnover (CA, haemolysis, inflamm disease, renal dialysis)
  3. malabsorption [coeliac]
  4. alcohol
  5. drugs [antiep, methotrex, trimeth]
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24
Q

management of folate deficiency

Ix + Mx

A

assess for poor diet
coeliac serology

folic acid + B12

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25
Q

causes of glossitis

A 
B12 deficiency
iron def
contact derm/ food allergy
crohns, coeliac
drugs
alcoholism
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26
Q

causes of B12 deficiency

A

diet [vegan]

malabsorp [PA, crohns, resection]

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27
Q

food sources of B12

A

meat
fish
dairy products

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28
Q

describe how absorption of B12 occurs

A

intrinsic factor from the stomach binds B12, allowing it to be absorbed in the terminal ileum

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29
Q

clinical features of B12 deficiency

A

lemon tinged skin [pallor + jaundice]
glossitis
anaemia Sx
psych: irritable, dementia, depression, psychosis
parasthesia, peripheral neuropathy
subacute combined degeneration of the spinal cord

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30
Q

classical triad of subacute combined degeneration of the spinal cord - seen in B12 deficiency

A

extensor plantars
absentknee jerks
absent ankle jerks

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31
Q

describe briefly the patholgy behind pernicious anaemia

A

autoimmune
atophic gastritis
leading to reduced secretion of intrinsic factor from the parietal cells
unbound B12 therefore not absorbed

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32
Q

other diseases associated with pernicious anaemia

A

autoimmune: thyroid, addisons, vitiligo, hypoparathyroidsim

gastric carcinoma

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33
Q

Ix in pernicious anaemia

A 
FBC [Hb, MCV, WCC, platelets]
haematinics
parietal cell autoantibodies
intrinsic factor antibodies
blood film [hypersegmented neutrophils]
marrow
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34
Q

Mx of B12 deficiency

A

treat cause

B12 IM/ PO

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35
Q

why is there a marked continuing high MCV after initiating B12 treatment for deficiency

A

reticulocytosis

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36
Q

normal lifespan of a RBC

A

120 days

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37
Q

haemolysis can occur intravascularly or extravascularly. Explain extravascular haemolysis

A

macrophages in liver, spleen, bone marrow (reticuloendothelial system)

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38
Q

investigation findings that would support incerased red cell breakdown

A
  1. raised bilirubin
  2. low Hb, normal or high MCV
  3. high urinary urobilinogen
  4. high serum LDH (released from red cells)
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39
Q

what blood test finding would suggest increased red cell production?

A

high MCV [reticulocytosis]

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40
Q

an examinatin finding that may suggest extravascular haemolysis

A

splenomegaly

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41
Q

important aspects of the history in suspected haemolytic anaemia

A 
FH
previous anaemia
ethnicity
dark urine
drugs
travel
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42
Q

important aspects of the examination in suspected haemolytic anaemia

A

jaundice
hepatosplenomegaly
gallstones [^bili]
leg ulcers

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43
Q

Ix in haemolytic anaemia

A 
FBC
LFT [bili]
LDH
urinary urobilinogen
haptoglobin
blood film

if travel Hx - malaria thick + thin films

extras:
osmotic fragility testing
direct coombs test
Hb electrophoresis

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44
Q

what does coombs test identify

A

immune causes of haemolytic anaemia

identifies RBCs coated with antibody

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45
Q

acquired causes of haemolytic anaemia

A 
infection
autoimmune
malignancy CLL, lymphoma
TTP, HUS
drugs
DIC
transfusion
hep B+C
vaccinations
pre-eclampsia
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46
Q

hereditary causes of haemolytic anaemia

A

enzyme defect: G6PD deficiency, PKD

membrane defect: hereditary spherocytosis

haemoglobinopathy: sickle cell, thalasaemia

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47
Q

how is sickle cell inherited

A

autosomal recessive

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48
Q

pathophysiology of sickle cell

A

abnormal haemoglobin results in deformed RBCs (sickle cells). these haemolyse -> vaso-occlusive crises

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49
Q

investigation findings in sickle cell

A

FBC - low Hb, ^reticulocytes/MCV
blood film - sickle cells + target cells
LFT - high bili

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50
Q

triggers for a vaso-occlusive ‘painful’ crisis in sickle cell

A

cold
hypoxia
dehydration
infection

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51
Q

presentation of vaso-occlusive ‘painful’ crisis

A 
severe pain
dactylitis in <3 yr olds
acute abdomen [mesenteric ischaemia]
stroke, seizure, cognitive defects
avascular necrosis (e.g. femoral head)
leg ulcers
priapism
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52
Q

what is a sequestration crisis in sickle cell

and Mx?

A

pooling of blood in spleen and liver > organomegaly, shock, severe anaemia

transfusion

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53
Q

what is a aplastic crisis in sickle cell

A

parvovirus B19 infection leads to sudden reduction in marrow production of RBCs

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54
Q

complications of sickle cell

A 
splenic infarction
poor growth
CKD
gallstones
retinal disease
iron overload
lung hypoxia -> fibrosis -> pULM HTN
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55
Q

Mx of chronic sickle cell

A 
analgesia for crises
hydroxycarbamide
Abx prophylaxis + immunisations [splenic infarct]
transfusions
bone marrow transplant
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56
Q

Mx of sickle cell crisis

A 
analgesia
septic screen
fluids
O2
Abx if pyrexial
transfusion/ exchange transfusion
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57
Q

Sx of acute chest syndrome in sickle cell

A 
wheeze
dyspnoea
pain
fever
cough
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58
Q

what causes the infiltrates in acute chest syndrome in sickle cell

A

infection

fat embolism from bone marrow

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59
Q

Mx of acute chest syndrome in sickle cell

A 
O2
analgesia 
Abx [cephalosporin + macrolide]
bronchodilators in wheeze]
transfusion/ exchange
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60
Q

examples of macrolide Abx

A

azithromycin
clarithromycin
erythromycin

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61
Q

examples of cephalosporin Abx

A

cefuroxime

ceftriaxone

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62
Q

what is thalasaemia

A

reduced production of one globin chain

leads to haemolysis

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63
Q

where in the world is thalassaemia common?

A

med to far east

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64
Q

Ix in beta thalasaaemia

A 
FBC
haematinics
film
Hb electrophoresis
MRI [for myocardial siderosis]
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65
Q

clinical features of patient with beta thalassaemia

A 
presents in 1st yr of life
severe anaemia
failure to thrive
hepatosplenomeg
skull deformity
osteopenia
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66
Q

mx of beta thalassaemia

A

life long regular transfusions
folate
iron chelators [deferipone + desferrioxamine]
ascorbic acid -> iron excretion
splenectomy
Mx of endrocrine complications [DM, thyroid]
marrow transplant

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67
Q

side effect / risk of regular transfusions in beta thalassaemia, and the consequences of this

A

iron overload
endocrine: pituitary, thyroid, pancreatic failure [DM]. liver disease
cardiac toxicity

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68
Q

what are the 3 processes that halt bleeding after injury? (and therefore the 3 types of bleeding disorder)

A

vasoconstriuction
platelet plugging
coag cascade

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69
Q

bleeding disorders - platelet/vascular vs coagulation disorder. What is the pattern of bleeding in platelet/vascular disorders?

A
  1. prolonged bleeding from cuts
  2. bleeding into skin (bruising, purpura)
  3. Mucous membranes (epistaxis, gums, menorrhagia)
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70
Q

bleeding disorders - platelet/vascular vs coagulation disorder. What is the pattern of bleeding in coagulation disorders?

A

into joionts and muscles

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71
Q

bleeding disorders: give 4 examples of platelet disorders

A 
decreased production: 
leukaemia, myeloma
aplastic anaemia (marrow failure)
cytotoxic drugs
radiotherapy

destruction:
ITP (anti-platelet antibodies)
SLE
drugs e.g. heparin

non-immune:
DIC
TTP
HUS

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72
Q

bleeding disorders: congenital coagulation disorders

A

haemophilia

VWd

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73
Q

bleeding disorders: acquired coagulation disorders

A

anticoagulants
liver disease
DIC
vit K deficiency [diet, absorption]

74
Q

what are haemophilia A + B

A

A =factor 8 deficiency

B= factor 9 def

75
Q

what is the pattern of inheritance in haemophilia A + B

A

X linked recessive

76
Q

how does haemophilia A present

A

early life or post-surg/trauma
bleeds into joints - arthropathy
and into muscles - haematomas (+nerve palsies, compartment syndrome)

77
Q

how is haemophilia A diagnosed

A

^APTT

low factor VIII assay

78
Q

Mx of haemophilia A

A 
desmopressin [^s factor VIII]
compression and elevation in minor bleeds
avoid IM injection, NSAIDs
recombinant factor VIII
genetic councelling
79
Q

Mx of haemophilia B

A

recombinant factor IX

80
Q

what is acquired haemophilia

and how is it managed

A

factor VIII autoantibodies suddenly appear and cause big mucosal bleeds

steroids

81
Q

why does liver disease produce a bleeding disorder

A
  1. reduced synthesis of clotting factors
  2. reduced absorption of vitamin K
  3. abnormalities in platelet function
82
Q

why does malabsorption lead to bleeding disorder?

A

reduced uptake of vit K (needed for factor synth)

83
Q

what is the final product of the clotting cascade?

A

fibrin

84
Q

how does chronic ITP present (immune thrombocytopenia)

A 
bleeding 
purpura (esp. pressure areas)
menorrhagia
epistaxis
usually women
85
Q

Mx of ITP

A 
none if mild
pred
IV Ig for temporary e.g. surgery
splenectomy
ritux
86
Q

when would a D-dimer be raised

A 
fibrin degradation product so...
DVT
PE
DIC
inflammation e.g. infection, malignancy
87
Q

pre-op patient - what questions mioght you ask to assess their risk of excessive bleeding?

A

previous unexplained big/prolonged bleed
liver disease
SLE
drugs e.g. anticoags

88
Q

complications of massive blood transfusion

A 
thrombocytopenia
hypocalc
low clotting factors
hyperkal
hypothermia
89
Q

how would you transfuse a HF patient without overloading?

A

give with furosemide

90
Q

what is an acute haemolytic reaction in blood transfsuion and what Sx

A

ABO/Rh incompatibility

pyrexia
agitation
low BP
abdo/chest pain
flushing
oozing venepuncture sites
DIC
91
Q

why do you need to be wary using heparin in renal failure patinet and how would you combat this?

A

accumulates

lower dose

92
Q

contraindictations to giving heparin e.g. for DVT prophylaxis

A 
bleeding disorders
low platelets on bloods
peptic ulcer
cerebral haemoprrhage
severe HTN
neurosurg
93
Q

contraindictations to giving warfarin

A

peptic ulcer
bleeding disorders
severe HTN
pregnancy [terat]

94
Q

contraindications to NOACs

A

renal/ liver failure
active bleeding
lesion at risk of bleeding
low clotting factors

95
Q

management of patinet on warfarin with minor or major e.g. intracranial bleed

A

minor - vit K

major - prothromin complex concentrate and vit K (or FFP if PCC unavailable)

96
Q

what is tumour lysis syndrome and what are the dangerous consequences

A

chemo -> cell death -> ^urate, ^K+, ^phosphate, low calcium

arrhythmia, renal failure

97
Q

how do you prevent tumour lysis syndrome complications

A

hydration

allopurinol

98
Q

causes of DIC

A

malignancy
trauma
sepsis
obstetric emergencies

99
Q

DIC Mx

A

treat cause
platelets
cryo [fibrinogen]
FFP [coag factors]

100
Q

pathology behind ALL

A

malignancy of lymphoid cells in the bone marrow leading to proliferation of immature blasts
∴ marrow failure

101
Q

ALL and AML, more common in adult or child?

A

ALL childhood

AML adult

102
Q

clinical features in ALL

A 
anaemia Sx e.g. pallor SOB
bleeding (brusing/epistaxis)
infection
lymphadenopathy
hepatosplenomegaly
orchidomegaly
CNS involvment - cranial nerve palsy/meningism
103
Q

how is acute leukaemia diagnosed

A

blood film - blast cells

bone marrow biopsy - blast cells

104
Q

auer rods within blast cells are pathognomic of which leukaemia

A

AML

105
Q

Ix in acute leukaemias

A 
FBC [anaemia, thrombocytopenia, WCC↑]
blood film
bone marrow biopsy
LP
fever - CXR, cultures
CXR/CT lymphadenopathy
106
Q

Mx of ALL

A
  1. chemo +/- intrathecal
  2. transfusion for anaemia
  3. platelets for thrombocytopenia
  4. IV Abx for infection (+prophylaxis)
  5. fluids + allopurinol to prevent tumour lysis syndrome
  6. bone marrow transplant
107
Q

ALL has an increased risk of CSF involvement. How would you combat this?

A

give chemo into csf

108
Q

common infection site in ALL

A

chest
mouth
perianal
skin

109
Q

clinical features in AML

A 
anaemia
bleeding
infections
hepatosplenomegaly
gum hypertrophy
skin involvement
110
Q

tests in AML

A

bone marrow biopsy

FBC [WCC↑/↓/↔]

111
Q

complications of AML and its treatment

A

infections, sepsis
tumour lysis syndrome from chemo
leukostasis

112
Q

Mx of AML

A
  1. chemo
  2. transfusion for anaemia
  3. platelets for thrombocytopenia
  4. IV Abx for infection (+prophylaxis)
  5. fluids + allopurinol to prevent tumour lysis syndrome
  6. bone marrow transplant
113
Q

CML chromosome

A

philadelphia

114
Q

CML Sx

A 
weight loss
tired
fever
sweats
gout
bleeding
abdo discomfort [splenomeg]
115
Q

signs in CML

A

splenomegaly
hepatomeg
anaemia
bruising

116
Q

Ix in CML

A 
FBC [^WCC]
urate
B12
bone marrow biopsy
genetic for Phili
117
Q

Mx for CML

A

imatinib
hydroxycarbamide
chemo
marrow transplant

118
Q

CLL Sx

A

often none

anaemia, infection prone, weight loss, sweats, anorexia if seevre

119
Q

signs in CLL

A

tender rubbery lymhadenopathy

hepatosplenomeg

120
Q

Ix in CLL

A

FBC [^lymphocytes]

later marrow infiltration causes anaemia, neutropenia, throbocytopaenia

121
Q

complications of CLL

A

autoimmune haemolysis
infections [hypogammaglobulinaemia]
marrow failure

122
Q

Mx of CLL

A 
chemo if symptomatic
steroids for autoimmune haemolysis
radiotherapy [lymphadenopathy/splenomeg]
stem cell transplant
transfusions
IVIg for recurrent infections
123
Q

what is lymphoma

A

malignant proliferation of lymphocytes in lymph nodes

also in peripheral blood and infiltrate organs

124
Q

characteristic cell of hodgkins l;ympohoma

A

reed-sternberg

125
Q

risk factors for hodgkins lymphoma

A

affected sibling
EBV
SLE
post transplant

126
Q

what symptoms might mediastinal lymph nodes in hodgkins lymphoma cause by mass effect

A

bronchial obstruction

SVC obstruction

127
Q

complications of hodgkins Tx

A

radio: lung/breast/stomach/thyroid CA, melanoma, sarcoma, IHD, hypothyroid, lung fibrosis.
chemo: myelosuppression, infection, nausea, alopecia
both: AML, non-hodgkins, infertility

128
Q

what is non-hodgkins lymphoma

A

all lymphomas [malignant proliferation of lymphocytes] without reed-sternberg cells

129
Q

causes of non-hodgkins lymphoma

A 
HIV
EBV
immunosuppressive drugs
H.pylori
congenital
130
Q

sites for non-hodgkins lymphoma

A
  1. lymphadenopathy
  2. gastric MALT [h.pylori]
  3. non-MALT gastric
  4. Small bowel
  5. skin
  6. oropharynx
  7. other: bone, CNS, lung
131
Q

Sx of non-hodgkins lymphoma

A
  1. lymphadenopathy
  2. gastric: dyspepsia, dysphagia, vomiting
  3. bowel: diarrhoea, vomiting, abdo pain
  4. oropharynx: sore throat, obstructed breathing

all: fever, night sweats, weight loss
marrow involvement: anaemia, infection, bleeding

132
Q

tests in non-hodgkins lymphoma

A 
FBC, U+E, LFT, LDH
node biopsy
marrow
CT/PET for staging
effusion - cytology
LP > csf cytology
133
Q

Tx non-hodgkins lymphoma

A

radio
chemo - R-CHOP
ritux

134
Q

the myeloproliferative disorders. Name the disorders caused by proliferation of each of the following cell types: RBC, WBC, platelets, fibroblasts

A

RBC - polycythaemia vera
WBC - CML
platelets - essential thrombocythaemia
fibroblasts - myelofibrosis

135
Q

what is relative polycythaemia

A

normal RBC mass, low plasma vol e.g. acute - dehydration or chronic - obesity, HTN, alc/smoking

136
Q

what is absolute polycythaemia and its causes

A

^RBC mass

primary [PRV] or secondary [smoking, CHD, lung disease, high altitude]

OR inappropriately ^EPO production [RCC, HCC]

137
Q

what is the mutation present in >95% of polycythaemia vera?

A

JAK2

138
Q

presentation of polycyth RV

A

asymp
hyperviscosity > headache, dizzy, tinitus, visual disturbance
itching after hot bath, erythromelalgia
gout, arterial + venous thrombosis

139
Q

what age is polycythaemia vera commomer

A

> 60

140
Q

why might polycythaemia patient get gout?

A

^urate from ^RBC turnover

141
Q

signs in polycythaemia

A

splenomeg

flushed face

142
Q

Ix in polycythaemia vera

A

FBC
haematinics
marrow
EPO [low]

143
Q

Mx of polycythaemia vera

A

reduce haematocrit by:
venesection
hydroxycarbamide
alpha interferon

aspirin

144
Q

complications of polycythaemia vera

A

thrombosis
haemorrhage [defective platelets]
myelofibrosis
acute leukaemia

145
Q

what is essential thrombocythaemia, and what problems does it cause

A

proliferation in bone marrow -> ^platelets, with abnormal fn.

bleeding, thrombosis [arterial and venous], microvascular occlusion

146
Q

Tx of essential thrombocythaemia

A

aspirin

hydroxycarbamide

147
Q

Sx of essential thrombocythaemia

A

headache
CP
light-headed
erthromelalgia

148
Q

what is myelofibrosis

A

marrow fibrosis leading to haematopoiesis in spleen + liver -> massive hepatosplenomeg

149
Q

presentation of myelofibrosis

A

hypermetabolic Sx: night sweats, fever, weight loss
abdo discomfort from hepatosplenomeg
marrow failure: anaemia, infections, bleeding

150
Q

Mx of myelofibrosis

A

marrow support - transfusions, neutropenic regimen

marrow transplant

151
Q

causes of thrombocytosis

A 
essential thrombocythaemia
bleeding
infection
malignancy
trauma
post-surg
iron deficiency
chronic inflamm e.g. collagen disorders
152
Q

what is myeloma

A

abnormal proliferation of plasma cells -> secretion of Ig

153
Q

what effect does the excess Ig secreted in myeloma have ?

A

organ dysfunction e.g. kidney

154
Q

what are the symtoms/ presentation of myeloma

A
  1. bone lesions: backache, fractures
  2. hypercalc: many Sx e.g. constipation, abdo pain, confusion, stones
  3. anaemia Sx
  4. bleeding/ bruising
  5. infection!
  6. renal impairment [Ig + hypercalc]
155
Q

why do myeloma patients get anaemia and thrombocytopenia

A

bone marrow infiltration by plasma cells

156
Q

why do myeloma patients get ^infections

A
  1. immunoparesis
  2. bone marrow infiltration
  3. chemo
157
Q

why do myeloma patients get hypercalcaemia

A

myeloma cells signal osteoclasts -> increased osteoclast activation

158
Q

what is immunoparesis in myeloma

A

the Ig secreted by the myeloma cells is very high e.g. IgG. But the rest of the immunoglobulins are very low.

159
Q

Ix in myeloma

A 
FBC
film
ESR
U+E
marrow
serum/urine electrophoresis ->monoclonal band
XR
[CT/MRI]
ECG - hyperkal/hypercalc
160
Q

what would be seen on bone marrow biopsy in myeloma

A

many plasma cells with abnormal forms

161
Q

what might be seen on an XR in myeloma

A

punched out lytic lesions
pepper pot skull
fractures, vertebral collapse
osteoporosis

162
Q

what aspects are required for diagnosis of myeloma

A
  1. monoclonal band [serum/urine]
  2. ^plasma cells on marrow
  3. end organ damage [hypercalc/renal/anaemia]
  4. bone lesions
163
Q

Mx for myeloma

A 
supportive: 
analgesia
bisphos
local radio
orthopedics
transfusion [anaemia]
fluids 3L/day
(dialysis)
Abx for infections
IVIg [recurrent inf]

chemo
stem cell transplant

164
Q

usual cause of death in myeloma

A

renal failure

infection

165
Q

acute complications of myeloma

A 
infection
hypercalc
spinal cord compression
hyperviscosity [light chains]
AKI
166
Q

casues of hyperviscosity

A

polycythaemia
leukaemia
myeloma
drugs: OCP, diuretics, IVIG, EPO, chemo, contrast

167
Q

how do you combat hyperviscosity in each of the following:
polycythaemia

leukaemia

myeloma

A

polycythaemia - venesection
leukaemia - leukapheresis
myeloma - plasmapheresis [removes Ig]

168
Q

give 4 causes of splenomegaly

A 
infection [malaria, EBV, TB]
CML
myelofibrosis
portal HTN/cirrhosis
haemolytic anaemia
lymphoma
169
Q

Ix in splenomegaly

A

FBC
LFT
ESR
(liver biopsy, marrow biopsy, lymph node biopsy)

170
Q

the most common type of inherited thrombophilia

A

Factor V Leiden

171
Q

acquired casues of thrombophilia

A

antiphospholipid syndrome
OCP/HRT
polycthaemia
thrombocytosis

172
Q

risk factors for arterial thrombosis

A

smoking
HTN
hyperlipidaemia
DM

173
Q

risk factors for venous thrombosis

A 
surgery
trauma
immobility
preg
OCP/HRT
age
obesity
varicose veins
HF
malignancy
IBD
nephrotic syndrome
inherited
174
Q

why must long term steroids not be stopped suddenly?

A

addisonian crisis

175
Q

how can you combat steroid side effect osteoporosis

A

give calcium and vit D
consider bisphos
exercise and smoking cessation

176
Q

why should steroid patient avoid NSAIDs?

A

^risk of duodenal ulcer

177
Q

name 5 side effects of steroids

A

GI: pancreatitis, candidiasis, oesoph ulcer, peptic ulcer

MSK: myopathy, osteoP, fractures, growth suppression

endocrine: adrenal suppression, cushings

CNS: triggers epilepsy, depression, psychosis

eye: glaucoma, cataracts, papilloedema

^INFECTIONS

178
Q

in a patient with iron deficiency, with travel Hx, what other Ix would you do and why?

A

travel Hx - stool microscopy for ova [hookworm]

179
Q

Bleeding hx includes…

A

Obs (PPH) & surgical hx

Vaccinations e.g. haematomas

180
Q

APTT vs PT abnormalities

A

APTT: (intrinsic) vWf, factor 8,9,10,11

PT: (extrinsic) 7

Both: 5, 2, 10,

Anticoagulant, DIC, liver disease

3B GH (16 decks)

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