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fourth year > medicine 3 > Flashcards

medicine 3 Flashcards

1
Q

RBCs develop from

A

from reticulocytes that comes from the myeloid stem cells.

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2
Q

platelets are made from

A

megakaryocytes

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3
Q

myeloid stem cells become promyelocytes that can then become

A 
Monocytes then macrophages
Neutrophils
Eosinophils
Mast Cells
Basophils
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4
Q

anisocytosis refers too

A

variation in the size of red blood cells

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5
Q

target cells are seen in

A

iron deficiency anaemia and post-splenectomy.

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6
Q

heniz bodies cells are seen in

A

G6PD and alpha-thalassaemia.

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7
Q

howell-jolly bodies are seen in

A

post-splenectomy and in patients with severe anaemia where the body is regenerating red blood cells quickly.

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8
Q

howell jolly bodies specifically refer too

A

blobs of DNA inside the RBC

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9
Q

reticulocytes appear when there is

A

haemolytic anaemia

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10
Q

schistocytes are present when there is

A

haemolytic uraemic syndrome, disseminated intravascular coagulation (DIC) or thrombotic thrombocytopenia purpura, metallic heart valves or haemolytic anaemia

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11
Q

sideroblasts refer too

A

immature RBC’s with blobs of iron

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12
Q

sideroblasts are present in

A

myelodysplasic syndrome.

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13
Q

smudge cells are present in

A

chronic lymphocytic leukaemia.

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14
Q

spherocytes are present in

A

autoimmune haemolytic anaemia or hereditary spherocytosis.

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15
Q

causes of microcytic anaemia

A 
T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia
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16
Q

causes of normocytic anaemia

A 
A – Acute blood loss
A – Anaemia of Chronic Disease
A – Aplastic Anaemia
H – Haemolytic Anaemia
H – Hypothyroidism
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17
Q

causes of macrocytic anaemia and megaloblastic anaemia

A

B12 deficiency

Folate deficiency

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18
Q

causes of normoblastic macrocytic anaemia

A 
Alcohol
Reticulocytosis (usually from haemolytic anaemia or blood loss)
Hypothyroidism
Liver disease
Drugs such as azathioprine
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19
Q

symptoms of anaemia

A 
Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations
Worsening of other conditions such as angina, heart failure or peripheral vascular disease
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20
Q

specific symptoms of iron deficiency anaemia

A

Pica describes dietary cravings for abnormal things such as dirt and can signify iron deficiency
Hair loss can indicate iron deficiency anaemia
koilonychia
angular chelitis
atrophic glossitis

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21
Q

signs of anaemia

A

Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate

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22
Q

anaemia Ix

A 
Haemoglobin
Mean Cell Volume (MCV)
B12
Folate
Ferritin
Blood film
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23
Q

iron is absorbed in the

A

duodenum and jejunum

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24
Q

what medication could affect iron absorption

A

PPI

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25
Q

what chronic conditions could effect iron absorption

A

Crohn’s disease or coeliac disease

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26
Q

transferrin saturation =

A

serum iron/total iron binding capacity.

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27
Q

low serum ferritin indicates

A

iron deficiency anaemia

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28
Q

what marker could be used to indicate how much serum transferring there is

A

total iron binding capacity

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29
Q

what injury can give the impression of iron overload

A

acute liver damage

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30
Q

new iron deficiency in an adult with a underlying cause requires

A

oesophago-gastroduodenoscopy (OGD) and a colonoscopy to look for cancer of the gastrointestinal tract.

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31
Q

management of iron deficiency anaemia is with

A

blood transfusion, iron infusion or oral iron ferrous sulfate 200mg three times daily

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32
Q

pernicious anaemia refers too

A

low B12

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33
Q

pathophysiology of pernicious anaemia

A

parietal cells of the stomach produce a protein called intrinsic factor that is essential for vitamin B12 absorption in the ileum. autoantibodies are against parietal cells or intrinsic factor.

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34
Q

Vitamin B12 deficiency symptoms

A

Peripheral neuropathy with numbness or paraesthesia (pins and needles)
Loss of vibration sense or proprioception
Visual changes
Mood or cognitive changes

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35
Q

if there is a concurrent folate deficiency with a B12 deficiency what is the procedure

A

TREAT THE B12 FIRST

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36
Q

treating patients with folic acid when they have a B12 deficiency this can lead too

A

subacute combined degeneration of the cord

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37
Q

pernicious anaemia Tx is with

A

They can be treated with 1mg of intramuscular hydroxycobalamin

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38
Q

inherited haemolytic anaemias

A 
Hereditary Spherocytosis
Hereditary Elliptocytosis
Thalassaemia
Sickle Cell Anaemia
G6PD Deficiency
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39
Q

features of haemolytic anaemia

A

splenomegaly, jaundice and anaemia

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40
Q

acquired haemolytic anaemias

A 
Autoimmune haemolytic anaemia
Alloimmune haemolytic anaemia (transfusions reactions and haemolytic disease of newborn)
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Prosthetic valve related haemolysis
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41
Q

Ix for haemolytic anaemias

A

Full blood count shows a normocytic anaemia
Blood film shows schistocytes (fragments of red blood cells)
Direct Coombs test is positive in autoimmune haemolytic anaemia

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42
Q

hereditary spherocytosis inheritance

A

autosomal dominant

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43
Q

presentation of hereditary spherocytosis

A

jaundice, gallstones, splenomegaly and notably aplastic crisis in the presence of the parvovirus.

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44
Q

dx of hereditary spherocytosis is by

A

presence of spherocytes on blood film
raised mean corpuscular haemoglobin concentration
raised reticulocytes

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45
Q

Tx for hereditary spherocytosis

A

folate supplementation
splenectomy
removal of the gall bladder if necessary

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46
Q

hereditary elliptocytosis inheritance

A

autosomal dominant

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47
Q

G6PD inheritance

A

X-linked recessive

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48
Q

G6PD crises can be triggered by

A

fava (broad beans) or medications (ciproloxacin, primaquine or sulfonylureas)

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49
Q

G6PD diagnosis is by

A

heinz bodies on blood film,

and a G6PD enzyme assay

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50
Q

symptoms of G6PD

A

jaundice (usually in the neonatal period), gallstones, anaemia, splenomegaly

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51
Q

two types of autoimmune haemolytic anaemia are

A

warm or cold

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52
Q

causes of warm autoimmune haemolytic anaemia

A

idiopathic

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53
Q

causes of cold autoimmune haemolytic anaemia

A

lymphoma, leukaemia, systemic lupus erythematosus and infections such as mycoplasma, EBV, CMV and HIV.

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54
Q

management of autoimmune haemolytic anaemia

A

Blood transfusions
Prednisolone (steroids)
Rituximab (a monoclonal antibody against B cells)
Splenectomy

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55
Q

alloimmune haemolytic anaemia causes

A

transfusion reaction or haemolytic disease of the newborn

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56
Q

Paroxysmal Nocturnal Haemoglobinuria pathology

A

mutation that results in loss of proteins on the RBC that inhibit complement cascade and destruction of RBC’s

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57
Q

presentation of Paroxysmal Nocturnal Haemoglobinuria

A

presentation is red urine in the morning containing haemoglobin and haemosiderin. The patient becomes anaemic due to the haemolysis. They are also predisposed to thrombosis (e.g. DVT, PE and hepatic vein thrombosis) and smooth muscle dystonia (e.g. oesophageal spasm and erectile dysfunction).

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58
Q

Mx of paroxysmal nocturnal haemoglobinuria

A

eculizumab or bone marrow transplantation

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59
Q

Microangiopathic Haemolytic Anaemia (MAHA) pathology

A

structural abnormalities in small vessels that causes haemolysis

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60
Q

normal haemoglobin consists of

A

two alpha and 2 beta chains

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61
Q

thalassaemia inheritance

A

autosomal recessive

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62
Q

signs and symptoms of thalassaemia

A 
Microcytic anaemia (low mean corpuscular volume)
Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly
Poor growth and development
Pronounced forehead and malar eminences
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63
Q

Dx of thalassaemia

A

Full blood count shows a microcytic anaemia.
Haemoglobin electrophoresis is used to diagnose globin abnormalities.
DNA testing can be used to look for the genetic abnormality

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64
Q

iron overload symptoms

A 
Fatigue
Liver cirrhosis
Infertility and impotence
Heart failure
Arthritis
Diabetes
Osteoporosis and joint pain
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65
Q

alpha thalassaemia is caused by a mutation of chromosome

A

16

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66
Q

Mx of alpha thalassaemia

A 
Monitoring the full blood count
Monitoring for complications
Blood transfusions
Splenectomy may be performed
Bone marrow transplant can be curative
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67
Q

beta thalassaemia is caused by a mutation on chromosome

A

11

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68
Q

thalassaemia beta minor causes

A

mild microcytic anaemia

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69
Q

thalassaemia beta intermedia genetic pathology

A

This can be either two defective genes or one defective gene and one deletion gene.

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70
Q

thalassaemia major genetics are

A

homozygous for the deletion genes.

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71
Q

thalassaemia major causes

A

Severe microcytic anaemia
Splenomegaly
Bone deformities

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72
Q

thalassaemia major requires

A

regular transfusions, iron chelation and splenectomy. Bone marrow transplant can potentially be curative.

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73
Q

sickle cell anaemia transmission

A

autosomal recessive

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74
Q

sickle cell anaemia effects which gene

A

beta globin on chromosome 11

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75
Q

sickle cell screening

A

newborn screening heel prick test

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76
Q

general management of sickle cell anaemia

A

antibiotic prophylaxis to protect against infection with penicillin V (phenoxymethypenicillin)
Hydroxycarbamide can be used to stimulate production of fetal haemoglobin (HbF).
vaccines
blood transfusion, bone marrow transplant, avoid dehydration

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77
Q

sickle cell crises Mx

A

NSAIDS, keep warm, hydrated

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78
Q

vaso occlusive crisis is caused by

A

clogging capillaries causing distal ischaemia.

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79
Q

vaso occlusive crisis can cause what emergency?

A

priapism

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80
Q

splenic sequestration crises refers too

A

red blood cells blocking blood flow within the spleen. This causes an acutely enlarged and painful spleen. The pooling of blood in the spleen can lead to a severe anaemia and circulatory collapse (hypovolaemic shock).

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81
Q

Mx of splenic sequestration crisis

A

preventative splenectomy, blood transfusion and fluid resus.

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82
Q

aplastic crisis refers too and is caused by what?

A

parvovirus B19

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83
Q

acute chest syndrome diagnosis requires

A

Fever or respiratory symptoms with

New infiltrates seen on a chest xray

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84
Q

management of acute chest syndrome requires

A

Antibiotics or antivirals for infections
Blood transfusions for anaemia
Incentive spirometry using a machine that encourages effective and deep breathing
Artificial ventilation

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85
Q

Age ranges for ALL

A

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)

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86
Q

age ranges for CLL

A

Over 55 – chronic lymphocytic leukaemia (CeLLmates)

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87
Q

age ranges for CML

A

Over 65 – chronic myeloid leukaemia (CoMmon)

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88
Q

age ranges for AML

A

Over 75 – acute myeloid leukaemia (AMbitions)

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89
Q

presentation of leukaemia

A 
Fatigue
Fever
Failure to thrive (children)
Pallor due to anaemia
Petechiae and abnormal bruising due to thrombocytopenia
Abnormal bleeding
Lymphadenopathy
Hepatosplenomegaly
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90
Q

differentials for petechiae

A 
Leukaemia
Meningococcal septicaemia
Vasculitis
Henoch-Schonlein Purpura (HSP)
Idiopathic Thrombocytopenia Purpura (ITP)
Non-accidental injury
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91
Q

how to diagnose leukaemia

A

FBC, blood film, LDH, bone marrow biopsy, CXR, lymph node biopsy, lumbar puncture, CT, MRI, PET

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92
Q

what are the different types of bone marrow biopsy

A

aspiration, trephine or biopsy

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93
Q

Acute lymphoblastic leukaemia pathology

A

acute proliferation of a single type of lymphocyte, usually B-lymphocytes. Excessive proliferation of these cells causes them to replace the other cell types being created in the bone marrow, leading to a pancytopenia.

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94
Q

Acute lymphoblastic leukaemia is associated with

A

down syndrome

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95
Q

Acute lymphoblastic leukaemia blood film shows

A

blast cells

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96
Q

Acute lymphoblastic leukaemia is associated with which gene

A

Philadelphia chromosome (t(9:22) translocation

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97
Q

Chronic lymphocytic leukaemia pathology

A

chronic proliferation of a single type of well differentiated lymphocyte, usually B-lymphocytes

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98
Q

Chronic lymphocytic leukaemia can cause

A

warm autoimmune haemolytic anaemia

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99
Q

Chronic lymphocytic leukaemia presents with

A

asymptomatic, infections, anaemia, bleeding and weight loss.

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100
Q

Chronic lymphocytic leukaemia can transform into

A

high-grade lymphoma

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101
Q

Chronic lymphocytic leukaemia blood film shows

A

smear or smudge cells

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102
Q

Chronic Myeloid Leukaemia

has what phases?

A

chronic, accelerated and blast

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103
Q

Chronic Myeloid Leukaemia chronic phase presentation

A

raised WCC and asymptomatic

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104
Q

Chronic Myeloid Leukaemia accelerated phase

A

develop anaemia and thrombocytopenia and become immunocompromised.

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105
Q

Chronic Myeloid Leukaemia blast phase

A

severe symptoms and pancytopenia. It is often fatal.

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106
Q

Chronic Myeloid Leukaemia genetics

A

Philadelphia chromosome, which is a translocation of genes between chromosome 9 and 22: it is a t(9:22) translocation.

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107
Q

acute myeloid leukaemia may arise from

A

myeloproliferative disorder such as polycythaemia ruby vera or myelofibrosis.

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108
Q

acute myeloid leukaemia blood film shows

A

high proportion of blast cells. These blast cells can have rods inside their cytoplasm that are named auer rods.

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109
Q

tumour lysis syndrome refers too

A

release of uric acid from cells that are being destroyed by chemotherapy.

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110
Q

complications of tumour lysis syndrome

A

crystals in the interstitial tissue and tubules of the kidneys and causes acute kidney injury.

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111
Q

Mx of tumour lysis syndrome

A

Allopurinol or rasburicase are used to reduce the high uric acid levels with monitoring of calcium and potassium.

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112
Q

Hodgkin’s Lymphoma is caused by

A

by proliferation of lymphocytes

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113
Q

Hodgkin’s Lymphoma age distribution

A

bimodal age distribution with peaks around aged 20 and 75 years.

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114
Q

risk factors for hodgkin’s lymphoma

A

HIV
Epstein-Barr Virus
Autoimmune conditions such as rheumatoid arthritis and sarcoidosis
Family history

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115
Q

presentation of hodgkin’s lymphoma

A

Lymphadenopathy is the key presenting symptom. pain on drinking alcohol.

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116
Q

B symptoms of hodgkin’s lymphoma

A

Fever
Weight loss
Night sweats

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117
Q

other symptoms of hodgkin’s lymphoma

A 
Fatigue
Itching
Cough
Shortness of breath
Abdominal pain
Recurrent infections
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118
Q

Ix for hodgkin’s lymphoma

A

lymph node biopsy, LDH, CT, MRI, PET

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119
Q

key finding from hodgkin’s lymphoma biopsy

A

Reed-Sternberg cells, they are large B cells with multiple nuclei and nucleoli

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120
Q

what is the staging system for lymphoma

A

ann arbor

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121
Q

stage 1 ann arbor

A

Confined to one region of lymph nodes.

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122
Q

stage 2 ann arbor

A

In more than one region but on the same side of the diaphragm (either above or below).

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123
Q

stage 3 ann arbor

A

Affects lymph nodes both above and below the diaphragm.

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124
Q

stage 4 ann arbor

A

Widespread involvement including non-lymphatic organs such as the lungs or liver.

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125
Q

notable non-hodgkin’s lymphomas include

A

Burkitt lymphoma is associated with Epstein-Barr virus, malaria and HIV.
MALT lymphoma affects the mucosa-associated lymphoid tissue, usually around the stomach. It is associated with H. pylori infection.
Diffuse large B cell lymphoma often presents as a rapidly growing painless mass in patients over 65 years.

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126
Q

Tx for non-hodgkin’s lymphoma

A 
Watchful waiting
Chemotherapy
Monoclonal antibodies such as rituximab
Radiotherapy
Stem cell transplantation
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127
Q

myeloma is a cancer of the

A

plasma cells

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128
Q

Monoclonal gammopathy of undetermined significance (MGUS) refers too

A

incidental finding of excessive antibody/components without features of myeloma

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129
Q

Smouldering myeloma is where there is

A

progression of MGUS to a premalignant state.

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130
Q

Waldenstrom’s macroglobulinemia is a type of smouldering myeloma where there is excessive

A

IgM

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131
Q

what immunoglobulin is commonly produced in myeloma

A

IgG monoclonal paraprotein

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132
Q

what protein can be found in the urine of a myeloma patient?

A

“Bence Jones protein” that can be found in the urine of many patients with myeloma is actually a part (subunit) of the antibody called the light chains.

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133
Q

why does anaemia arise in myeloma?

A

The cancerous plasma cells invade the bone marrow. This is described as bone marrow infiltration.

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134
Q

myeloma bone disease is the result of

A

increased osteoclast activity and suppressed osteoblast activity. This is caused by cytokines released from the plasma cells and the stromal cells (other bone cells) when they are in contact with the plasma cells.

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135
Q

common sites for myeloma bone disease is

A

the skull, spine, long bones and ribs

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136
Q

the bone appearance in myeloma bone disease is

A

These patches of thin bone can be described as osteolytic lesions. These weak points in bone lead to pathological fractures.

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137
Q

what biochemical sign is associated with myeloma bone disease?

A

hypercalcaemia due to osteoclast activity

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138
Q

people with myeloma can also develop with concurrent cancer?

A

plasmacytomas. These are individual tumours made up of the cancerous plasma cells. They can occur in the bones,

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139
Q

myeloma renal disease factors

A

High levels of immunoglobulins (antibodies) can block the flow through the tubules
Hypercalcaemia impairs renal function
Dehydration
Medications

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140
Q

raised plasma viscosity in myeloma may cause

A

Easy bruising
Easy bleeding
Reduced or loss of sight due to vascular disease in the eye
Purple discolouration to the extremities (purplish palmar erythema)
Heart failure

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141
Q

four key features of myeloma

A

C – Calcium (elevated)
R – Renal failure
A – Anaemia (normocytic, normochromic) from replacement of bone marrow.
B – Bone lesions/pain

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142
Q

myeloma Ix

A 
FBC (low white blood cell count in myeloma)
Calcium (raised in myeloma)
ESR (raised in myeloma)
Plasma viscosity (raised in myeloma)
serum protein electrophoresis
 urine bence-jones protein
bone marrow biopsy
imaging
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143
Q

BLIP testing for myeloma

A

B – Bence–Jones protein (request urine electrophoresis)
L – Serum‑free Light‑chain assay
I – Serum Immunoglobulins
P – Serum Protein electrophoresis

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144
Q

X-ray signs of myeloma

A

Punched out lesions
Lytic lesions
“Raindrop skull” caused by many punched out (lytic) lesions throughout the skull that give the appearance of raindrops splashing on a surface

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145
Q

first line for myeloma

A

chemotherapy with:

Bortezomid
Thalidomide
Dexamethasone

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146
Q

additional treatment of myeloma includes

A

stem cell transplant and VTE prophylaxis

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147
Q

Mx for myeloma bone disease

A

RT, orthopaedic surgery, bisphosphonates, cement augmentation

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148
Q

proliferating cell line: haematopoietic stem cell disease name is

A

primary myelofibrosis

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149
Q

proliferating cell line: erythroid cells disease name

A

polycythaemia vera

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150
Q

proliferating cell line: megakaryocyte disease name

A

essential thrombocythaemia

151
Q

myeloproliferative disorders have a risk of progressing into

A

acute myeloid leukaemia

152
Q

myeloproliferative disorders are associated with which genes

A

JAK2
MPL
CALR

153
Q

what drug targets JAK2

A

ruxolitinib.

154
Q

Myelofibrosis cytokine

A

fibroblast growth factor.

155
Q

when the bone marrow is replaced by scar tissue in myelofibrosis what process may occur?

A

extramedullary haematopoiesis and can lead to hepatomegaly and splenomegaly. This can lead to portal hypertension. If it occurs around the spine it can lead to spinal cord compression.

156
Q

presentation of myeloproliferative disorders systemically

A

Fatigue
Weight loss
Night sweats
Fever

157
Q

signs and symptoms of the underlying complications of myeloproliferative disorders

A

Anaemia (except in polycythaemia)
Splenomegaly (abdominal pain)
Portal hypertension (ascites, varices and abdominal pain)
Low platelets (bleeding and petechiae)
Thrombosis is common in polycythaemia and thrombocythaemia
Raised red blood cells (thrombosis and red face)
Low white blood cells (infections)

158
Q

A blood film in myelofibrosis can show

A

teardrop-shaped RBCs, varying sizes of red blood cells (poikilocytosis) and immature red and white cells (blasts).

159
Q

Management of Primary Myelofibrosis

A

allogeneic stem cells transplant, chemotherapy, supportive management

160
Q

Management of Polycythaemia Vera

A

venesection, aspirin, chemotherapy

161
Q

Management of Essential Thrombocythaemia

A

aspirin and chemotherapy

162
Q

Myelodysplastic syndrome is caused by the

A

myeloid bone marrow cells not maturing properly and therefore not producing healthy blood cells

163
Q

Myelodysplastic syndrome may progress too

A

acute myeloid leukaemia

164
Q

myelodysplastic syndrome is common in what demographic of patients?

A

60 years of age and in patients that have previously had treatment with chemotherapy or radiotherapy.

165
Q

presentation of myelodysplastic syndrome

A

anaemia (fatigue, pallor or shortness of breath), neutropenia (frequent or severe infections) or thrombocytopenia (purpura or bleeding).

166
Q

Dx of myelodysplastic syndrome

A

Full blood count will be abnormal. There may be blasts on the blood film.

The diagnosis is confirmed by bone marrow aspiration and biopsy.

167
Q

thrombocytopenia production problems

A 
Sepsis
B12 or folic acid deficiency
Liver failure causing reduced thrombopoietin production in the liver
Leukaemia
Myelodysplastic syndrome
168
Q

thrombocytopenia destruction problems

A 
Medications (sodium valproate, methotrexate, isotretinoin, antihistamines, proton pump inhibitors)
Alcohol
Immune thrombocytopenic purpura
Thrombotic thrombocytopenic purpura
Heparin induced thrombocytopenia
Haemolytic-uraemic syndrome
169
Q

differentials for abnormal or prolonged bleeding

A

Thrombocytopenia (low platelets)
Haemophilia A and haemophilia B
Von Willebrand Disease
Disseminated intravascular coagulation (usually secondary to sepsis)

170
Q

ITP management

A

Prednisolone (steroids)
IV immunoglobulins
Rituximab (a monoclonal antibody against B cells)
Splenectomy

171
Q

thrombotic thrombocytopenia purpura pathology

A

tiny blood clots develop throughout the small vessels which is due to the specific protein ADMTS13 without it VWF cannot be inactivated.

172
Q

Tx for thrombotic thrombocytopenia purpura

A

plasma exchange, steroids and rituximab

173
Q

heparin induced thrombocytopenia involves

A

development of antibodies against platelets in response to exposure to heparin

174
Q

von willebrand disease inheritance is

A

autosomal dominant

175
Q

what specific VWF is effected in von willebrand disease

A

glycoprotein

176
Q

presentation of von willebrand disease

A

Bleeding gums with brushing
Nose bleeds (epistaxis)
Heavy menstrual bleeding (menorrhagia)
Heavy bleeding during surgical operations

177
Q

Mx of von willebrand disease

A

Desmopressin can be used to stimulates the release of VWF
VWF can be infused
Factor VIII is often infused along with plasma derived VWF

178
Q

haemophilia A is caused by a deficiency with

A

Factor 8

179
Q

haemophilia B is caused by a deficiency with

A

factor 9

180
Q

inheritance of haemophilia

A

X-linked recessive

181
Q

signs and symptoms of haemophilia

A

spontaneous haemorrhage without any trauma.
haemoathrosis) and muscles are a classic feature of severe haemophilia.
Abnormal bleeding can occur in other areas:

Gums
Gastrointestinal tract
Urinary tract causing haematuria
Retroperitoneal space
Intracranial
Following procedures
182
Q

Mx of haemophilia

A

The affected clotting factors (VIII or IX) can be replaced by intravenous infusions.
Infusions of the affected factor (VIII or IX)
Desmopressin to stimulate the release of von Willebrand Factor
Antifibrinolytics such as tranexamic acid

183
Q

RF for DVT are

A 
Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen (combined oral contraceptive pill and hormone replacement therapy)
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia
184
Q

thrombophilia conditions

A 
Antiphospholipid syndrome (this is the one to remember for your exams)
Antithrombin deficiency
Protein C or S deficiency
Factor V Leiden
185
Q

VTE prophylaxis is with

A

low molecular weight heparin such as enoxaparin

186
Q

DVT presentation is with

A 
unilateral Calf or leg swelling
Dilated superficial veins
Tenderness to the calf (particularly over the site of the deep veins)
Oedema
Colour changes to the leg
187
Q

what is the score for predicting risk of DVT

A

wells

188
Q

Dx for DVT

A

D-dimer, US, CTPA for PE, V/Q for PE

189
Q

Budd-Chiari syndrome is where a blood clot (thrombosis) develops in the

A

hepatic vein causing acute hepatitis

190
Q

budd chiari triad

A

Abdominal pain
Hepatomegaly
Ascites

191
Q

risk factors for osteoarthritis

A

obesity, age, occupation, trauma, being female and family history.

192
Q

key X-ray changes for osteoarthritis

A

L – Loss of Joint Space
O – Osteophytes
S – Subarticular Sclerosis (increased density of the bone along the joint line)
S – Subchondral Cysts (fluid filled holes in the bone, aka geodes)

193
Q

presentation of OA

A

joint pain and stiffness. This pain and stiffness tends to be worsened by activity. reduced function, instability and deformity.

194
Q

hand signs in OA

A 
Haberdens nodes (in the DIP joints)
Bouchards nodes (in the PIP joints)
Squaring at the base of the thumb at the carpo-metacarpal joint
Weak grip
Reduced range of motion
195
Q

Mx for OA

A

Oral paracetamol and topical NSAIDs or topical capsaicin (chilli pepper extract).
Add oral NSAIDs and consider also prescribing a proton pump inhibitor (PPI) to protect their stomach such as omeprazole. They are better used intermittently rather than continuously.
Consider opiates such as codeine and morphine. These should be used cautiously as they can have significant side effects and patients can develop dependence and withdrawal. They also don’t work for chronic pain and result in patients becoming depending without benefitting from pain relief.

196
Q

holistic support for OA includes

A

weight loss, PT, and OT, orthotics

197
Q

procedures for OA

A

intra-articular steroid injections and joint replacement

198
Q

genetic associations with rheumatoid arthritis

A 
HLA DR4 (a gene often present in RF positive patients)
HLA DR1 (a gene occasionally present in RA patients)
199
Q

rheumatoid factor in RA binds to what

A

an autoantibody that targets the Fc portion of the IgG antibody.

200
Q

rheumatoid factor is what type of immunoglobulin

A

IgM

201
Q

other than Rheumatoid Factor what is another autoantibody in rheumatoid arthritis

A

Anti-citrullinated cyclic peptide antibodies

202
Q

presentation of Rheumatoid arthritis

A

symmetrical distal polyarthropathy
Pain
Swelling
Stiffness

203
Q

systemic symptoms of Rheumatoid arthritis

A

Fatigue
Weight loss
Flu like illness
Muscles aches and weakness

204
Q

key history finding in rheumatoid arthritis

A

pain from an inflammatory arthritis is worse after rest but improves with activity. Pain from a mechanical problem such as osteoarthritis is worse with activity and improves with rest.

205
Q

what joints are almost never effected by rheumatoid arthritis

A

distal interphalangeal joints are almost never affected by rheumatoid arthritis

206
Q

what crisis may arise from atlantoaxial subluxation?

A

spinal cord compression

207
Q

hand sings in rheumatoid arthritis

A 
Z shaped deformity to the thumb
Swan neck deformity (hyperextended PIP with flexed DIP)
Boutonnieres deformity (hyperextended DIP with flexed PIP)
Ulnar deviation of the fingers at the knuckle (MCP joints)
208
Q

Boutonnieres deformity are due to

A

a tear in the central slip of the extensor components of the fingers. This means that when the patient tries to straighten their finger, the lateral tendons that go around the PIP (called the flexor digitorum superficialis tendons) pull on the distal phalynx without any other supporting structure, causing the DIPs to extend and the PIP to flex.

209
Q

extra-articular manifestations of rheumatoid arthritis

A

Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
Bronchiolitis obliterans (inflammation causing small airway destruction)
Felty’s syndrome (RA, neutropenia and splenomegaly)
Secondary Sjogren’s Syndrome (AKA sicca syndrome)
Anaemia of chronic disease
Cardiovascular disease
Episcleritis and scleritis
Rheumatoid nodules
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis

210
Q

Ix for rheumatoid arthritis

A

Check rheumatoid factor
If RF negative, check anti-CCP antibodies
Inflammatory markers such as CRP and ESR
X-ray of hands and feet
Ultrasound scan of the joints can be used to evaluate and confirm synovitis.

211
Q

X-ray changes present for rheumatoid arthritis

A

Joint destruction and deformity
Soft tissue swelling
Periarticular osteopenia
Boney erosions

212
Q

diagnostic rheumatoid arthritis criteria are

A

The joints that are involved (more and smaller joints score higher)
Serology (rheumatoid factor and anti-CCP)
Inflammatory markers (ESR and CRP)
Duration of symptoms (more or less than 6 weeks)

213
Q

DAS28 score triad

A

Swollen joints
Tender joints
ESR/CRP result

214
Q

Mx of rheumatoid arthritis

A

short course of steroids, NSAIDs and a PPI

215
Q

DMARDS for RA

A

First line is monotherapy with methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in mild disease and is considered the “mildest” anti rheumatic drug.
Second line is 2 of these used in combination.
Third line is methotrexate plus a biological therapy, usually a TNF inhibitor.
Fourth line is methotrexate plus rituximab

216
Q

biological therapies for RA

A

TNF inhibitors adalimumab, infliximab and etanercept and it is also worth remembering rituximab.

217
Q

risk of use with biological therapies for RA

A

immunosuppression so patients are prone to serious infections. They can also lead to reactivation of dormant infections such as TB and hepatitis B.

218
Q

methotrexate mechanism

A

Methotrexate works by interfering with the metabolism of folate and suppressing certain components of the immune system.

219
Q

methotrexate requires what to be co-prescribed

A

folic acid 5mg

220
Q

SE of methotrexate

A 
Mouth ulcers and mucositis
Liver toxicity
Pulmonary fibrosis
Bone marrow suppression and leukopenia (low white blood cells)
It is teratogenic
221
Q

leflunomide mechanism

A

mmunosuppressant medication that works by interfering with the production of pyrimidine. Pyrimidine is an important component of RNA and DNA.

222
Q

leflunomide SE

A 
Mouth ulcers and mucositis
Increased blood pressure
Rashes
Peripheral neuropathy
Liver toxicity
Bone marrow suppression and leukopenia (low white blood cells)
It is teratogenic
223
Q

Hydroxychloroquine mechanism

A

It acts as an immunosuppressive medication by interfering with Toll-like receptors, disrupting antigen presentation and increasing the pH in the lysosomes of immune cells.

224
Q

SE of hydroxychloroquine

A

Nightmares
Reduced visual acuity (macular toxicity)
Liver toxicity
Skin pigmentation

225
Q

rituximab mechanism

A

monoclonal antibody that targets the CD20 protein on the surface of B cells

226
Q

Sulfasalazine SE

A

male infertility (reduces sperm count)

227
Q

rituximab SE

A 
Vulnerability to severe infections and sepsis
Night sweats
Thrombocytopenia (low platelets)
Peripheral neuropathy
Liver and lung toxicity
228
Q

psoriatic arthritis is part of what group of conditions?

A

“seronegative spondyloarthropathy”

229
Q

Spondylitic pattern

A

Back stiffness
Sacroiliitis
Atlanto-axial joint involvement

230
Q

signs of psoriatic arthritis

A

Plaques of psoriasis on the skin
Pitting of the nails
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the full finger)
Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)Plaques of psoriasis on the skin
Pitting of the nails
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the full finger)
Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)

231
Q

other associations with psoriatic arthritis

A 
Eye disease (conjunctivitis and anterior uveitis)
Aortitis (inflammation of the aorta)
Amyloidosis
232
Q

x-ray changes with psoriatic arthritis

A

Periostitis is inflammation of the periosteum causing a thickened and irregular outline of the bone
Ankylosis is where bones joining together causing joint stiffening
Osteolysis is destruction of bone
Dactylitis is inflammation of the whole digit and appears on the xray as soft tissue swelling
Pencil-in-cup appearance

233
Q

pencil cup appearance X-ray with psoriatic arthritis refers to

A

This is where there are central erosions of the bone beside the joints and this causes the appearance of one bone in the joint being hollow and looking like a cup whilst the other is narrow and sits in the cup.

234
Q

Arthritis Mutilans refers too

A

severe form of psoriatic arthritis. This occurs in the phalanxes. There is osteolysis

235
Q

arthritis mutilans may lead too

A

This leads to progressive shortening of the digit. The skin then folds as the digit shortens giving an appearance that is often called a “telescopic finger”.

236
Q

MX for psoriatic arthritis is with

A

NSAIDs for pain
DMARDS (methotrexate, leflunomide or sulfasalazine)
Anti-TNF medications (etanercept, infliximab or adalimumab)
Ustekinumab is last line (after anti-TNF medications) and is a monoclonal antibody that targets interleukin 12 and 23

237
Q

Reiter Syndrome is known as

A

Reactive arthritis is where synovitis occurs in the joints or acute monoarthritis

238
Q

Reiter Syndrome presents as

A

warm, swollen and painful joint.

239
Q

common infections that could cause reactive arthritis are

A

gastroenteritis or sexually transmitted infection. Chlamydia

240
Q

associations with reactive arthritis

A

Bilateral conjunctivitis (non-infective)
Anterior uveitis
Circinate balanitis is dermatitis of the head of the penis

“can’t see, pee or climb a tree”.

241
Q

Mx of reactive arthritis

A

exclude septic arthritis

NSAIDs
Steroid injections into the affected joints
Systemic steroids may be required, particularly where multiple joints are affected

242
Q

ankylosing spondylitis is a part of what group of conditions

A

seronegative sponyloarthropathy

243
Q

ankylosing spondylitis affects which joints

A

acroiliac joints and the joints of the vertebral column.

244
Q

ankylosing spondylitis progressively leads too

A

fusion of the spine and sacroiliac and bamboo spine on X-ray

245
Q

ankylosing spondylitis is associated with

A

HLA B27 gene.

246
Q

ankylosing spondylitis presents with

A

lower back pain and stiffness and sacroiliac pain in the buttock region. The pain and stiffness is worse with rest and improves with movement. The pain is worse at night and in the morning and may wake them from sleep. It takes at least 30 minutes for the stiffness to improve in the morning and it gets progressively better with activity throughout the day.

247
Q

key complication of ankylosing spondylitis is

A

vertebral fractures

248
Q

ankylosing spondylitis is associated with

A

chest pain, enthesitis, dactylitis, anaemia, anterior uveitis, aortitis, heart block, restrictive lung disease, pulmonary fibrosis and inflammatory bowel disease

249
Q

what examination test is used in ankylosing spondylitis

A

Schober’s test

250
Q

Schobers test involves

A

finding L5, marking 10cm above and 5 cm below and having the patient bend forward, if less than 20cm it is likely ankylosing spondylitis

251
Q

Ix of ankylosing spondylitis

A

Inflammatory markers (CRP and ESR) may rise with disease activity
HLA B27 genetic test
Xray of the spine and sacrum
MRI of the spine can show bone marrow oedema early in the disease before there are any xray changes

252
Q

X-ray of ankylosing spondylitis

A

Squaring of the vertebral bodies
Subchondral sclerosis and erosions
Syndesmophytes are areas of bone growth where the ligaments insert into the bone. They occur related to the ligaments supporting the intervertebral joints.
Ossification of the ligaments, discs and joints. This is where these structures turn to bone.
Fusion of the facet, sacroiliac and costovertebral joints

253
Q

medication for ankylosing spondylitis

A

NSAIDS, steroids, Anti-TNF medications such as etanercept or a monoclonal antibody against TNF such as infliximab, adalimumab or certolizumab pegol are known to be effective in treating the disease activity in AS.
Secukinumab is a monoclonal antibody against interleukin-17

254
Q

leading causes of death in lupus

A

Cardiovascular disease and infection

255
Q

pathophysiology of lupus is

A

anti-nuclear antibodies target cell nucleus

256
Q

presentation of lupus

A 
Fatigue
Weight loss
Arthralgia (joint pain) and non-erosive arthritis
Myalgia (muscle pain)
Fever
Photosensitive malar rash. This is a “butterfly” shaped rash across the nose and cheek bones that gets worse with sunlight.
Lymphadenopathy and splenomegaly
Shortness of breath
Pleuritic chest pain
Mouth ulcers
Hair loss
Raynaud’s phenomenon
257
Q

Ix for lupus

A

Autoantibodies (see below)
Full blood count (normocytic anaemia of chronic disease)
C3 and C4 levels (decreased in active disease)
CRP and ESR (raised with active inflammation)
Immunoglobulins (raised due to activation of B cells with inflammation)
Urinalysis and urine protein:creatinine ratio for proteinuria in lupus nephritis
Renal biopsy can be used to investigate for lupus nephritis

258
Q

autoantibodies associated with lupus

A

Anti-double stranded DNA (anti-dsDNA) and anti-nuclear antibodies, anti-smith

259
Q

limited cutaneous systemic sclerosis autoantibody

A

Anti-centromere antibodies

260
Q

Sjogren’s syndrome autoantibody

A

Anti-Ro and Anti-La

261
Q

systemic sclerosis autoantibody

A

Anti-Scl-70

262
Q

dermatomyositis autoantibody

A

Anti-Jo-1

263
Q

what syndrome can occur secondary to SLE

A

Antiphospholipid antibodies and antiphospholipid syndrome

264
Q

first line Tx for lupus are

A

NSAIDs
Steroids (prednisolone)
Hydroxychloroquine (first line for mild SLE)
Suncream and sun avoidance for the photosensitive the malar rash

265
Q

biological therapies for SLE

A

Rituximab is a monoclonal antibody that targets the CD20 protein on the surface of B cells
Belimumab is a monoclonal antibody that targets B-cell activating factor

266
Q

immunosuppressants used for SLE

A 
Methotrexate
Mycophenolate mofetil
Azathioprine
Tacrolimus
Leflunomide
Ciclosporin
267
Q

Discoid Lupus Erythematosus may progress too

A

SLE or rarely squamous cell carcinoma

268
Q

presentation of discoid lupus erythematosus

A

The lesions typically occur on the face, ears and scalp. They are photosensitive, meaning that they are made worse by exposure to sunlight. They are associated with scarring alopecia (hair loss in affected areas that does not grow back) and hyper-pigmented or hypo-pigmented scars.

The appearance of the lesions are:

Inflamed
Dry
Erythematous
Patchy
Crusty and scaling
269
Q

DX of discoid lupus erythematosus is with

A

skin biopsy

270
Q

discoid lupus erythematosus Tx

A

Sun protection
Topical steroids
Intralesional steroid injections
Hydroxychloroquine

271
Q

Systemic sclerosis is an

A

autoimmune inflammatory and fibrotic connective tissue disease.

272
Q

Systemic sclerosis two patterns

A

Limited cutaneous systemic sclerosis

Diffuse cutaneous systemic sclerosis

273
Q

Limited Cutaneous Systemic Sclerosis presentation

A 
C – Calcinosis
R – Raynaud’s phenomenon
E – oEsophageal dysmotility
S – Sclerodactyly
T – Telangiectasia
274
Q

Diffuse Cutaneous Systemic Sclerosis presentation

A

includes the features of CREST syndrome plus many internal organs causing:

Cardiovascular problems, particularly hypertension and coronary artery disease.
Lung problems, particularly pulmonary hypertension and pulmonary fibrosis.
Kidney problems, particularly glomerulonephritis and a condition called scleroderma renal crisis.

275
Q

Sclerodactyly describes

A

kin tightens around joints it restricts the range of motion in the joint and reduces the function of the joints. As the skin hardens and tightens further the fat pads on the fingers are lost. The skin can break and ulcerate.

276
Q

autoantibodies associated with systemic sclerosis

A

Antinuclear antibodies (ANA)

Anti-centromere antibodies are most associated with limited cutaneous systemic sclerosis.

Anti-Scl-70 antibodies are most associated with diffuse cutaneous systemic sclerosis

277
Q

Ix for raynaud’s phenomenon

A

Nailfold Capillaroscopy to exclude systemic sclerosis

278
Q

diffuse disease systemic sclerosis is usually treated with

A

Steroids and immunosuppressants

279
Q

symptoms of Raynaud’s phenomenon Tx

A

Nifedipine

280
Q

Polymyalgia rheumatica is associated with

A

giant cell arteritis

281
Q

features of polymyalgia rheumatica

A

Bilateral shoulder pain that may radiate to the elbow
Bilateral pelvic girdle pain
Worse with movement
Interferes with sleep
Stiffness for at least 45 minutes in the morning

282
Q

other features of polymyalgia rheumatica

A

Systemic symptoms such as weight loss, fatigue, low grade fever and low mood
Upper arm tenderness
Carpel tunnel syndrome
Pitting oedema

283
Q

Tx with polymyalgia rheumatica

A

Initially patients are started on 15mg of prednisolone per day.

284
Q

steroid rules

A

don’t STOP

make them steroid aware
sick day rules
treatment card
osteoporosis prevention 
PPI
285
Q

key complication of giant cell arteritis is

A

vision loss

286
Q

symptoms of giant cell arteritis

A

The main presenting feature is a headache:

Severe unilateral headache typically around temple and forehead
Scalp tenderness my be noticed when brushing hair
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly

287
Q

diagnosis of giant cell arteritis

A

Clinical presentation
Raised ESR: usually 50 mm/hour or more
Temporal artery biopsy findings

288
Q

additional investigations for giant cell arteritis

A

Full blood count may show a normocytic anaemia and thrombocytosis (raised platelets)
Liver function tests can show a raised alkaline phosphatase
C reactive protein is usually raised
Duplex ultrasound of the temporal artery shows the hypoechoic halo sign

289
Q

giant cell artery biopsy shows

A

Multinucleated giant cells

290
Q

initial management for giant cell artery biopsy

A

Start steroids immediately before confirming the diagnosis to reduce the risk of permanent sight loss. Start 40-60mg prednisolone per day

291
Q

other medications for giant cell artery biopsy

A

Aspirin 75mg daily decreases visual loss and strokes

Proton pump inhibitor

292
Q

referrals for giant cell artery biopsy

A

vascular surgeons, rheumatology and ophthalmology

293
Q

long term complications of giant cell arteritis

A

Relapses of the condition are common
Steroid related side effects and complications
Cerebrovascular accident (stroke)
Aortitis leading to aortic aneurysm and aortic dissection

294
Q

key diagnosis for myositis is

A

creatine kinase

295
Q

Polymyositis or dermatomyositis can be caused by

A 
paraneoplastic syndromes for:
Lung
Breast
Ovarian
Gastric
296
Q

presentation for Polymyositis or dermatomyositis is

A

Muscle pain, fatigue and weakness
Occurs bilaterally and typically affects the proximal muscles
Mostly affects the shoulder and pelvic girdle
Develops over weeks

297
Q

Dermatomyositis Skin Features

A

Gottron lesions (scary erythematous patches) on the knuckles, elbows and knees
Photosensitive erythematous rash on the back, shoulders and neck
Purple rash on the face and eyelids
Periorbital oedema (swelling around the eyes)
Subcutaneous calcinosis

298
Q

Autoantibodies in dermatomyositis and polymyositis is

A

Anti-Jo-1 antibodies: polymyositis (but often present in dermatomyositis)
Anti-Mi-2 antibodies: dermatomyositis.
Anti-nuclear antibodies: dermatomyositis.

299
Q

Dx of dermatomyositis and polymyositis

A 
Clinical presentation
Elevated creatine kinase
Autoantibodies
Electromyography (EMG)
Muscle biopsy
300
Q

Mx dermatomyositis and polymyositis

A

corticosteroids
Immunosuppressants (such as azathioprine)
IV immunoglobulins
Biological therapy (such as infliximab or etanercept)

301
Q

Antiphospholipid syndrome pathology

A

hyper-coagulable state. The main associations are with thrombosis and complications in pregnancy, particularly recurrent miscarriage.

302
Q

Antiphospholipid syndrome associated with what autoantibodies

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

303
Q

Antiphospholipid syndrome Livedo reticularis refers too

A

a purple lace like rash that gives a mottled appearance to the skin.

304
Q

Antiphospholipid syndrome Libmann-Sacks endocarditis refers too

A

on-bacterial endocarditis where there are growths (vegetations) on the valves of the heart.

305
Q

Mx of anti-phospholipid syndrome

A

Long term warfarin with an INR range of 2-3 is used to prevent thrombosis. during pregnancy women are started on low molecular weight heparin.

306
Q

Sjogren’s Syndrome refers too and causes

A

autoimmune condition that affects the exocrine glands. It leads to the symptoms of dry mucous membranes, such as dry mouth, dry eyes and dry vagina.

307
Q

Sjogren’s is associated with what autoantibodies

A

anti-Ro and anti-La antibodies.

308
Q

Sjogren’s key examination test

A

Schirmer test (<10mm is significant)

309
Q

Mx of Sjogren

A

Artificial tears
Artificial saliva
Vaginal lubricants
Hydroxychloroquine is used to halt the progression of the disease.

310
Q

small vasculitis types

A

Henoch-Schonlein purpura
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
Microscopic polyangiitis
Granulomatosis with polyangiitis (Wegener’s granulomatosis)

311
Q

medium vessel vasculitis types

A

Polyarteritis nodosa
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
Kawasaki Disease

312
Q

large vessel vasculitis types

A

Giant cell arteritis

Takayasu’s arteritis

313
Q

presentation of vasculitis

A

Purpura. These are purple-coloured non-blanching spots caused by blood leaking from the vessels under the skin.
Joint and muscle pain
Peripheral neuropathy
Renal impairment
Gastrointestinal disturbance (diarrhoea, abdominal pain and bleeding)
Anterior uveitis and scleritis
Hypertension

314
Q

systemic features of vasculitis

A 
Fatigue
Fever
Weight loss
Anorexia (loss of appetite)
Anaemia
315
Q

Tests for vasculitis

A

Inflammatory markers (CRP and ESR), Anti neutrophil cytoplasmic antibodies (ANCA)

316
Q

p-ANCA (MPO antibodies) associated with

A

Microscopic polyangiitis and Churg-Strauss syndrome

317
Q

c-ANCA (PR3 antibodies) associated with

A

Wegener’s granulomatosis

318
Q

management of vasculitis is with

A 
steroids,
 Cyclophosphamide
Methotrexate
Azathioprine
Rituximab and other monoclonal antibodies
319
Q

Henoch-Schonlein Purpura (HSP) is what specific type of vasculitis

A

IgA

320
Q

four classic features of henoch-schonlein purpura is

A

purpura (100%), joint pain (75%), abdominal pain (50%) and renal involvement

321
Q

Eosinophilic granulomatosis with polyangiitis used to be called Churg-Strauss syndrome - presents with

A

lung and skin problems, often with severe asthma in later years

322
Q

characteristic blood finding with churg-strauss syndrome is

A

elevated eosinophil levels on the full blood count

323
Q

main feature of Microscopic polyangiitis is

A

renal failure effecting the lungs causing SOB and haemoptysis

324
Q

Granulomatosis with polyangiitis effects

A

respiratory tract and kidneys: epistaxis, hearing loss and sinuses causing sinusitis, saddle shaped nose, cough, wheeze, haemoptysis and glomerulonephritis

325
Q

Polyarteritis Nodosa is associated with

A

hepatitis B but can also occur without a clear cause or with hepatitis C and HIV.

326
Q

features of kawasaki disease

A

Clinical features are:

Persistent high fever > 5 days
Erythematous rash
Bilateral conjunctivitis
Erythema and desquamation (skin peeling) of palms and soles
“Strawberry tongue” (red tongue with prominent papillae)

327
Q

key complication of kawasaki disease is

A

coronary artery aneurysms

328
Q

coronary artery aneurysms Tx

A

aspirin and IV immunoglobulins.

329
Q

Takayasu’s arteritis can cause

A

aneurysms or become narrowed and blocked arteries

330
Q

the other name for Takayasu’s arteritis is

A

pulseless disease

331
Q

Takayasu’s arteritis present as

A

fever, malaise and muscle aches, or with more specific symptoms of arm claudication or syncope.

332
Q

Dx with takayasu’s disease is with

A

CT or MRI angiography. Doppler ultrasound of carotids.

333
Q

Behçet’s disease characteristic feature

A

recurrent genital and mouth ulcers

334
Q

Behçet’s skin presentation

A

Erythema nodosum
Papules and pustules (similar to acne)
Vasculitic type rashes

335
Q

Behçet’s eye presentation

A

Anterior or posterior uveitis
Retinal vasculitis
Retinal haemorrhage

336
Q

Behçet’s MSK presentation

A

Morning stiffness
Arthralgia
Oligoarthritis often affecting the knee or ankle. This causes swelling without joint destruction.

337
Q

Behçet’s veins presentation

A

Budd Chiari syndrome
Deep vein thrombosis
Thrombus in pulmonary veins
Cerebral venous sinus thrombosis

338
Q

Behçet’s CNS presentation

A

Memory impairment
Headaches and migraines
Aseptic meningitis
Meningoencephalitis

339
Q

Behçet’s investigation and method

A

pathergy test involves using a sterile needle to create a subcutaneous abrasion on the forearm. This is then reviewed 24 – 48 hours later to look for a weal 5mm or more in size. It tests for non-specific hypersensitive in the skin. It is positive in Behçet’s disease, Sweet’s syndrome and pyoderma gangrenosum.

340
Q

Behçet’s Mx

A

topical/systemic steroids, colchicine, topical anaesthetics, immunosupressants azathioprine and biologic therapy infliximab

341
Q

prognosis of Behcet’s

A

relapsing remitting condition

342
Q

gout pathology

A

crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing it to become hot, swollen and painful.

343
Q

what joint is most commonly affected in the hands with gout

A

DIP joints

344
Q

RF of gout

A 
Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history
345
Q

typical joints effected in gout

A

Base of the big toe (metatarsophalangeal joint)
Wrists
Base of thumb (carpometacarpal joints)

346
Q

aspiration of a gout joint will reveal

A

No bacterial growth
Needle shaped crystals
Negative birefringent of polarised light
Monosodium urate crystals

347
Q

joint presentation of gout on an X-ray

A

Typically the space between the joint is maintained
Lytic lesions in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanging edges

348
Q

acute gout flare Tx

A

NSAIDs (e.g. ibuprofen) are first-line
Colchicine second-line
Steroids can be considered third-line

349
Q

prophylaxis with gout is

A

Allopurinol is a xanthine oxidase inhibitor used for the prophylaxis of gout and lifestyle

350
Q

the rule for allopurinal prophylaxis is

A

wait until after an acute attack

351
Q

pseudogout is

A

crystal arthropathy caused by calcium pyrophosphate crystals (also called chondrocalcinosis)

352
Q

presentation with pseudogout

A

hot, swollen, stiff, painful knee. Other joints that are commonly affected are the shoulders, wrists and hips.

353
Q

pseudogout aspirated fluid will reveal

A

No bacterial growth
Calcium pyrophosphate crystals
Rhomboid shaped crystals
Positive birefringent of polarised light

354
Q

X-ray presentation of pseudogout

A

L – Loss of joint space
O – Osteophytes
S – Subarticular sclerosis
S – Subchondral cyst

Chondrocalcinosis is the classic xray change in pseudogout. It appears as a thin white line in the middle of the joint space caused by the calcium deposition.

355
Q

Mx for pseudogout

A 
NSAIDs
Colchicine
Joint aspiration
Steroid injections
Oral steroids
Joint washout (arthrocentesis) is an option in severe cases.
356
Q

RF for osteoporosis

A 
Older age
Female
Reduced mobility and activity
Low BMI (<18.5 kg/m2)
Rheumatoid arthritis
Alcohol and smoking
Long term corticosteroids
357
Q

fragility fracture risk assessment is with

A

FRAX tool

358
Q

T score of -1 to -2.5

A

osteopenia

359
Q

T score less than -2.5

A

osteoporosis

360
Q

T score less than 2.5 plus a fracture

A

osteoporosis

361
Q

Mx of osteoporosis

A 
Activity and exercise
Maintain a health weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption
362
Q

first line medication for osteoporosis for

A

Bisphosphonates such as Zolendronic acid 5 mg once yearly (intravenous)

363
Q

SE for bisphosphonates

A

Reflux and oesophageal erosions. Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this.
Atypical fractures (e.g. atypical femoral fractures)
Osteonecrosis of the jaw
Osteonecrosis of the external auditory canal

364
Q

osteomalacia pathophysiology

A

Inadequate vitamin D leads to a lack of calcium and phosphate in the blood. Since calcium and phosphate are required for the construction of bone, low levels result in defective bone mineralisation. Low calcium causes a secondary hyperparathyroidism as the parathyroid gland

365
Q

vitamin D is created by

A

cholesterol by the skin in response to the UV radiation

366
Q

presentation with vitamin D

A 
Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures
367
Q

Ix for osteomalacia

A

Serum 25-hydroxyvitamin D
Serum calcium is low
Serum phosphate is low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high (secondary hyperparathyroidism)
Xrays may show osteopenia (more radiolucent bones)
DEXA scan shows low bone mineral density

368
Q

Tx with osteomalacia

A

supplementary vitamin D

369
Q

Paget’s disease refers too

A

excessive bone turnover (formation and reabsorption) due to excessive activity of both osteoblasts and osteoclasts.

370
Q

presentation of Paget’s disease

A

Bone pain
Bone deformity
Fractures
Hearing loss can occur if it affects the bones of the ear

371
Q

X-ray findings for paget’s disease

A

Bone enlargement and deformity
“Osteoporosis circumscripta” describes well defined osteolytic lesions that appear less dense compared with normal bone
“Cotton wool appearance” of the skull describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
“V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone

372
Q

biochemistry for paget’s disease of bone

A

Raised alkaline phosphatase (and other LFTs are normal)
Normal calcium
Normal phosphate

373
Q

Mx for paget’s disease

A

bisphosphonates
NSAIDs for bone pain
Calcium and vitamin D supplementation, particularly whilst on bisphosphonates
Surgery is rarely required for fractures, severe deformity or arthritis

374
Q

two key complications for paget’s disease of bone

A 
Osteogenic sarcoma (osteosarcoma)
Spinal stenosis and spinal cord compression

fourth year (12 decks)

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