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Path Flashcards

1
Q

What is the deficiency in Haemophilia A?

A

Factor VIII

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2
Q

What is the deficiency in Haemophilia B?

A

Factor IX

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3
Q

What does the APTT, PT and bleeding time do in Haemophilia A?

A

APTT increases
PT normal
bleed time normal

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4
Q

Management in Haemophilia A?

A

Avoid NSAIDs and IM injections
Desmopressin (releases FVIII from vessel walls)
IV recombinant/plasma FVIII

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5
Q

Management in Haemophilia B?

A

IV Factor IX

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6
Q

Type 1 vWD is a qualitative or quantitative deficiency?

A

partial quantitative

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7
Q

Type 2 vWD is a qualitative or quantitative deficiency?

A

qualitative

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8
Q

Type 3 vWD is a qualitative or quantitative deficiency?

A

Total deficiency!!

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9
Q

What does the APTT do in vWD?

A

APTT increases

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10
Q

What does the INR do in vWD?

A

INR is normal.

INR is the PT, i.e. the extrinsic pathway, which is unaffected in vWD

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11
Q

What can you give in vWD?

A

Desmopressin (increases vWF release)

vWF/FVIII concentrates

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12
Q

Causes of disseminated intravascular coagulation?

A

“PTT GONe Mad”
Pancreatitis ???
Trauma
Transfusion (ABO incompatibility)

Gram negatives (i.e. sepsis)
Obstetric Complications (e.g. pre-eclampsia, amniotic fluid embolism or placental abruption)
Nephrotic syndrome???
Malignancy

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13
Q 
What happens to the following in DIC:
PT
FDP
Platelets
Fibrinogen
A

PT (INR) is prolonged
FDP (Fibrin degradation products) are raised. D-Dimer is a FDP so that can be raised too.
Platelets are low
Fibrinogen is low

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14
Q

Management of DIC?

A

Treat underlying cause

Consider transfusions, FFP, platelets, cryoprecipitate.

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15
Q

What does vitamin K activate?

A

Factors II, VII, IX, X

Protein C + S

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16
Q

Causes of DVT?

A

“SICC PT”

Surgery
Immobilisation
Cancer
Contraception

Pregnancy
Trauma

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17
Q

What to consider with heparin in antithrombin deficiency?

A

thrombin binds antithrombin to form thrombin-antithrombin complex (TAT) = anticoagulant.

Heparin enhances this binding. Need higher dose of heparin in people with AT deficiency.

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18
Q

What clotting factors does protein C inhibit?

A

V and VIII

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19
Q

What are the different types of Protein C deficiency?

A

Type 1 = Quantitative (Quan rhymes with 1!)

Type 2 = Qualitative

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20
Q

Management of Protein C deficiency?

A

prophylaxis in familial/previous clotters = LMWH, heparin or warfarin

Homozygous protein C defect = supplemental protein C concentrates. Liver transplant is supposedly curative.

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21
Q

What’s the inheritance pattern of Factor V Leiden?

A

Autosomal dominant with incomplete penetrance (i.e. not everyone who has the mutation will develop the disease)

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22
Q

What happens to APTT in FV Leiden and why?

A

APTT is low
Leiden variant is unable to be degraded by activated Protein C (which usually inhibits FV activity) therefore there is increased clotting.

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23
Q

Mechanism of heparin?

A

Potentiates Antithrombin III (AT) and inactivates thrombin as well as coagulation FIX, X and XI.

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24
Q

How is LMWH usually adminstered?

A

Subcut OD

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25
Q

How is unfractionated heparin usually administered?

A

IV, loading dose then infusion.

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26
Q

Side effects of heparin?

A

Bleeding
Heparin-induced thrombocytopenia
Osteoporosis

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27
Q

What is the antidote for heparin overdose?

A

Protamine sulfate

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28
Q

Mechanism of Warfarin?

A

Vitamin K antagonist which leads to reduced activation of Factors II, VII, IX and X. Plus proteins C and S.

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29
Q

What to use in warfarin reversal?

A

IV vitamin K

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30
Q

Typical target INR for a person on Warfarin?

A

2.0-3.0

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31
Q

Typical INR of a healthy person?

A

0.8-1.2

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32
Q

What investigation to order to definitively diagnose ALL, what are you looking for?

A

Bone marrow biopsy
Use Wright or Giemsa stain.
Looking for >20-30% lymphoblasts.

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33
Q

Management of ALL?

A

Steroid (prednisolone/dexamethasone) with chemo (vincristine, asparaginase)
CNS prophylaxis too
Hydration plus allopurinol - prevent formation of uric acid and hence tumour lysis syndrome
Antibiotic prophylaxis
Transfusion, if indicated

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34
Q

What is the role of consolidation therapy in ALL?

A

To eliminate clinically undetectable residual leukaemia, hence preventing relapse and the development of drug-resistant cells.

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35
Q

What is the goal of maintenance therapy in ALL?

A

eliminate minimal residual disease (MRD)

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36
Q

Complications of ALL and the chemo?

A

Quite a few, some include:

“PaNTInG”: Pancytopenia; Neutropenia; Tumour lysis syndrome; Infertility; Gastrointestinal Toxicity.

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37
Q

What is the induction chemotherapy of choice for acute promyelotic leukaemia?

A

oral tetinoin (aka all-trans-terinoic acid - ATRA)

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38
Q

What is the definitive diagnostic method for AML and what are you looking for?

A

Bone marrow biopsy/aspiration
>20% blast cells
Blast cells with granulated and Auer rod content

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39
Q

What is philadelphia chromosome?

A

Fusion oncogene, BCR-ABL, resulting from t(9;22)

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40
Q

In terms of blast cells in peripheral blood/BM, how is the accelerated phase defined?

A

10-20% blast cells

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41
Q

In terms of blast cells in peripheral blood/BM, how is the blast phase defined?

A

> 20% blast cells

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42
Q

What are the three phases of CML?

A

“CAB” like the Fresh Prince took a cab to Philadelphia

Chronic
Accelerated
Blast

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43
Q

What cell markers are you looking for in CLL?

A

CD5, CD19 and CD23 +ve

CD5 is usually found on T cells but can be expressed on B cells in CLL.

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44
Q

What might you see on a blood film in CLL?

A

Smudge/smear cells

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45
Q

What are good prognostic factors in CLL?

A

Low Zap-70 expression
13q14 deletion
hypermutated Ig gene

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46
Q

What are bad prognostic factors in CLL?

A

11q23 deletion
CD38 +ve
raised LDH

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47
Q

The Binet staging system is used for what condition?

A

CLL

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48
Q

The Rai staging system is used for what condition?

A

CLL

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49
Q

What autoantibodies are associated with SLE?

A 
Anti-dsDNA
Anti-Sm
Anti-nRNP
Anti-cardiolipin
Anti-Nuclear Antigens
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50
Q

What autoantibodies are associated with RA?

A

Anti-CCP
RF
Anti-Nuclear antigens

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51
Q

What autoantibodies are associated with Sjogren’s syndrome

A

Anti-Ro

Anti-La

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52
Q

What autoantibodies are associated with Wegener’s granulomatosis?

A

c-ANCA

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53
Q

What autoantibodies are associated with Microscopic polyangitis?

A

p-ANCA

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54
Q

What autoantibodies are associated with Diffuse cutaneous systemic sclerosis?

A

Anti-Scl 70 aka anti-topoisomerase I

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55
Q

What autoantibodies are associated with Polymyositis?

A

Anti-Jo1

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56
Q

What autoantibodies are associated with CREST syndrome?

A

Anti-centromere

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57
Q

What autoantibodies are associated with drug induced lupus?

A

Anti-histone

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58
Q

ACR criteria for diagnosing SLE? (mnemonic!)

A 
Need 4 out of the 11:
"A RASH POINts MD"
Arthritis
Renal disease (proteinuria, cast cells)
ANA positive
Serositis (pleurisy/pericarditis)
Haematological disorders (haemolytic anaemia, leucopenia, lymphopenia, thrombocytopenia)
Photosensitivity
Oral ulcers
Immunological disorder (Anti-Sm, Anti-dsDNA, Anti-ANA, Anti-cardiolipin, AntinRNP)
Neurological (seizures/psychosis in absence of other diagnosis)
Malar rash
Discoid rash
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59
Q

What are the antibodies associated with limited cutaneous systemic sclerosis?

A

ANA

Anti-centromere/nucleolar patterns

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60
Q

What does CREST stand for?

A 
Calcinosis
Raynaud's
Esophageal symptoms
Sclerodactyly
Telangiectasia
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61
Q

What are patients with Sjogren’s syndrome at risk of developing?

A

Non-Hodgkin’s Lymphoma

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62
Q

Clinical features of henoch schonlein purpura?

A

Nephropathy (IgA)
Arthritis
GIT disturbances
Extensor surface (arm/legs) rash

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63
Q

What ‘size’ of vasculitis is Takayasu’s arteritis?

A

Large - it affects places like the aorta

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64
Q

What ‘size’ of vasculitis is Giant-cell arteritis?

A

Large - places like the temporal artery

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65
Q

What ‘size’ of vasculitis is Polyarteritis nodosa?

A

Medium - renal and lung involvement

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66
Q

What ‘size’ of vasculitis is Kawasaki’s disease?

A

Medium

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67
Q

What ‘size’ of vasculitis is Buerger’s disease?

A

Medium - arteries of extremities

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68
Q

What ‘size’ of vasculitis is Wegener’s granulomatosis?

A

Small

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69
Q

What ‘size’ of vasculitis is Churg-Strauss syndrome?

A

Small

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70
Q

What ‘size’ of vasculitis is Microscopic polyangiitis?

A

Small

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71
Q

What ‘size’ of vasculitis is Henoch Schonlein Purpura?

A

Small

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72
Q

What vascular signs might a person with Takayasu’s arteritis have on examination?

A

Absent pulse with bruits and claudication

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73
Q

What histopathological findings might you find with Temporal arteritis?

A

Granulomatous transmural inflammation
Giant cells
Skip lesions

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74
Q

What infection is polyarteritis nodosa associated with?

A

Hep B

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75
Q

What might you find on angiography in a patient with polyarteritis nodosa?

A

microaneurysms

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76
Q

What is strongly associated with Buerger’s disease?

A

Smoking

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77
Q

What are typical signs and symptoms of Buerger’s disease?

A

Pain and claudication upon walking

Inflammation and thrombosis affects vessels of hands and feet

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78
Q

What appearances might you see on angiograms in patients with Buerger’s disease?

A

corkscrew appearances

tree root or spider leg appearances

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79
Q

What is the triad of findings in a patient with Wegener’s granulomatosis?

A

Upper respiratory tract: sinusitis, epistaxis, saddle nose
Lower respiratory tract: cavitation, pulmonary haemorrhage
Kidneys: crescentic glomerulonephritis

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80
Q

What immunological finding would increase your suspicion of Wegener’s granulomatosis?

A

cANCA anti-proteinase3 positive

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81
Q

What findings make up Churg Strauss?

A

Asthma
Allergic rhinitis
Eosinophilia

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82
Q

What immunological finding would increase your suspicion of Churg Strauss?

A

pANCA anti-myeloperoxidase positive

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83
Q

What syndrome can you see in microscopic polyangitis?

A

Pulmonary renal syndrome:

  • Pulmonary haemorrhage
  • Glomerulonephritis
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84
Q

What immunological finding would increase your suspicion of microscopic polyangitis?

A

pANCA anti-myeloperoxidase positive

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85
Q

What age and gender does Hodgkin’s lymphoma tend to affect?

A

M>F

bimodal age incidence 20-29 and >60 year olds

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86
Q

What are the risk factors for Hodgkin’s lymphoma?

A

history of EBV infection

Family history

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87
Q

What are the symptoms of Hodgkin’s lymphoma?

A

Painless lymphadenopathy +/- obstructive symptoms
B symptoms: Fever; lethargy; weight loss; night sweats
Pain in nodes after alcohol

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88
Q

What is Pel-Ebstein fever?

A

A cyclical fever which intensifies and remits over a typically 2 week period, it is associated with Hodgkin’s lymphoma.

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89
Q

What specific investigations would you order for Hodgkin’s lymphoma?

A

PET/CT scan - establish baseline extent

lymph node biopsy - characteristic Reed-Sternberg cells

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90
Q

How is Hodgkin’s lymphoma staged?

A

Stage 1: one LN region (LN region can include spleen)
Stage 2: two or more LN regions on the same side of the diaphragm
Stage 3: two or more LN regions on opposite sides of the diaphragm
Stage 4: extranodal sites (liver, BM)

A: No constitutional symptoms
B: Constitutional symptoms

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91
Q

What treatment can you give for patient’s with Hodgkin’s lymphoma?

A

ABVD chemotherapy

  • Adriamycin (aka doxorubicin)
  • Bleomycin
  • Vinblastine
  • Dacarbazine
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92
Q

Which lymphoma type produces pain after alcohol?

A

Hodgkin’s lymphoma

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93
Q

What are the hallmark cells of Anaplastic large cell lymphoma associated with?

A

CD30
Clusterin
Characteristic golgi staining
Alk-1 protein expression

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94
Q

What are the risk factors for adult T cell lymphoma?

A

Caribbean and Japanese

HTLV-1 infection

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95
Q

What is a risk factor for enteropathy-associated T cell lymphoma?

A

longstanding coeliac disease

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96
Q

What is a risk factor for cutaneous T cell lymphoma?

A

Mycosis fungoides

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97
Q

What are the three main clinical variants of Burkitt’s lymphoma? What patient population do they typically affect and where is the site of lymphoma usually?

A

Endemic - children living in malaria endemic regions. Jaw/facial bone, ileum/cecum, ovaries, kidney, breast.

Sporadic - non-Malaria endemic regions. Jaw less commonly involved, ileocaecal region more so.

Immuno-deficiency - associated with HIV or post-transplant.

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98
Q

What typical histological appearance can be seen with Burkitt’s lymphoma?

A

“Starry sky” appearance

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99
Q

What age group does diffuse large B cell lymphoma tend to affect?

A

middle aged and >60

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100
Q

What is Richter’s transformation?

A

Conversion of CLL to diffuse large B-cell lymphoma

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101
Q

What histological finding can be seen in diffuse large B-cell lymphoma?

A

“sheets of large lymphoid cells”

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102
Q

What genetic factor is mantle cell lymphoma associated with and what is the implication of that genetic factor?

A

t(11;14) - overexpression of cyclin D1

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103
Q

What genetic factor is follicular lymphoma associated with and what is the implication of that genetic factor?

A

t(14;18) - overexpression of the bcl-2 gene which is therefore anti-apoptotic

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104
Q

What histological findings might you see in follicular lymphoma?

A

“follicular pattern or nodular appearance”

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105
Q

What are two risk factors for mucosal associated lymphoid tissue lymphoma?

A

H. pylori –> gastric MALT lymphoma

Sjogren’s syndrome –> parotid lymphoma

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106
Q

What is the affected cell type in multiple myeloma?

A

plasma cells

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107
Q

What is paraprotein?

A

a monoclonal immunoglobulin

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108
Q

What are the clinical features of multiple myeloma?

A

“CRAB”
Caclium high - stones, bones, moans, groans and thirst
Renal failure - plus amyloidosis + nephrotic syndrome
Anaemia + pancytopenia
Bones - pain, osteoporosis, osteolytic lesions, fractures

+hyperviscosity

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109
Q

What specific investigations would you order for multiple myeloma?

A

serum electrophoresis - looking for narrow band

Blood film - rouleaux (RBC stacking)

Urine - Bence Jones protein

ESR - v high

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110
Q

What staging system is used for multiple myeloma?

A

Durie-Salmon

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111
Q

What are risk factors for multiple myeloma?

A

monoclonal gammopathy of undetermined significance (MGUS)

Obesity

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112
Q

What are the values of plasma cells in BM for Multiple Myeloma, Smouldering myeloma and for MGUS?

A

MM: >10% in BM
MGUS: 10%

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113
Q

What would the serum paraprotein levels be for smouldering myeloma and for MGUS?

A

Smouldering: >30g/L
MGUS:

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114
Q

What is the pathological factor that contributes to Waldenstrom’s macroglobulinaemia?

A

IgM that infiltrates LNs and BM

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115
Q

What are the symptoms of Waldenstrom’s macroglobunlinaemia?

A 
weakness
fatigues
weight loss
vision changes
confusion
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116
Q

How would you treat Waldenstrom’s macroglobunlinaemia?

A

plasmapheresis for hyperviscosity

chemotherapy

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117
Q

What are the 4 C’s of Wegener’s Granulomatosis?

A
  • cANCA
  • corticosteroids
  • cyclophosphamide
  • crescentic glomerulonephritis

Think of Wegener’s as Wecener’s!

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118
Q

How do Wegener’s and Microscopic polyangiitis differ in the regions of the body affected?

A

Wegener’s - upper respiratory tract down to lungs with kidneys

MPA - No upper resp tract but still involves lungs and kidneys

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119
Q

Using ANCAs - how can we tell the difference between Wegener’s and microscopic polyangiitis?

A

Wegener’s - cANCA

MPA - pANCA

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120
Q

What is different between biopsies in patients with Wegener’s and microscopic polyangiitis?

A

No granulomas formed in MPA unlike Wegener’s.

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121
Q

How can chronic bronchitis be defined clinically?

A

Cough and sputum on most days for 3 months over 2 years

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122
Q

What are the histological features of chronic bronchitis?

A

Dilatation of the airways
Goblet cell hyperplasia
Mucous gland hypertrophy

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123
Q

Dilatation of the airways, goblet cell hyperplasia and mucous gland hypertrophy are histological features of what condition?

A

Chronic bronchitis

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124
Q

What are Curschmann spirals and what condition do they indicate?

A

spiral shaped mucus plugs from subepithelial mucous glands - seen in asthma (but also other lung disease)

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125
Q

What condition are Charcot-Leyden crystals seen in?

A

eosinophilic conditions like allergies or asthma

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126
Q

What are the characteristic histopathologic findings seen in idiopathic pulmonary fibrosis?

A
  • Interstitial fibrosis in a “patchwork pattern”
  • honeycomb change
  • fibroblast foci
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127
Q

What is the pathogenesis of “honeycomb change”

A

Hyperplasia of type II pnemocytes causing cyst formation

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128
Q

Name the four stages of lobar pneumonia.

A
  1. Congestion - first 24 hours, vascular engorgement, intra-alveolar fluid, neutrophils and bacteria.
  2. Red hepatization or consolidation - red cells extravasate into alveolar spaces. Exudate consolidates alveolar parenchyma.
  3. Grey hepatization - red cells disintegrate
  4. Resolution - exudate cleared
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129
Q

What are risk factors for squamous cell carcinoma?

A

being Male

smoking

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130
Q

What region of the lung does squamous cell carinoma tend to affect?

A

Proximal bronchi

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131
Q

Describe the progression of squamous cell carinoma of the lung beginning with epithelium.

A
  1. Epithelium
  2. Hyperplasia
  3. Squamous metaplasia
  4. angiosquamous dysplasia (B.M. thickening)
  5. carcinoma in situ
  6. invasive carcinoma
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132
Q

What histological features might you see with squamous cell carcinoma?

A 
Keratinsation
intercellular prickles (desmosomes)
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133
Q

A lung biopsy shows keratinisation with intercellular prickles. What could this be?

A

Squamous cell carcinoma

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134
Q

What region of the lung do adenocarcinomas tend to affect?

A

The peripheral regions

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135
Q

how do SCCs and adenocarcinomas compare in terms of when they metastasise in the lung?

A 
SCCs = late
adenocarcinomas = early
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136
Q

What histological appearance do lung adenocarcinomas tend to have?

A

Glandular differentiation with mucin production

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137
Q

What is the most common gene mutation in lung adenocarcinomas?

A

EGFR

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138
Q

What is the typical progression of lung adenocarcinomas, starting from ‘atypical adenomatous hyperplasia’.

A
  1. Atypical adenomatous hyperplasia
  2. non-mucinous bronchoalveolar carcinoma (BAC)
  3. mixed-pattern adenocarcinoma
139
Q

What are the main different types of non-small cell lung cancers?

A

Adenocarcinoma
Squamous Cell Carcinoma
Large cell carcinoma

140
Q

What are the cytological appearances of the cells in Large Cell Carcinoma?

A

Large cell size
Higher cytoplasmic to nuclear size ratio
Lack of salt-and-pepper chromatin

141
Q

What histological appearance do large cell carcinomas have?

A

LCC is a diagnosis of exclusion so they do not have the appearance of other non-SCLCs, i.e. no glandular or squamous differentiation

142
Q

What region of the lung does small cell carcinoma tend to affect?

A

Central airways, proximal bronchi

143
Q

What cell type do small cell lung cancers arise from?

A

neuroendocrine

144
Q

What are two paraneoplastic syndromes associated with small cell lung cancer?

A

SIADH

Lambert-Eaton myasthenic syndrome (proximal leg+arm weakness relieved through use)

145
Q

What genetic mutations are common in small cell carcinomas?

A

p53

RB1

146
Q

p53 and RB1 genetic mutations, common in what type of lung cancer?

A

small cell lung cancer

147
Q

How do you interpret the following result from a dexamethasone test:

Low ACTH
Cortisol not suppressed by high or low dose dex

A

Cushing’s syndrome (anything but pituitary)

148
Q 
How do you interpret the following result from a dexamethasone test:
Elevated ACTH (in hundreds)
Cortisol not suppressed by high or low dose dex
A

Ectopic ACTH production, e.g. adrenal/chest/abdo tumour

149
Q

How do you interpret the following result from a dexamethasone test:
Normal or slightly elevated ACTH
Cortisol not suppressed by low dose dex
Cortisol suppressed by high dose dex

A

Cushing’s disease because pituitary still retains some feedback control

150
Q

How can the causes of Addison’s disease be categorised?

A

Adrenal dysgenesis - genetic abnormalities
Impaired steroidogenesis - genetic/enzyme problems
Adrenal destruction - autoimmune/TB

151
Q

What effect does aldosterone have on electrolytes and fluid?

A

Increase Na and water retention

Deplete plasma K

152
Q

What is the mechanism behind the metabolic acidosis in Addison’s Disease?

A

Addison’s –> low aldosterone –> reduced reabsorption of Na in distal tubule therefore increased H+ retention in serum

153
Q

What test for Addison’s disease?

A

synACTHen test

154
Q

Describe the two tests involved in the synACTHen test

A
  1. Short test: measure cortisol before and after admin IM 250mcg synacthen. 1 hour later cortisol levels should reach designated threshold level ~700nmol/l. If normal, it excludes primary adrenal failure. If abnormal, need to do long test ….
  2. Long test: 1mg IM synacthen. Measure cortisol at 1, 4, 8 and 24 hours. Normal should reach 1000nmol/l by 4 hours. In primary adrenal failure = reduced at all stages. In secondary corticoadrenal insufficiency it is delayed but normal response seen.
155
Q

What are the high uptake hyperthyroid conditions?

A

Graves
Toxic multinodular goitre (uneven uptake)
Toxic adenoma (hot nodule)

156
Q

What are the low uptake hyperthyroid conditions?

A 
Subacute DeQuervains thyroiditis (think, 'sub' = below)
Postpartum thryoiditis (think, they'll be tired after labour so too tired to take up)
157
Q

A ‘hot nodule’ on radioactive iodine uptake test indicates what condition?

A

toxic adenoma

158
Q

What are the autoimmune variants of hypothyroidism?

A

Primary atrophic hypothyroidism

Hashimotos thyroiditis

159
Q

What is the normal range for the anion gap?

A

14-18mmol/l

160
Q

What is the mnemonic for elevated anion gap metabolic acidosis?

A

“KULT”

  • Ketoacidosis
  • Uraeamia (Renal Failure)
  • Lactic acidosis
  • Toxins (ethylene glycol, methanol, paraldehyde, salicylate)
161
Q

Asparate aminotransferase is found in which part of the liver?

A

Hepatocytes

162
Q

Alanine aminotransferase is found in which part of the liver?

A

Hepatocytes

163
Q

Alkaline phosphatase is found in which part of the liver?

A

Bile canaliculi

164
Q

AST:ALT = 1 is associated with what?

A

ischaemia (CCF and ischaemic necrosis/hepatitis)

165
Q

AST:ALT >2.5 is associated with what?

A

Alcoholic hepatitis

166
Q

AST:ALT

A

Hepatocellular damage
Paracetamol overdose with hepatocellular necrosis
Viral hepatitis, ischaemic necrosis, toxic hepatitis

167
Q

What would you expect the AST:ALT to be in alcoholic hepatits?

A

> 2.5 (basically raised)

168
Q

What would you expect the AST:ALT to be in toxic/viral hepatitis?

A
169
Q

What can cause increased ALP?

A

Liver - biliary obstruction (e.g. malignancy/infection)
Pregnancy (non-pathological) - released from placenta in late pregnancy
Hyperparathyroidism
Bone - Osteomalacia; bone metastasis; Pagets disease; Deficiency induced Ricket’s
Blood type O and B (non-pathological) release from small intestine after fatty meal
and many more!

170
Q

Normal range of AST?

A
171
Q

Which is more specific for liver damage - AST or ALT?

A

ALT (It’s got ‘L’ for liver in it)

172
Q

Normal range for ALT?

A
173
Q

Normal range for ALP?

A

30-150iu/L

174
Q

Normal range for GGT?

A

30-150iu/L

175
Q

What dye can be used to measure hepatic perfusion levels?

A

Indocyanine green

176
Q

What is indocyanine green used for?

A

Measuring hepatic/splanchnic perfusion

177
Q

What is Bromsulphthalein used for?

A

A dye used to measure liver function - measuring the rate of removal of the dye.

178
Q

What body system do acute porphyrias usually affect?

A

Nervous system

179
Q

What are the major symptoms of a porphyria’s acute attack?

A

abdominal pain
vomiting
hypertension
tachycardia

180
Q

What two distinct patterns are there of skin disease seen in the cutaneous porphyrias?

A 
Immediate photosensitivity (pain, burning, discomfort but not always visible)
Vesciulo-erosive skin disease (blistering and open sores)
181
Q

What enzyme is deficient in Porphyria Cutanea Tarda?

A

Uroporphyrinogen decarboxylase

182
Q

What enzyme is deficient in Acute Intermittent Porphyria?

A

Hydroxymethylbilane synthase

183
Q

Which acute porphyrias have skin lesions?

A

Hereditary coproporphyria

Variegate porphyria

184
Q

What enzyme is deficient in hereditary coproporphyria?

A

Coproporphyrinogen oxidase

185
Q

What enzyme is deficient in variegate porphyria?

A

Protoporphyrinogen oxidase

186
Q

What dietary measures should be taken in an acute attack of porphyria?

A

High carbohydrate diet, in severe cases a dextrose infusion

187
Q

What are skin features in guttate psoriasis and what is the onset/resolve time?

A

multiple small scaly plaques - ‘tear drops’ - on the trunk and arms.

Quick onset following an infection, typically streptococcal throat, which will usually resolve spontaneously completely.

188
Q

Name that derm condition:

Thick, silvery-white scale over well-defined red thickened skin located on the back of the head.

A

Scalp Psoriasis

189
Q

Treatment for scalp psoriasis?

A

Shampoos , e.g. coal tar or antifungal shampoos.
Short hair - helps treatment application
Phototherapy

190
Q

What is subungal hyperkeratosis?

A

Scaling under the nail due to excessive proliferation of keratinocytes in the nail bed and hyponychium

191
Q

What are the two types of plaque psoriasis?

A

Large plaque psoriasis

Small plaque psoriasis

192
Q

What are the plaques like in Large plaque psoriasis?

A

thick, well-demarcated, red with silvery scale.

193
Q

What are the plaques like in Small plaque psoriasis?

A

numerous small (mm to few cm) thin, pinkish with a fine scale

194
Q

How do Large and Small plaque psoriasis compare in terms of: age of onset; family history; treatment options.

A

Large plaque: early onset (under 40); positive family history; treatment resistant.

Small plaque: Any age (usually over 40); less relevant family history; responds well to phototherapy

195
Q

How does flexural psoriasis look compared to typical psoriasis?

A

Usually no silvery scale - instead is shiny and smooth.
Possibly a fissure in skin crease

Still has deep red colour and well-defined borders

196
Q

What health conditions are associated with psoriasis?

A 
Psoriatic arthritis
IBD
Uveitis
Coeliac disease
Metabolic syndrome (obesity, hypertension, hyperlipidaemia, T2DM
Pustulosis
197
Q

What is Auspitz’s sign?

A

bleeding spots when psoriasis scales are scraped off

198
Q

What is koebner phenomenon?

A

When skin lesions form at sites of trauma

199
Q

What are the characteristic histological findings in psoriasis?

A

Rete ridges

Epidermal thickening

Munro’s microabscesses

Granular layer loss

Parakeratosis

200
Q

What are Rete Ridges?

A

epidermal projections that extend into the underlying dermis - seen in psoriasis

201
Q

What is Munro’s microabscess?

A

Abscess in the stratum corneum of the epidermis due to infiltration of neutrophils from papillary dermis - cardinal sign of psoriasis.

202
Q

What is the PASI score?

A

Psoriasis Area and Severity Index (PASI) score

203
Q

What treatment options are there for a person with psoriasis?

A

Conservative: stop smoking; drink less; maintain optimal weight.

Medical:

  • Topical: emollients, coal tar; salicylic acid; steroids
  • Phototherapy
  • If severe, methotrexate or ciclosporin
  • avoid systemic steroids because of withdrawal flare risk
  • biologics like infliximab reserved for severe treatment resistant variants
204
Q

What can precipitate erythrodermic psoriasis?

A

Infections; low calcium; steroid withdrawal; strong coal tar preparations; excess alcohol

205
Q

Treatment for erythrodermic psoriasis?

A

Hospitalisation - fluids and temperature regulation
Bed rest
Emollients and wet dressings
Low-dose methotrexate or ciclosporin
Treat complications - Abx, diuretics, etc.

206
Q

What are the six P’s of Lichen Planus?

A 
Lesions are :
Pruritic 
Purple
Polygonal
Papules
Plaques
Mother-of-Pearl sheen
207
Q

What are Wickham striae?

A

fine white lines that cross the plaques in Lichen Planus

208
Q

Where is Lichen Planus usually distributed?

A

Front of wrists
Lower back
Ankles

209
Q

You look inside the patient’s mouth and see white streaks in a lacy pattern which are painless along with painful erosions and inflammation. What is the diagnosis?

A

Oral lichen planus with erosions

210
Q

What histological appearances might you see with lichen planus?

A

hyperkeratosis with saw-toothing of rete ridges

211
Q

Rete ridges are histological findings in what condition? and saw-toothing rete ridges?

A

Rete ridges = psoriasis

Saw-toothing rete ridges = lichen planus

212
Q

What treatment is there for lichen planus?

A

topical steroids

topical retinoids

213
Q

What is the prognosis for lichen planus?

A

Cutaneous form likely to clearly within a couple of years - unpredictable.

Oral - persist for a decade or so.

214
Q

What can trigger erythema multiforme?

A

Infection with HSV (commonly 1 rather than 2) or Mycoplasma pneumoniae

Drugs - v. uncommon e.g. penicillins, salicylates.

215
Q

What is the clinical progression of the erythema multiforme skin lesions? What characteristic lesions can be seen? What area of the body does it affect?

A

erupt within 24 hours and evolve over 72 hours.

demarcated, red/pink macules –> papules –> plaques which eventually develop blistering/crusting.

Target lesions: dusky centre, paler middle ring, outer bright ring.

Start peripherally then to trunk
a/w pruritis

216
Q

Target lesions are associated with what condition?

A

Erythema Multiforme

217
Q

Who gets Erythema multiforme?

A

Usually the young adults (20-40s) but anyone can.

M>F

218
Q

What might a skin biopsy of erythema multiforme show?

A

apoptotic keratinocytes

blisters within/under the epidermis

219
Q

What is the treatment for Erythema Multiforme?

A

Rash usually settles over few weeks

Treat any underlying cause (aciclovir for HSV, erythromycin for M pneumoniae)

Supportive

220
Q

What condition is associated with dermatitis herpetiformis?

A

Coeliac disease

221
Q

What are the risk factors for dermatitis herpetiformis?

A

Predominantly caucasian 15-40 year olds

M>F

222
Q

Dermatitis Herpetiformis has associations with which HLAs?

A

DQ2 and DQ8

223
Q

What’s the pathophysiology of dermatitis herpetiformis?

A

Dermal autoantibodies similar to those seen in Coeliac

224
Q

What are the clinical features of dermatitis herpetiformis?

A

Itchy vesicles in groups on the scalp, shoulders, buttocks, elbows or knees.

225
Q

What might you see on histology for dermatitis herpetiformis?

A

subepidermal bullae

IgA deposits at tips of dermal papillae

226
Q

What treatment would you give for dermatitis herpetiformis?

A

Gluten-free diet

Dapsone (it’s a sulphone antibiotic) to reduce itch

227
Q

What causes the bullae in pemphigoid?

A

IgG binding the hemidesmosomes of the epidermal basement membrane –> subepidermal bullae

228
Q

How do the location of bullae in pemphigoid and pemphigus differ?

A

Pemphigoid bullae are subepidermal (PemphigoiD = Deep)

Pemphigus bullae are intraepidermal (PemphiguS = Superficial)

229
Q

What are the clinical features of Pemphigoid?

A

Large tense bullae which rupture –> crusted erosions
Severe itch
Usually affects skin fold areas

230
Q

What histological findings might there be in pemphigoid?

A

Subepidermal bullae with eosinophils

Linear deposition of IgG along the basement membrane

231
Q

You see a skin biopsy come back with subepidermal bullae with eosinophils and deposits of IgG. What’s the diagnosis?

A

Pemphigoid

232
Q

What causes the bullae in Pemphigus?

A

IgG binding desmosomal proteins

233
Q

How do Pemphigoid and Pemphigus differ in terms of how readily the bullae rupture?

A

Pemphigoid - difficult to rupture

Pemphigus - easily ruptured

234
Q

Where can the bullae of pemphigus be found?

A

skin and mucosa

235
Q

What ages tend to get seborrhoeic keratoses?

A

begin 30s/40s

Most people over 60 have them

236
Q

Where can seborrhoeic keratoses be found/not found on the body?

A

Any area of skin except palms, soles and mucous membranes

237
Q

What colour do seborrhoeic keratoses tend to have?

A

Yellow to brown to black

238
Q

What dermatoscopic findings would suggest a seborrhoeic keratosis?

A

orange or brown clods
white ‘milia-like’ clods
curved thick ridges and furrows forming a brain-like pattern

239
Q

Seborrhoeic Keratosis is classified as benign, premalignant or malignant?

A

benign

240
Q

Actinic keratosis is classified as benign, premalignant or malignant?

A

premalignant

241
Q

Keratoacanthoma is classified as benign, premalignant or malignant?

A

premalignant

242
Q

Bowen’s Disease is classified as benign, premalignant or malignant?

A

premalignant

243
Q

What’s are risk factors for developing actinic keratosis?

A

Sun exposure - geography/photoageing/sunburn/fair skin

Poor immune function

244
Q

What’s the mechanism for development of actinic keratosis?

A

DNA damage by UVB

245
Q

What region of the body do actinic keratoses tend to form?

A

Sun-exposed areas, e.g. back of hands, face, balding scalp

246
Q

What appearance do actinic keratoses tend to have?

A

Flat/thickend papule or plaque
White/yellow, scaly, warty surface
Skin coloured/pigmented
Tender/asymptomatic

247
Q

What is the main concern with actinic keratoses?

A

Development of squamous cell carcinoma

248
Q

A Rosette sign is seen on dermoscopy, what condition does this suggest?

A

Actinic Keratosis

249
Q

What dermoscopic features might you see in actinic keratosis?

A

Rosette sign - four bright white points like a four leaf clover

250
Q

What are the histological features of actinic keratosis?

A 
"SPAIN"
Solar elastosis 
Parakeratosis 
Atypia/Dysplasia
Inflammation
Not full thickness
251
Q

What is solar elastosis?

A

Accumulation of elastin in the dermis

252
Q

What is parakeratosis?

A

Keratinisation characterised by retention of nuclei in the stratum corneum.

253
Q

What type of cells do keratoacanthomas arise from?

A

hair follicle skin cells

254
Q

A small pimple that grows rapidly to about 2cm with a central crusted area on a region of sun-damaged skin is suggestive of what?

A

Keratoacanthoma

255
Q

How can keratoacanthomas present?

A

Rapidly growing nodule
Central crusted region
Located on sun-damaged skin

256
Q

How can you treat keratoacanthomas?

A

Removal with cryotherapy, curettage and cautery, excision or radiotherapy.

257
Q

Why should you treat keratoacanthomas?

A

Obtain pathology - r/o SCC

Cosmetic - get rid of ugly lesion and minimise scar which can be worse if left to spontaneously resolve

258
Q

What is Bowen’s disease?

A

Intra-epidermal squamous cell carcinoma in situ

259
Q

What are risk factors for Bowen’s Disease?

A

sun exposure
arsenic ingestion
HPV infection
Immunosuppression

260
Q

What are the clinical features of Bowen’s disease?

A

one or more (asymmetrical) irregular scaly plaques, red/pigemented

261
Q

What dermoscopic features support a diagnosis of Bowen’s disease?

A

crops of rounded/coiled blood vessels

262
Q

What histological findings would support a diagnosis of Bowen’s disease?

A

full thickness dysplasia of the epidermis - no dermis involvement

263
Q

What is your main concern with Bowen’s disease?

A

development of invasive SCC

264
Q

What layers of the skin does SCC affect?

A

Derived from epidermis and has invaded beyond, i.e. to the dermis.

265
Q

Which gene mutation is commonly associated with SCC?

A

mutation of the p53 tumour suppression gene

266
Q

What are the clinical features of SCC?

A

enlarging scaly/crusted lumps arising from pre-existing actinic keratosis/Bowen’s disease.

Located on sun-exposed areas
May be tender/painful
May ulcerate

267
Q

What is known as a rodent ulcer?

A

Basal Cell Carcinoma

268
Q

What are the main clinical characteristics of a basal cell carcinoma?

A

Slow growing plaque or nodule
Skin coloured, pink/pigmented
Spontaneous bleeding/ulceration

269
Q

What histological features are typical of basal cell carcinomas?

A

Mass of basal cells pushing down into dermis

Palisading - nuclei align in outermost layer

270
Q

A ‘buckshot’ appearance is associated with what condition? and what is this appearance

A

Melanoma

atypical epithelioid melanocytes found singly or in clusters scattered throughout the epidermis

271
Q

A mass of basal cells pushing down into the dermis are features associated with what condition?

A

basal cell carcinoma

272
Q

Breslow thickness is used for what?

A

Staging melanoma

273
Q

What system can we use for staging Melanoma?

A

Breslow thickness

274
Q

Where does lentigo maligna melanoma occur?

A

Sun-exposed areas

275
Q

What age group does nodular malignant melanoma tend to affect?

A

younger folks

276
Q

Where does acral lentiginous melanoma tend to affect?

A

Palms, soles and subungal areas

277
Q

What triggers Stevens Johnson Syndrome/Toxic Epidermal Necrolysis?

A

Reactions to Drugs/Medications - technically any but some are more common than others, e.g. antibiotics or anticonvulsants

278
Q

What are the clinical symptoms of Stevens Johnson Syndrome?

A

Prodromal ‘flu-like’ illness (fever, sore throat, aches)

Abrupt onset of tender/painful red skin rash on the trunk which extends rapidly to limbs and face - usually reached a max by 4 days

Blisters –> sheets of skin detachment with oozing dermis.

279
Q

What is Nikolsky sign and what condition is it associated with?

A

Blisters/erosions appear in response to gentle skin rubbing.

A/w Stevens Johnson Syndrome

280
Q

How do the classifications of Stevens Johnson Syndrome and Toxic Epidermal Necrolysis compare?

A

SJS = Skin detachment less than 10% body surface area

TEN = detachment greater than 30%

281
Q

What blood test can be predictive of Stevens Johnson Syndrome/Toxic Epidermal Necrolysis?

A

elevated serum granulysin

282
Q

Elevated serum granulysin in the first few days of a drug eruption may indicate what?

A

Stevens Johnson Syndrome/Toxic Epidermal Necrolysis

283
Q

What are the histopathological features of Stevens Johnson Syndrome/Toxic Epidermal Necrolysis?

A

Keratinocyte necrosis
Full thickness epidermal necrosis
Minimal inflammation
Negative antibodies

284
Q

Keratinocyte necrosis, full thickness epidermal necrosis, minimal inflammation and negative antibodies on a skin biopsy indicate what condition?

A

Stevens Johnson Syndrome/Toxic Epidermal Necrolysis

285
Q

The SCORTEN system is used for what condition?

A

Stevens Johnson Syndrome/Toxic Epidermal Necrolysis

286
Q

How to treat Stevens Johnson Syndrome?

A 
Cease suspected causative drug
Admit
Nutritional and fluid support
Temperature maintenance
Analgesia
287
Q

What triggers pityriasis rosea?

A

viral illness

288
Q

How might pityriasis rosea present clinically?

A

Post-viral illness
Herald patch - oval pink/red plaque with scale inside the edge
Secondary rash in Christmas tree distribution - scaly patches/plaques appear on chest and back

289
Q

What does a herald patch look like and what condition is it associated with?

A

Oval pink/red plaque with a scale inside the edge.

Pityriasis Rosea

290
Q

What is the causative agent in erythema infectiosum?

A

Parvovirus B19

291
Q

Parvovirus B19 causes which condition?

A

Erythema infectiosum

292
Q

What is the treatment for erythema infectiosum?

A

Supportive

293
Q

Can children with erythema infectiosum go to school?

A

yes

the infectious stage has passed by the time the rash is evident.

294
Q

What age do infants typically develop seborrhoeic dermatitis and when will it usually resolve?

A

Less than 3 months, resolve by 6-12 months.

295
Q

What are the clinical features of infantile seborrhoeic dermatitis?

A

Cradle cap (diffuse, greasy scaling on scalp)
Salmon-pink patches that may flake or peel
Non-itchy, i.e. calm baby

296
Q

How do you treat infantile seborrhoeic dermatitis?

A

Reassurance
Regular washing with baby shampoo
Emollient during nappy changes

297
Q

What causes molluscum contaiosum?

A

Poxvirus - molluscum contagiosum virus

298
Q

How can molluscum contagiosum be spread?

A

Skin-to-skin contact
shared towels/other items
Auto-inoculation by scratching into another site
Sexual transmission in adults

299
Q

What is the incubation period for molluscum contagiosum?

A

2 weeks to 6 months

300
Q

What are the clinical features of molluscum contagiosum?

A

Clusters of small white/pink/brown papules
Shiny with a small central pit
Warm places like armpit or groin

301
Q

How long does molluscum contagiosum usually last?

A

1-2 years

302
Q

What typically causes non-bullous impetigo?

A

Staphylococci and/or streptococci invasion of minor trauma site

303
Q

What typically causes ecthyma?

A

Streptococcus pyogenes

co-infection with Staph. aureus may occur

304
Q

What typically causes bullous impetigo?

A

Staphylococcal infection

305
Q

What is the progression of skin lesions in non-bullous impetigo?

A

pink macule –> vesicle/pustule –> crusted erosion –> untreated will heal without scarring

306
Q

What is the progression of the skin lesion in ecthyma?

A

pink macule –> punched-out necrotic ulcer –> heals slowly, leaving scar

307
Q

What is the clinical progression of bullous impetigo?

A

small vesicles –> flaccid transparent bullae –> heals without scarring

308
Q

How to treat impetigo?

A 
Cleanse wound using moist soaks
Avoid close contact with others 
Apply antiseptics or Abx ointment
Cover affected areas
If extensive, oral Abx
309
Q

Can children with impetigo go to school?

A

Stay away from school until crusts have dried out

310
Q

Clinical features of chickenpox in children?

A

itchy rash of red papules –> vesicles on trunk

311
Q

When is a person with chickenpox contagious?

A

1-2 days before the rash appears and all the way until every single blister has formed scabs (approx 5-10 days)

312
Q

Which plasmodium species works by sequestration?

A

P. Falciparum

313
Q

Which plasmodium:

early trophozoites
absence of mature trophozoites or schizonts

A

Plasmodium falciparum

314
Q

What are the treatment options for plasmodium falciparum?

A

Quinine with doxcycline for seven days

Artemisinin-based combination therapy

315
Q

Schuffner’s dots are seen on microscopy. What organism does this indicate?

A

Plasmodium ovale or Plasmodium vivax

316
Q

What drug would you give to prevent relapse of P. vivax or P. ovale?

A

Primaquine

317
Q

What drug would you give for P. vivax or ovale?

A

Artemisinin-based combination therapy

or Chloroquinine

318
Q

What are the fever intervals for the plasmodium species?

A

P. falciparum, vivax and ovale - 48 hours

P. malariae - 72 hours (quartan fever)

319
Q

Which plasmodium species is characterised by a compact parasite that does not alter host erythrocyte shape or size?

A

P. malariae P. knowlesi

320
Q

What are the reasons for performing a thick and thin film in Malaria management?

A

Thick - to identify parasites

Thin - distinguish malarial species

321
Q

Botulinum toxin acts on what family of proteins to mediate its effects?

A

SNARE family of proteins - involved in vesicle fusion and NT release

322
Q

What is the mechanism of action of botulinum toxin?

A

Cleavage of SNARE proteins

Inhibition of ACh release

323
Q

What are the signs/symptoms of botulism?

A

bulbar palsy and descending paralysis
apyrexial
clear sensorium (normal senses and mental state)

324
Q

What are potential sources of Clostridium Botulinum?

A

Canned foods

325
Q

What are potential sources of Clostridium Perfringens?

A

Poorly prepared meat/poultry

Long standing prepared food

326
Q

Which agent is the most common cause of gas gangrene?

A

Clostridium Perfringens

327
Q

What is the treatment for botulism?

A

Supportive care

Botulism antitoxin

328
Q

Common cause for pseudomembranous colitis?

A

Clostridium dificile

329
Q

What does C. dificile require in order to cause pseudomembranous colitis?

A

Toxin A or Toxin B

330
Q

Treatment for C. dificile?

A

Oral metronidazole 10-14 days

if severe, Oral Vancomycin 10-14 days

331
Q

A few weeks after an infection a symmetrical ascending muscle weakness begins.

A

Guillan-Barre Syndrome

332
Q

What is the ‘big danger’ with Guillan-Barre Syndrome?

A

Respiratory Failure

333
Q

What are the two main modalities of treatment for Guillan-Barre Syndrome?

A

Plasmapheresis and IV immunoglobulin

334
Q

What type of antibodies are involved in myasthenia gravis?

A

Post-synaptic acetylcholine receptor antibodies

335
Q

What type of antibodies are involved in Lambert-Eaton syndrome?

A

Pre-synaptic voltage-gated calcium channel antibodies

336
Q

What muscle groups tend to be affected first in myasthenia gravis?

A

Ocular

337
Q

What muscle groups tend to be affected first in Lambert-Eaton syndrome?

A

Legs

338
Q

What is a medical treatment in myasthenia gravis and what is its mechanism of action?

A

Pyridostigmine - acetylcholinesterase inhibitor thus increases ACh duration in synaptic cleft

339
Q

How might you treat a myasthenic crisis?

A

Identify trigger for relapse (infection, medications, etc.)
?Ventilate
Treat with plasmapharesis or IV Ig

340
Q

What surgical treatment is available for myasthenia gravis?

A

Thymectomy - if thymoma present

341
Q

A muscle weakness that improves after exercise.

A

Lambert-Eaton syndrome

342
Q

A muscle weakness that worsens with use and improves upon resting.

A

Myasthenia Gravis

343
Q

What skin and eye signs can be present in neurofibromatosis type 1?

A

Cafe-au-lait spots
Lisch nodules - brown mounds on iris
Freckling

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