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eMRCS questions > Pathology Book > Flashcards

Pathology Book Flashcards

1
Q

Types of necrosis

A

Coagulative - denaturing of intracytoplasmic proteins- occurs after ischaemia except brain- tissue becomes firm and swollen

Colliquative- seen in brain - hypoxia

Caseous - tuberculosis

Fat- trauma to apdipsoedue to lipase

Fibrinoid - arteriole smooth muscle wall due to malignant HTN

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2
Q

Cause of inflammation cellular wise

A

Contraction of endothelial cytoskeleton in venules

Due to release of chemical mediators

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3
Q

Main cell in acute inflammation

A

Neutrophil

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4
Q

Main cell in chronic inflammation

A

Macrophages

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5
Q

IL1,2 IF and TNF fucntion

A

IL1 neutrophil adhesion
IL2- differentiation of B and NK cells
IF- activation of macrophages and NK cells
TNF- fever, neutrophil adhesion

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6
Q

What is formed at inflammation sites that can limit spread of pathogen

A

Fibrin

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7
Q

What is a histological diagnostic feature of acute inflammation

A

Neutrophil polymorphs

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8
Q

Sequale of acute inflammation

A

Resolution - minimal injury, stimulus removed

Organisation - delayed removal of exudate

Suppuration - abscess, large quantity of dead neutrophils

Progression to chronic inflammation- usually when inadequately managed

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9
Q

Causes of chronic inflammation generally

A

Persisting infection
Prolonged exposure to non biodegradable substances
AI conditions

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10
Q

Vascular changes in chronic inflammation

A

Angiogenesis

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11
Q

Cells in chronic inflammation

A

Macrophages
Plasma
Lymphocytes

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12
Q

Resolution of chronic inflammation

A

Healing by fibrosis

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13
Q

What is a granuloma

A

Aggregation of macrophages
Large giant cells found at periphery

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14
Q

How TNFa induces apoptosis

A

TNF-alpha binds to both the p55 and p75 receptor

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15
Q

Reversible cell injury microscopically

A

Cellular swelling
Swelling of cell and organelles
Blebbing of plasma membrane
Detachment of ribosomes from ER
Clumping of chromatin
Fatty changes - hypoxic injury- in cells involved in and are unable to fat metabolism- hepatocytes and myocardial cells

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16
Q

Ulcer associated with burns

A

Curling

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17
Q

Microscopic changes in irreversible cell damage

A

Swelling and disruption of lysosomes
Presence of large amorphous densities in swollen mitochondria

Membrane disrupted

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18
Q

Which organelle is self replicating

A

Mitochondria

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19
Q

Which pigment is involved in ageing cells

A

Lipofuscin

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20
Q

Phases of bone healing

A

Reactive - haematoma forms
Fibroblasts, macrophages and new vessels invade area forming granulation tissue

Reperative- osteoblasts and chondroblasts in haematoma forming woven bone and fibrocartilage forming callus
Woven bone is replaced by lamellar bone

FInal- lamellar bone is replaced by compact bone

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21
Q

Hypertrophic vs keloid scars

A

Hypertrophic - within margins of wound - thick raised scar

Keloid- extend margins

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22
Q

Collagen in wound healing

A

Type 3 in early phase
1 in maturation phase, which is stronger

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23
Q

Rule of closing the abdomen

A

Suture 4x length of wound
1cm deep and apart

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24
Q

Primary vs secondary intuition of wound healing

A

Primary- margins closely brought together

Secondary- margins not apposed
Granulation tissue forms that contracts
Mylofibroblasts contract reducing scar size

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25
Q

Where keloid scars most commonly form

A

Sternum and deltoid area
Dorsal surfaces

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26
Q

4 stages of wound healing

A

Coagulative - vasoconstriction, platelet adhesion, fibrin clot

Inflammatory - vasodilation, exudation, phagocytosis

Fibroblastic/proliferative- granulation, contraction, epitheliasagtion

Remodelling - scar tissue and reorganising

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27
Q

Factors contributing to poor wound healing

A

Local- poor blood supply, infection, FB, haematoma, mechanical stress

Systemic- old age, anaemia, drugs, DM, malnutrition, obesity, infection, uraemia

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28
Q

Immediate complications of Central venous lines

A

Pneumothorax, tamponade, chlythorax, arryhtmia

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29
Q

RF of aortic dissection

A

Atheroscelrosis
HTN
Aortic valve defects
Turners
Marfans
Ehlers Danlos

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30
Q

Milroy disease

A

Congenital hereditary primary lymphedema- casted by aplasia of lymph trunks

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31
Q

Diabetic ulcer features

A

Pressure areas
Painless

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32
Q

Protein C and S function

A

Inhibit factor V and VIII

Therefore deficiency increases clot risk

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33
Q

What ascites type does a psuedomyoxoma cause

A

Exudative
Tumour of appendix

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34
Q

Types of acquired aneursym

A

Atherosclerotic
Mycotic
Dissecting
AV

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35
Q

Areas with stratified squamous cells

A

Keratonised - skin , tongue, outer lips

Non keratinised- cornea, oesophagus, rectum, vagina

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36
Q

Areas with pseudo stratified columnar

A

Epipidymis and trachea
Prostate

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37
Q

Areas with simple columnar

A

Colon and uterus

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38
Q

Characteristics of dysplasia

A

Pre cancerous
Increased cell growth and decreased cell differential

Increased mitotic activity
Hyperchromatic nuclei with high nuclear to cytoplasm ratio

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39
Q

Define metaplasia

A

Reversible cell change due to environmental stress

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40
Q

Types of gangrene and pathology

A

Wet- arterial and venous obstruction causing stagnation and rapid infection and sepsis

Dry- arterial obstruction - lack of blood- reduced infection

Gas- clostridium perfrigens

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41
Q

Haemochromatosis, Wilson and a1at disease inheritance

A

HC- AD- 6
Wilson- AR- 13
A1AT- AR

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42
Q

Haemachromatosis vs Wilsons symptoms

A

HC- increased iron absorption in cells - myocytes, pancreas and liver- cardiac, liver failure, DM, pancreatitis

Wilsons- accumulation of copper in brain, liver and cornea

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43
Q

Familial cancer syndrome and their affected genes

A

Li-Fraumeni- p53
Retinoblastoma- Rb1
FAP- APC
vHL- VHL
MEN- RET
Familail breast cancer- BRCA1,2

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44
Q

Types of gene mutation for Down syndrome

A

Non disjunction- most common
Translocation- rare
Mosaicism- very rare- non disjunction in blastocysts formation- some normal some trisomy 21

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45
Q

What is a giant cell
Physiological examples and pathological

A

Union of small cells to formate a multinuclear cell

Physio- osteoclast, skeletal muscle, synctiotrophoblasts, oocytes

Pathological- reed steenberg, langerhans (sarcoid, TB, Crohns), CMV

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46
Q

Time for irreversible damage to neutrons vs myocytes

A

Neurons- 3-5 mins
Myocyes- 1-2 hrs

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47
Q

Which necrosis preserves tissue architecture

A

Coagulative necrosis

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48
Q

Types of cell degradation due to enzymes

A

Heterolysis - outside

Autolysis- inside cell

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49
Q

Compostiosn of amyloid and arrangement

A

Minor constant- amyloid p protein

Major
Chronic inflammation- Amyloid A protein
Monoclonal cell proliferation- myeloma- Amyloid light chain

Arranged in B pleats

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50
Q

Staining of amyloid

A

Congo red

“apple-green birefringence” when viewed under polarized microscopic light.

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51
Q

What happens in apoptosis

A

Energy dependent process
Cells- shrink and undergo fragmentation to form apoptotic bodies
Apoptotic bodies
Nuclear shrinking
Membrane integrity is preserved
No inflammatory response

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52
Q

Morphogenic apoptosis

A

During embryological development
Involved in alteration of tissue form

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53
Q

Hyperplasia vs hypertrophy and reversibility

A

Hyperplasia- increase number of cells
Hypertrophy- increase size of cells

Both reversible when stimulus removed

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54
Q

Change in bone marrow cells at altitude

A

Hyperplasia

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55
Q

Stages of cell cycle

A

G0- resting phase
G1- 1st gap- increase in size
S- DNA synthesis
G2- second gap - further increase in size
M- mitosis (pro, meta, ana, telophase)

56
Q

Viruses that cause cancer

A

HPV 16,18- cervical
EBV- Burkitt lymphoma, hodgkin, nasopharyngeal
Herpes- lymphoma
Human T lymph virus- T cell lymphoma
Hep B- HCC
HIV- karposi

57
Q

Rhabdomyosarcoma vs leimyosarcoma

A

Rhabdo- skeletal
Leio- smooth

58
Q

Marker in seminoma

A

bhCG

59
Q

Marker in teratoma

A

aFP

60
Q

What is an adenoma

A

Tumour of glandular tissue

61
Q

Most common area for prostate cancer to develop

A

Posterior side

62
Q

Most common type of male breast cancer

A

Invasive ductal carcinoma

63
Q

Types of paraneoplastic syndrome

A

Humoral
Cushing
SIADH
PTrP- high calcium
Carcinoid

Immuno- AI
Dermatomyositis
Membranous glomerulnepritis

64
Q

Bacertial and fungal infections associated with cancer

A

H pylori- gastric lymphoma
Aspergillus- HCC
Schisto- bladder cancer
Clonorchis- cholangiocarcinoma

65
Q

Transcolaemic transmission of cancer and examples

A

Across a body cavity
Lung- to pleura- pleural effusion
Stomach - to ovaries- Krunkenberg tumour
Ovarian - to omentum and peritoneum- ascites
Colon

66
Q

Krunkenburg tumour arises and spread to were

A

From stomach to ovaries
Transcolemic spread
Adenocarcinoma

67
Q

Most common bone cancer

A

Osteoscarcoma

68
Q

Plummer Vinson sx and risks

A

Webbed oesophagus
IDA
Splenomegaly

Rf for SCC of oesophagus

69
Q

Dukes staging

A

A- limited to mucosa
B1- MP, 2- through
C1- LN, C2- >4
D- distant mets

70
Q

FNA results breast

A

C1- insufficient
2- benign
3- uncertain
4- suspected cancer
5- cancer

71
Q

TNM for breast cancer

A

T1- <2cm
2- 2-5cm
3- >5cm
4- spread to chest wall or skin

N0- no LN
1- ipsilateral axillary mobile
2- ipsilateral fixed, or internal mammary
3- LN supra or infraclavicular

M1- distant mets

72
Q

Types of hypersensitivites

A

Type 1- immediate allergic reaction- IgE
2- AB on cell surface
3- deposition of AB- antigen complex in tissues
4- delayed- T lymph

73
Q

Which cell kills viral infected cells and tumour cells

A

Nk cells

74
Q

AB Production order and timescale

A

IgM
IgG- 3w
Change due to T cell switch

75
Q

What happens if you’re IgA deficient

A

Mucosal infections
Since that is where IgA is secreted

Also need IgA deficient blood or else react against it

76
Q

Types of transplant rejection

A

Hyperacute- preformed ABs to HLA or ABO

Acute T cell- type 4, epithelial damage
Antibody- anti HLA AB-endothelial damage

Chronic- may be antigen AB mismatches not suppressed by immunosuppressant

77
Q

Complement activation pathway

A

Classical
Antigen AB complex binds to C1,4,2
C3- which activates C5

Alternative
Activated by cell wall

Mannose binding
Activated by c​ ell surface carbohydrates
Activates cascade via the classical pathway - via​ C2 and C4 (but NOT C1)

Final
C5- activates others for MAC

78
Q

Features of leucocyte adhesion deficiency

A

Neuts unable to migrate
High neuts in blood
No pus

79
Q

Features of chronic granulomatous disease

A

Failure of oxidative killing
Granuloma formation
Abnormal dihydrorhodamine test (-ve)​

80
Q

Di George syndrome characteristics

A

● Low T-cells, low IgA, low IgG
● Normal B-cell levels, normal IgM
Alter facial characteristics
Cardiac defects

81
Q

Selective IgA def features

A

● - IgA provides mucosal immunity
● Associated with other AI diseases e.g. coeliac, SLE
● Risk of a​ naphylaxis after blood transfusion (​ anti-IgA Abs

82
Q

Endogenous pyrogens

A

TNFa
IL1

83
Q

Chemoattractant for neutrophils

A

IL8

84
Q

Cause of thrombocytopaenia

A

Aplastic
Viral infections
Myelodysplasia
Myeloma
ITP
Post transfusion
DIC
Hypersplenism

DIAPHM

85
Q

Blood film of myelodysplasia

A

Pelger Huet abnormality
(hyposegmented neutrophils) - bilobed & dumbbell shaped nucleus

86
Q

Function of apoptosis

A

Morphogenesis
Removal of cells with DNA damage
Removal of viral infected cells
Induction of tolerance in immunity

87
Q

Medaitors of apoptosis

A

p53- tumour suppressor gene
bcl2- inhibits apoptosis
fas- receptor that leads
caspases

88
Q

Mechanism of skin graft take

A

Adherence- fibrin bonds graft to recipient <12h
Plasmic imbibition- graft absorbs nutrients- 24-48
Insoculation- revascularisation- 28-72

89
Q

Stages of formation of blood clot

A

Platelets sticking to endothelium- vWF
Fibrin and leucocytes adhere
Fibrin and red cells develop on this layer
Secondary layer of platelets
Adherence to wall- mural thrombus
Second stage- further platelets lay down on initial aggregate
Contraction of platelets and fibrin cause ridged- lines of Zahn

90
Q

Fate of thrombi

A

Lysis- resolution
Recanalisation- new vessels
Propagation- causing further thrombi
Embolisation

91
Q

Causes of non thromboembolic vascular insufficiency

A

Atherome
Torsion
Spasm
Steal- AV fistula- flow goes through cephalic instead of radial- poor perfusion distally
External pressure- tumour

92
Q

Red vs white infarct

A

Red- venous - lung
White- arterial- e.g heart and spleen

93
Q

Adenoma vs papilloma

A

Adenoma- glandular
Papiloma- non glandular

94
Q

Blastoma meaning

A

Histological resemblance to embryonic form of origin

95
Q

Harmatoma constituants

A

Usually 2 or more matures cells- but abnormally organised

96
Q

Examples of premalignant conditions

A

Pagets- osteogenic sarcoma
Cirrhosis- HCC
Xeroderma pig- skin cancer
UC- colon adenoma, bile duct
Cervical dysplasia
Hyperplasia of breast
Colorectal polyp

97
Q

Oncogenes examples

A

Genes that stimulate the development of cancer
May only need 1 to become abnormal

sis
ras
abl
myc

MARS

98
Q

Tumour suppressor genes examples

A

Gatekeepers- inhibit proliferation or promote death with DNA damage
p53
Rb1
APC

Caretakers- maintain integrity of DNA by repairing damage
BRCA1,2

99
Q

Steps of metastatic cascade

A

Detachment of tumour cells
Invasion of surrounding tissue
Intravasation into lumen of vessels
Evasion of defence
Adherence to endothelium at remote location
Extravascularisation
Survival
Establish blood supply

100
Q

Which cancers spread often to bone

A

Breast
Bronchus
Kidney
Thyroid
Prostate

Spread via haematogenous

101
Q

How do sarcomas spread

A

Haematogenous

102
Q

How can cancers cause jaundice

A

Invasion of nodes in portal hepatis
Causing obstruction of hepatic bile duct

103
Q

What is bad prognosis of malignant melanoma

A

> 4cm on breslow thickness

104
Q

Composition of an antibody

A

Heavy- y, u, a, b, e
Light- k or l

Fab- contains binding site
Fc

N terminal region of the end of Fab fragment - variable region- specific to antigen

105
Q

Which antibody crosses placenta

A

IgG

106
Q

How many antigen binding sites are there in IgG, IgM, IgA

A

IgG-2
IgA- 4
IgM- 10

107
Q

Role of IgG

A

Crosses placenta
Opsination
Neutralise toxins

108
Q

Role of IgM

A

Primary response
Great agglutination

109
Q

Types of T cell

A

CD4- helper
CD8- cytotoxic

110
Q

Classification of MHC

A

1- A, B, C (all nucleated cells)
2- DP, DR, DQ (B cells, activated T cells and APC)

111
Q

How T cells recognise antigens

A

T cells have TCR

Will only recognise an antigen as part of a complex of the antigenic peptide and MHC

Endogenous antigens are presented by MHC class 1 to CD8 cells
Exogenous antigens are presented by MHC class 2 to CD4

112
Q

Structure of lymph node and where cells are located

A

Cortex- primary follicles of B cells, dendritic cells- APC

Paracortex- T cells

Medulla- contained lymphocytes less packed, with macrophages, plasma cells
Sinuses lined with macrophages that phagocytose

Primary follicles turn into secondary on antigen stimulation which contain germinal centre of B cells (antigen activated) and a few CD4 cells

Activated B cell migrate from follicle to medulla- develop into plasma cells and release AB into efferent limb

113
Q

Organisation of spleen

A

Lymphoid tissue is in white pulp arranged around arterioles

T cells surround central arteriole

B cells in white pulp- may form germinal centres when activated
Produce ABs

Red pulp- remove old RBC, abnormal WC, phagocytosis by macrophages

114
Q

Types of T helper cell

A

Th1- secrete TNFa and IFNy and mediate cellular immunity

Th2- secrete IL4,5,10,13- stimulate B cell to produce AB

115
Q

Types of immunosuppressive dugs

A

Corticosteroids- inhibit T cell activation, neutrophil pahgocytosing, anti inflammatory effects

Antiproliferative
Azathioprine - interferes with nucleic acid- purine- T cells prolif
Mycophenolate- prevents guanine synth- more effective for acute- prevents both T and , prevents smooth muscle prolif

Calcinerin- inhibit T cell activation- prevent IL2 release from helper cells
Ciclosporin
Tacrolismus

116
Q

Clinical features of haemolytic anaemia

A

Palloe
Jaundice
Gallstones
Splenomegaly - more susceptible to infection due to reduced function
Frontal bone bossing
Bone marrow expansion- weaken

117
Q

Sickle pathophysiology

A

HbS
glutamic replaced by valine
Causing them to polymerise on deoxygenation
Sickle in venous blood- due to lower O2 levels

Increased rigidity- plug small vessels- infarction and painful crisis

Anaesthetist needs to avoid hypoxia

118
Q

Hereditary spheorcytosis features and tx

A

Defect on cell membrane
Raised bilirubin
Cholecystitis
Splenectomy- as prevents destruction of RBC- Hb rise, reduce bilirubin

119
Q

Degradation of fibrin

A

Tissue plasminogen activator released by endothelial cells
This is inhibited by PAI1- plasminogen inhibitor 1
This is also released by endothelial cells

TPA activated it to plasmin which degrades fibrin into degradation products.
This process is inhibited by antiplasmin

120
Q

Min level of plts for surgery

A

70

121
Q

Days before surgery that each anticoagulant needs to be stopped

A

Warfarin- 5d, Vit K should be given day before if INR >1.5

LMWH- 24 hrs before, started 48hrs after if high risk for bleeding

DOAC- 24 hrs before low risk, 48 in high

122
Q

Cause of massive splenomegaly

A

CML
Myelofibrosis
Lymphoma

123
Q

Which vaccines are required for patients who are undergoing splenectomy

A

Pneumococcal
H influenza
Meningococcal

Needs to be at least 2w before surgery

124
Q

Conditions causing abnormal growth in thymus

A

MG
SLE
Dermatomyositis
Aplastic anaemia

125
Q

Indication of platelet transfusion

A

Haemorrhage with thrombocytopaenia
Thrombo prior to procedure
Consumption coagulopathy- DIC

126
Q

Indication for FFP transfusion

A

Replace clotting factors in major haemorrhage
Liver disease, rapid reversal of warfarin
Prophylaxis with specific deficiency

127
Q

Indication for cryoprecipitate transfusion

A

Rich in VIII, fibrinogen, vWF
Haemophillia
vWD
Fibrinogen disease

128
Q

Staph aureus shape and staining

A

Gram + cocci arranged in clusters
Coagulase positive

129
Q

Streptococci Shape and stain

A

Gram + cocci arranged in pairs or chains

130
Q

Gram + cocci coagulase neg

A

S epididimis- prosthetics, HV
S Saprolyticus- UTI

131
Q

Gram positive rods

A

Actino
Bacillis
Clostridium
Listeria

132
Q

Gram negative cocci

A

Neisseria

133
Q

Gram negative bacilli

A

Anaerobes
E coli
Klebsiella
Salmonella
Shigella

Aerobes
Psudomonas

Campylobacter- curved or spiral rods
H influenza
H pylori - spiral

134
Q

Definition of when SIRS can be diagnosed

A

Temp >38 or <36
Tachycardic >90
Tachypnoeic >20 or CO2 <4.
WCC >12/ <4

135
Q
A

eMRCS questions (45 decks)

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