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1
Q

Lines of Zahn

A

Ridges present on surface of thrombi

Alternate layers of platelets and blood clots form a lamina arrangement

Causes a differential contraction of platelets and fibrin and gives a rippled appearance

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2
Q

Phlegmasia cerulea dolens

A

Severe form of deep vein thrombosis with venous engorgement such that venous gangrene may supervene

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3
Q

Sequence of infarction

A

Dead tissue undergoes progressive autolysis of parenchymal cells and haemolysis of red cells

Living tissue surrounding the infarct undergoes an acute inflammatory response

Demolition phase: when there is an increase in the polymorphs, and after a few days macrophage infiltration

Repair phase: gradual ingrowth of granulation tissue
and the infarct is eventually organized into a fibrous
scar

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4
Q

Red or white infarct

A

Infarcts may either be described as red or white
(pale)

White infarcts: arterial occlusion of ‘end’ arteries in solid tissues, e.g. heart, spleen, kidneys

Red infarcts: venous infarcts and occur in loose tissues, e.g. the lung, where the bronchial arteries continue to pump in blood

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5
Q

Low flow water-shed areas

A

Splenic flexure: SMA - IMA

Deep myocardium: perfused directly from ventricles

Portal vasculature
-anterior pituitary is perfused by blood that has passed through hypothalamus

Tissues distal to stenosis / narrowing e.g. atherosclerotic areas

Metabolically active areas: undergo ischaemia first

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6
Q

Coagulative necrosis

A

Typically ischaemic injury (with exception of brain)

Denaturation of intracytoplasmic proteins

Dead tissue initially swollen and firm

Later becomes soft: e.g. ventricular rupture post MI

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7
Q

Colliquative necrosis

A

Seen in brain tissue - lack fof supportinh stroma

Necrotic brain tissue liquefies

Glial reaction at periphery with eventual cyst formation

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8
Q

Caseous necrosis

A

Characteristic of TB

Macroscopically cheese-like (caseous)

Microscopically structureless

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9
Q

Gangrenous necrosis

A

Necrosis with putrefaction of tissues due to presence bacteria
=e.g. clostridia, streptococci

Tissuesblack = iron sulphide from degraded haemoglobin

Gas gangrene = clostridium perfringens

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10
Q

Fibrinoid necrosis

A

Malgnant hypertension

Necrosis of arteriole smooth muscle wall
Seepage of plasma into tunica media and deposition of fibrin

=smudgy eosinophillic appearance on H&E

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11
Q

Fat necrosis

A

2 Types:

Direct trauma to adipose tissue
Extracellular relase of lipids e.g. Fat necrosis in breast

Enzymatic lysis of fat by lipases, e.g. pancreatic
lipase in acute pancreatitis
Fats split into fatty acids, which combine with calcium to precipitate as soaps

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12
Q

Mediators of apoptosis

A

p53: tumour suppressor, switches cells with damaged DNA into apoptosis

bcl-2: inhibits apoptosis, over-expressed in malignancy

fas (CD 95): death receptor (NK cells trigger when cells dont express self) - Plasma membrane receptor coupled to the activation of intracellular proteases

Caspaces: Present in all cells and unless inhibited lead to morphological changes of apoptosis.

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13
Q

p53

A

Tumour suppressor

Switches cells with damaged DNA into apoptosis

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14
Q

bcl-2

A

Inhibits apoptosis

Over-expressed in malignancy

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15
Q

Pernament cells

A

Never divide

If lost, lost forever

e.g. nerve cells, striated muscle cells, myocardial cells.

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16
Q

Labile cells

A

Have capacity to regenerate

e.g. surface epithelial cells constantly being replaced from deeper layers, e.g. skin, oesophagus vagina

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17
Q

Skin graft take process

A

Adherence:

  • fibrin bonds the graft to the recipient site
  • occurs in < 12 h.

Plasmic imbibition:

  • graft absorbs essential nutrients from recipient bed
  • occurs at 24–48 h.

Inosculation:

  • revascularization of the graft via growth of vascular buds
  • occurs at 48–72 h.
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18
Q

Random pattern flaps

A

Relies on dermal/subdermal plexus of vessels

Has maximum length:width ratio of 2:1 for safety

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19
Q

Non-random axial flaps

A

Non-random axial pattern flap: based on specific artery

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20
Q

Non-random island flaps

A

Non-random island flap: isolated on a vascular pedicle and can be moved to another site

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21
Q

Anterolateral thigh flap

A

—branches of lateral femoral circumflex artery and skin paddle

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22
Q

Radial forearm flap

A

-branch of radial artery and skin pedicle

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23
Q

DIEP / TRAM flap

A

DIEP/TRAM flap— branches of the deep inferior epigastric artery and skin paddle

TRAM: take muscle

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24
Q

Hydrofluoric acid burn

A

Requires calcium gluconate

Causes hypocalcaemia

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25
Jackson's burn wound model
Zone of necrosis: = area of maximum damage -suffers rapid and irreversible cell death due to coagulation of cellular proteins Zone of stasis: =adjacent to the zone of necrosis -compromised tissue perfusion due to damaged microcirculation - can progress to necrotic tissue if left untreated or inadequately resuscitated Zone of hyperaemia: =outermost burn zone, adjacent to zone of stasis -tissue perfusion is increased due to local inflammatory mediator release -will usually completely recover
26
Treatment of CO poisoning
Hyperbaric oxygen Treatment is by displacing COHb with oxygen – COHb has a half-life of 250 minutes in room oxygen levels and 40 minutes with 100% oxygen.
27
Superifical partial thickness burn
Papillary demris only
28
Deep partial thickness burn
Papillary dermis AND Reticular dermis (adnexal structures involved)
29
Phases of the cell cycle
M phase: - mitosis: nuclear division - cytokinesis: cytoplasmic division G1: gap varies between different cell types S phase: DNA synthesis G2: gap 2 G0 phase: cells can leave the cell cycle temporarily and re-enter later; said to be in the G0 phase
30
G1 phase
Variation in replication frequency occurs due to duration in G1 Cells can leave the G1 phase permanently, lose the ability to undergo mitosis, and become terminally differentiated cells
31
Go
G0 phase: cells can leave the cell cycle temporarily and re-enter later; said to be in the G0 phase Growth factords act on cells in G0 --> G1 --> undergo protein synthesis and replication Stimulated by growth factors: PDGF, EGF, IGF1 & 2
32
Renal agenesis
Unilateral or bilateral Failure of mesonephric duct to give rise to ureteric bud, with failure of induction of metanephric blastema
33
β-naphthylamine
--> bladder cancer high exposure in dye and rubber industry
34
Cyclophosphamide increases risk of which cancer
Alkylating agents e.g. cyclophosphamide Small risk of leukaemia
35
Cancer developing at the sites of previous radiotherapy treatment for breast cancer
Angiosarcoma
36
Clonorchis sinesis
Liver fluke Sits in biliary system --> cholangiocarcinoma
37
Nickel exposure cancer
Nickel exposure is associated with nasal and | bronchial carcinoma
38
Betel nut
Chewing betel nut is associated with increased | risk of neoplasms of oral cavity
39
Li-Fraumeni
p53 Breast carcinoma Ovarian carcinoma Astrocytomas Sarcomas
40
Retinoblastoma
Rb1 Genetically associated --> bilateral Sporadic --> unilateral Retinoblastoma Osteosarcoma
41
Familial polyposis coli
APC gene Chromosomal location 5q 21 Mainly colon cancer Other GI tract malignancies
42
von Hippel-Lindau
VHL Renal carcinoma Phaochromocytoma Haemangioblastoma
43
MEN syndromes
RET
44
Familial breast cancer
BRCA1 BRCA2 Breast caricnoma Ovarian syndrome Prostatic carcinoma
45
p53
Tumour supressor gene Short arm of chromosome 17 Functions - Arrest cycle in G phase to allow repair of damanaged DNA before S - Apoptotic cell death if DNA damage is extensive Inherited germ line mutations of p53 occur in the rare Li–Fraumeni syndrome, giving an inherited predisposition to a wide range of tumours.
46
Krukenberg tumours
Spread of stomach carcinoma --> ovaries Signet ring cells - primary is gastric adenocarcinoma which are mucinous signet ring cell
47
Autoimmune disease trigerred by malignancy
Dermatomyositis Membranous glomerulonephritis
48
Cervical screnning
Women aged 25–49 years old, screened every 3 years Women aged 50–64 years old, screened every 5 years
49
Breast screening
Women aged 50–70 years old (currently being extended to women aged 47–73 years old in some areas of the UK as a trial extension of the programme). Repeated 3-yearly
50
C5a
Chemotactic for neutrophils Increase vascular permeability Release of histamine from mast cells
51
C4b, 2a, 3b
Opsonification bacteria
52
Kinin system
Activated by factor XII Converts: prekallikrein --> kallikrein Kallikrein cleaves kininogen --> bradykinin Bradykinin controls vascular permeability and is a chemical mediator of pain
53
Serous inflammation
Abundant protein-rich fluid -little cellular material Inflammation of serous cavities e. g. peritonitis e. g. synovitis e. g. conjunctivitis
54
Catarrhal inflammation
hyper-secretion of mucous in acute inflammation of mucous membrane E.g. common cold
55
Fibrinous inflammation
Exudate contains much fibrinogen Fibrin forms a thick coating, e.g. acute pericarditis, fibrinous peritonitis.
56
Haemorrhagic inflammation
Accompanying vascular injury or coagulopathy e. g. acute haemorrhagic pancreatitis due to proteolytic digestion of vessel walls e. g. meningococcal septicaemia, resulting from associated disseminated intravascular coagulation (DIC).
57
Suppurative inflammation
Production of pus i.e. dying and degenerate neutrophils, organisms and liquefied tissues May become walled-off by fibrin or fibrous tissue to produce an abscess, i.e. a localised collection of pus May form an empyema (a collection of pus in a hollow viscus, e.g. gall bladder)
58
Membranous inflammation
Epithelium coated with layer of fibrin, desquamated epithelial cells and inflammatory cells e.g. grey membrane seen in pharyngitis due to diphtheria
59
Pseudomembranous inflammation
Superficial mucosa inflammation and ulceration with sloughing of mucosa, fibrin, mucus and inflammatory cells e.g. pseudomembranous colitis in C.Difficile
60
Necrotising inflammation
Tense oedema may cause vascular occlusion and thrombosis -->septic necrosis e.g. gangrenous appendicits
61
Types of giant cell
Histocytic: ingestible material by macrophages e. g. silica e. g. tuberculosis Langhans: horseshoe arrangement of peripheral nuclei at one pole of cell -characteristically seen in tuberculosis Foreign body: large cells with nuclei scattered randomly Touton: ring of central nuclei -clear peripheral cytoplasm with accumulated lipid, seen at sites of adipose tissue breakdown and in xanthomas
62
Drugs causing hepatic granulomatous
Allopurinol Phenylbutazone Sulphonamides
63
Petechial haemorrhages in corpus callosum and cerebellar peduncles
= diffuse axonal injuries
64
Blood in CSF
= subarachnoid haemorrhage Fibrous obliteration of subarachnoid space --> hydrocpehalus in those that survive
65
Most common cause of intracerebral haemorrhage
Hypertensive vascular disease
66
Diffuse petechial haemorrhage https://www.brainscape.com/decks/7516133/cards/quick#
Small pin-point haemorrhages scattered throughout brain Result from disruption of wall of small cerebral blood vessels Causes include: - vasculitis - acute hypertensive encephalopathy - fat embolism - head injury
67
Brain abscess sites
Temporal lobe or cerebellum - otitis media Frontal love - paranasal sinus spread Parietal lobe - haematogenou spread
68
Salmonella osteomyelitis
= sickle cell disease
69
Sickle cell osyteomyelitis
= Salmonella
70
Brucella abortis
Intervertebral discitis
71
Charcot joints
Degenerative joint disease which occurs due to loss of sensory nerve supply Tabes dorsalis: knee or hip joints Syringomyelia: shoulder or elbow joint - -> recurrent swelling - -> degenerative changes in ligaments and tendons, resulting in subluxation of the joint
72
HLA B27
Ankylosing spondylitis
73
HLA DR2
Goodpastures
74
HLA DR3
Addison's Hashimotos thyroidits Myasthenia gravis
75
HLA D4
Insulin dependent diabetes
76
Classical complement
Antigen-antibody complex mediated
77
Alternative complement pathway
Bacteria cell surface mediated
78
C3b
Opsonification +removal of immune complexes
79
C5a C4a C3a
Chemotactic Inflammatory Increase vascular permeability Histamine release from mast cells
80
C5 - C9
MAC Membrane attack complex
81
DiGeorge
T cell deficiency Thymic aplasia
82
MHC complex
Chromosome 6
83
Cytokines important in graft rejection
IL-2 | gamma interferon
84
Induction immunosuppression
IL-2R monoclonal antibodies - basiliximab - daclizumab
85
Acute rejection prophylaxis regimen
Calcineurin inhibitor: tacrolimus or ciclosporin AND Anti-metabolite: mycophenolate motefil or azathioprine AND Prednisolone
86
Maintenance therapy
Wean down doses of calcineurin inhibitor and anti-metabolite Stop steroids, after weaning If tacrolimus or ciclsporin not tolerated --> sirolimus used as a substitute e.g. if nephrotoxicity occurs
87
Anti-rejection therapy in suspected active rejection
Cell mediated: =Three pulses IV methylprednisolone ATG given if steroid resistant Antibody-mediated =plasmapheresis, IV IG AND retuximab anti CD-52 --> B cells
88
Genetic mutation in HbS
Glutamic acid replaced by valine
89
Mx of hereditary spherocytosis
Delayed spelectomy until 10 years of age --> reduced likelihood of post-splenectomy sepsis After spelnectomy: - Life-span of red cells increase - Jaundice resolves - Reduced pigment stones - Hb increases
90
Extinsic pathway requires...
Tissue thromboplastin | -released by damaged endothelial cells
91
Intrinsic pathway requires...
Nothing additional Formed by normal constituents of ciruclating bloods
92
Convergence of intrinsice and extrinsic pathway
Converge at Factor X --> Xa
93
Outline of intrinsic pathway
Vessel injury exposes collagen -collagen initates first step Circulating twelveE --> XII a EleveN ---> XIa NinE --> IXa Eight --> + IXa + platelet phospholipid = convergence on X
94
Outline of extrinsic pathway
Damaged endothelium released tissue thromboplastin Thromboplastin + Factor VII Converge on X
95
Factor V
Facilitates Xa acting on Porthrombin --> thrombin -hence common pathway Inatcivated by protein C + S
96
Production of clotting factors
All soluble clotting factors produced in liver EXCEPT Factor VIII (8) - produced in endothelium
97
Plasmin
Breaks fibrin down into soluble fibrin breakdown products Derived from plasminogen Activated by tissue plasminogen activator released from endothelium INHIBITION: Control of activation of plasminogen is provided by plasminogen-activator inhibitor 1 (PAI-1) -PAI-1 is released by endothelial cells and rapidly inactivates tissue plasminogen activator.
98
Platelet count needed for surgery
70
99
Spontaenous bleeding level for platelet count
20
100
Prolonged bleeding time
= platelet dysfunction Normal bleeding time - adequate platelet count - adequate platelet function - adeqaute vascular contraction
101
Whole-blood clotting time
Whole blood in glass tube Measures: - platelet ufnction - intrinsic pathwya - common pathway
102
Prothrombin time
Measure integrity of extrinsic pathway AND final common pathway Factor VII I, II, V and X
103
Activated partial thromboplastic time APTT
Tests intrinsic system AND final common pathway All factors with exception of Factor VII
104
Bleeding + APTT and PT normal
= platelet dysfunction
105
Bleeding + APTT and PT abnormal
=defect in common pathway
106
Bleeding + APTT normal and PT abnormal
= defect in factor VII | factor VII deficiency
107
Bleeding + APTT abnormal and PT normal
= defect in intrinsic system
108
Thrombin time
Note difference to prothombin time Increased if there is an inadequate concentration of fibrinogen. Prolonged by heparin and presence of fibrin degradation products.
109
von Willebrand's disease
Due to deficiency of von Willebrand’s factor. AD inheritance Vascular endothelium releases decreased amounts of Factor VIII Platelet count usually normal, but platelet interaction with endothelium is defective because of deficiency of von Willebrand’s factor
110
Haemophilia A
Inherited deficiency of Factor VIII X-linked recessive disorder affecting males and carried by females Severity of the disease depends upon the degree of Factor VIII deficiency ``` Prothrombin time (PT) normal but activated partial thromboplastin time (APTT) prolonged ```
111
Antithrombin III deficiency
AD inheritance Heterozygotes may suffer from recurrent deep vein thrombosis (DVT), pulmonary embolism (PE) and mesenteric thrombosis. Homozygotes present in childhood with severe arterial and venous thrombosis
112
Protein C
Degrades Factors Va and VIIIa Promotes fibrinolysis by inactivating plasminogen-activator inhibitor 1 (PAI-1)
113
Phenylbutazone
Inhibits warfarin-albumin binding
114
Cimetinide
Inhibits hepatic microsomial degredation of warfarin
115
MOA Clopidogrel
Inhibits activation and aggregation of platelets by blocking the glycoprotein IIa/IIIb pathway Stop 7 days pre-op
116
Cortex of lymph
Primary and secondary lymphoid follicles Secondary = stimulated Tightly packed
117
Paracortex of lymph
T-cell dependent area
118
Medulla of lymph gland
Contains the medullary cords and sinuses Contains lymphocytes, which are much less densely packed than in the cortex together with macrophages, plasma cells and a small number of granulocytes
119
Haematological changes post splenectomy
Red cell count does not change but red cells with cytoplasmic inclusion, e.g. Howell–Jolly bodies, may appear. Granulocytosis occurs immediately after splenectomy but is replaced in a few weeks by lymphocytosis and monocytosis. he platelet count is usually increased and may stay at levels of 400 000–500 000 × 109/L for over a year A thrombocytosis in excess of 1000 × 109/L may occur --> anti-platelets
120
Most common cause of post-splectomy spesis
= pneumooccus
121
Splenectomy vaccines
Polyvalent pneumococcal PPV Men ACWY Hib Influenza Re-immunization every 5 years + 2 years penicillin
122
Infusion of platlets
Infuse rapidly via short-giving set with no filter Usual adult dose is 6 units, which should raise the count by 40 000 × 109/L
123
Indications for cryoprecipitate
Haemophilia Von Willebrand’s disease Fibrinogen deficiency e.g. DIC Rich in factor VIII, fibrinogen and vWF

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