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MRCS > Path > Flashcards

Path Flashcards

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 of supporting 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

Malignant 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 release 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
Q

Jackson’s burn wound model

A

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

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26
Q

Treatment of CO poisoning

A

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.

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27
Q

Superifical partial thickness burn

A

Papillary demris only

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28
Q

Deep partial thickness burn

A

Papillary dermis

AND

Reticular dermis (adnexal structures involved)

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29
Q

Phases of the cell cycle

A

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

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30
Q

G1 phase

A

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

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31
Q

Go

A

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

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32
Q

Renal agenesis

A

Unilateral or bilateral

Failure of mesonephric duct to give rise to ureteric
bud, with failure of induction of metanephric blastema

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33
Q

β-naphthylamine

A

–> bladder cancer

high exposure in dye and rubber industry

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34
Q

Cyclophosphamide increases risk of which cancer

A

Alkylating agents e.g. cyclophosphamide

Small risk of leukaemia

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35
Q

Cancer developing at the sites of previous radiotherapy treatment for breast cancer

A

Angiosarcoma

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36
Q

Clonorchis sinesis

A

Liver fluke

Sits in biliary system –> cholangiocarcinoma

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37
Q

Nickel exposure cancer

A

Nickel exposure is associated with nasal and

bronchial carcinoma

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38
Q

Betel nut

A

Chewing betel nut is associated with increased

risk of neoplasms of oral cavity

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39
Q

Li-Fraumeni

A

p53

Breast carcinoma
Ovarian carcinoma
Astrocytomas
Sarcomas

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40
Q

Retinoblastoma

A

Rb1

Genetically associated –> bilateral
Sporadic –> unilateral

Retinoblastoma
Osteosarcoma

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41
Q

Familial polyposis coli

A

APC gene
Chromosomal location 5q 21

Mainly colon cancer

Other GI tract malignancies

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42
Q

von Hippel-Lindau

A

VHL

Renal carcinoma
Phaochromocytoma
Haemangioblastoma

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43
Q

MEN syndromes

A

RET

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44
Q

Familial breast cancer

A

BRCA1
BRCA2

Breast caricnoma
Ovarian syndrome

Prostatic carcinoma

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45
Q

p53

A

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.

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46
Q

Krukenberg tumours

A

Spread of stomach carcinoma –> ovaries

Signet ring cells - primary is gastric adenocarcinoma which are mucinous signet ring cell

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47
Q

Autoimmune disease trigerred by malignancy

A

Dermatomyositis

Membranous glomerulonephritis

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48
Q

Cervical screnning

A

Women aged 25–49 years old, screened every 3
years

Women aged 50–64 years old, screened every 5 years

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49
Q

Breast screening

A

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

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50
Q

C5a

A

Chemotactic for neutrophils

Increase vascular permeability

Release of histamine from mast cells

51
Q

C4b, 2a, 3b

A

Opsonification bacteria

52
Q

Kinin system

A

Activated by factor XII

Converts: prekallikrein –> kallikrein

Kallikrein cleaves kininogen –> bradykinin

Bradykinin controls vascular permeability and is a chemical mediator of pain

53
Q

Serous inflammation

A

Abundant protein-rich fluid
-little cellular material

Inflammation of serous cavities

e. g. peritonitis
e. g. synovitis
e. g. conjunctivitis

54
Q

Catarrhal inflammation

A

hyper-secretion of mucous in acute inflammation of mucous membrane

E.g. common cold

55
Q

Fibrinous inflammation

A

Exudate contains much fibrinogen

Fibrin forms a thick coating, e.g. acute pericarditis,
fibrinous peritonitis.

56
Q

Haemorrhagic inflammation

A

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
Q

Suppurative inflammation

A

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
Q

Membranous inflammation

A

Epithelium coated with layer of fibrin, desquamated epithelial cells and inflammatory cells

e.g. grey membrane seen in pharyngitis due to diphtheria

59
Q

Pseudomembranous inflammation

A

Superficial mucosa inflammation and ulceration with sloughing of mucosa, fibrin, mucus and inflammatory cells

e.g. pseudomembranous colitis in C.Difficile

60
Q

Necrotising inflammation

A

Tense oedema may cause vascular occlusion and thrombosis
–>septic necrosis

e.g. gangrenous appendicits

61
Q

Types of giant cell

A

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
Q

Drugs causing hepatic granulomatous

A

Allopurinol

Phenylbutazone

Sulphonamides

63
Q

Petechial haemorrhages in corpus callosum and cerebellar peduncles

A

= diffuse axonal injuries

64
Q

Blood in CSF

A

= subarachnoid haemorrhage

Fibrous obliteration of subarachnoid space –> hydrocpehalus in those that survive

65
Q

Most common cause of intracerebral haemorrhage

A

Hypertensive vascular disease

66
Q

Diffuse petechial haemorrhage https://www.brainscape.com/decks/7516133/cards/quick#

A

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
Q

Brain abscess sites

A

Temporal lobe or cerebellum - otitis media

Frontal love - paranasal sinus spread

Parietal lobe - haematogenou spread

68
Q

Salmonella osteomyelitis

A

= sickle cell disease

69
Q

Sickle cell osyteomyelitis

A

= Salmonella

70
Q

Brucella abortis

A

Intervertebral discitis

71
Q

Charcot joints

A

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
Q

HLA B27

A

Ankylosing spondylitis

73
Q

HLA DR2

A

Goodpastures

74
Q

HLA DR3

A

Addison’s

Hashimotos thyroidits

Myasthenia gravis

75
Q

HLA D4

A

Insulin dependent diabetes

76
Q

Classical complement

A

Antigen-antibody complex mediated

77
Q

Alternative complement pathway

A

Bacteria cell surface mediated

78
Q

C3b

A

Opsonification

+removal of immune complexes

79
Q

C5a C4a C3a

A

Chemotactic

Inflammatory

Increase vascular permeability

Histamine release from mast cells

80
Q

C5 - C9

A

MAC

Membrane attack complex

81
Q

DiGeorge

A

T cell deficiency

Thymic aplasia

82
Q

MHC complex

A

Chromosome 6

83
Q

Cytokines important in graft rejection

A

IL-2

gamma interferon

84
Q

Induction immunosuppression

A

IL-2R monoclonal antibodies

  • basiliximab
  • daclizumab
85
Q

Acute rejection prophylaxis regimen

A

Calcineurin inhibitor: tacrolimus or ciclosporin

AND

Anti-metabolite: mycophenolate motefil or azathioprine

AND

Prednisolone

86
Q

Maintenance therapy

A

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
Q

Anti-rejection therapy in suspected active rejection

A

Cell mediated:
=Three pulses IV methylprednisolone
ATG given if steroid resistant

Antibody-mediated
=plasmapheresis, IV IG
AND retuximab and anti CD-52 (alemtuzumab) –> B cells

88
Q

Genetic mutation in HbS

A

Glutamic acid replaced by valine

89
Q

Mx of hereditary spherocytosis

A

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
Q

Extinsic pathway requires…

A

Tissue thromboplastin

-released by damaged endothelial cells

91
Q

Intrinsic pathway requires…

A

Nothing additional

Formed by normal constituents of ciruclating bloods

92
Q

Convergence of intrinsice and extrinsic pathway

A

Converge at Factor X –> Xa

93
Q

Outline of intrinsic pathway

A

Vessel injury exposes collagen
-collagen initates first step

Circulating twelveE –> XII a

EleveN —> XIa

NinE –> IXa

Eight –> + IXa + platelet phospholipid = convergence on X

94
Q

Outline of extrinsic pathway

A

Damaged endothelium released tissue thromboplastin

Thromboplastin + Factor VII

Converge on X

95
Q

Factor V

A

Facilitates Xa acting on Porthrombin –> thrombin
-hence common pathway

Inatcivated by protein C + S

96
Q

Production of clotting factors

A

All soluble clotting factors produced in liver

EXCEPT Factor VIII (8) - produced in endothelium

97
Q

Plasmin

A

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
Q

Platelet count needed for surgery

A

70

99
Q

Spontaenous bleeding level for platelet count

A

20

100
Q

Prolonged bleeding time

A

= platelet dysfunction

Normal bleeding time

  • adequate platelet count
  • adequate platelet function
  • adeqaute vascular contraction
101
Q

Whole-blood clotting time

A

Whole blood in glass tube

Measures:

  • platelet ufnction
  • intrinsic pathwya
  • common pathway
102
Q

Prothrombin time

A

Measure integrity of extrinsic pathway AND final common pathway

Factor VII
I, II, V and X

103
Q

Activated partial thromboplastic time APTT

A

Tests intrinsic system AND final common pathway

All factors with exception of Factor VII

104
Q

Bleeding + APTT and PT normal

A

= platelet dysfunction

105
Q

Bleeding + APTT and PT abnormal

A

=defect in common pathway

106
Q

Bleeding + APTT normal and PT abnormal

A

= defect in factor VII

factor VII deficiency

107
Q

Bleeding + APTT abnormal and PT normal

A

= defect in intrinsic system

108
Q

Thrombin time

A

Note difference to prothombin time

Increased if there is an inadequate concentration of fibrinogen.

Prolonged by heparin and presence of fibrin degradation
products.

109
Q

von Willebrand’s disease

A

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
Q

Haemophilia A

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
Q

Antithrombin III deficiency

A

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
Q

Protein C

A

Degrades Factors Va and VIIIa

Promotes fibrinolysis by inactivating plasminogen-activator inhibitor 1 (PAI-1)

113
Q

Phenylbutazone

A

Inhibits warfarin-albumin binding

114
Q

Cimetinide

A

Inhibits hepatic microsomial degredation of warfarin

115
Q

MOA Clopidogrel

A

Inhibits activation and aggregation of platelets by
blocking the glycoprotein IIa/IIIb pathway

Stop 7 days pre-op

116
Q

Cortex of lymph

A

Primary and secondary lymphoid follicles

Secondary = stimulated

Tightly packed

117
Q

Paracortex of lymph

A

T-cell dependent area

118
Q

Medulla of lymph gland

A

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
Q

Haematological changes post splenectomy

A

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
Q

Most common cause of post-splectomy spesis

A

= pneumooccus

121
Q

Splenectomy vaccines

A

Polyvalent pneumococcal PPV

Men ACWY

Hib

Influenza

Re-immunization every 5 years

+ 2 years penicillin

122
Q

Infusion of platlets

A

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
Q

Indications for cryoprecipitate

A

Haemophilia
Von Willebrand’s disease
Fibrinogen deficiency e.g. DIC

Rich in factor VIII, fibrinogen and vWF

MRCS (24 decks)

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