Path Flashcards
Lines of Zahn
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
Phlegmasia cerulea dolens
Severe form of deep vein thrombosis with venous engorgement such that venous gangrene may supervene
Sequence of infarction
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
Red or white infarct
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
Low flow water-shed areas
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
Coagulative necrosis
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
Colliquative necrosis
Seen in brain tissue - lack fof supportinh stroma
Necrotic brain tissue liquefies
Glial reaction at periphery with eventual cyst formation
Caseous necrosis
Characteristic of TB
Macroscopically cheese-like (caseous)
Microscopically structureless
Gangrenous necrosis
Necrosis with putrefaction of tissues due to presence bacteria
=e.g. clostridia, streptococci
Tissuesblack = iron sulphide from degraded haemoglobin
Gas gangrene = clostridium perfringens
Fibrinoid necrosis
Malgnant hypertension
Necrosis of arteriole smooth muscle wall
Seepage of plasma into tunica media and deposition of fibrin
=smudgy eosinophillic appearance on H&E
Fat necrosis
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
Mediators of apoptosis
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.
p53
Tumour suppressor
Switches cells with damaged DNA into apoptosis
bcl-2
Inhibits apoptosis
Over-expressed in malignancy
Pernament cells
Never divide
If lost, lost forever
e.g. nerve cells, striated muscle cells, myocardial cells.
Labile cells
Have capacity to regenerate
e.g. surface epithelial cells constantly being replaced from deeper layers, e.g. skin, oesophagus vagina
Skin graft take process
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.
Random pattern flaps
Relies on dermal/subdermal plexus of vessels
Has maximum length:width ratio of 2:1 for safety
Non-random axial flaps
Non-random axial pattern flap: based on specific artery
Non-random island flaps
Non-random island flap: isolated on a vascular pedicle and can be moved to another site
Anterolateral thigh flap
—branches of lateral femoral circumflex artery and skin paddle
Radial forearm flap
-branch of radial artery and skin pedicle
DIEP / TRAM flap
DIEP/TRAM flap— branches of the deep inferior epigastric artery and skin paddle
TRAM: take muscle
Hydrofluoric acid burn
Requires calcium gluconate
Causes hypocalcaemia
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
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.
Superifical partial thickness burn
Papillary demris only
Deep partial thickness burn
Papillary dermis
AND
Reticular dermis (adnexal structures involved)
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
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
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
Renal agenesis
Unilateral or bilateral
Failure of mesonephric duct to give rise to ureteric
bud, with failure of induction of metanephric blastema
β-naphthylamine
–> bladder cancer
high exposure in dye and rubber industry
Cyclophosphamide increases risk of which cancer
Alkylating agents e.g. cyclophosphamide
Small risk of leukaemia
Cancer developing at the sites of previous radiotherapy treatment for breast cancer
Angiosarcoma
Clonorchis sinesis
Liver fluke
Sits in biliary system –> cholangiocarcinoma
Nickel exposure cancer
Nickel exposure is associated with nasal and
bronchial carcinoma
Betel nut
Chewing betel nut is associated with increased
risk of neoplasms of oral cavity
Li-Fraumeni
p53
Breast carcinoma
Ovarian carcinoma
Astrocytomas
Sarcomas
Retinoblastoma
Rb1
Genetically associated –> bilateral
Sporadic –> unilateral
Retinoblastoma
Osteosarcoma
Familial polyposis coli
APC gene
Chromosomal location 5q 21
Mainly colon cancer
Other GI tract malignancies
von Hippel-Lindau
VHL
Renal carcinoma
Phaochromocytoma
Haemangioblastoma
MEN syndromes
RET
Familial breast cancer
BRCA1
BRCA2
Breast caricnoma
Ovarian syndrome
Prostatic carcinoma
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.
Krukenberg tumours
Spread of stomach carcinoma –> ovaries
Signet ring cells - primary is gastric adenocarcinoma which are mucinous signet ring cell
Autoimmune disease trigerred by malignancy
Dermatomyositis
Membranous glomerulonephritis
Cervical screnning
Women aged 25–49 years old, screened every 3
years
Women aged 50–64 years old, screened every 5 years
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