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Exam 1 > MoD week 4-7 > Flashcards

MoD week 4-7 Flashcards

1
Q

what is fibrous repair?

A

inflammatory, endothelial & fibroblasts cells infiltrate
blood clot forms (cytokines)
acute inflammation becomes chronic
clot is digested and replaced by granulation tissue
local hypoxia initiates angiogenesis (VEGF)
fibro/myofibroblasts produce ECM causing a scar
maturation is long lasting, cell population falls, collagen increases
myfibroblasts contract to reduce size
blood vessel differentiate and reduce

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2
Q

what are the 3 types of regeneration?

A

labile e.g. epithelial, in active cell division ATT
stable e.g. hepatocytes, enter cell cycle when required
permanent e.g. nerves, no stem cells to mitose

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3
Q

what is regeneration controlled by?

A

GF, hormones, proteins, contact between BM (e-cadherin) and between cells (integrin) - contact inhibition (cells stop growing when they meet)

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4
Q

what is healing by primary intention?

A

clean incised wound, apposed edges, minimal granulation & bleeding, loss of contact inhibition, epidermis regenerated, dermis undergoes fibrous repair
the wound closes first (epidermis) before dermis so can trap bacterial / infection

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5
Q

what is healing by secondary intent?

A 
large skin defect, infarct or ulcer
unopposed edges
granulation tissue from wound edges
loss of contact inhibition
epidermis repairs from base up
more myofibroblasts
large scar
takes longer
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6
Q

what are local factors which affect healing?

A 
type, size, location
apposition
blood supply
infection
foreign material
radiation
surgery
mechanical stress
necrosis
protection
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7
Q

what are general factors which affect healing?

A

age, drugs, diet, anaemia, obesity, general health, malignancy, genes, CVS status

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8
Q

how does the cardiac system heal?

A

limited, forms scar

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9
Q

how does the liver heal?

A

regeneration

enlargement of loves to compensate growth + replication of cells

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10
Q

How does a peripheral nerve heal?

A

schwann cells 1-3mm/day
regenerates proximal axon (elongate)
distal axon degenerates (wallerian degeneration)
use vacated schwann cells to guide axon growth

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11
Q

how does CNS heal?

A

gliosis
no healing as it is permanent
when damaged, support cells proliferate (glial cells)

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12
Q

how does muscle regenerate?

A

satellite cells (support)

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13
Q

what are some of the complications of healing?

A
  1. insufficient fibrosis
  2. excessive fibrosis (keloids)
  3. excessive contraction - contracture (pull on muscle) / stricture (narrowing of opening)
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14
Q

what is haemostasis?

A

body’s response to blood loss

cessation of bleeding, halting of blood loss

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15
Q

what are the stages of haemostasis?

A
  1. severed artery contracts to decrease pressure downstream
  2. platelet plug forms
  3. platelet plug stabilised by fibrin
  4. organisation and replaced by granulation tissue
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16
Q

how is haemostasis regulated? (think about thrombin, what stimulates and what inhibits)

A

positive feedback from thrombin (prothrombin –> thrombin –> fibrinogen –> fibrin)
thrombin inhibited by: antithrombin III & a-1 antitrypsin & protein C

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17
Q

what is haemostasis regulated by? (breakdown of fibrin)

A

plasmin breaks downs fibrin clots
plasminogen –(t-PA),(streptokinase)–> plasmin –> fibrin –> fibrin fragment
heparin enhances antithrombin III
warfarin –> antagonises vit K (needed for clotting)

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18
Q

what is thrombosis

A

formation of a solid mass in the blood stream during life

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19
Q

what is thrombosis caused by?

A

virchow’s triad, abnormalities in:
blood flow
blood component
endothelium wall (vessels)

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20
Q

what do arterial thrombosis look like?

A

pale, granular, lines of zhan, low cell content

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21
Q

what do venous thrombosis look like?

A

deep red, soft, gelatinous, high cell content

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22
Q

what are the fates of thrombus?

A

PORER
Propagation: thrombus spread and travel in direction of blood flow
Organisation: ingrowth of fibroblasts
Resolution: break down
Embolism: break off to lodge at different location
Recanalisation: blood vessels go through thrombus - supply

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23
Q

what is DIC?

A

clots everywhere - widespread around the body

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24
Q

what is embolism?

A

blockage of a blood vessel by a solid, liquid or gas at a site distant from its origin

25
Q

what are the types of embolism?

A 
DVT
pulmonary embolism
thromboembolism
paradoxical
atheroma emboli causing TIA (stroke)
fat and bone marrow post fracture
gas: air, amniotic fluid, nitrogen
26
Q

what is paradoxical embolism?

A

in arteries through arteriovenous anastomoses (AVA) or PDF (patent foramen ovale)

27
Q

what is an atheroma?

A

accumulation of intra and extra cellular lipid in intima & media of large and medium sized arteries

28
Q

what is an atherosclerosis?

A

thickening and hardening of arterial walls from formation of atheroma

29
Q

what is arteriosclerosis

A

thickening of arterial & arterioles walls from hypertension and DM

30
Q

what are macroscopic changes of atherosclerosis? (simple & complicated plaque)

A 
fatty streak, 
simple plaque (irregular outline, raised yellow / white enlarge & coalesce)
complicated plaque (calcification, thrombosis, haemorrhage, aneurysm formation)
31
Q

what are microscopic changes of atherosclerosis

A

early changes: accumulation of foam cells from SMC

intermediate: fibrosis, necrosis, cholesterol clefts
later: disruption extends to internal elastic lamina, media, ingrowth of blood vessels & plaque fissuring)

32
Q

what happens during endothelial damage?

A

platelets (plug) releases PDGF which stimulates smooth muscle cells to proliferate and migrate, taking up LDL causing them to become foam cells
macrophages also come and take up oxidised LDL to become foam cells

33
Q

what are the risks of atheroma?

A

age, gender, genes, hyperlipidaemia, smoking, diabetes, alcohol, infection, obesity, homocysteinuria

34
Q

which markers are shown in atheroma?

A

ApoE: changes in LDL

ACE increases chances of atheroma

35
Q

what are the complications of atheroma?

A

coronary artery (MI), cerebral ischaemia (stroke), mesenteric ischaemia (gut), PVD, ulceration, calcification, aneurysm, haemorrhage, stenosis

36
Q

what is aneurysm?

A

local dilations of an artery due to weak wall
saccular
dissecting
AAA

37
Q

What are the markers of MI?

A

CK-MB

cTnT / cTnI

38
Q

cardiogenic shock

A

caused by MI death to part of LV decreasing heart

39
Q

PAD

A

intermittent claudication
changes on affected limb
impotence and thigh pain mean occlusion higher e.g. le riche syndrome

40
Q

what regulates the cell cycle?

A

G1, S, G2 - all growth phases regulated by cyclin & CDK
cyclin-CDK complex phosphorylates protein RB
allowing progress onto next stage of cell cycle
p53 triggered by damaged DNA
GF stimulates cyclins and inhibits cdki

41
Q

what is regeneration?

A

multiply to replace loss

42
Q

what is reconstitution?

A

replacement of a lost part

43
Q

what is hyperplasia?

A

increase in cell number

physiological: endometrium
pathological: goitre

44
Q

what is hypertrophy?

A

increase in cell size

physio: muscle uterus
patho: ventricular cardiac cells, prostate

45
Q

cardiac hypertrophic

A

increase in capillaries but not enough so relative ischaemia

46
Q

compensatory hypertrophy

A

kidney

47
Q

atrophy

A

decreased in cell size or number

physiological: thymus gland / ovaries
pathological: denervation, disuse, ischaemic

48
Q

what is metaplasia?

A

REversible change from 1 cell type to another replacement of phenotype

adaptive: splenic issuing bone marrow tissue due to disease
detrimental: barrett’s oesophagus

49
Q

what is aplasia?

A

failure of a tissue or organ to develop

aplastic anaemia of BM

50
Q

what is hypoplasia?

A

abnormal maturation of cells within a tissue often precancerous
disordered organisation
reversible

51
Q

what is involution?

A

normal programme shrinkage, thymus in early life

52
Q

what is atresia?

A

no orofice (opening)

53
Q

what is neoplasm?

A

abnormal growth of cells that persist after removal of initial stimulus

54
Q

what is benign neoplasia?

A

rounded mass due to pushing growth at site of origin
cells are well differentiated
minimal pleiomorphism (viariation in size & shape)
low mitotic count with normal form

55
Q

what is malignant neoplasia?

A 
invades and spreads to distant sites
irregular mass infiltration growth edges
range of cells with varying differentiation
nuclear pleiomorphism 
abnormal mitotic figures
56
Q

tumour

A

any clinically detectable lump

57
Q

cancer

A

any malignant neoplasm

58
Q

insitu

A

all the features of malignant neoplasm but no invasion of BM

59
Q

what is dysplasia?

A

pre-cancerous, reversible changes
the enlargement of an organ or tissue by the proliferation of cells of an abnormal type, as a developmental disorder or an early stage in the development of cancer
e.g. cellular change of cells lining the uterus

Exam 1 (39 decks)

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