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Easter revision 2018 > PP > Flashcards

PP Flashcards

1
Q

Are pale cells or pink cells alive or dead?

A

Pale cells are alive, pink cells are dead (have taken up eosin stain)

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2
Q

Name free radicals and how they cause damage

A

Superoxide, OH-

Damage cell membranes by stealing electrons from neighbours

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3
Q

How do anti-oxidants work

A

vits ACE donate an electron

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4
Q

Name three things that can happen to a nucleus in necrosis

A

Pyknosis- nucleus shrinks and dark
Karyorrhexis- breaks into bits
Karyolysis- nucleus dissolves

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5
Q

Describe features of a dying cell

A

Swollen, chromatin clumps, blebs, ER and mito swell, ribosomes detach

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6
Q

Difference between oncosis and necrosis

A

Oncosis is process of dying, necrosis is changes after death 12-24hours

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7
Q

4 types of necrosis

A

Coagulative (e.g. heart, kidney), liquefactive (brain), caseous (TB), fat (breast)

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8
Q

Describe how to prepare slides

A

Add formalin to prevent auto lysis, put in casettes, processor adds water and paraffin wax, blocking, microtome cuts 3-4microns thick, float on warm water bath to remove creases, stain, mount on medium

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9
Q

Explain dystrophic and metastatic calcification

A

Dystrophic- localised calcium crystals from dying/damaged tissue e.g. athero plaques, TB LNs. Crunchy. Normal Ca metabolism
Metastatic- systemic abnormal Ca metabolism e.g. increased breakdown of bone from excess PTH or destruction of bone e.g. Paget’s disease of bone, immobilisation

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10
Q

What is mallory’s hyaline?

A

Keratin clumps in alcholic liver disease

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11
Q

What do HSPs do?

A

Fix misfolded proteins e.g. ubiquitin

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12
Q

Apoptosis definition and process

A

programmed cell death with shrinkage, membrane integrity maintained. p53 activated and outer membrane becomes leaky, cytochrome C released from mito which activates caspases (or TNFa from Tc binds to death R to activate caspases), apoptotic bodies made which express surface proteins, no inflam

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13
Q

Define gangrene (and dry, wet, gas)

A

Gangrene is visible necrosis. Dry is exposed to air, wet is infection, gas is infection with anaerobes (soil e.g. motorbike accident)

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14
Q

What are red and white infarcts?

A

White: in solid organs with occluded end artery
Red: in loose tissues with collateral circulation, or if re-perfused or haemorrhage

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15
Q

What’s ischaemia-reperfusion injury?

A

Reperfusion can make it worse as brings ROS, brings neuts (inflam and damage), and increases complement

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16
Q

Give examples of when K, enzymes, and myoglobin are released from damaged cells

A

K in MI, AST and ALT in liver damage, myoglobin in rhabdomyolysis

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17
Q

Stem cells show ____ replication and are __potent

A

Asymmetrical replication (one stays a stem cell) and unipotent

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18
Q

Describe process of repair/resolution

A

Healing by secondary intention
Haemostasis
Acute inflam
Chronic inflam
Granulation tissue (new capillaries from endo cell prolif, fibroblasts make ECM and myofibroblasts contract)
Early scar (can’t lay down elastin, no melanocyte regen)
Scar maturation

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19
Q

Compare healing by primary and secondary intention

A

Primary is incised, non-infected wound with minimal tissue loss, low granulation tissue, v minimal scar. Basal epidermal cells creep and deposit BM to undermine scab
Secondary is excisional, large tissue loss, or infected, lots of granulation tissue, leaves scar, takes longer, needs big contraction

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20
Q

Components of granulation tissue?

A

Fibroblasts, myofibroblasts, endothelial cells (angiogenesis), macrophages

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21
Q

What cell connecting molecules are there?

A

Cell:cell is cadherin, cell:ECM is integrins

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22
Q

What are the principles of haemostasis?

A

Vasoconstriction, platelet plug blocks, blood coag and fibrin clot (makes clot stable), fibrinolysis

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23
Q

Haemostasis =

A

stopping bleeding whilst maintaining fluidity of blood

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24
Q

What normally inhibits coagulation in blood

A

Endothelial prostacyclin and NO inhibit platelet aggregation
Plus nothing for platelets to bind to: vWF not expressed

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25
Q

How do platelets work?

A

Block the hole- have cytoskeleton proteins to change shape, have pseudopodia to help sealing. Release granules. Have a fibrin R to cross-link with other platelets

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26
Q

What granules do platelets have?

A

Dense: adrenaline, ATP, ADP, calcium, 5HT
Alpha: fibrinogen, thromboxane A2 (vasoconstricts and platelet aggregation)

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27
Q

Describe the fibrinolytic system

A

Plasminogen —TPA—> plasmin which breaks down fibrin. Protein C (protein S is a cofactor) decreases fibrin formation, antithrombin III and TFPI

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28
Q

What are PT and APTT?

A

PT is extrinsic, APTT intrinsic + common

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29
Q

What do D-dimers measure

A

Released from fibrin of clot as it hardens

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30
Q

What does thrombin time measure

A

Fibrinogen –> fibrin

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31
Q

What’s thrombocytopenia?

A

<150 x 10^9/L

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32
Q

Causes of thrombocytopenia

A

Increased destruction: Immune thrombyocytopenic purpura, thrombotic thrombocytopenic purpur, disseminated intravascular coagulation, haemolytic uremic syndrome, splenic pooling
Reduced production: from megakaryocyte- B12/folate def, cancer/fibrosis in BM, chemo/antibiotics

Either peripheral destruction or marrow failure

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33
Q

Name inherited bleeding disorders

A

Haemophilia A: deficient factor 8. Elevated APTT (intrinsic), normal PT, diagnosed prenatal/birth, muscle haematomas, haemarthoses, post op bleeds. X linked AR
Haemophilia B: deficient factor 9
vWD: AD, most common. vWF carries VIII & role in platelet adhesion so increased APTT and normal PT. Measure VIII cofactor binding. Skin, mucosal bleeding
Thrombophilia: loves to clot e.g. protein C or S deficiency, ATIII deficiency. Cause DVT, PE, stroke

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34
Q

What is DIC?

A

Widespread activation of clotting cascade following trigger e.g. virus (EBV,HCV,CMV), malignancy, ABO transfusion reaction, with microthrombi +++ formed in circulation, using up clotting factors and platelets to cause haemolytic anemia. RBC damage from moving through clots. Increased PT and APTT and D-dimers. Treatment is platelet infusions and LMWH

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35
Q

Name anti-coagulant and anti-platelet drugs

A

Anti-coagulant: heparin (binds to ATIII and increases its activity by x1000) and warfarin (inhibits vit K dep factors)
Anti-platelet: aspirin (inhibits COX which catalyses thromboxane which aggregates platelets), clopidogrel (inhibits ADP from binding to platelets so blocks aggregation)

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36
Q

What should you give for anticoagulant OD?

A

Vit K, FFP, RBCs

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37
Q

What protein drives the stages of the cell cycle?

A

Cyclins! Eg. G1 cyclin for G phase

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38
Q

What are CDKs?

A

Activated by cyclins to drive activity in a particular cell cycle stage

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39
Q

What is p53?

A

Tumour suppressor gene- can induce growth arrest, DNA repair and apoptosis

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40
Q

What is the R point?

A

Near end of G1 and is the point of no return where the cell is committed to completing the cell cycle and no longer requires growth factors. Activates p53

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41
Q

Give examples of physio and patho hyperplasia

A

Physio endometrium from oestrogen

Patho eczema

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42
Q

Give examples of physio and patho hypertrophy

A

Physio uterus in pregnancy

Patho LV hypertrophy

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43
Q

Give examples of physio and patho atrophy

A

Physio breast, muscle

Patho AD cerebral atrophy

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44
Q

Define atherosclerosis

A

Hardening and thickening of arteries as a result of the process of atheroma

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45
Q

Define arteriosclerosis

A

Hardening and thickening of arteries and arterioles NOT DUE to atheroma e.g. diabetes mellitus, HTN

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46
Q

Define atheroma

A

Deposit of lipid intracellularly and extracellularly in the tunica intima and media of medium and large sized arteries

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47
Q

Describe cellular events leading to atherosclerotic lesions

A

Chronic endothelial injury, platelet adhesion, monocytes accumulate, release of growth factors and cytokines
SM cells migrate from media to intima
Macrophages and and SM cells engulf lipid to form foam cells
SM cells proliferate, collagen and matrix deposited, extracellular lipid deposition, neovascularisation

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48
Q

Describe the macroscopic appearance of atherosclerosis

A

Fatty streak, simple plaque, complicated plaque (calcification, thrombosis, haemorrhage, aneurysm)

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49
Q

What’s a complicated plaque?

A

If it calcifies, thrombosis, aneurysm, haemorrhage

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50
Q

Describe microscopic appearance of atherosclerosis

A

Early changes are foam cells, extracellular lipid deposition, SM proliferation
Later changes are fibrosis, necrosis, disruption of elastic lamina, ingrowth of blood vessels, plaque fissuring (breaking), extension into media

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51
Q

Common sites for atherosclerosis

A

Aorta (esp. abdo aorta), carotid, cerebral, coronary, leg

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52
Q

Describe some severe effects of atherosclerosis

A

If in coronary arteries –> IHD –> MI, angina, cardiac arrest
If in carotid –> cerebral –> ischaemic stroke, TIA
If in abdo aorta –> AAA –> rupture –> death
If in leg –> PVD –> intermittent claudication, gangrene, DVT
If in SI –> mesenteric ischaemia –> necrosis/death, ischaemic colitis

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53
Q

Describe different theories of atherogenesis

A

Insudation: endothelial damage and inflam, vessel more permeable, lipid enters
Reaction to injury: endothelial damage cause plaques to form, vessel more permeable, platelet adhesion, monocytes penetrate endothelium, SM cells proliferate and migrate
Monoclonal: each plaque is monoclonal, SM proliferation is key, do they represent abnormal growth like a tumour?
Unifying: endothelial injury (from HTN, raised LDL, smoke) leads to platelet adhesion, SM proliferation, insudation, PDGF release, SM cells make matrix and collagen, SM and macrophages become foam cells, cytokines released

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54
Q

What cells are involved in atherogenesis?

A

SM cells, macrophages, endothelial, platelets, neutrophils, lymphocytes

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55
Q

Name risk factors for atherosclerosis

A

Age, sex, hyperlipidemia, exercise, diet (high fat bad),smoking, hypertension, apoE genotype (affects LDL levels), familial hyperlipidemia, DM doubles risk, >5 units/day alcohol, CMV and H.pylori

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56
Q

Why are platelets important in atherogenesis?

A

Adhesion plus they release PDGF which stimulates SM cell proliferation and migration

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57
Q

Which cells produce collagen in atherogenesis?

A

Endothelial and SM

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58
Q

Associated signs with familial hyperlipidemia?

A

Xanthelasma (hands), xanthoma (eyes), corneal arcus

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59
Q

Atherosclerosis prevention?

A

Stop smoking, decrease fat intake, treat HTN/DM, reduce alcohol intake, regular exercise, lipid lowering drugs if needed, aspirin anti-platelet

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60
Q

Define sepsis, severe sepsis and septic shock

A

Sepsis = SIRS (systemic inflammatory response syndrome) + suspected/confirmed infection. SIRS is RR >20/min, temp >38.5, HR >90bpm
Severe sepsis = sepsis + 1 organ failure
Septic shock = severe sepsis + MAP <60mmHg despite fluids, lactate >4mmol/L

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61
Q

Define neoplasia, dysplasia, anaplasia, metaplasia

A 
Dysplasia = disordered tissue organisation, pre-neoplastic so still reversible
Neoplastic = abnormal growth of cells persisting after initial stimulus removed, irreversible 
Anaplasia = no resemblance to any tissue
Metaplasia = change of one cell to another cell type
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62
Q

Cancer =

A

malignant neoplasm

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63
Q

Atresia =

A

absence of normal opening

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64
Q

Pleomorphism =

A

Variation in size and shape of cells and their nuclei

65
Q

Progression =

A

accumulation of mutations in a monoclonal population

66
Q

Describe macro and micro and behavioural differences in benign and malignant tumours

A

Benign is well differentiated, confined to site of origin, edges well demarcated, regular appearance
Malignant is irregular appearance, have potential to metastasise, areas of necrosis and ulceration, dysplastic or anaplastic, pleomorphic, hyperchromatic, more mitotic figures, increasing nuclear size

67
Q

Difference between in situ and invasive malignancy

A

In situ is before invasive carcinoma which is when it has gone through BM

68
Q

What clonality are neoplasms?

A

Monoclonal. Neoplasm means mutations in a monoclonal population

69
Q

What types of genes are involved in neoplasia?

A

TSGs e.g. p53

Proto-oncogenes are normal genes which if mutated could become oncogenes

70
Q

Name types of benign neoplasms

A

Papilloma, adenoma, leiomyoma, lipoma, glioma, benign teratoma (dermoid cyst), osteoma, fibroma, chondroma, neuroma, neurofibroma, melanocytoma

71
Q

Name types of malignant neoplasms:

A

Osteosarcoma, melanoma, chondrosarcoma, leukaemia, lymphoma, seminoma, malignant teratoma, myeloma, fibrosarcoma, nephroblastoma, carcinoma (breast, lung, prostate, colon), adenocarcinoma (stomach, SI, colon, PTH), leiomyosarcoma, lipsarcoma, sarcoma

72
Q

Invasion =

A

Past the BM

73
Q

How to histologically identify Hodgkin’s?

A

Reed-Sternberg cell (from B cells), pale cytoplasm, one/2 large nuclei, many eosinophils because RS cells release factors that trap them

74
Q

Describe process leading to metastasis

A

Dysplasia (reversible), irreversible carcinoma in situ, invasive carcinoma though BM, can spread through lymph or blood or spaces (transcoelomic spread), grow in secondary site

75
Q

What changes are needed for invasion

A

Altered adhesion: reduced E-cadherin expression (cell-cell), reduced integrin to detach from stroma
Altered proteolysis: MMPs
Altered motility: changes in actin expression
These changes in adhesion, proteolysis and motility is called epithelial-to-mesenchymal transition (EMT)

76
Q

What are micrometastases?

A

Surviving deposits of failed colonisation that can be dormant

77
Q

What is the seed and soil phenomenon?

A

Unpredictable mets because depends on cell-niche environment

78
Q

What’s a sarcoma?

A

Malignant tumour of non-epi tissue

79
Q

Common sites of blood-born mets?

A

Liver, brain, lungs, bone

80
Q

Which neoplasms most frequently spread to bone?

A

Lung, breast, prostate, kidney

81
Q

Which neoplasms that spread to bone cause sclerotic, and which cause lytic, bone lesions?

A

Sclerotic: breast and prostate carcinomas
Lytic: squamous cell carcinoma

82
Q

Describe local effects of neoplasms

A

Pressure/compression, invasion, destruction, ulceration, bleeding, obstruction of tubes and orifices

83
Q

Describe systemic effects of neoplasms

A 
Paraneoplastic syndromes: 
Hypercoagulability
Endocrine tumour hormone production
Cachexia, malaise, anorexia, febrile, hypercalcemia 
DIC
84
Q

Name extrinsic carcinogens and how they work

A

2-napthylamine is purple dye causing bladder carcinoma. Asbestos causes mesothelioma
Ionising radiation strips electron to damage directly e.g. DNA breaks or indirectly by making free radicals
HPV cervical carcinoma (expresses E6 and E7 which inhibit p53 and pRB
HBV/HCV chronic hepatocyte injury
H pylori chronic gastric inflam
HIV lowers immunity so allows carcinogenic infections

85
Q

How much of cancer risk is environmental?

A

85%

86
Q

What is a complete carcinogen?

A

Acts as a both an initiator (mutate) and promoter (proliferate). A carcinogen can only be one of those things

87
Q

What are proto-oncogenes, oncogenes, TSGs and caretaker genes?

A

Proto-oncogenes could acquire a mutation to become oncogenes, oncogenes enhance neoplastic growth, TSGs inhibit neoplastic growth (have 2 alleles), caretaker genes promote genome stability

88
Q

Name some oncogenes

A

RAS, c-myc, HER-2

89
Q

What is the 2 hit hypothesis?

A

TSGs have two alelles so both need to be inactivated

90
Q

Name some inherited tumours

A

HNPCC- AD germline mutation that causes DNA mismatch
Familial breast carcinoma- BRCA1/2 that repairs DSBs
Xeroderma pigmentosum- AR from NER problem so very sensitive to UV, early skin cancer
Retinoblastoma- AD two hit hypothesis
Familial adenomatous polyposis: colorectal cancer.

91
Q

Describe stages in carcinogenesis:

A

Initiators initiate, promoters proliferate, progression occurs (accumulation of mutations in monoclonal population)
May involve adenoma to carcinoma sequence as in the colon, where intestinal epithelium acquires mutations to become an adenoma and further mutations such as p53 to become carcinoma

92
Q

Hallmarks of cancer

A

Immortal (no limit to divisions), grow without growth factors, invasive, resistance to stop signals, angiogenesis, apoptosis resistant

93
Q

What virus can cause Kaposi’s sarcoma?

A

HHV8

94
Q

What virus and parasite causes Burkitt’s lymphoma?

A

EBV. Infects B cells, dysregulates c-myc, cell survives longer
Malaria also, because it reduces resistance to EBV

95
Q

Commonest cancer in adults

A

Prostate, breast, lung, bowel

96
Q

Commonest cancer in children

A

Retinoblastoma, leukaemia, lymphoma, neuroblastoma

97
Q

Leading causes of cancer-related death

A

Lung 10%, , bowel, oesophageal 15%, breast and prostate

98
Q

What’s TNM staging

A

Tumour size, LN involement, mets?

99
Q

What staging system for lymphoma?

A

Hodgy podgy Ann Arbor. Stage for lymph involvement (III is both sides of diaphragm, IV extra-lymphatic) plus a B for B symptoms (weight loss, night sweats, fever)

100
Q

What staging system for colorectal cancer?

A

Duke’s poop. A is into bowel, B is through bowel, C is LN, D is distant mets.

101
Q

What does tumour grading tell you?

A

How well differentiated it is

102
Q

What staging system for breast cancer?

A

Bloom Richardson. Assesses tubule formation (how much normal tubule is left versus cancer), nuclear pleomorphism (how uniform are nuclei), mitotic count (how much division)

103
Q

How does radiotherapy work

A

Ionising radiation that damages cells to trigger apoptosis at checkpoints

104
Q

Name mechanisms of chemotherapy

A

Alkylating- cross links DNA strands (cyclophosphamide)
Antimetabolites- mimic DNA substrates (5FU)
Antibiotics- e.g. bleomycin causes DSBs
Vincristine blocks microtubule assembly

105
Q

Name an anticancer hormone therapy

A

SERM like tamoxifen binds to ER

Androgen blockade for prostate cancer

106
Q

Name a targeted molecular cancer therapy

A

Herceptin binds to HER-2

107
Q

What are neo-adjuvant and adjuvant treatments?

A

Neo-adjuvant: reduce tumour size prior to surgical excision

Adjuvant = after surgical removal to eliminate subclinical disease

108
Q

Describe use of tumour markers

A 
HCG from testicular tumour (testicles trying to be pregnant) 
CEA for CC
AFP for hepatcellular (like AST)
PSA for prostate 
CA125 ovarian (125 eggs)
109
Q

Describe UK screening programmes for colorectal, breast, and cervix

A

Cervix is 25-64 every 3 years
Breast is 50-70 every 3 years
Colorectal is occult blood screening 60-74 every 2 years

110
Q

What’s a struma ovarii?

A

Dermoid cyst (ovarian teratoma) that is mostly thyroid tissue

111
Q

What are fibroids?

A

Uterine leiomyoma

112
Q

For bone pain in a young person, what are your cancer differentials?

A

Osteosarcoma most likely if young. If older then myeloma.

113
Q

Why in osteosarcoma would bone pain increase after exertion?

A

Periosteum containing the blood vessels is stretching by tumour so already a bit ischaemic, increases ischamia in exercise

114
Q

Describe symptoms you might get from a neuroendocrine tumour in the SI

A

For symptoms to occur it must metastasise to liver too otherwise hormones will be metabolised. 5-HT produced by tumour can increase bowel transit to cause diarrhoea, vasodilation from bradykinin, thickened bowel wall causing intermittent ado pain.

115
Q

What does an early first pregnancy do to rates of cancer?

A

Reduces breast cancer because earlier terminal differentiation of breast cells. Increases risk of cervical cancer due to early exposure to HPV

116
Q

What infection can increase risk of bladder cancer?

A

Schistosomiasis because eggs embed into bladder wall

117
Q

What makes asbestos dangerous?

A

Microscopic easily inhaled rigid fibres that aren’t easily metabolised, induces necrosis, generates free radicals, can cause mesothelioma, lung cancer, or asbestosis

118
Q

What is mesothelioma?

A

Cancer of pleura/peritoneum

119
Q

Describe the appearance of squamous cell and basal cell carcinomas

A

Squamous cell has irregular margin and crusted centre

Basal cell from UV exposure, volcano appearance, very rarely metastasises.

120
Q

Name some small cell and non-small cell lung cancers

A

Non-small: large cell, adenocarcinoma, squamous cell carcinoma, neuroendocrine
Small: mesothelioma, carcinoid tumours (a type of neuroendocrine)

121
Q

Which testicular cancers will affect boys at which ages

A

<20: non-seminomatous
20-30: teratoma (positive for AFP and HCG)
30-40: seminoma

122
Q

What’s the difference between a teratoma and seminoma?

A

Teratoma- all 3 germ cell layers

Seminoma- uniform cell type of germ cell epithelium only

123
Q

What cancers is Tamoxifen good and bad for?

A

Binds to ER and inhibits in breast cancer but activates in endometrium so increases risk of endometrial cancer

124
Q

What grading system for prostate cancer?

A

Gleason (gleasy prostate)

125
Q

When is PSA raised?

A

Prostate cancer, prostate hyperplasia, prostatitis,

126
Q

What is cancer staging and grading?

A

Staging is size & spread (TNM, Ann Arbor, Duke,)

Grading is how well differentiated (Bloom Richardson, Gleason,

127
Q

Name the three zones of the acinus

A

Furthest from central vein is periportal, then midzonal/transition zone, inner is centrilobular

128
Q

What microscopic findings occur from paracetamol OD?

A

Coagulative necrosis (ghost outlines), karyorrhexis (breaking nucleus), neutrophil infiltrate

129
Q

Describe effects of excessive alcohol intake

A

Cirrhosis, fatty liver (because breaking down acetaldehyde converts NAD to NADH, which is used in FA synthesis), alcoholic hepatitis, elevated AST, hypoalbuminemia

130
Q

Which areas get liquefactive necrosis?

A

If low connective tissue (brain) or in areas of infection with neutrophils +++ (abscess)

131
Q

What happens in hereditary haemochromatocytosis?

A

Body absorbs too much iron so deposited in skin, joints, bones, heart, liver. Fatigue, joint pain, arthritis, cirrhosis, diabetes, heart failure, osteoporosis.

132
Q

What’s coal worker’s pneumoconiosis?

A

Coal dust inhaled, macrophages trap and transport to LNs, trigger immune response. Fibroblasts activated, can become ischaemic and necrotic and create lung cavities. Can cause COPD, chronic bronchitis, cor pulmonale

133
Q

Causes of meningitis at different ages

A

Newborns: strep pneumoniae, e coli, listeria
Infants/children: strep pneumoniae, neisseria meningitidis
Adults: step, neisseria, listeria

134
Q

Complications of meningitis

A

Hearing loss, vision loss, epilepsy, amputation if sepsis, DIC

135
Q

What bugs often implicated in ascending cholangitis?

A

E.coli and klebsiella

136
Q

Describe stages of lobar pneumonia

A

Day 1-2 is red/purple from dilation of blood vs
Day 3-4 red hepatisation (red/brown), accumulation of fibrin
Day 5-7 grey hepatisation, alveoli filled with exudate (neuts and MO)
Day 8-3 weeks: resolution, exudate drained via lymphatics and productive cough)

137
Q

What’s hereditary angioedema?

A

Recurrent attacks of oedema (face, limbs, airway, GI) due to lack of C1 inhibitor

138
Q

What’s CGD?

A

Chronic Granulomatous Disease, AR defective NADPH oxidase in neuts

139
Q

What are rheumatoid nodules?

A

Granulomas with T & B cells, multinucleate giant cells, due to immune complexes deposition

140
Q

What signs occur in RA

A

LESS: loss of joint space, erosion, soft tissue swelling, soft bones (osteopenia).

141
Q

Complications of Crohn’s and UC

A

Crohn’s: bowel fistulas, anal lesions

UC: colon cancer

142
Q

Tell me about sarcoidosis

A

Presents with tiredness, cough, CXR enlarged hillier LNs, biopsy iwht non caseating granulomas (can still see individual cells), raised calcium and ACE because granulomas secrete it

143
Q

When might a foreign body giant cell arise?

A

After silicone implant rupture causing fibrosis

144
Q

What is traumatic neuroma?

A

Following trauma to axon attempts to connect to distal axon, searches for place to go forming tangled mass –> nodule in that area (regeneration without a direction)

145
Q

Describe Seddon’s classification of nerve injury

A

Neurapraxia: damage to myelin (loss of conduction)
Axonotmesis: damage to myelin and axon. Wallerian degeneration, will regenerate
Neurotmesis: damage to myelin, axon, endoneurium. Wallerian regeneration, will only regenerate with surgery

146
Q

Alport syndrome

A

Defect with type IV collagen. Glomerulonephritis, haematuria and proteinuria

147
Q

How do you treat proud flesh?

A

With cauterisation

148
Q

Immune thrombocytopenic purpura

A

Autoantibodies to platelet membrane glycoproteins to target for destruction

149
Q

Thrombophilia

A

At increased risk of VTE due to absence of anti-coagulation factors e.g. protein C, protein S, antithrombin III

150
Q

DIC?

A

Systemic coagulation caused by trigger e.g. EBV, cancer, sepsis, transfusion reactions. Thrombosis leads to infarction (e.g. renal) but also using of coagulation factors leads to haemorrhagic damage too.

151
Q

Why is an MI red and then white?

A

Red from inflammatory reaction and white from death/fibrosis

152
Q

What’s a paradoxical embolism?

A

Passes from venous to arterial circulation through a defect e.g. patent foramen ovale, septal defect

153
Q

How might fat embolism present?

A

Post surgery that has released fat from BM that has travelled to pulmonary circulation and caused dyspnea

154
Q

PVD presentation

A

Intermittent claudication, gangrene, erectile dysfunction, pain at rest from chronic ischaemia

155
Q

In an AAA, which parts of the wall become thicker and thinner?

A

Thicker- tunica intima

Thinner- tunica media

156
Q

Causes of LV hypertrophy?

A

AV stenosis, aortic regurg, HTN,

157
Q

What cell type changes occur in smoking?

A

Columnar bronchus epithelium changes to squamous to cope with smoke better. Risk of squamous cell carcinoma

158
Q

What’s traumatic myositis ossificans?

A

When bone grows in muscle following trauma because fibroblasts become osteoblasts

Easter revision 2018 (11 decks)

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