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MRCS part B- JMB > Surgical Pathology > Flashcards

Surgical Pathology Flashcards

1
Q

Function of plasma proteins?

A 
Albumin- binds and transports calcium, on oncotic pressure
Immune system
Completement cascade
Clotting
Enzymes
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2
Q

Causes of raised urate?

A

Idiopathic
Inborn errors of metabolism

Alcohol
Diuretics
Protein rich foods

Causes
Gout
Renal failure
Renal calculus

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3
Q

Role liver?

A 
Bike production and conjugation
Clotting factor production
Drug metabolism
Glycogen storage
Plasma proteins 
Reticulendothelium system
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4
Q

Life cycle of bilirubin

A

RBCs broken down to haem and then biliverdin
Converted to bilirubin
Conjugated by binding to albumin by hepatocytes
Excreted in bile
Excreted in kidneys as urobilin- yellow
Farces- sterobiliogen- brown

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5
Q

Commonest renal stones?

A 
Calcium oxalate- 77%
Struivate- 15%
Uris acid -5% (radiolucent)
Cystine- 2%
Xanthine- 1%
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6
Q

Gall stone commonest?

A

Mixed-85%- fat femal fair forty
Cholesterol-10%
Pigment-5% haemolysis

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7
Q

Bile volume per day and composition?

A

1500ml/day

Bike pigments
Bike salts
Cholesterol
Electrolytes
Water and bicarbonate
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8
Q

Amyloid definition?

A

A group of degradation resistant proteins with a beta pleated structure

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9
Q

How to diagnose amyloidosis?

A

Biopsy
Stain with Congo red
Apple green birefringence under polarised light

Isotope scan for hotspots

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10
Q

Types of amyloid?

A

AL- myeloma leading to global production of Ig amyloid
AA- chronic inflammation- macrophages releasing interleukins. Ra/ibd/tb
PrP- prion diseaze

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11
Q

Consequences of amyloid?

A

Organ failure
Localised deposits- larynx and thyroid
Medullary thyroid cancer
Organomegally

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12
Q

Cause of death in amykoidosis?

A

Myocardial amyloid

Leads to arrhythmia sand heart failure

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13
Q

Aetiology of microcytic anaemia?

A

Iron deficiency- bleeding, poor intake, low absorption, increase demand
Thalassaemia
Sideroblastic anaemia

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14
Q

Aetiology of macrocyclic anaemia?

A 
B12/folate deficiency- megloblasts on blood film
Alcohol
Hypothyroidism
Myelodysplasia 
All normoblasts on blood film
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15
Q

Normocytic anaemia aetiology

A

Chronic disease
Renal failure- epo
Sickle cell anaemia- hydrolysis
Spherocytosis

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16
Q

Microscopy of b12 anaemia?

A

Macrocytosis
Howell jolly bodies
Hypersegmented neuclei in neutrophils

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17
Q

Aetiology of b12

A

Poor intake
Pernicious anaemi
Ileal/ gastric resection
Crohns

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18
Q

Aetiology of folate deficiency

A

Decrease intake
High demand- pregnancy/cancer
Drugs- methotrexate
Malabsorption-coeliac

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19
Q

Sickle cell pathogenesis?

A

Autosomal recessive
10-20 day turnover of rbcs
Defective beta chains in HbA leads to less soluble hbS. Which leads to sickle cells

Veno-occlusive disease
Ischaemia
Pain crises

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20
Q

Blood film findings of sickle cell

A 
Normochrmia
Normocytic
Reticulocytes
Sickle cells
Target cells
Howell jolly bodies
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21
Q

Causes of sickle cell crises?

A

Infective
Low o2
Hypothermia
Dehydration

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22
Q

Thalassaemia features?

A 
Autosomal recessive haemolytic disease
3 types
Alpha
Beta
Delta
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23
Q

Beta thalassaemia blood film?

A 
Hypochromic
Microcytic
Reticulocytes
Target cells
Howell jolly bodies
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24
Q

Process of haemostasis?

A

Vasoconstriction
Platelet aggregation and activation
Clotting cascade- secures platelet plug

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25
Q

Function of platelets?

A

Primary haemostasis

vWF and TXA2 for platelet activation
Phagocytosis
Cytokines signalling

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26
Q

Draw clotting cascade

A

https://www.osmosis.org/answers/coagulation-cascade

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27
Q

Which clotting factor is calcium?

A

Factor 4

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28
Q

What are the moa of heparin, clopidogrel and txa?

A

Heparin- inhibited factor 10a- potentiates antithrombin III
Clopidogrel- ADP receptor inhibitor- prevents platelet aggregation
TXA- inhibits plasmin, prevents clots from breaking down

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29
Q

How is blood processed to be ready for transfusion?

A

Viral screening
Centrifugation
Leucofiltration- decreases cmv reaction
Irradiation- optional- prevent gvhd

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30
Q

What is FFP and cryoprecipitate

A

FFP- top layer of centrifuged blood- plasma, contains clotting factors, compliment, fibrinogen, vWF and albumin

Cryo- precipitate of ffp, factors 8, 13 and vWF.

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31
Q

Definition of oedema?

A

Generalised or localised collection extracellular fluid

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32
Q

Aetiology of lymphoedema?

Surgical treatment?

A

1- milroys
2- iatrogenic, malignancy, infection

Treatment surgical- homans/Charles/lympho anastomoses

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33
Q

What is starlings law of the capillaries?

A

Governs the net filtration across capillaries

= capillary pressure- interstitial hydrostatic pressure

  • capillary pressure - oncotic pressure

Taking into account lymphatic drainage

Hydrostatic pressure- pressure blood exerts on the wall

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34
Q

Oedema aetiology?

A

Increase hydrostatic pressure- heart failure, fluid overload

Decrease oncotic pressure- liver/kidney failure

Capillary leakage- inflamm/anaphylaxis

Lymphatic failure

Drugs- nifedipine

Gravitational

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35
Q

Types of hypersensitivity reactions?

A

Acids

Type 1- allergic 
Type 2- cytotoxic- good pastures 
Type 3- immune complexes- sle
Type 4- delayed- transplant related 
Type 5- stimulatory- graves
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36
Q

Name some cell mediators of the immune response?

A

Bradykinin- vasodilation and permeability
Histamine- same as above + puritus + gastric acid secretion
Leukotrines c4- bronchoconstriction + vascular permeability
Prostaglandins d2- neutrophil recruitment, vasodilation, bronchoconstriction
TXA2- vasoconstriction, bronchoconstriction, platelet aggregation

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37
Q

Name some cytokines?

A

Il4- cd4 t helper cell proliferator
B cell ige synthesis

Il5 histamine and leukotrine release
B cell proliferation, eosinophil recruitment

Il13 cd4 t helper cell proliferation

Tnfalpha neutrophil activation

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38
Q

What is the complement cascade?

A

Part of the innate immune system
Involved in the clearance of pathogens via production of MAC
4 pathways
Classic
Lectin- independent of ab-ag complexes
Alternative- same as above
Final common- leads to MAC production, opsonisation, chemotaxsis

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39
Q

What is the composition of Ig?

A

Fab region- heavy and light chains- fragment bindings region- variable region

Fc region- interacts with cell surface fc receptors- contstant

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40
Q

Types of immune response?

A

Cell mediated- T cell mediated- production of cd4 T cells, macrophages and NKCs

Humoral- B cell mediated- ab release, complement, opsonisation, phagocytosis

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41
Q

Roles of the Ig?

A 
IgM- first released
IgG- majority of humoral response
Crosses placenta
IgD on b lymphocytes and bind to Ag
IgA primary Ab in bodily secretions
IgE binds to basophils and mast cells to promote degranulations of cytokines and mediators
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42
Q

What is leukocyte margination and emigration?

A

Normally flow in centre of blood stream
Margination- move to plasmatic peripheral zone
Emigration- pavementing then active migration across endothelium

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43
Q

What is a granuloma?

A

Collection of modified macrophages +- time of surrounding lymphocytes
Seen in TB/sarcoid

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44
Q

What is the cellular process during chronic inflamm?

A 
Lymphokine production- IFN gamma
Activate macrophages release growth factors
Fibroblast proliferation
Neovascularisation
Tissue destruction
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45
Q

What is a cyst and pseudo cyst?

A

Cyst abnormal membrane lined sac containing fluid- epithelial cells

Abnormal collection of fluid surrounded by granuloma/fibrous tissu

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46
Q

What is an abscess?

Why?

A

Localised collection of pus surrounded by granulation tissue

Neutrophils/macrophages release enzymes that split large molecules to small ones increasing the oncotic pressure

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47
Q

What is a fistula / sinus

A

Fistula is an abnormal communication between two epithelial surfaces

Sinus- blinding ending tract in communication with an epithelial surfsce

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48
Q

What is pus?

A

Pus is made out of fluid and solid components
Fluid- exudate of plasma proteins, water

Solid- live and dead- macrophages/neutrophils/bacteria

Dead human cellS
Fibrin

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49
Q

Describe the process of wound healing?

A

Cutting is pleasing repetitive
Coagulation- seconds
Inflammatory days
Proliferation weeks- granulation and epithelisation
Remodelling- years- reorganisation, regression, scar tissue

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50
Q

Epidemiology of SSIs?

A

5% of cases
Superficial skin
Muscle/fascia
Organ/cavity

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51
Q

What are endotoxins?

A

Proteins released by gram - bacteria. Lead to pyrexia/shock/dic

Activate clotting/complement
Cause fibrin degradation
Lead to cytokines formation

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52
Q

What are exotoxins?

A

Formed by gram + can lead to tetanus and gangrene

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53
Q

What are nosocomial infections?

A

Hospital acquired infections

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54
Q

Phases of the cell cycle

A

G0 resting phase
G1 regulation of the duration of cell cycle
R restriction point in G1. Rb tumour suppression gene
S synthesis phases
G2 rapid growth and 2nd check point p53
M mitosis

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55
Q

What stimulates and inhibits the cell cycle?

A

Stimulation
Cyclins d&e
Cyclin dependent kinase

Inhibition
P53
Rb gene

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56
Q

Difference between dysplasia, metaplasia and neoplasia?

A

Dysplasia is abnormal cell development. Premalignant
Metaplasia is replacement of one fully differentiated cell type with another
Neoplasia is an abnormal mass of tissue due to uncontrolled and progressive cell division

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57
Q

Tumour markers for testicular teratoma? And breast/pancreas/ovary?

A

Testicle- bhcg, afp

Breast ca153
Pancreas ca199
Ovary ca125

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58
Q 
Carcinogens?
Bladder
Burkitts
Cervix
Cholangiocarcinoma
HCC
Kaposi
Leukaemia
Lymphoma
Lung
Nose
Skin
A 
Dyes and nitrosamines
Ebv
Hpv
Liver flukes
Afalatoxin, HBV HCV
HHV8
HTLV
Cyclophosphamide
Asbestos and tobacco
Sawdust
UV light
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59
Q

Cellular features of malignancy

A 
Macroscopic
Growth
Necrosis
Infiltration
Metastasis
Haemorrhage
Microscopic
High mitotic rate
Pleomorphism
Hyperchromatism
High nucleus to cytoplasmic ratio
60
Q

Commonest cancers and highest mortality?

A

Skin, lung, prostate, breast colorectal

Lung, colorectal, breast, prostate, oesophageal

61
Q

Endocrine paraneoplastic syndromes?

A

Cushings- small cells lung and pancreas
SIADH- small cell lung cancer
Hypercalcaemia- squamous lung cancer, breast, ovarian, rcc
Carcinoid- lymphoma, gastric, pancreatic

62
Q

Haematological paraneoplastic syndromes

A 
Aplastic anaemia (pan cytopeni) - thymus
Polycythaemia- RCC/HCC
63
Q

MSK paraneoplastic syndromes

A

Acanthodians nigracans- gastric/lung cancer- EGF

Dermatomyositis (skin rash, muscle weakness) -breast/ lung

64
Q

Neurological paraneoplastic syndromes?

A

Cerebellum degeneration- lung overian breast

Lamber Eaton syndrome- lung prostate cervix

65
Q

Definition of of clot thrombus and embolus

A

A clot describes a collection of solid material (made of the constituents of blood) found in stagnant blood

Thrombosis is the progression of a clot with Virchow triad in the same place as it formed in flowing blood

Embolus is a clot distant to where it was formed

66
Q

What is Virchow triad?

A

Endothelial damage
Hypercoagulable stage
Stasis or turbulent blood flow

Leads to thrombosis

67
Q

Trauma triad?

A

Hypothermia
Acidosis
Coagulopathy
(Hypocalcaemia?- citrate theory)

68
Q

Definition and RFs of an atheroma

A

Lipid collection within the tunica intima of arteries. May have foam cells

Congenital- fhx, make, familial hyperlipidaemia

Acquired- diabetes, smoking, hypertension, hyperlipidaemia

69
Q

Theories of the formation of an atheroma?

A

Imbition- circulating lipoproteins
Proliferation- smooth muscle hyperplasia
Encrustations- lipid portion of atheroma derived from pre existing thrombus

70
Q

Definitions of infarction and ischaemia?

A

Ischaemia- abnormal reduction in blood supply/drainage

Infarction- tissue/organ necrosis due to poor blood supply

71
Q

Definition of an aneurysm?

A

Abnormal vessel dilation by more than 50%

72
Q

Classification of aneurysms?

A

Aetiology- congenital/acquired- infection/trauma/hypertension

Morphology- saccular vs fusiform

Pathology- true/false/dissecting

73
Q

Aetiology of aneurysms?

A 
Congenital
Atherosclerosis
Htn
Infective
Ischaemia
Traumatic
Iatrogenic
74
Q

Difference between true, dissecting and false aneurysms?

A

True involve all three layers of arterial wall
False does not

Dissecting- blood running through media/adventitia. Can lead to vessel occlusion

75
Q

Composition of bones?

A

Cellular- osteoprogenitor cells
Osteoclasts, osteoblasts

Matrix- inorganic- calcium hydroxapitate
Organic- type 1 collagen

76
Q

Types of bone

A

Anatomically- Flat vs Long bone

Macroscopically- Cortical vs Cancellous

Microscopically- Lamellar vs woven

Flat bone- irregular structure- skull/scaphoid
Long- regular structure- diaphysos, metaphysis, epiphysis- femur/tibia

Woven- haphazardly organised collagen fibres, pathological/immature
Lamellar- regular parallel alignment of collagen fibres

Cortical- hard outer layer of bones. Composed of tightly tightly packed osteons with Haversian canals
Cancellous- porous central layer of bone, high turnover

77
Q

What is the process of fracture healing?

A

Coagulation- haematoma formation
Inflammatory- granulation and fibroblasts proliferation
Proliferation- callous- woven bone- chondroblasts and osteoblasts. Lamellar bone formation.
Remodelling- cortical bone replaces woven bone

78
Q

Principles of fixation principles

A

Reduce
Restrict
Rehab

79
Q

Why does smoking lead to poor bone healing?

A

Decreased calcium absorption
Decreased vit d
Increased non union and malunion

80
Q

Osteomyelitis aetiology
< 4 months
4months- teenager
Adults

DM
Immunocomprimised
HIV
Sickle cell

A

Vaginal flora- staph a/strep/ E. coli
Staph a/gas/hi
Staph a/enterococcus/gbs

Anaerobes
Aspergillosis/candida
TB
salmonella

81
Q

Pathogenesis of osteomyelitis?

A

Acute inflam leads to compression of capillaries
Osteonecrosis
Dead bone fracture separate off necrosis
New bone formation around this

82
Q

Aetiology of septic arthritis?

A

Direct trauma
Haematogenous spread
Dissemination- osteomyelitis/cellulitis
Iatrogenic

83
Q

What is the reconstructive ladder?

A

Secondary intention
Primary closure
Skin graft
Flap (free vs pedicled)

Adjuncts- negative pressure dressings

84
Q

What are the different types of graft?

A

Split skin graft- takes epidermis and portion of dermis- poor colour/contracts

Full skin graft- takes epidermis and Dermis- requires a well vascularised bed

85
Q

Differences between keloid and hypertrophic scars?

A

Keloid- thick and raised. Extends beyond boarders. Appears over years. Afro Caribbean. Increased collagen synthesis

Hypertrophic- thick and raised. Within boarders, appears in weeks, regresses

86
Q

Types of muscles

A

Skeletal- located at joints- striated and voluntary
Type 1- slow twitch, type 2 fast twitch

Cardiac- striated and voluntary
Smooth- vessels and viscera. Greater stretch ability and prolonged contraction. Calmodulling is binding agent

87
Q

Draw a sarcomere and describe the sliding protein theory and muscle contraction

A
88
Q

Types of cartilage

A

Fibrocartillage- type 1 collagen. Pubic symphysis. High tensile strength

Hyaline- type 2 collagen. Hard. Smooth articular surfaces

Elastic- lots of elastin. Pinna. Epiglottis.

Fibroelastic- meniscus

Physeal

89
Q

Features of Men 1

A

Pancreatic tumour
Pituitary adenoma
Primary hyperparathyroidism

90
Q

Features of men 2a/b

A

2a- phaeochrmocytoma, medullary thyroid ca, 1o hyperparathyroidism

2b- phaeochromyocytoma, medullary thyroid cancer, multiple neuromas, marfanoid habitus

91
Q

Aetiology of gynaecomastia

A

Raised oestrogen to androgen ratio

Physiological- puberty/old age

Pathological- cirrhosis, hyperthyroidism, hypogonadism, kleitfelters, testicular tumours.

Pharmacological- steroids, spironolactone (anti androgen)

92
Q

Draw out the pth and calcium homeostasis

A

https://www.researchgate.net/figure/Calcium-Homeostasis-and-Selected-Causes-of-Hypercalcemia-in-Pediatric-Patients-The-serum_fig1_49822084

93
Q

Embryological Origins of superior and inferior parathyroid glands

A

Superior- 4th pharyngeal pouch

Inferior - 3rd pharyngeal pouch

94
Q

Aetiology of hyperparathyroidism?

A

1o- single parathyroid adenoma (85%)
Parathyroid hyperplasia (10%)
Carcinoma (1%)

2o - physiological response to chronic hypocalcaemia secondary to renal failure

3o - hyperplasia of parathyroids from 2o leading to raised pth

95
Q

Cushing’s syndrome clinical features?

A 
Ulcers
Cataracts
Diabetes
Fluid retention
Atrophy
Pancreatitis
96
Q

Aetiology of Cushing’s syndrome?

A

ACTH dependent- cushings disease- pituitary adenoma. Paraneoplastic cancer

Independent- steroids, adrenal cortex neoplasm

97
Q

Carcinoid syndrome definition?

A

Neuroendocrine tumour arising from APUD cells
Intestinal- appendix/ small bowel
Extra intestinal- lung ovary testis

98
Q

Classical carcinoid syndrome and diagnosis?

A 
Abdo cramps
Bronchoconstriction 
Cardiac failure
Diarrhoea
Flushing

24 hr urinary 5-HIAA
octreo scan- hot spots
Ct/mri
Laparotomy

99
Q

Draw the thyroid hormone homeostasis

A
100
Q

Aetiology of hyper and hypo thyroid

A

Hyper- iodine excess, graves (anti tsh receptor abs), toxic nodule, subacute thyroiditis

Hypo- iodine deficiency, hashimoto’s (anti tpo abs anti thyroglobulin abs)

101
Q

Role of thyroid hormone

A

Cellular metabolism and glycogenolysis
Growth and development
Increased sensitivity to adrenaline
Increased gut motility

102
Q

Types of amyloid disease?

A

AL amyloid- Clonal expansion of plasma cells producing amyloid Ig
AA amyloid- chronic inflam lead to macrophages stimulating hepatocytes to produce precursor to amyloid
Prions disease

103
Q

Complications of EVAR?

A

Intraop- rupture, failure of op- endo leak

Post op- mesenteric/renal ischaemia, infection, MI

104
Q

Causes of appendicitis?

A

Faecoliths
Tumours- carcinoid
Lymphoid tissue
Foreign object

105
Q

Ascites aetiology? More detail

A

Exudate- increased vascular permeability
4Ps- peritonitis, post irradiation, peritoneal mets, pancreatitis

Transudate
Increased interstitial pressure- cirrhosis, budd chiari, RHF
Decreased oncotic pressure- liver/renal failure

106
Q

Underlying process of atherosclerosis?

A

Endothelial damage leading to inflam response (caused by trauma/htn)
Foam cells and lipid core (aided by hypercholesterolaemia)
Stenosis/thrombosis

107
Q

What is the carcinogenic version of fibroadenoma?

A

Phyllodes tumour

Worry if rapid growth and in >35yo

108
Q

Management of breast abscesses?

A

Lactational vs non lactational (smoking association)

USS + Drain for MCS
IV Abx

109
Q

Causes of gynaecomastia?

A

Physiological
Lower testosterone- testicular tumour/atrophy
Raised oestrogen- leydig cell tumour, liver disease, obesity, adrenal tumours
Medication- spironolactone, antipsychotics, chemo
Idiopathic

110
Q

Causes of nipple discharge?

A 
Physiological
Prolactinoma
Duct ectasia
Intra-ductal papilloma
Hyperplasia
111
Q

Causes of a cholangiocarcinoma?

A

Developed world- PSC
Non developed- Liver flukes

HIV/Chronic liver disease

112
Q

Difference between PSC and PBC?

A

PBC- interlobar ducts affected
Chronic granulomatous disease leading to cirrhosis/cholestasis
AMA +ve

PSC- intra and extrahepatic ducts
Fibrosis and stenosis
pANCA

113
Q

Types of bone tumours?

A

Benign- osteochondroma (10-20yrs old), giant cell tumours
1o- multiple myeloma
Osteosarcoma
Ewings- onion skin, 5-20 yo

2o- mets
Breast
Lung
Thyroid
Kidney Prostate

BLT and a packet of KP crisps

114
Q

Layers of the GI tract?

A

Mucosa (epithelium, lamina propria, musclaris mucosa)
Submucosa
Musclaris propria
Adventitia

115
Q

What is the adnoma carcinoma sequence?

A

A series of mutations leading to hyperproliferation metaplasia and dyslplasia

APC, KRAS, p53

116
Q

What is a neoplasm?

A

A tumour
Abnormal mass of tissue
Demonstrating uncoordinated growth
And continued growth despite removal of the stimulus

117
Q

What is metaplasia and dysplasia?

A

Reversible change in cell type

Dysplasia- uncoordinated cellular development, no basement membrane invasion, mitosis and pleomorphism

118
Q

What type of cells involve a carcinoma and a sarcoma?

A

Carcinoma- epithelial cells

Sarcoma- connective tissue

119
Q

Causes of hypoparathyroidism and hypothyroidism?

A

Iatrogenic- surgery/ DTx

Autoimmune- Parathyroid- addison’s, thyroid- hashimotos

PTH- hypomagmanesia
Thyroid- iodine deficiency

120
Q

What is the LN drainage of the tongue?

A

Tip- submental
Ant 2/3- submandibular
Post 1/3- deep cervical LNs

121
Q

How does H pylori evade destruction?

A

Burrows into mucus lining
Produces urease which neutralises HCL
Forms Ammonia- which cause inflammation of gastric lining

122
Q

How to Dx h pylori?

A

Urea breath test
Stool Ag
Biposy + CLO testing

123
Q

Are chief cells and oxyphyill cells present in normal parathyroid tissue?

A

Yes

124
Q

Components of the corpus callosum?

A

Rostrum
Genu
Body
Sternium

125
Q

What are the stages of acute inflammation?

A

Rubor, Dolor, Calor, Tumour

Vascoconstriction then dilation
Permeability
Neutrophil migration
Phagocytosis
Resolution/chronicity/abscess/death
126
Q

Which cells are present in chronic inflammation?

A

Macrophages
Lymphocytes
Plasma cells

127
Q

What is a granuloma and giant cell?

A

Granuloma- collection of epitheloid macrophages (lots of giant cells)
Giant cell- fusion of epitheloid cells (derived from macrophages)

128
Q

Difference between branchial cyst, dermoid cyst and cystic hygromas

A

Branchial cyst- anterior triangle, failure of obliteration of branchial arch
Dermoid cyst- teratomas, neck midline

Cystic hygroma- lymphatic system blockage, lymphangioma
Post triangle- kids

129
Q

What is the procedure called to remove a thryoglossal cyst?

A

Sistrunk’s- removal of middle part of hyoid bone

130
Q

Types of necrosis?

A 
Coagulative- MI in heart
Liquefactive- Stroke in brain
Caseous- TB
Fat- Breast trauma
Fibrinoid- Type III hypersensitivity
131
Q

Examples of hypertrophy and hyperplasia?

A

Hypertrophy- exercise and muscles, uterus in preg
HOCM

Hyperplasia- grave’s, bph
Breasts in puberty/thyroid in pregnancy

132
Q

What does the glasgow score for pancreatitis tell you?

A

> /3 in 48 hours- ITU discussion- severe pancreatitis

133
Q

Difference classically between a DU and GU?

A

DU- pain relieved by eating, returns after 3 hours

GU- pain related to meals

134
Q

Dumping’s syndrome?

A

Rapid gastric emptying of undigested foods
Leading to fluid shifts (secondary to increased intestinal osmolality)
Hypotension, bloating, flushing, abdo pain

135
Q

Types of intestinal polyps?

A

Benign- harmatomas, inflammatory
Neoplastic- commonest- tublar, villous, tublovillous
Malignant potential- tublovillous, villous, tubular

136
Q

What is PSA?

A

Prostate specific antigen
Tumour marker for Prostate cancer
Enzyme that liquifies semen

137
Q

Types of dialysis?

A

Haemodialysis- cheaper, simpler, diffusion across PPM
Haemofiltration- convection of fluid, iTU
Peritoneal dialysis

138
Q

Complications of renal transplants?

A 
Rejection- dx via biopsy
Delayed function
Thrombosis/stenosis of artery/vein
Ureteric stricture
Infection
Lymphocele
Failure of anastamosis
139
Q

What tumour markers do testicular tumours produce?

A

Teratomas- bHCG and AFP

Seminomas- bHCG

140
Q

What is the role of the white and red pulp of the spleen?

A

Red pulp- filtration of rbc/wbc/platelets

White pulp- Ab production

141
Q

Causes of splenomegaly?

A 
Infective- EBV, TB, malaria
Portal HTN
Lymphoma/leukaemia
Sickle cell/thalassaemia
Systemic- sacroid/amyloid/RA
142
Q

Difference between staging and grading of cancers?

A

Staging- size and spread

Grading- differnetiation of a tumor from original cells

143
Q

Causes of SqCC of the bladder?

A

Chronic inflam
Schisto
Catheter- long term
Bladder stones

144
Q

How does hypercalcaemia lead to groans?

A

Leads to increased HCL release- ulcers

145
Q

How to Dx TB?

A

Active disease- biopsy + PCR, CT/CXR

Latent- quanterferon gold/mantoux test

146
Q

Causes of granulomas?

A

INfective- TB/schisto/fungal

Non infective- sarcoid/RA/Crohn’s

147
Q

Types of bones?

A

Long vs flat
Macroscopically- cortical vs cancellous
Microscopically- lamellar (organised), woven (pathological/growing)

MRCS part B- JMB (10 decks)

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