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Clinical Conditions > Pathology > Flashcards

Pathology Flashcards

1
Q

Hypoxia?

A

Decreased oxygen supply to tissues

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2
Q

Ischaemia?

A

Decreased blood supply to tissues

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3
Q

Oncosis?

A

Cell death with swelling, changes occurring in injured cells before death

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4
Q

Necrosis?

A

Morphological changes occurring in a cell after it has been dead for 12-24 hours

  • Coagulative (protein denaturation & clumping - solid tissue)
  • Liquefactive (enzyme degradation - loose CT tissue e.g. Brain and infected areas with lots of neutrophils)
  • Caseous (TB) and fat (adipose tissue)
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5
Q

Apoptosis?

A

Controlled cell death with shrinkage, induced by caspases

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6
Q

Gangrene?

A

Necrosis visible to naked eye

  • Dry (coagulative necrosis - air exposure)
  • Wet (Liq necrosis - infections)
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7
Q

Infarction?

A

Necrosis caused by reduction in blood supply
Infarct-area of necrotic tissue due to loss of blood supply
- White –> occlusion of end artery
- Red –> dual blood supply, loose tissue

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8
Q

Ischaemia reperfusion injury?

A

When blood flow is returned to a damaged but not necrotic tissue, it can cause further damage, worse than if no blood flow had been returned to tissue at all.
Causes: oxygen free radicals, more neutrophils leading to more inflammation, complement proteins and pathway

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9
Q

Anthracosis?

A

Caused by long exposure to coal dust
Inhaled and phagocytosed by alveolar macrophages
Travel to peribrochial lymph nodes - blackened lungs and nodes
Usually harmless

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10
Q

Coal worker’s pneumoconiosis?

A

Large amounts of anthracosis - fibrosis and emphysema

Blackened lungs and peri bronchial nodes

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11
Q

Hepatitis?

A

Acute or chronic (over 6 months) inflammation and necrosis of liver
Tests:
High ALT, AST, LDH, bilirubin, PT, ammonia
Low albumin

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12
Q

Alcoholic liver disease?

A 
Acute: similar to hepatitis 
Chronic: fulminant liver failure
-Mallory's hyaline (damaged keratin)
Tests: high bilirubin, alkaline phosphatase, gamma GT, 
Low
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13
Q

Acute pancreatitis?

A

Inflammation of pancreas
Tests
High: serum amylase (24hrs), lipase (72-96hrs)
Could lead to hypocalcaemia - due to precipitation of Ca salts in fat necrosis

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14
Q

Acute appendicitis?

A

Swelling of appendix
Causes coag. necrosis -> perforation -> spreading of inflammation through peritoneum > peritonitis -> septicaemia
Complications: septic shock, fistula
Predisposing factors: family history, high fibre diet, CF, gender

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15
Q

Steatosis?

A

Accumulation of triglycerides
Often seen in liver
Due to: alcohol, diabetes mellitus, obesity, toxins

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16
Q

Inherited angio-oedema?

A

Rare AD deficiency of C1-esterase inhibitor (part of complement). Causes reduced level of C2/4, C3 normal
Symptoms: acute inflammation - non itchy cutaneous angio-oedema (dermis , subcutaneous tissue, mucosa, submucosal tissue), recurrent abdo pain

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17
Q

Chronic granulomatous disease?

A

X-linked or AR genetic deficiency of NADPH oxidase responsible for generating ROS
No ROS for oxygen dependent killing in phagocytes (neutrophils, macrophages)
Causes:
-Chronic suppurative granulomas, abscesses of skin & lymph nodes & lung & liver -> cirrhosis
-Increased susceptibility to bacterial infections, pneumonia, impetigo, cellulitis

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18
Q

Alpha1-antitrypsin deficiency?

A

Liver produces incorrectly folded protein
Accumulates within ER
Does not break down elastase - so elastase breaks down alveolar walls resulting in emphysema
Leads to acute inflammation -> cirrhosis

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19
Q

Hereditary haemochromatosis?

A

AR genetic disorder
Mutation in gene HFE on chromosome 6
Normally HFE competes with Transferrin to bind to receptor. Mutated-> doesn’t bind, transferrin has no competition
Too much Fe absorbed in intestine/cells -> Fe then deposited by skin, liver, pancreas, heart causing haemosiderosis
Symptoms: liver damage, heart dysfunction, pancreatic failure
Treatment: venesection/repeated bleeding

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20
Q

Cirrhosis?

A

Chronic inflammation with fibrosis of the liver, with no normal function
Due to: alcohol, HBV infection, immunological, fatty liver disease, drugs, toxins, obesity
Microscopic: regenerating nodules surrounded by fibrotic tissue

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21
Q

Jaundice?

A

Accumulation of bilirubin - bright yellow
Bile flow obstructed - bilirubin levels rise
It is a breakdown product of haem, stacks of porphyrin rings, formed in all body cells
Usually bilirubin taken from tissues by albumin to liver - excreted in bile
Signs: yellow sclera

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22
Q

Dystrophic calcification?

A

Localised calcification occurring in area of dying tissue, atherosclerosis plaque, ageing/damaged heart vessels, lymph nodes
It is a local change which favours nucleation of hydroxyapatite crystals

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23
Q

Metastatic calcification?

A

Generalised calcification due to hypercalcaemia, which in turn is due to calcium metabolism problems
Hydroxyapatite crystals deposited in normal tissues

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24
Q

Hypercalcaemia?

A 
High calcium
Due to: 
Increased secretion of PTH resulting in bone resorption 
- primary, secondary and ectopic
Destruction of bone tissue
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25
Q

Acute inflammation?

A

Stereotyped, local, vascular, immediate response of living tissues to injury
Symptoms:
Rubor, calor, tumor, Dolores, loss of function
Causes: infection, physical agents, chemicals, tissue necrosis, hypersensitivity reactions

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26
Q

Bacterial meningitis?

A

Acute inflammation in meninges
Exudate of fluid causes swelling, brain compresses because skull is rigid. Could lead to death
Damage of blood vessels by the exudate
Causes vascular thrombosis leading to reduced cerebral perfusion
Caused by: Nisseria meningitidis, streptococcus pneumoniae

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27
Q

Lobar pneumonia?

A

Alveoli gets filled up with exudate, where it should only contain air. Involves one lobe on one lung
Caused by: streptococcus pneumoniae
Effects: worsening fever, prostration, hypoxaemia, dry couch, breathlessness
Complications: lung abscess, empyema, pleural effusion, lung fibrosis, bacteraemia
Can be completely resolved if treated

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28
Q

Bronchopneumonia?

A

Especially seen in young and old patients
Patchy distribution
Involves more than one lobe on lungs

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29
Q

Ulcer?

A

Breach in mucosa to level of submucosa or deeper

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30
Q

Skin blister?

A

Due to inflammation in the skin. Collection of fluid strips off overlying epithelium. Clear exudate (few inflammatory cells)
Causes: heat, sunlight, chemicals
Completely treatable (may leave scarring)

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31
Q

Abscess?

A

Localised acute inflammation that the body can’t control - scarring?
In solid tissues, inflammatory exudate forces tissues apart. Liq necrosis in centre
Causes high pressure and pain, tissue damage (squash adjacent structures)

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32
Q

Chronic cholecystitis?

A

Very common repeated attacks of acute inflammation of gall bladder - chronic inflammation takes over (scarring)
Very thickened fibrotic wall, jaundice, pain
Due to: obstruction by gall stones
Treatment: removal of gall bladder

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33
Q

Gall stones?

A

Block bile duct- gets infected ( bacteria travel from duodenum into bile duct-enough time for invasion because it is blocked) -> ascending cholangitis
Other complications: obstructive jaundice, gall bladder cancer

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34
Q

Inflammatory bowel disease?

A

Family of idiopathic diseases - bowel inflammation
Repeated attacks of acute and chronic inflammation together
Causes diarrhoea, rectal bleeding, weight loss

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35
Q

Ascending cholangitis?

A

Gall stones -> block bile duct- gets infected ( bacteria travel from duodenum into bile duct-enough time for invasion because it is blocked)
Usually E. coli

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36
Q

Ulcerative colitis?

A

Autoimmune inflammation of colon and rectum - usually distal colon
Symptoms: Superficial inflammation only, crypt abscess, distorted crypts, diarrhoea, bleeding, sclerosing colongitis (leads to cirrhosis)
Increases risk of colon cancer
Treatment: colectomy

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37
Q

Crohn’s disease?

A

Inflammation of digestive system lining (any part of GI)
Symptoms: transmural inflammation, discontinuous distribution, cobblestone appearance, granulomas, anal lesions, fistulae, strictures, diarrhoea (crypt architecture not affected)

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38
Q

Gastritis?

A

Caused by helicobacter pylori - stimulates pro-inflammatory cytokines, direct epithelial injury & acid secretions
Microscopically: chronic inflammation, lamina propria fibrosis, mucosal atrophy, intestinal metaplasia
Can cause: Gastro adenocarcinoma, MALT lymphoma

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39
Q

Tuberculosis?

A

Infection caused by Mycobacteria tuberculosis –> produces no toxins
Disease caused by persistence –> chronic inflammation
Affects apexes of lung
Symptoms: Cough, chest pain, fever etc
Granuloma - Langhans giant cells
Caseous central necrosis
Test: Zeil-Neelsen stain, acid-fast

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40
Q

Sarcoidosis?

A

Idiopathic disease causing granulomas
Symptoms: tiredness, cough, enlarged hilar lymph nodes (not found in TB)
Similar presentation to TB, but non-caseating necrosis
Common in young female adults

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41
Q

Keloid scar?

A

Complication of fibrous repair - overgrowth of fibrous scar tissue due to overproduction of collagen -> grows beyond scar borders
Common with Caribbean descent

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42
Q

Scurvy?

A

Vit C deficiency
Reduced cross linking of collagen –> defective helix
collagen lacks strength, is vulnerable
- Unable to heal wounds properly, tooth loss, old scars break (form fresh wounds)
- Less bone formation

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43
Q

Ehlers-Danlos syndrome?

A 
Heterogenous group, inherited disorders
Defective conversion of procollagen to tropocollagen (Type 5 mutation)
Low tensile strength, poor wound healing
-Skin hyperextensive, thin
-Joints hypermobile
-Colon rupture, retinal detachment
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44
Q

Osteogenesis imperfecta?

A

Type 1 collagen deficiency
Too little bone tissue
-fragile skeleton, deformation of long bones
-blue sclera
-hearing impairment, dental abnormalities

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45
Q

Alport syndrome?

A

Type 4 collagen abnormal -X linked disease
Dysfunction of glomerular basement membrane, eye
Presents with haematuria (kids), renal failure (teens), neural deafness, eye disorders

46
Q

Haemophilia A?

A

X linked recessive genetic disorder - lack of factor 8
Excessive bleeding into muscles, joints, post-op, on small cuts
Treatment: recomb factor 8

47
Q

Haemophilia B?

A

X linked recessive disorder - lack of factor 9

Similar to Haemophilia A

48
Q

Von Willebrand’s disease?

A

Usually AD congenital disease - reduced vWF production
Abnormal platelet adhesion, reduced factor 8 activity
Signs: skin/mucosal/gum/nose bleeding, bruising, prolonged bleeding after trauma, menorrhagia

49
Q

Hereditary Haemorrhagic Telangiectasia (HHT)?

A

AD inherited disorder affecting vessel walls
Dilated microvascular swellings increase with time
GI Haemorrhage -> iron deficiency anaemia

50
Q

Immune thrombocytopenic purpura?

A

Autoantibodies act against glycoproteins IIb/IIIa and Ib/IX - decrease in platelets
Can be secondary to immune diseases
Test: PT/APTT normal, bleeding time abnormal
Treatment: immunosuppressants
(Platelet transfusions don’t work - destroyed)

51
Q

Thrombocytopenia?

A

Deficiency of platelets
Due to increased removal (immune destruction [ITP], non-immune [DIC]) or decreased production (virus, drugs, B12/folate deficiency, cancer)
Symptomatic when platelets <30
Causes easy bruising, petechiae, purpura, severe bleeding after trauma, intracranial haemorrhage

52
Q

Disseminated Intravascular Coagulopathy (DIC)?

A

Pathological activation of coagulation
Due to: infection, neoplasia, trauma etc
Many microthrombi formed in blood -> consumption of clotting factors/platelets
Abnormal fibrin clots in RCBs -> microangiopathic haemolytic anaemia (due to abnormal RBCs squeezing through constricted vessels)
Causes haemorrhage, necrosis etc
Tests:
Raised PT/INR, APTT, D-dimers. Low fibrinogen

53
Q

Thrombosis?

A

Formation of solid mass of blood in circulatory system
Due to problem in: vessels walls blood flow, blood components - Virchow’s triad
Outcomes: lysis, propagation, organisation, recanalisation, embolism
Effects: arterial, infarct, oedema (veins)

54
Q

Embolism?

A

Blockage of BV by solid/liquid/gas at site distant from origin
Could be by: air, amniotic fluid, N, tumour cells, thrombus

55
Q

Deep vein thrombosis?

A

Thrombus in deep veins of calf
Stasis -> venous pooling -> abnormal flow -> thrombus
Usually not severe unless causes pulmonary embolism
Risks: immobility, post-op, burns
Symptoms/signs: pain, swelling, tenderness, warmth, oedema, pyrexia , red-blue discolouration
Treatment: IV heparin, oral warfarin (prevents thrombus propagating)

56
Q

Thrombophillia?

A

Inherited defects of haemostasis resulting is predisposition to thrombosis (eg DVT)

  • Factor V Leiden deficiency
  • Antithrombin deficiency
  • Protein C/S deficiency
  • Antiphospholipid syndrome
57
Q

Trousseau’s syndrome?

A

Recurrent episodes of inflammation of BVs due to a thrombus - appearing at different locations
Prevalent in pancreatic cancer

58
Q

Paradoxical embolus?

A

Embolism that travels from vein to artery due to a congenital septal heart defect (hole)
Happens when RA pressure increases due to pulmonary hypertension
Paradox - seems to be moving from low to high pressure

59
Q

Atherosclerosis?

A

Accumulation of intra and extracellular lipid in intima and media of large and medium arteries/thickening of arterial walls due to atheroma
Common in: abdominal aorta, coronary/carotid/cerebral/femoral arteries
Microscopic: prolif. of smooth muscle cells/foam cells, extracellular lipid, fibrosis, necrosis, cholesterol clefts, inflammation, ingrowth of BVs, plaque rupture (leads to thrombosis)
Clinical effects: IHD (MI), stroke, multi infarct dementia, mesenteric ischaemia, peripheral vascular disease, aneurysm
Risk factors: age, gender, familial hyperlipidaemia, smoking, high BP, diabetes, alcohol, infection, diet, family history, obesity

60
Q

Arteriosclerosis?

A

Thickening of arterial walls due to hypertension or diabetes mellitus

61
Q

Peripheral vascular disease?

A

Blood supply to legs affected due to atherosclerosis

Effects: intermittent claudication, ischaemic rest pain, gangrene

62
Q

Familial hyperlipdaemia?

A

Genetically determined abnormalities of lipoproteins
Leads to early development atherosclerosis
Assc. physical signs: arcus, tendon xanthoma, xanthelasma

63
Q

Hyperplasia?

A

Increase in tissue/organ size by increased cell number
In labile, stable tissues
Caused by increased functional demand/hormonal stimulation
Exposes cells to risk of mutations ad neoplasia
Physiological: uterus endometrium (oestrogen influence), bone marrow (hypoxia -> more RBCs)
Pathological: eczema, thyroid goitre

64
Q

Hypertrophy?

A

Increase in tissue/organ size due by increased cell size
Labile, stable and permanent tissues
Caused by increased functional demand/hormonal stimulation
Physiological: skeletal muscle, pregnant uterus
Pathological: heart, bladder

65
Q

Compensatory hypertrophy?

A

Eg If one kidney is small or inactive from birth, other one enlarges (hypertrophies) to compensate for the function

66
Q

Atrophy?

A

Shrinkage of tissue/organ by ether decrease cell size or number
Tissue atrophy reversible only up to a point
Physiological: menopausal ovaries, uterus after child brith
Pathological: atrophy of disuse (muscles), denervation atrophy, inadequate blood supply, inadequate nutrition (muscles), endocrine stimuli loss (breast), persistent injury, senile atrophy, pressure (around benign tumour)

67
Q

Metaplasia?

A

Reversible change of one differentiated cell type to another due to altered stem cell differentiation
Labile, stable tissues
Reversible process, but sometimes prelude to dysplasia and cancer
Does not happen across germ layers
Eg change in epithelium due to cigarette smoke or persistent acid reflux (Barrett’s oesophagus), bone marrow damage (spleen takes over), bone deposition in muscles (fibroblasts->osteoblasts)

68
Q

Traumatic myosistis ossification?

A

Metablastic bone develops in skeletal muscles after trauma
Fibroblasts in muscle undergo metaplasia to osteoblasts
Often in young people

69
Q

Aplasia?

A

Complete failure of specific tissue/organ to develop

Or organ whose cells have ceased to proliferate (bone marrow in aplastic anaemia)

70
Q

Hypoplasia?

A

Congenital condition of under/incomplete development of tissue/organ at embryonic stage

71
Q

Involution?

A

Normal programmed shrinkage of an organ

Eg uterus after child birth, thymus in early life

72
Q

Reconstitution?

A

Replacement of lost body part

73
Q

Atresia?

A

Congenital imperforation of an opening (no orifice)

Eg anus, vagina, small bower

74
Q

Dysplasia?

A

Abnormal maturation of cells within a tissue - disordered tissue organisation, altered differentiation
Potentially reversible so not neoplastic
Often pre-cancerous/neoplastic

75
Q

Benign prostatic hyperplasia?

A

Enlargement of the prostate gland - periurethral area most commonly affected
Nodules press on urethra, obstruct urine flow
Effects: bladder muscle hypertrophy/distension, urinary retention

76
Q

Psoriasis?

A

Common inflammatory dermatitis - skin scaly and bleeds easily
T cell mediated disease -> they produce growth factors for keratinocytes -> proliferation
Elbows, knees, scalp, ears most commonly affected
Signs: pink plaques covered with silver scales, yellow/pitting nails, arthiritis
Effects: epidermal thickening, absent granular layer, microabscesses of neutrophils, multiple bleeding points under scales

77
Q

Barrett’s oesophagus?

A

Metaplasia of oesophageal stratified squamous epithelium to gastric glandular epithelium due to stress on the epithelium - metaplasia to more tolerant epithelium
Predisposes to dysplasia and then oesophageal adenocarcinoma due to rapid proliferation

78
Q

Tumour?

A 
Any clinically detectable lump or swelling
Non neoplastic (abscess, haematoma etc) or neoplastic (benign or malignant)
79
Q

Neoplasia?

A

Type of tumour - abnormal growth of cells that persists after stimulus is removed (irreversible)
Caused by both initiators (chemicals, infections, radiation) and promoters
Can have direct local (destruction of normal tissue, ulceration->bleeding, compression of adj. structures, blocking tubes) and indirect systemic effects (increasing tumour burden-reduced appetite, weight loss, malaise, immunosupression, thrombosis, hormone production, brain and skin problems)

80
Q

Malignant neoplasia/cancer?

A

Abnormal growth of cells that persists after stimulus is removed and invades surrounding tissue with potential to spread to distant sites
Have potential to metastasise (Stages 1-4)
Irregular outer margin & shape
Areas of necrosis & ulceration
Cells range from well to poorly differentiated

81
Q

Benign neoplasia?

A

Abnormal growth of cells that persists after stimulus is removed that remains confined to site of origin
Does not metastasise
Pushing outer margin
Cells closely resemble parent tissue. Well differentiated, looks normal

82
Q

Metastasis?

A

A malignant neoplasm that has spread from it’s original site (primary) to a new non-contiguous site (secondary)

83
Q

Transient ischaemic attacks?

A

Mini strokes which are resolved within 24 hours
Secondary to microemboli originating from heart or carotid/vertebral arteries
Could be earthed ischamic or haemorrhagic
Could lead to a full stroke
Symptoms: eg; weakness down one arm lasting about 1 minute, then resolved

84
Q

Colorectal adenocarcinoma?

A

Malignant glandular bowel epithelia tumour
Can cause: ulceration, strictures, perforation, haemorrhage
Presentation: rectal bleeding (due to ulceration), abdominal pain, unexplained weight loss
Staging system: Dukes (A - D)

85
Q

Uterine leiomyoma?

A

Benign tumour of the endometrial smooth muscle uterine cells
Also called fibroids
Presentation: abdo pain, heavy/painful periods
Microscopic: proliferation in bundles of smooth muscle cells in random orientation
Can cause: torsion -> twisted polyp -> high capillary pressure -> haemorrhage -> red infarct

86
Q

Osteosarcoma?

A

Malignant stromal bone tumour - makes abnormal osteoid
Arises from osteoblasts
Common in young age
Usually in metaphysis of long bones
Can cause: fractures, microfractures in abnormal bone
Presentation: pain in bones (due to fractures)

87
Q

Teratoma?

A 
Germ cell tumour of ovary or testes 
Also called dermoid cyst (looks like skin)
Can contain hair, sebum etc
Ovarian - commonly benign
Testicular - commonly malignant
Can also occur in embryonic crest
88
Q

Strumsa ovarii?

A

Ovarian dermoid tissue compromised almost entirely of thyroid tissue
Can cause hyperthyroidism

89
Q

Chronic lymphocytic leukaemia?

A

Cancer of B lymphocytes caused by primary tumour in the BM secreting abnormal cells
Presentation: lethargy, breathlessness, pale conjuctiva, hepatomegaly, splenomegaly, enlarged neck/groin/axillary lymph nodes, anaemia

90
Q

Glioma?

A

Tumour of glial cells
Usually a metastasis from breast, lung, colon
Presentation: body weakness on one side
Can cause: haemorrhage, raised ICP, brain midline shift

91
Q

Malignant melanoma?

A

Malignant tumour of melanocytes
Increased risk with UV light, no. of moles
Macro: irregularly shaped mole
Micro: brown staining cells (melanin deposits)
Metastasises to: brain, lung, bone, bowel, across placenta foetus
Presentation: enlarged lymph nodes, mole
Test: Sentinel lymph node biopsy

92
Q

Carcinoid tumour?

A

Tumour of neuroendocrine system
Produces hormones
Presentation if serotonin being produced and metastasised to liver: intermittent abdominal pain, diarrhoea, sweating, flushing
-Carcinoid syndrome: systemic release of hormones (they bypass the liver if there is a metastasis there and cause systemic effects)

93
Q

Cannonball lesions?

A

Large round pulmonary tumours - grow lime benign tumours

94
Q

Pancreatic adenocarcinoma?

A

Tumour of exocrine pancreas glands
Presentation: DVT (Trousseau’s sign->abnormal blood constituents causes sticky platelets), jaundice, hepatomegaly
Metastasis to liver -> jaundice etc

95
Q

Familial adenomatous polyposis?

A

AD - 1000s of colonic polyp adenomas due to genetic change on APC gene (normally binds microtubule bundles preventing proliferation)
Macro: sessile polyps blanketing colon

96
Q

Kaposi’s sarcoma?

A

Malignant vascular stromal tumour cased by HIV - lowers immunity allowing other carcinogens to act

97
Q

Xeroderma pigmentosum?

A

AR germ line mutation -> affects DNA NER -> increased susceptibility to UV damage -> high chance of skin cancer at young age
Presentation: intense photosensitivity, pigment changes, premature skin ageing

98
Q

Hereditary non-polyposis colon cancer syndrome (HNPCC)?

A

AD germiline mutation -> affects DNA mismatch repair gene

Assc. with colon carcinoma

99
Q

Familial breast carcinoma?

A

Most common cancer in females (87% 5 year survival rate)
Mutations affecting BRCA1 or BRCA2 genes which are important for DNA double strand break repair
Causes malignant tumours
Macro: breast lump, sunken nipple
Staging (TNM): I (2cm), II (<5cm), III (>5cm), IV (distant metastasis)
Grading system: Bloom-Richardson (asseses tubule formation, nuclear variation and mo. of mitoses)
Grading correlates well with survival
Treatment: tamoxifen (SERMs) - has side effects, Herceptin, monoclonal antibodies

100
Q

Retinoblastoma?

A

AD inheritance pattern or can occur sporadically, mutation of retinoblastoma gene (tumour suppressor)
(2 mutations in same cell req)
Inherited - more likely because germ line mutation already present
Sporadic - less likely because no germ line mutation present
Presentation: “cat’s eye reflex”

101
Q

Burkitt’s lymphoma?

A

Neoplasia of B cells

Increased risk with EBV (because this infects B cells) and malaria (decreased immunity)

102
Q

Liver cell carcinoma?

A

Increased risk with Hep B
- chronic infection acts s a promoter
Increased risk with aflatoxins (created by fungi on nuts in moist conditions)
Tumour markers: alpha feroprotein, oncofetal antigens

103
Q

Cervical carcinoma?

A

Cancer of cervical epithelium
Increased risk with early first pregnancy (because it correlates to early first sexual intercourse) and HPV - E6 mutates p53 and E7 mutates pRb

104
Q

Bladder carcinoma?

A

Usually squamous cell carcinoma

Increased risk with schistosomiasis - lay eggs in bladder causing metaplasia to squamous cell epithelium

105
Q

Malignant mesothelioma?

A

Malignant tumour of lining of pleura (mesothelia)
Increased risk with asbestos (usually develops 30 years after exposure) - can be an initiator, promoter or mutagenic
Macro: visceral pleural layer covered with small nodule, rind formed obliterating pleural space

105
Q

Basal cell carcinoma?

A

Increased risk with UV light exposure
Causes abnormal patterning of hair follicles
Invasive but rarely metastatic (forms ulcers) and so is still malignant
Macro: open sore, red arches, shiny nodule, pink growth with rolled edges
Micro: very blue

106
Q

Squamous cell carcinoma of skin?

A

Risk factors: UV exposure etc

Good prognosis

108
Q

Lung cancer?

A

Types - small cell, squamous cell, adenocarcinoma
Predisposing factors - smoking etc
Not a good prognosis

109
Q

Hodgkin’s lymphoma?

A 
Malignant tumour of Reed Sternberg cells
Presentation: enlarged lymph nodes, fever, night sweats
Stageing - Ann Arbour:
-I: 1 lymph node
-II: 2 adj. lymph nodes above diaphragm
-III: 2 lymph nodes, 1 below diaphragm
-IV: visceral organ spread
B symptoms: night fevers, sweats etc - worsening prognosis
110
Q

Prostate cancer?

A

PSA elevated to diagnose (also found in BPH)
Gleason grading system (1-5): >2 is cancer
Usually asymptomatic because it is slow growing and doesn’t obstruct urethra
Symptoms: back pain because cancer often metastasises to bone via blood - blood supply to prostate is close to spinal cord

111
Q

Testicular cancer?

A
  • Seminoma (differentiating towards sperm)
  • Non-seminoma (differentiating towards embryonic cells): teratomas etc
  • Stromal (Leydig etc)
  • Tumour markers: AFP (yolk sac tumour), hCG (coricarcinoma)

Clinical Conditions (6 decks)

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