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Kofi: Pure clinical conditions > Pathology conditions > Flashcards

Pathology conditions Flashcards

1
Q

What is the effect of alcohol on the liver?

A

Cause cause a fatty liver and mallory’s hyaline accumulation in hepatocytes

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2
Q

What is the laboratory diagnosis of excessive alcohol intake?

A

Isolated elevation of Gamma GT

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3
Q

What is the presentation of hepatitis B?

A
  • Jaundice
  • Fatigue
  • Abdominal pain
  • Anorexia
  • Nausea
  • Vomiting
  • Arthralgia
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4
Q

What is the laboratory diagnosis for Hepatitis B?

A
  • Viral antigen present
  • ALT, AST, LDH are all raised
  • Bilirubin elevated
  • Albumin and clotting factors lowered due to impaired hepatic function
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5
Q

What is the laboratory diagnosis for acute pancreatitis?

A

Elevated serum amylase and lipase

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6
Q

What is hereditary haemochromatosis?

A

Genetic disorder resulting in increased intestinal absorption of dietary iron

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7
Q

What is the presentation of hereditary haemochromatosis?

A
  • May be asymptomatic

- May present with multiple organ related symptoms

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8
Q

What are complications of hereditary haemochromatosis?

A
  • Liver damage
  • Heart dysfunction
  • Multiple endocrine failure especially pancreas, arthropathy, hypogonadism
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9
Q

What is the treatment of hereditary haemochromatosis?

A

Therapeutic phlebotomy

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10
Q

What is Alpha-1 antitrypsin deficiency?

A

Autosomal recessive condition involving low levels of alpha-1 antitrypsin leading to destruction of elastin in alveoli which results in emphysema. Can also cause cirrhosis as abnormal proteins accumulate in hepatocytes

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11
Q

What is the presentation for alpha-1 antitrypsin deficiency?

A
  • Coughing
  • Wheezing
  • Sputum production
  • General respiratory work evident
  • Tachypnoea
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12
Q

What are the complications of alpha-1 antitrypsin deficiency?

A
  • Emphysema
  • COPD
  • Cirrhosis
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13
Q

What is coal workers’ pneumoconiosis?

A

Anthracosis and blackened peribronchial lymph nodes caused by inhalation of coal particles.

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14
Q

What is the presentation of coal workers’ pneumoconiosis?

A

Usually asymptomatic but may have cough or sputum production

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15
Q

What is complication of coal workers’ pneumoconiosis?

A

-Fibrosis
-Emphysema
If prolonged exposure or large quantities

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16
Q

What are the pathological stages of Lobar pneumonia?

A
  • Consolidation (capillaries congest, cellular exudates neutrophils)
  • Red Hepatisation (capillaries engorge, erythrocytes enter alveoli, lung resembles liver)
  • Grey Hepatisation (Red cell death, leukocyte enter alveoli, fibrinopurulent exudates)
  • Resolution ( restoration of architecture, large number of macrophages)
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17
Q

What is the difference between lobar pneumonia and bronchopneumonia?

A
  • Patchy foci of consolidation in broncho

- Entire lobe or lung inflammation in lobar

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18
Q

What is the common causative organisms of pneumonia?

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Mycobacterium tuberculosis
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19
Q

What are the complications of lobar pneumonia?

A
  • Death
  • Pleural effusion
  • Difficulty breathing
  • Abscess
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20
Q

What is the macroscopic appearance of acute appendicitis?

A
  • Swollen
  • Pus
  • Gangrene
  • Darker/Redder colour
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21
Q

What is the microscopic appearance of acute appendicitis?

A
  • Inflamed mucosa
  • Polymorphs
  • Macrophages present
  • Mucosal ulceration
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22
Q

What are possible causes acute appendicitis?

A
  • Pinworms
  • Faecal obstruction
  • Lymphoid hyperplasia
  • Adenocarcinoma
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23
Q

What are the complications of acute pancreatitis?

A
  • Perforation leading to peritonitis
  • Bacteraemia
  • Sepsis
  • Fistulae
  • Abscess
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24
Q

What is macroscopic appearance of bacterial meningitis?

A
  • Swollen

- Pus

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25
Q

What is the microscopic appearance of bacterial meningitis?

A
  • Polymorph accumulation

- RBC accumulation adjacent to brain

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26
Q

What are the causative organism of bacterial meningitis?

A

Neonates: Group B Strep, Strep pneumoniae
Children: Neisseria meningitidis, Pneumococcus, Haemophilus influenza
Young adults: Neisseria meningitidis, Strep pneumoniae
Older: Pneumococcus, Neisseria meningitidis, Haemophilus influenza

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27
Q

What are the complications of bacterial meningitis?

A
  • Sepsis

- Raised intracranial pressure leading to death

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28
Q

What are the complications Gallstones?

A
  • Hepatic abscess due to blocked duct allowing bacteria into liver
  • Pancreatitis
  • Fistulae
  • Perforation
  • Adult colic Carcinoma
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29
Q

What is the link of ascending cholangitis with gallstones?

A

Obstruction of bile duct by gallstones allows bacteria from duodenum to enter bile duct and gall bladder

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30
Q

What are the most common causative organisms of ascending cholangitis?

A
  • E.coli
  • Clepcilla
  • Streptococcus
  • Staphlycoccus
  • Enterobacter
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31
Q

What are the complication of ascending cholangitis?

A
  • Perforation
  • Cholecystitis
  • Peritonitis
  • Pancreatitis
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32
Q

What is hereditary angio-oedema?

A

Rare autosomal dominant condition in which sufferers have an inherited deficiency of C1-esterase inhibitor (complement). Patients have attacks of non-itchy cutaneous angio-oedema, recurrent abdominal pain due to intestinal oedema

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33
Q

What are the complication of hereditary angio-oedema?

A

Sudden death due to laryngeal involvement

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34
Q

What is chronic granulomatous disease?

A

Genetic condition

  • Phagocytes are unable to generate superoxide, therefore cannot kill bacteria
  • Leads to many chronic infections in the first year of life. –Numerous granulomous and abscesses affecting skin, lymph nodes, and sometimes the lung, liver and bones
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35
Q

What are the complications of chronic granulomatous disease?

A
  • Anaemia

- Malsorption syndrome

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36
Q

What is the presentation of rheumatoid arthritis?

A
  • Painful, warm, stiff joints
  • Reduced range of movement
  • Deformity
  • Worse in the morning
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37
Q

What is the microscopic features of rheumatoid arthritis?

A
  • Plasma cells
  • Lymphocytes
  • Pannus
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38
Q

What are rheumatoid nodules?

A

Subcutaneous lumps on extensor aspect, microscopically, shell of fibrous tissue surrounding centre of fibrinoid necrosis

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39
Q

What is the presentation of ulcerative colitis?

A
  • Abdominal pain
  • Diarrhoea
  • Weight loss
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40
Q

What is differential diagnosis of ulcerative colitis?

A
  • Crohns disease
  • Bowel cancer
  • Diverticulitis
  • Anorexia Nervosa
  • Inflammatory bowel disease
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41
Q

What is the macroscopic appearance of ulcerative colitis?

A
  • Continuous distribution
  • Oedema
  • Mucopurulent exudate
  • Ulceration
  • Mucosal bleeding
  • Polyps
  • Mucosal scarring
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42
Q

What is the microscopic appearance of ulcerative colitis?

A
  • Superficial
  • Crypt abscesses
  • Distorted crypt architecture
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43
Q

What are the complications of ulcerative colitis?

A
  • Joint pain
  • Psoriases
  • Erythema nodosum
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44
Q

What is the presentation of Crohn’s disease?

A
  • Abdominal pain
  • Diarrhoea
  • Weight loss
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45
Q

What is the differential diagnosis of Crohn’s disease?

A
  • Ulcerative colitis
  • Bowel cancer
  • Diverticulitis
  • Anorexia Nervosa
  • Inflammatory bowel disease
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46
Q

What is the macroscopic appearance of Crohn’s disease?

A
  • Cobblestone appearance
  • Fistulae
  • Strictures
  • Anal lesions
  • Discontinuous distribution
  • Any part of GI tract affect
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47
Q

What is the microscopic appearance of Crohn’s disease?

A
  • Transmural inflammation

- Granuloma

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48
Q

What are the complications of Crohn’s disease?

A
  • Perforation
  • Fistulae
  • Intestinal bleeding
  • Malabsorption
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49
Q

What is the macroscopic appearance of Chronic cholecystitis?

A
  • Strawberry-like appearance
  • Wall thickening
  • Gallstones
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50
Q

What is the microscopic appearance of Chronic cholecystitis?

A
  • Fibrosis
  • Muscular hypertrophy of wall
  • Lymphocytes
  • Entrapped epithelial crypts
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51
Q

What is the role of helicobacter in chronic gastritis?

A

Injures mucosa so cannot protect against stomach acid

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52
Q

What is the microscopic appearance of chronic gastritis?

A
  • Granuloma
  • Mucosal atrophy
  • Goblet cell metaplasia
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53
Q

What are the complications of chronic gastritis?

A

Cancer

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54
Q

What is cirrhosis?

A

Scarring of the liver

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55
Q

What is macroscopic appearance of cirrhosis?

A
  • Nodular hobnailed appearance
  • Change in size and colour
  • Often small and yellowish but can be enlarged and yellow or green
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56
Q

What is microscopic appearance of cirrhosis?

A
  • Nodules
  • Fibrous septa
  • Effacement of architecture
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57
Q

What are the causes of cirrhosis?

A
  • Alcohol excess
  • Hepatitis B
  • Hepatitis C
  • Non-acoholic fatty liver disease
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58
Q

What are the complications of cirrhosis?

A
  • Cancer
  • Oedema
  • Ascites- (fluid accumulation in the peritoneal cavity)
  • Peritonitis
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59
Q

What is the microscopic appearance of tuberculosis?

A
  • Caseous necrosis

- Langhan’s cells

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60
Q

What is the pathophysiology of tuberculosis?

A
  • Neutrophils migrate early and phagocytose the bacteria
  • Monocytes differentiate into macrophages which use PRRs to recognise PAMPS. They release cytokines to attract epithelioid cells which mature
  • Laghan’s Giant cells are present by day 9
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61
Q

What is the presentation of sarcoidosis?

A
  • Tiredness

- Cough

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62
Q

What is the microscopic appearance of sarcoidosis?

A

Alveolar granuloma (non-caseating)

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63
Q

What is the difference between TB and sarcoidosis?

A

TB

  • Caused by mycobacterium tuberculosis
  • Caseating granulomas
  • Chronic cough + Haemoptysis
  • Acid fast stain, PCR, culture
  • Antibiotics

Sarcoidosis

  • Immune-mediated
  • Non-Caseating granulomas
  • Difficulty breathing
  • Elevated ACE and calcium
  • Steroids
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64
Q

What is the cause of scurvy?

A

Vitamin C deficiency causes weak collagen fibres

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65
Q

What is the pathophysiology of scurvy?

A

Vitamin C needed for pro collagen hydroxylation which allows cross-linkage

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66
Q

What is the presentation of scurvy?

A
  • Fatigue
  • Poor healing
  • Tendency to bleed
  • Tooth loss
  • Old scars open
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67
Q

What is Ehler’s danlos syndrome?

A

Defective conversion of pro collagen to tropocollagen leading to poor tensile strength of collagen

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68
Q

What is the clinical presentation of Ehler’s Danlos syndrome?

A
  • Hyperextensible
  • Fragile skin
  • Hypermobile
  • Easily dislocated joints
  • Retinal detachement
  • Colon rupture
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69
Q

What is osteogenesis imperfector and clinical manifestations ?

A

Type 1 collagen mutation leading to insufficient bone tissue resulting in easily fractured bones and deformed bones. Blue sclera is also present

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70
Q

What is the macroscopic appearance of a keloid scar?

A

Large, raised scar tissue which exceeds the bounds of the previous wound

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71
Q

What is the microscopic appearance of keloid scars?

A

Excessive collagen network laid down beneath an otherwise relatively normal epidermis

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72
Q

What is alport syndrome?

A

X-linked recessive condition involving abnormal type IV collagen synthesis causing dysfunction of glomerular basement membrane, lens of the eye and cochlea of the ear

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73
Q

\what is the clinical presentation of alport syndrome?

A
  • Haematuria in children progressing to renal failure
  • Eye defects
  • Deafness
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74
Q

What is haemophilia A?

A

X-linked recessive deficiency in clotting factor VIII

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75
Q

What is the presentation of a patient with haemophilia A?

A
  • Poor clotting
  • Sudden joint swelling
  • Prolonged headache
  • Vomiting
  • Changes in vision
  • Stiffness
  • Easy bruising
  • Massive haemorrhage
  • Haemarthrosis
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76
Q

What is the lab abnormalities of haemophilia A

A

Increased APTT

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77
Q

What is Haemophilia B?

A

X-linked recessive deficient of clotting factor IX

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78
Q

What is the presentation of a patient of Haemophilia B?

A
  • Poor clotting
  • Sudden joint swelling
  • Prolonged headache
  • Vomiting
  • Changes in vision
  • Stiffness
  • Easy bruising
  • Massive haemorrhage
  • Haemarthrosis
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79
Q

What are the lab abnormalities of Haemophilia B?

A

Increased APTT

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80
Q

What is Von-Willebrand disease?

A

Deficiency in Von-Willebrand factor, which stabilises factor VIII and assists platelet plug formation by attracting circulating platelets to site of damage

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81
Q

What is the presentation of Von-Willebrand disease?

A
  • Mucosal bleeding
  • Can be asymptomatic
  • Easy bruising
  • Prolonged bleeding
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82
Q

What are lab abnormalities for Von-Willebrand disease?

A
  • Low factor VIII and VWF

- Increased APTT

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83
Q

What is immune thrombocytopaenic purpura?

A

Autoimmune disease against platelets causing isolated low circulating platelet count

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84
Q

What is the presentation of immune thrombocytopaenic purpura?

A
  • Widespread petechiae
  • Headache
  • Easy bruising
  • Vision changes
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85
Q

What are the lab abnormalities of Immune thrombocytopaenic purpura?

A

Bleeding time is long

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86
Q

What are the types of thrombophilias?

A
  • Factor V leidan
  • Prothrombin 20210 mutation
  • Protein C deficiency
  • Antithrombin deficiency
  • Antiphospholid syndrome
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87
Q

What is the pathophysiology of thrombophilias?

A

Increased coagulability of blood due to clotting factor imbalance

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88
Q

What is the presentation of thrombophilias?

A
  • Pain
  • Swelling
  • Tenderness of lower limbs (DVT)
  • Shortness of breath
  • Chest pain (PE)
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89
Q

What are the causes of Disseminated Intravascular Coagulation?

A

Sepsis, bacteraemia

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90
Q

What is the pathophysiology of Disseminated Intravascular Coagulation?

A
  • Bacterial endotoxin binds to macrophages, causing them to release cytokines to stimulate inflammatory response.
  • Cytokines eventually released into circulation and stimulate growth factors and platelets to control infection
  • If uncontrolled, cytokines lead to activation of humoral cascades and RES to cause circulatory insult.
  • Cytokines initiate thrombin production
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91
Q

What is treatment for Disseminated Intravascular Coagulation?

A
  • Treat cause
  • Replacement therapy
  • Sometime heparin
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92
Q

How is diagnosis for Disseminated Intravascular Coagulation made?

A
  • Platelet count low
  • PT (normal to long)
  • APTT (long)
  • Plasma Fibrinogen (low)
  • Plasma D-dimer (high)
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93
Q

What is the role of thrombosis in a myocardial infarction?

A
  • Thrombi can form from complicated atherosclerotic plaques, causing occlusion of coronary artery
  • Alternatively, a thrombus can form in the heart (left side most likely) and then a thrombo-embolus may occlude coronary artery
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94
Q

What is the laboratory diagnosis for myocardial infarction?

A
  • Increased Troponin(I)

- Increased creatinine

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95
Q

What are the complications of a myocardial infarction?

A
  • Death
  • Cardiac Tamponade
  • Arrhythmia
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96
Q

What is the pathophysiology of Deep Vein Thrombosis?

A

Thrombus forms in deep veins of leg causing oedema and pain.

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97
Q

What are the predisposing factors of Deep Vein Thrombosis?

A
  • Contraceptive pill
  • Sedentary behaviour
  • Pulmonary embolism
  • Trauma
  • Burns
  • Surgery
  • Pregnancy
  • Obesity
  • Smoking
98
Q

What is the presentation of Pulmonary Thromboembolism?

A
  • Shortness of breath
  • Localised
  • Sharp chest pain
99
Q

What is the pathophysiology of pulmonary thromboembolism?

A

Part or entirety of thrombus from venous side breaks and gets lodged in capillaries of lungs causing congestion and damage to vessels and alveoli

100
Q

What are the risk factors for a pulmonary thromboembolism?

A
  • Deep vein thrombosis
  • Hypercoagulability
  • Endothelial injury
101
Q

What is pathophysiology of an air embolism?

A

Air travels in arterial or venous system until it reaches smaller vessels and capillaries which it then blocks, with larger gas emboli, the blood can become frothy preventing circulation

102
Q

What is the presentation of a fat embolism?

A
  • Tachypnea
  • Tachycardia
  • Elevated temperature
  • Hypoxemia
  • Hypercapnia
  • Thrombocytopenia
  • Occasionally mild neurological symptoms
103
Q

What is the pathophysiology of a fat embolism?

A

Often follow trauma such as long bone fractures. Fatty material enters the bloodstream and blocks blood vessels. Biochemical injury also ensues as a result of endothelial injury following the release of fatty acids form the embolus.

104
Q

What is the pathophysiology of an amniotic fluid embolism ?

A

Amniotic fluid enter mother’s bloodstream via placental bed in the uterus triggering an allergic-like reaction resulting in cadiorespiratory collapse and massive bleeding

105
Q

What is heterozygous familial hypercholesterolaemia?

A

Genetic disorder of LDL receptor, leading to very high levels of LDL

106
Q

What are the consequence of familial hypercholesterolaemia?

A
  • Xanthoma
  • Xanthelesma
  • Corneal arcus
  • Increased risk of atherosclerosis
107
Q

What is the role of atherosclerosis in Ischaemia heart disease?

A

Atherosclerotic deposits narrow coronary arteries leading to ischaemia of the myocardium. Usually exercebated by exercise.

108
Q

What is the role of atherosclerosis in bowel ischaemia?

A

Atheroma occludes mesenteric artery. (embolus entrapment or plaque rupture)

109
Q

What is the role of atherosclerosis in peripheral vascular disease?

A

Occlusion of peripheral arteries

110
Q

What is the presentation peripheral valvular disease?

A
  • Claudication
  • Aching calves
  • Lehriche’s Syndrome
  • Cold
  • Pale limb
111
Q

What is the cause of Left ventricular Hypertrophy?

A
  • Aortic valve stenosis
  • Hypertension
  • Valve regurgitation
  • Hypertrophic cardiomyopathy
112
Q

What is the complications of left ventricular hypertrophy?

A
  • Death. through loss of cardiac output
  • Cardiogenic shock
  • Ischaemia
  • Arrhythmia
  • Myocardial infarction
113
Q

What is Barrett’s Oesophagus?

A

-Oesophageal reflux lead to metaplasia of stratified squamous epithelium to simple columnar

114
Q

What is the cause of Barrett’s Oesophagus?

A

Chronic gastric reflux

115
Q

What is the complication of Barrett’s Oesophagus?

A

Oesophageal adenocarcinoma

116
Q

What is traumatic myositis Ossificans?

A

Inappropriate differentiation of fibroblasts into osteoblasts in muscle following trauma resulting in a calcified mass.

117
Q

What is the macroscopic appearance of a benign prostatic hyperplasia?

A

Larger and nodular compared with normal

118
Q

What are the complications of a benign prostatic hyperplasia?

A
  • Bladder hypertrophy
  • UTIs
  • Urinary retention
  • Kidney damage
  • Bladder stones
119
Q

What is the pathophysiology of Psoriases?

A

T-cell mediated hyperproliferaton of keratinocytes.

120
Q

What is the presentation of Psoriasis?

A

Silvery white coat on red raised patches

Pruritus

121
Q

What is the macroscopic appearance of Psoriasis?

A

Silvery white ‘scales’ on red raised patches of skin on extensor aspects, scalp, glans, lower back and gluteal region

122
Q

What is the microscopic appearance of Psoriasis?

A
  • Hyperplasia of keratinous layer
  • Neutrophils in epidermis, -Thinning of epidermis overlying dermal papillae
  • Vessels close to epidermis dilate
  • Elongate rete ridges
  • Acanthosis
  • Parakeratosis – incompletely formed keratin forms black dots in cells
123
Q

What is the role of atherosclerosis in abdominal aortic aneurysm?

A
  • In oder to overcome stenotic effects of atheroma, the media tries to widen the artery to normalise lumen. Arterial remodelling occurs
  • Alternatively possible direct causative effect from plaque that damages the artery
124
Q

What are the complications of an abdominal aortic aneurysm?

A
  • Nervous or Visceral impingement
  • Death following rupture
  • Peripheral vascular disease
  • Fistulae
  • Aortic dissection
125
Q

What is the role of atherosclerosis in a Transient ischaemic attach and Cerebral Vascular accident?

A

-Atheroma in cerebral arteries causes partial occlusion therefore emboli has more chance of lodging and complicated plaque rupture leading to thrombus likely

126
Q

What is the pathophysiology of TIA+CVA?

A
  • TIA resolves in 24 hours

- Ischaemia of brain cells due to occlusion. Can result in necrosis

127
Q

What is the distinction between ischaemic and haemorrhage stroke?

A
  • Ischaemic causes hypoxic injury due to cessation of adequate perfusion
  • Haemorrhagic causes causes physical injury as the bleed compresses surrounding brain tissue
128
Q

What are the macroscopic features of benign tumours and malignant tumours?

A

Benign

  • Confined to site of origin
  • Pushing outer margin

Malignant

  • Irregular outer margin
  • Irregular shape
  • Areas of necrosis and ulceration (if on surface)
129
Q

What are the microscopic features of benign and malignant tumours?

A

Benign
-Closely resemble the parent tissue so well differentiated

Malignant tumours
-Range from well differentiated to poorly differentiated

130
Q

What are anaplastic cells?

A

Cells with no resemblance to any tissue

131
Q

How does worsening differentiation appears?

A
  • Increasing nuclear size
  • Increasing nuclear to cytoplasmic ratio
  • Increasing nuclear staining
  • More mitotic figues
  • Increasing variation ins size and shape of cells and nuclei (pleomorphism)
132
Q

What does hIgh grade and low grade mean?

A
  • High grade - poorly differentiated

- Low Grade - well differentiated

133
Q

What is a neoplasm?

A

An abnormal growth of cells that persist after the initial stimulus (and invades surrounding tissue with potential to spread to distant sites - of malignant)

134
Q

What is dysplasia?

A

A reversible pre-neoplastic change in which cells show disordered tissue organisation.

135
Q

How does signalling through inter grins occur?

A

Via small G proteins such as member of the Rho family

136
Q

Why would a malignant neoplasm replaces years after an apparent cure?

A
  • Tumour dormancy

- A micrometastases starts to grow

137
Q

How do carcinomas typically spread first?

A

By lymphatics

138
Q

How do sarcomas typically spread first?

A

By bloodstream

139
Q

What are the common site of blood borne metastasis?

A

Lung, Bone, Liver and Brain

140
Q

Which neoplasms most frequently spread to bone?

A

Breast, Bronchus, Kidney, Thyroid and Prostate

141
Q

What did 2-naphthylamine show about malignant neoplasms?

A
  • Long delay between between carcinogen exposure and malignant neoplasm onset
  • Risk of cancer depends on total carcinogen dosage
  • There is sometimes organ specificity for particular carcinogens
142
Q

Why doesn’t tobacco smoke have a signifiant effect on other members of the public?

A

-The dosage is not enough

143
Q

How does radiation damage DNA bases?

A
  • Directly
  • Indirectly - Generation of free radicals

Ionising radiation causes single and double strand DNA breaks.

144
Q

What is the most important type of radiation and why?

A
  • UV radiation as it carries increased risk of skin cancer

- Exposure daly from sunlight

145
Q

What is mechanism of action of ionising radiation and its main route of exposure ?

A
  • Strips electrons from atoms

- Natural background radiation from radon which seeps from earth crust

146
Q

What is the relationship between HPV and cervical carcinoma?

A
  • HPV is a direct carcinogen
  • Expresses E6 protein that inhibits p53 protein function
  • Expresses E7 protein that inhibits pRB protein function
  • These proteins are important in cell proliferation as they regulate the cell cycle
147
Q

What is the relationship between Hepatitis C and B and carcinoma of the liver?

A
  • Virus infects liver cells
  • Action of cytoxic T cells leads to chronic Hepatocellular injury and regeneration. Acts as an
  • Direct effect through transactivating gene which alters level of transcription
148
Q

What is the relationship between Epstein-Barr virus and Burkitt’s lymphoma?

A
  • EBV stays dormant in B cells
  • Acts as a polyclonal B cell mitogen
  • Causes B cells to divide rapidly for a long period of time and increases chance of mutation which can be in the tumor suppressor or proto-oncongene in replication
149
Q

What is the relationship between EBV and malaria in relation to Burkitt’s Lymphoma?

A

Malaria can cause a degree of incompetence that allows the EBV infected B cells to proliferate and gives them a risk of mutation.

150
Q

What is the association between helicobacter pylori and gastric carcinoma?

A

-Chronic gastric inflammation increased the risk of gastric carcinoma

151
Q

What is the association between parasitic flukes (schistomsoma haemotabium) and cholangiocarcinoma as well as bladder cancer?

A
  • Inflammation of bile ducts

- Inflammation of the bladder mucosa

152
Q

What is mechanism of action of HIV and neoplasms?

A
  • Lowers immunity

- Allows other potentially carcinogenic infections to occur

153
Q

What is the function of the RAS proto-oncogene?

A
  • Encodes a small G protein that relays signals into the cell
  • Pushes the cell past the cell cycle restriction point
  • Mutant RAS encodes a protein that is always active so produces a contact signal to pass through the cell cycle’s restriction point
154
Q

What is the role of c-Myc in neoplasm?

A
  • Codes for transcription factor
  • Mutated version of Myc causes Myc to be constitutively (persistently) expressed.
  • Leads to the unregulated expression of many genes, some of which are involved in cell proliferation, and results in the formation of cancer
155
Q

What is the role of Her-2 in relation to breast cancer?

A
  • It is a growth factor receptor
  • Amplification or over-expression of this oncogene has been shown to play an important role in the development and progression of certain aggressive types of breast cancer.
156
Q

Describe the role of tumour suppressor genes in the formation of a retinoblastoma?

A
  • Retinoblastoma gene restrains cell proliferation by inhibiting passage through the restriction point.
  • Inactivation of both RB alleles therefore allows unrestrained passage through the restriction point
  • The first hit is delivered though the germ line and the second hit is a somatic mutation in familial cancers.
157
Q

What is the two hit hypothesis?

A
  • Tumour suppressor genes require both allelles to be inactivated before a tumour can grow
  • Proto-oncogenes need only one allele to be inactivated to encourage neo-plastic growth
158
Q

How does the 2 hit hypothesis present in a sporadic retinoblastoma?

A

Both hits have to be a somatic mutation

159
Q

What is role of P53 as a tumour suppressor gene?

A
  • Levels of p53 rise after DNA damage leading two two main effects which is cell cycle arrests by transcription of an inhibitor of CDK or cell death by apoptosis
  • Cell cycle arrest allows repair to take place before cell division completes
  • If the p53 is affects, cells can be produced that are defective which can result in tumour cells
160
Q

What are the hallmarks of cancer?

A
  • Self sufficiency in Goth signals
  • Resistance to Growth stop signals
  • No limit on the number of times a c ell can divide
  • Sustained ability to induce blood vessels
  • Resistance to apoptosis
  • Ability to invade and produce metastases (exclusive to malignant neoplasms)
161
Q

What is the association between asbestos and malignancy?

A

-Lung carcinoma, Mesothelioma, Gastrointestinal carcinoma

Due to

  • Chronic physical irritation
  • Initiator and promoter
  • Generates free radicals
  • Absorbs toxins
162
Q

What is the inheritance pattern of hereditary non-polyposis colon cancer syndrome?

A
  • Autosomal dominant
  • Associated with increased risk of colorectal and extra intestinal cancer. Early presentation of adenomas
  • The germline mutations affects one of several DNA mismatch repair genes.
163
Q

Describe the inheritance of familial breast cancer?

A
  • Associated with either BRCA1 or BRCA2 genes

- These are important for repairing double strand DNA breaks

164
Q

Describe the inheritance of xeroderma pigmentosum?

A
  • Autosomal recessive

- Due to mutations in one of the 7 genes that affect DNA nucleotide excision repair. XP gene

165
Q

What are the commonest types of cancer in adults?

A

Lung, Bowel, Prostate and Breast carcinoma. 53% and cluster around 40000 incidences

166
Q

What are the commonest types of cancer in children?

A

Leukaemia, Central nervous system tumours and lymphomas

167
Q

What is the leading cause of cancer-related death?

A

Lung cancer

168
Q

What is adjuvant treatment?

A

Given after surgical removal of a primary tumour to eliminate subclinical disease

169
Q

What is neo-adjuvant treatment?

A

Given to reduce the size of a primary tumour prior to surgical excision

170
Q

What are principles of radiotherapy in treatment of malingnancies?

A
  • Focused on the tumour with shielding of surrounding healthy tissue
  • Given in fractionated doses to minimise damage to normal tissues
  • X-rays or ionising radiant giving which kills rapidly dividing cells especially in G2 of the cell cycle
  • High dosage cause direct or free radical induced DNA damage which is detect at cell cycle check points triggering apoptosis.
  • Double stranded DNA breaks causes damaged chromosomes that prevent the M phase from completing correctly
171
Q

What are the principle of chemotherapy?

A
  • Antimetabolites mimic normal substrates involved in DNA replication
  • Alkalyting and platinum-based drugs cross link the two strands of the DNA helix (cyclophosphamide and cisplatin)
  • Antibiotic act in different ways such as inhibiting DNA topoisomerase which is needed for DNA synthesis(doxorubicin) and bleomycin causes double stranded DNA breaks.
  • Plant served drugs (include vincristine) which block microtubule assembly and interfere with mitotic spindle formation
172
Q

What are the principles of hormone therapy?

A

Relatively non toxic treatment for certain malignancies

  • Selective oestrogen receptors modulators such as tamoxifen bind to oestrogen receptors preventing oestrogen from binding. Used to treat Hormone receptor-positive breast cancer
  • Androgen blockade is used for prostate cancer
173
Q

What are the principles of targeted molecular therapies?

A
  • Herceptin block Her-2 signalling. Her-2 is over expressed in over a quarter of breast cancers
  • Chronic myeloid leukaemia shows a chromosomal rearrangement creating an abnormal ‘Philadelphia’ chromosome in which an oncogenic fusion protein is encoded. Imatinib inhibits fusion protein
174
Q

What are the predisposing factors of colorectal carcinoma?

A
  • Obesity
  • Smoking
  • Alcohol
  • Age
  • Familial history
  • Previous colorectal carcinoma
175
Q

What is the presentation of colorectal carcinoma?

A
  • Blood in stool
  • Persistent abdominal pain/discomfort
  • Weakness
  • Fatigue
  • Unexplained weight loss
176
Q

What is the macroscopic appearance of colorectal carcinoma?

A
  • Ulceration
  • Irregular outline and surface
  • Possibly exocytic
177
Q

What is the microscopic appearance of colorectal carcinoma?

A
  • Irregular tubular structure with multiple lumens
  • Pleomorphism
  • Reduced stroma
178
Q

What are the principles of staging in association with a colorectal carcinoma?

A 
Dukes' Staging
A: Invasion, not through muscular propria
B: Invasion through muscular propria
C: Lymph node involvement 
D: Distant metastases
179
Q

What is the tumour marker for colorectal carcinoma?

A

CEA (carcinoembryonic antigen)

180
Q

What is the screen programme for colorectal carcinoma?

A
  • Faecal occult blood test
  • Every 2 years
  • Ages 60-74 years
181
Q

What is the presentation of a uterine leiomyoma?

A
  • Abdominal cramps/pains
  • Heavy/Painful periods
  • Lower back pain
182
Q

What is the macroscopic appearance of a uterine leiomyoma?

A

Circular or irregular masses in and around the uterus. (fibroids)

183
Q

What is the microscopic appearance of uterine leiomyoma?

A

Interwoven smooth muscle fibres

184
Q

What is the presentation of an osteosarcoma?

A

Pain in bone often following exertion, fractures and swelling

185
Q

What is the macroscopic appearance of an osteosarcoma?

A

Pale or haemorrhage, granular mass invading the marrow space

186
Q

What is the microscopic appearance of an osteosarcoma?

A
  • Abnormal osteoid
  • Pleomorphic osteoblasts
  • Vascular invasion
  • Necrosis
187
Q

What is the presentation of an ovarian teratoma?

A 
-Often asymptomatic and incidentally identified
however may have
-Abdominal pain
-Mass/Swelling
-Abnormal uterine bleeding
-GI disturbances
-Bladder symptoms
188
Q

What is the macroscopic appearance of an ovarian teratoma?

A

88% are unilocular

-Often filled with sebaceous material, hair, rudimentary tissues/organs (e.g. teeth)

189
Q

What is the microscopic appearance of ovarian teratoma?

A
  • Epithelial and glandular features

- Dermis

190
Q

What is chronic lymphocytic leukaemia?

A

Neoplasm of B lymphocytes resting in increased proliferation and release of functionally incompetent B lymphocytes

191
Q

What is the presentation of chronic lymphocytic leukaemia?

A
  • Lethargy
  • Breathlessness
  • Frequent/severe infections
  • Anaemia
  • Bleeding and bruising easily
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Unintentional weight loss
  • Enlarged hilar nodes
  • Heart failure
192
Q

What are the predisposing factors to malignant melanoma?

A
  • UV exposure e.g. agricultural worker
  • Gennetic predisposition
  • Fair skin
  • Co-morbidities
193
Q

What is the presentation of a malignant melanoma?

A
  • Pre-Existing mole has changed shape/colour
  • Itching
  • Non healing sores
194
Q

What is the macroscopic appearance of a malignant melanoma?

A
  • Irregularly shaped/asymmetrical mole
  • Multiple colours within the boundary
  • Larger than a 1/4 inch
195
Q

What is the microscopic appearance of a malignant melanoma?

A
  • Subtly grey/brown-staining cells
  • Melanin deposits
  • Pleomorphism of melanocytes
196
Q

What is the macroscopic appearance of a pancreatic adenocarcinoma?

A
  • Poorly defined
  • Fibrotic
  • White yellow masses
197
Q

What is the microscopic appearance of a pancreatic adenocarcinoma?

A

-Glandular differentiation of cancer cells all the way down to anaplasia

198
Q

What are the complications of a pancreatic adenocarcinoma?

A

Metastasis to the liver resulting in jaundice and hepatic symptoms
DVT secondary to increased hypercoagulability

199
Q

What is the presentation of a carcinoid tumour?

A
  • Intermittent abdominal pain
  • Diarrhoea
  • Sweating
  • Flushing

Differs depending the site

200
Q

What are the complications of a carcinoid tumour?

A
  • Ischaemia of bowel/surrounding tissue

- Metastasis to liver. Carcinoid syndrome due to inability of liver to metabolise hormones released

201
Q

What is Burkitt’s lymphoma?

A

Neoplasia of B cells. B cell proliferation

202
Q

What are the predisposing factors of Burkitt’s lymphoma?

A
  • EBV infection

- Malarial infection

203
Q

What is familial adenomatous polyposis?

A

Autosomal dominant condition 100s-1000s of colonic adenomas at or soon after birth which progress to cancer

204
Q

What is genetic changes of that result in familial adenomatous polyposis?

A

APC gene on chromosome 5q21 which is tumour suppressor gene which normally binds microtubule preventing proliferation

205
Q

What is the macroscopic appearance of familial adenomatous polyposis?

A

Sessile, plaque-like polyps blanketing colon

206
Q

What are the complications of familial adenomatous polyposis?

A
  • Colon cancer
  • Other cancers
  • Dental problems
207
Q

What is the treatment for familial adenomatous polyposis?

A

Supportive treatments e.g. NSAIDS but ultimately colectomy required

208
Q

What is the presentation of retinoblastoma?

A
  • Cat’s eye reflex

- Secondary conditions e.g. inflammation, glaucoma and proptosis

209
Q

what is the presentation of xeroderma pigmentosum?

A
  • Intense photosensitivity
  • Pigmentary changes
  • Premature skin ageing
  • Tumour development
210
Q

What is malignant mesothelioma?

A

Neoplasia of mesothelial cells lining serous membranes

211
Q

What are the predisposing factors for a malignant mesothelioma?

A
  • Previous asbestos exposure
  • Zeolites
  • Radiation
  • Possibly SV40 virus
212
Q

What is the macroscopic appearance of malignant mesothelioma?

A
  • Visceral layer of pleura covered with small nodules

- Rind forms around lung with obliterates pleural space

213
Q

What are the predisposing factors of cervical carcinoma?

A
  • HPV
  • Oestrogen-Progesterone contraceptives
  • HIV type 1
  • Smoking
214
Q

What is the screening programme of cervical carcinoma?

A

Women ages 25 and over are invited for smear test

215
Q

What are the predisposing factors of hepatocellular carcinoma?

A
  • Hepatitis B

- Aflatoxins

216
Q

What Is the tumour marker for haptocellular carcinoma?

A
  • Alpha fetoprotein

- Oncofetal antigens

217
Q

What are the predisposing factors of breast cancer?

A
  • Late pregnancy
  • Family history
  • Alcohol
  • Oestrogen-Progesterone contraceptives
  • Obesity
  • Radiation
218
Q

What is the macroscopic appearance of breast cancer?

A
  • Lumb in breast
  • Sunken nipple
  • Dimplin of skin of breast
  • Pale mass surrounded by normal fatty tissue
219
Q

What is the microscopic appearance of breast cancer?

A
  • Look for pleomorphism
  • Mitosis
  • Hyperchromasia
  • Anaplasia
220
Q

What is the screening programme for breast cancer?

A

Mammogram for ages 50-74 every 3 years

221
Q

What are the predisposing factors of squamous cell carcinoma of the skin?

A
  • UV exposure
  • Being male
  • Fair skin
  • Chronic skin inflammation
  • Previous skin cancer
222
Q

What are the predisposing factors of basal cell carcinoma?

A
  • UV exposure
  • Being male
  • Fair skin
  • Chronic skin inflammation
  • Previous skin cancer
223
Q

What is the macroscopic appearance of basal cell carcinoma?

A
  • Open sore
  • Red patches
  • Shiny bump/nodule
  • Pink growth with rolled edges and crusted centre
224
Q

What is the microscopic appearance of basal cell carcinoma?

A

-Very blue tumour histologically especially evident in basal layer

225
Q

What is the behaviour of a basal cell carcinoma?

A

Non-aggressive- almost never metastasises

226
Q

What are the main types of lung cancer?

A
  • Small cell
  • Squamous cell
  • Adenocarcinoma
227
Q

What is the relationship between lung cancer and smoking?

A

Smoking massively increases the risk of lung cancer due to polycyclic aromatic hydrocarbons in smoke

228
Q

What are the predisposing factors to bladder cancer?

A
  • Smoking

- Schistosomiasis

229
Q

What is kaposi’s sarcoma?

A

Systematic malignancy by a virus

230
Q

What is the cause of kaposi’s sarcoma?

A

Associated with EBV usually seen in people with HIB/AIDS

231
Q

What are the types of testicular cancer?

A

Germ cell:

  • Seminomas
  • Non-seminomas e.g. teratomas

Stromal

  • Leydig
  • Sertoli
232
Q

What is macroscopic appearance of testicular cancer?

A
  • Enlarged testis
  • Nodules
  • Cut surface is cream to grey-tan to pink
  • Lobulated
233
Q

What are the tumour makers of testicular cancer?

A
  • HCG

- Alpha fetoprotein

234
Q

What is the presentation of Hodgkins lymphoma?

A
  • Enlarged nodes
  • Fever without infection
  • Night sweats
  • Weight loss
235
Q

What is the microbic appliance of Hodgkin’s lymphoma?

A

Reed-Sternberg cells

236
Q

What are the principles of staging of Hodgkin’s lymphoma?

A

Ann Arbor

1: single node region
2: 2 regions on the same side of diaphragm
3: both sides of diaphragm
4: Diffuse/Disseminated involvement of 1 or more extra lymphatic organs

237
Q

What is the macroscopic appearance of prostate cancer?

A

Not usually apparent from gross inspection but may be enlarged or nodular

238
Q

What is the microscopic appearance of prostate cancer?

A
  • Disrupted architecture e.g. increased gland density or small circular glands
  • Basal cells lacking
  • Prominent nucleoli
  • Pleomorphism
239
Q

What is tumour marker of prostate cancer?

A

Increased PSA

240
Q

What are the colours of skin carcinoma?

A

Basal cell carcinoma - blue
Squamous cell carcinoma - pink
Melanoma - Grey/Brown

Kofi: Pure clinical conditions (8 decks)

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