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Clinical Conditions > 7. MoD > Flashcards

7. MoD Flashcards

1
Q

What is rhabdomyolysis?

A

Huge breakdown of skeletal muscle leading to release of myoglobin.

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2
Q

What are the consequence of rhabdomyolysis?

A

The release of myoglobin plugs renal tubules and causes renal failure.

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3
Q

What is a1 antitrypsin deficiency?

A

An autosomal recessive condition with a lack of antitrypsin molecule leading to increased trypsin activation.

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4
Q

How can a1 antitrypsin deficiency cause emphysema?

A

Increased elastase release by neutrophils be excess trypsin activation so areas of inflammation lead to excessive breakdown of elastin which destroys alveoli.

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5
Q

What is hereditary haemochromotosis?

A

Deficiency of hepcidin so Fe2+ isn’t stores and is deposited over the body.

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6
Q

What are the possible sequelae of hereditary haemochromotosis?

A

Damaged pancreas, heart etc.

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7
Q

How is hereditary haemochromotosis treated?

A

Bleeding.

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8
Q

What is coal worker’s pneumoconiosis?

A

Microscopic coal dust retained in alveoli and taken up by macrophages leading to an immune response that causes pulmonary fibrosis, which damaged lungs.

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9
Q

What are the consequence of coal worker’s pneumoconiosis?

A

Reduced air entry leading to persistent cough, breathlessness, fainting etc.

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10
Q

What is acute alcoholic hepatitis?

A

Serious binge drinking lead to toxins badly damaging the liver and formation of Mallory’s hyaline and targeted hepatic necrosis.

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11
Q

What are the symptoms of acute alcoholic hepatitis?

A

Fever, jaundice, and tenderness.

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12
Q

What is the outcome of acute alcoholic hepatitis?

A

It is usually reversible.

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13
Q

What is cirrhosis?

A

Irreversible severe damage to the liver.

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14
Q

What is the appearance of hepatocytes in cirrhosis?

A

Micronodules of hepatocytes surrounded by collagen bands.

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15
Q

What is the outcome of cirrhosis?

A

It is often fatal.

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16
Q

What causes lobar pneumonia?

A

Streptococcus pneumonae.

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17
Q

What is lobar pneumonia?

A

Acute inflammation of the lungs causing exudate to accumulate in the alveoli and loss of respiratory function.

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18
Q

What are the four stages of lobar pneumonia?

A 
Congestion phase (day 1-2) - vascular engorgement, clear exudate deposition into alveoli.
Red hepatisation (day 3-4) - RBCs leak into exudate, large fibrin deposits formed.
Grey hepatisation (day 5-7) - RBC disintegrate and exudate contains neutrophils and other WBCs.
Resolution (day 8+) - exudate drained through lymphatics and coughed up.
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19
Q

What is acute appendicitis caused by?

A

Fecaloma (calcified faeces) blocks part of the appendix causing inflammation and bacteria colonisation.

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20
Q

What can acute appendicitis lead to?

A

Abscess until rupturing, then causes peritonitis and systemic shock.

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21
Q

What is hereditary angio-oedema?

A

An autosomal dominant condition with mutation of C1 esterase inhibitor meaning the immune system is uncontrolled and there is huge generalised oedema throughout the body.

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22
Q

What are the results of hereditary angio-oedema on the airways?

A

Unable to breath so death.

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23
Q

How does hereditary angio-odema affect the intestines?

A

Oedema in intestines causes recurrent abdominal pain.

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24
Q

What is chronic granulomatous disease?

A

Neutrophils are unable to form superoxide radicals to eliminate phagocytosed pathogens so take them up by phagocytosis and stay there.

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25
Q

What is tuberculosis?

A

Chronic infection of the lung where macrophages phagocytose but can’t destroy bacteria due to mycolic acid coating so form granulomas, in which bacteria multiply.

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26
Q

What causes tuberculosis?

A

Mycobacterium tuberculosis.

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27
Q

How does tuberculosis spread?

A

By droplet infection.

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28
Q

What is a ghon focus?

A

The primary area of lungs that’s affected by tuberculosis.

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29
Q

What is a ghon complex?

A

Calcified hilar lymph node formed when tuberculosis infection begins to heal.

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30
Q

What is sarcoidosis?

A

Idiopathic granulomatous disease of the lungs without caseous necrosis.

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31
Q

What population is sarcoidosis common in?

A

Young women.

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32
Q

How is sarcoidosis managed?

A

Ease symptoms with steroids.

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33
Q

What is rheumatoid arthritis?

A

Autoimmune attack on the synovium of the joints, leading to granuloma formation and eroded articular surface of bones so decreased mobility and severe pain.

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34
Q

What are the features of rheumatoid arthritis on presentation?

A

Affects all joints but smaller ones first, common in younger people.

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35
Q

How is rheumatoid arthritis managed?

A

Steroids to mediate immune function.

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36
Q

What can cause chronic gastritis?

A

Helicobacter pylori or use of NSAIDs.

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37
Q

How can helicobacter pylori cause chronic gastritis?

A

Irritates the stomach lining and forms ulcers.

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38
Q

How can use of NSAIDs cause chronic gastritis?

A

Retard mucus defence and allow acid to erode the mucosa and come into contact with submucosa.

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39
Q

How is chronic gastritis treated?

A

If cause by helicobacter pylori - antibiotics to treat. Also give acid inhibitors.

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40
Q

What is the presentation of ulcerative colities?

A

Intermittent abdominal pain, diarrhoea (can be bloody and cause weight loss).

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41
Q

What is ulcerative colitis caused by?

A

Chronic autoimmune inflammation of the colon.

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42
Q

What are the histological features of ulcerative colitis?

A

Crypt abscesses, destruction of mucosa, and attack on submucosa.

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43
Q

What risk is increased with ulcerative colitis?

A

Risk of colon cancer.

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44
Q

How is ulcerative colitis managed?

A

Steroids given.

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45
Q

What is Crohn’s disease?

A

Autoimmune chronic inflammation of any part of the GI tract.

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46
Q

What is the presentation of Crohn’s disease?

A

Abdominal pain, diarrhoea (can be bloody), unexplained weight loss.

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47
Q

What are the histological features of Crohn’s disease?

A

Many granulomas and cobblestone bowel appearance.

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48
Q

What are some complications of Crohn’s disease?

A

Anal lesions and bowel fistulae.

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49
Q

How can Crohn’s disease be differentiated from ulcerative colitis?

A

Crohn’s isn’t restricted to the colon like UC and doesn’t show crypt abscesses.

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50
Q

How is Crohn’s disease treated?

A

With steroids.

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51
Q

What causes leprosy?

A

Mycobacterium leprae.

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52
Q

What is leprosy?

A

Chronic inflammation of the epidermis, nerves, eyes, and respiratory tract leading to neuropathy of epidermis, poor eyesight, and eventual loss of extremities from repeated unnoticed injury.

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53
Q

How is leprosy diagnosed?

A

Confirm bacteria with acid-fast test.

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54
Q

How is leprosy treated?

A

Antibiotics.

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55
Q

What is syphilis?

A

An infectious STD.

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56
Q

What is syphilis caused by?

A

Treponema pallidum.

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57
Q

What are the four stages of syphilis?

A

Painless ulcer on genital. Signs of second acute inflammatory response due to spread to other parts of the body - rash, fever, malaise etc. Latent stage, no symptoms but still infected. Tertiary syphilis, chronic inflammation in separate areas of the body, e.g. brain, liver, etc.

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58
Q

What is Wegener’s granulomatosis?

A

Autoimmmune chronic inflammation that causes a huge autoimmune attack on the epithelia of ears/nose/throat, lungs, and kidney. Leads to granuloma formation and fibrosis.

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59
Q

What are the untreated consequences of Wegener’s granulomatosis?

A

Renal and kidney failure.

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60
Q

How is Wegener’s granulomatosis treated?

A

With steroids.

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61
Q

What is the presentation of scurvy?

A

Bleeding gums.

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62
Q

What are keloid scars?

A

Scars that deposit an unusually large amount of grnaulation tissue so extends boundaries of original wound.

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63
Q

Which population is keloid scaring more common in?

A

Dark skinned.

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64
Q

What are oesophageal strictures?

A

Persistent acid reflux damages collagen framework of oesophagus so scar tissue formation - inflexible. Dysphagia is presenting complaint.

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65
Q

What are contractures?

A

Permanent shortening of the skin from second/third degree burn causing permanent damage to basal layer of epidermis so has granulation formation which is less flexible than skin.

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66
Q

What is the result of contractures over a joint?

A

It has a fixed flexed position.

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67
Q

What is deep vein thrombosis?

A

Formation of a thrombus within one of the deep veins of the body - usually in the leg.

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68
Q

What are the risk factors for DVT?

A

Inactivity, obesity, the pill, heart conditions.

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69
Q

How can DVT be prevented?

A

Subcutaneous heparin and TED stocking to prevent thrombus formation.

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70
Q

How can DVT be treated?

A

IV heparin/ oral warfarin.

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71
Q

What is the risk of DVT?

A

It can break off, migrate to the lungs and cause pulmonary embolism.

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72
Q

What is a pulmonary embolism?

A

Embolism that occlude the pulmonary arteries and leads to respiratory symptoms.

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73
Q

When is a pulmonary embolism fatal?

A

When >60% of the artery is occluded.

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74
Q

What are the symptoms of a major pulmonary embolism?

A

Shortness of breath, blood in sputum.

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75
Q

What are the symptoms of a minor pulmonary embolism?

A

Shortness of breath or asymptomatic.

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76
Q

How are pulmonary emboli treated?

A

With clot busters like streptokinase.

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77
Q

How can pulmonary emboli cause death?

A

Right sided heart failure due to severe pulmonary hypertension, mechanical shock due to severely decreased preload of the left heart, critical hypoxia due to ischaemia of a huge part of the lung.

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78
Q

What is an air embolism?

A

A bubble of air becomes trapped in a blood vessel.

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79
Q

What can cause an air embolism?

A

Care provider error like from cannulation, barotrauma (diver bursts up quickly), or decompression sickness.

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80
Q

What are the risks of air emboli?

A

Fatal is reaches the heart, occlude small arteries - risk of stroke, ischaemic limb.

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81
Q

How are air emboli treated?

A

Hyperbaric chamber (bring to high pressure to dissolve air and let pressure down slowly).

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82
Q

What is a fat embolism?

A

Embolism from a long bone breaking and releasing yellow marrow into the bloodstream.

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83
Q

How are fat emboli managed?

A

Wait for body to remove fat, fix the bone.

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84
Q

What is disseminated intravascular coagulation?

A

Widespread overactivation of the clotting cascade, leads to formation of many thrombi.

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85
Q

What are the sequelae of DIC?

A

Multiple organ damage and death from many thrombi. Consumes platelets and clotting factors so clotting at sides where it’s needed is less likely.

86
Q

How is DIC managed?

A

Platelet transfusion to prevent haemorrhage.

87
Q

What is thrombocytopenia?

A

Lack of thrombocytes in blood from decreased production of increased destruction.

88
Q

What can cause thrombocytopenia?

A

Decreased platelet production from folic acid deficiency, bone cancer, infection. Increased destruction from autoimmune conditions. Some medication.

89
Q

How is thrombocytopenia treated?

A

Treat underlying cause or give platelet transfusion.

90
Q

What is thrombophilia?

A

Excessive clotting throughout the body from genetic disorder, leading to overactivation of the clotting cascade.

91
Q

What does thrombophilia increase the risk of?

A

DVT.

92
Q

What is amniotic fluid embolism?

A

Embolism from a traumatic birth so amniotic fluid finds way into blood vessels.

93
Q

What is bowel infarction?

A

Death of the bowel due to occlusion of one of the mesenteric arteries from thrombus normally or atherosclerosis.

94
Q

What is a myocardial infarction?

A

Death of myocardium as a result of ischaemia, due to an occluded coronary artery.

95
Q

Why is the prognosis for myocardial infarction poor?

A

Myocardium is non regenerative so is dead forever.

96
Q

How are myocardial infarctions managed?

A

Coronary bypass and/or tenting to open a narrowed coronary artery.

97
Q

What is a transient ischaemic attack?

A

A mini stroke, cerebral ischaemia but not long enough to leave permanent damage.

98
Q

What is peripheral vascular disease?

A

Atheromas in the arteries of the legs leading to reduced capacity to perfuse the distal lower limb.

99
Q

What is the progression of symptoms in peripheral vascular disease?

A

Starts as intermediate claudication but then progresses to constant ischaemic pain and eventually ends up as dry gangrene when blood supply is completely lost.

100
Q

What is an abdominal aortic aneurysm?

A

Permanent dilation of the abdominal aorta from long term atheromas weakening and stretching it.

101
Q

What are the sequelae of an abdominal aortic aneurysm?

A

Rupture causing colossal haemorrhage and death. Lumen gets bigger each year, when past 4cm - operated on.

102
Q

How are abdominal aortic aneurysms detected?

A

Pulsatile mass in the abdomen if large enough.

103
Q

What is familial hypercholesterolaemia/hyperlipidaemia?

A

Disorders of the LDL mechanism which means LDL can’t be taken up into cells so left in blood causing hypercholesterolaemia or hyperlipidaemia.

104
Q

What are the clinical implications of hypercholesterolaemia/hyperlipidaemia?

A

Deposition of cholesterol and LDL at atheroma sites, tendons (tendon xanthoma), skin (xanthelasma), and cornea (corneal arcus).

105
Q

What is angina pectoris?

A

Sharp chest pain elicited on exertion due to narrowed coronary arteries being able to meet the demands of the heart at rest but not during exercise (so disappears after 10mins of rest).

106
Q

What is cardiac failure?

A

Inability of the heart to supply the needs of the body, it can’t pump enough blood.

107
Q

What are some contributing factors to cardiac failure?

A

Atherosclerosis, leading to ischaemic heart disease as the heart can’t get enough blood.

108
Q

What is a stroke?

A

Cerebral infarction from an embolism or atherosclerosis causing a wide range of symptoms, usually unilateral.

109
Q

What are the key signs of a stroke?

A

One side of face drops, can’t hold arms in the air, speech is slurred from paralysis of muscles involved in speech/muscles around the mouth.

110
Q

What is multi-infarct dementia?

A

Dementia from multiple cerebral infarctions.

111
Q

What is ischaemic colitis?

A

Impaired blood flow to the colon, either idiopathic or from atherosclerosis of either mesenteric artery.

112
Q

What are the results of ischaemic colitis?

A

Malabsorption, abdominal pain, progress to infarction - section of bowel needs removing.

113
Q

What is Leriche syndrome?

A

Peripheral vascular disease affecting the abdominal aorta at the point where it bifurcates into the common iliac arteries.

114
Q

What are the symptoms in men with Leriche syndrome?

A

Claudication in buttocks/thigh, weak/absent femoral pulses, and impotence.

115
Q

How is Leriche syndrome treated?

A

Stenting to re-open the artery.

116
Q

What is chronic eczema?

A

Relapsing/recurring inflammatory skin condition with a rash of excessive hyperplastic cells often found in skin creases often triggered by a specific allergen.

117
Q

What is psoriasis?

A

Extreme overproduction of skin cells leading to an excessive deposition of keratinocytes at the stratum corneum, from pathological hyperplasia, causing red scaling of the skin.

118
Q

What is a goitre caused by?

A

Pathological hyperplasia of the thyroid gland to compensate for its inefficiency.

119
Q

What is left ventricular hypertrophy?

A

Pathological hypertrophy, compensatory mechanism by heart to try to overcome increased afterload or aortic pressure (hypertension/aortic stenosis/aortic regurgitation).

120
Q

Why is left ventricular hypertrophy a bad thing?

A

Decreased compliance from thicker muscle leads to impaired contraction past a certain point.

121
Q

What is benign prostatic hypertrophy?

A

Actually benign prostatic hyperplasia - enlargement of the prostate so it presses on the urethra and causes problems with voiding bladder.

122
Q

What is Barrett’s oesophagus?

A

Metaplasia of the epithelium of the oesophagus from stratified squamous to simple columnar due to chronic acid reflux.

123
Q

What is the clinical significance of Barrett’s oesophagus?

A

Strongly associated with oesophageal adenocarcinoma.

124
Q

What is myositis ossificans?

A

Metaplasia of connective tissue inside the muscle into bone in response to fracture healing. From putting weight on incompletely healed fracture.

125
Q

What is endometrial hyperplasia?

A

Imbalance of oestrogen over progesterone so there is uncontrolled proliferation of the endometrial lining.

126
Q

What is the clinical significance of endometrial hyperplasia?

A

Predisposes to cancer due to more divisions - more chance of cancer developing.

127
Q

What is disuse atrophy?

A

Wastage of muscles due to lack of usage, reversed with proper usage again.

128
Q

What is disuse osteoporosis?

A

Atrophy - loss of bone density due to lack of usage of bone. Reduced osteoblast function, so less deposition of new bone.

129
Q

What is colorectal carcinoma?

A

Malignant bowel cancer with severe symptoms if it grows big enough to cause bowel obstruction.

130
Q

What is colorectal carcinoma linked with?

A

Ulcerative colitis.

131
Q

What is the five year survival for colorectal carcinoma?

A

65%.

132
Q

What is uterine leiomyoma?

A

Uterina fibroids. Benign tumour that arises from the smooth muscle of the uterus - myometrium.

133
Q

What are the symptoms of uterine leiomyoma?

A

Heavy/painful menstruation, painful sex, increasing urinary frequency.

134
Q

How may uterine leiomyoma be treated?

A

Elective hysterectomy.

135
Q

What is osteosarcoma?

A

Malignant bone cancer, likely to metastasise and form osteoids (uncalcified bone precursor) and makes pathological fractures likely.

136
Q

What populations is osteosarcoma common in?

A

Children and the elderly.

137
Q

What is the five year survival for osteosarcoma?

A

68%.

138
Q

What is mature cystic teratoma of the ovary?

A

Benign tumour that contains normal derivatives of more than one germ layer so may contain muscle tissue, teeth, skin, hair, etc.

139
Q

What are the symptoms of mature cystic teratoma of the ovary?

A

Normally asymptomatic but could have referred abdominal/pelvic pain from ovarian torsion.

140
Q

What is struma ovarii?

A

A rare type of benign ovarian neoplasm that contains mainly thyroid tissue.

141
Q

What is the clinical significance of struma ovarii?

A

Excess T3/4 and hyperthyroidism.

142
Q

What is chronic lymphocytic leukaemia?

A

Malignant cancer of the lymphocyte progenitor cells that leads to overproduction of B lymphocytes that are immature and useless.

143
Q

What is the clinical significance of chronic lymphocytic leukaemia?

A

Deposits of immature B lymphocytes in the blood crowd out RBC and WBC so anaemia results and potentially fatal infections.

144
Q

What are the average survivals for the types of chronic lymphocytic leukaemia?

A

If ZAP-70 is present, 8 years.

If ZAP-70 is absent, 25+ years.

145
Q

What is multiple myeloma?

A

Malignant cancer of the plasma cells.

146
Q

What is the clinical significance of multiple myeloma?

A

Excess plasma cells crowd out WBC and RBC. Bone lesions, adn susequent hypercalcaemia are present. The antibody paraprotein produced leads to kidney damage.

147
Q

What is the five year survival of multiple myeloma?

A

45%.

148
Q

What is lipoma?

A

Benign tumour composed of adipose tissue.

149
Q

What are the features of lipoma?

A

Soft to touch, mobile, and asymptomatic with no metastases.

150
Q

What is a seminoma?

A

Malignant tumour of the testicle.

151
Q

What is the five year survival of seminoma?

A

Over 95%, one of the most treatable and curable malignant cancers.

152
Q

What is angiosarcoma?

A

Malignant tumour of the endothelial lining of vessels in the lymphatic or circulatory system.

153
Q

What is the prognosis for angiosarcoma?

A

Poor as the location allows rapid metastasis.

154
Q

What is astrocytoma?

A

Tumour of the astrocytes (cells that makes up blood-brain barrier) that can be benign or malignant (benign can progress to malignant).

155
Q

What is the prognosis for astrocytoma?

A

Good if caught early enough to remove surgically. Very poor if later than that.

156
Q

What is melanoma?

A

A rare and aggressive (rapidly metastasising) cancer of the melanocytes int he skin.

157
Q

What is the five year survival of melanomas?

A

91% if it hasn’t penetrated the basement membrane.

158
Q

What is carcinoid tumour?

A

Slow growing neuroendocrine tumour that appears malignant microscopically but behaves in a benign fashion. Found in gut or lung and leads to excess production of serotonin, causing carcinoid syndrome.

159
Q

What are the features of carcinoid syndrome?

A

Flushing, wheezing, diarrhoea, abdominal cramps, and peripheral oedema.

160
Q

What is a carcinoma of the pancreas?

A

Malignant cancer of the exocrine portion of the pancreas that generally metastasis before a diagnosis is made.

161
Q

What are the signs of pancreatic cancer?

A

Nothing for a while, then weight loss, jaundice, abdominal pain - non-specific symptoms.

162
Q

What is a parathyroid adenoma?

A

Benign tumour of one of the parathyroid glands which leads to hypercalcaemia and phosphate deficiency.

163
Q

What are the signs of parathyroid adenomas?

A

Pathological fractures, kidney stones, abdominal pain and depression.

164
Q

How is a parathyroid adenoma treated?

A

Parathyriodectomy.

165
Q

What is pulmonary carcinoma?

A

The very common lung cancer, it is one of the four cancers that cause 54% of all cancer diagnoses. It is also the UK’s biggest killer of all cancers.

166
Q

What are the symptoms of lung cancer?

A

Haemoptysis, chest pain, weight loss, shortness of breath.

167
Q

Where does lung cancer metastasise to?

A

Through blood to the whole body or through the pleural cavity to other parts of the lung.

168
Q

What is lung cancer strongly linked with?

A

Smoking.

169
Q

What is the five year survival of lung cancer?

A

17%.

170
Q

What is squamous cell carcinoma of the skin?

A

The second most common type of skin cancer. Malignant and aggressive type from chronic sun exposure.

171
Q

What is basal cell carcinoma?

A

Malignant but not aggressive skin cancer that rarely metastasizes or kills.

172
Q

What are most gastric cancer?

A

Gastric carcinomas - developed from the endothelial lining of the stomach.

173
Q

What is a common cause of gastric carcinomas?

A

Helicobacter pylori infection that causes chronic infection, thus predisposing the individual to cancer.

174
Q

What are the symptoms of gastric cancers?

A

Non-specific and often confused with indigestion or GORD.

175
Q

What is the five year survival rate of gastric cancers?

A

28% due to misdiagnosis allowing for metastases before being detected.

176
Q

What is Burkett’s lymphoma?

A

A type of lymphoma focused on the destruction of B lymphocytes.

177
Q

What is Burkett’s lymphoma linked with?

A

Epstein-Barr virus.

178
Q

What is familial adenomatous polyposis?

A

Hereditary condition characterised by numerous polyps, which all can turn cancerous if untreated, from APC gene error that usually suppresses tumours by interacting with e-cadherin.

179
Q

What is retinoblastoma?

A

Cancer of the cells of the retina common in children.

180
Q

What is the hereditary element of retinoblastoma?

A

Involved a mutation in RB gene that usually acts as a tumour suppressor. If inherited, all germline cells will have this faulty alleles so only one mutation is needed to develop cancer.

181
Q

What is xeroderma pigmentosum?

A

A genetic defect that leads to the inability to perform excision DNA repair so cells are vulnerable to UV damage so patients are more likely to develop malignant melanomas or other skin cancer types.

182
Q

What is hereditary nonpolyposis colorectal cancer?

A

Autosomal dominant baseline mutation that leads to problems with mismatch repair that makes patients likely to develop colon cancer.

183
Q

What is bladder cancer strongly associated with and what did this prove about causality of cancer?

A

2-napthylamine - a dye used in industry. It proved cancers can take decades to develop after exposure, dose-response relationships are important, and different carcinogens can target specific organs.

184
Q

What is a hepatocellular carcinoma?

A

A very rare primary cancer of the liver.

185
Q

What causes hepatocellular carcinomas?

A

Hepatitis B or C acting as indirect carcinogens by causing chronic inflammation causing high cell turnover - makes mutation more likely by chancer and any mutation is more quickly promoted/proliferated.

186
Q

How is remission of hepatocellular carcinoma monitored?

A

By the presence of a-fetoprotein in the blood.

187
Q

What is malignant mesothelioma?

A

Cancer of the mesothelium (pleura) surrounding the lungs.

188
Q

What is malignant mesothelioma very strongly linked with?

A

Asbestos exposure. Asbestos is a complete carcinogen so initiates and promotes the mesothelioma.

189
Q

What is Kaposi’s sarcoma?

A

Cancer of the connective tissue due to infection with human herpesvirus 8.

190
Q

Which population is Kaposi’s sarcoma often found in?

A

HIV positive patients.

191
Q

How is HIV an indirect carcinogen?

A

It lowers immunological defences to allow an indirect carcinogen to cause cancer.

192
Q

What is cervical carcinoma?

A

Cancer of the cervix from infection by HPV virus.

193
Q

What are the T stages in TNM staging for cervical carcinoma?

A

1 - <2cm
2 - 2-5cm
3 - >5cm
4 - spread to wall/muscle/become inflamed

194
Q

What are the four cancer that makes up 54% of all cancer diagnoses?

A

Breast, prostate, bowel, and lung.

195
Q

What are breast carcinomas susceptible to?

A

Hormone targeted therapy as they are normally oestrogen sensitive.

196
Q

What is the Bloom-Richardson scale of differentiation for breast carcinomas?

A

Grade 1 - presence of tubules
Grade 2 - mitoses
Grade 3 - nuclear pleomorphism

197
Q

What is the problem with tumour marking with prostate cancer?

A

Prostate specific antigen isn’t specific to cancer, just disorder of the prostate.

198
Q

What is the tumour marker checking for remission of testicular cancer?

A

Beta-HCG.

199
Q

Why does testicular cancer have such a high survival rate?

A

Invention of cisplatin and relative ease with which a testicle can be removed allows over 90% five year survival rate.

200
Q

What is Hodgkin’s lymphoma?

A

A type of lymphoma focussing on the destruction of lymphocytes.

201
Q

What differentiates between Hodgkin’s and non-Hodgkin’s lymphoma?

A

The presence of Reed-Sternberg cells (large, moth eaten multinucleate) confirms it’s Hodgkin’s.

202
Q

What is the Ann-Arbor classification of Hodgkin’s lymphoma?

A

Stage I - one lymph node group
Stage II - multiple lymph node groups confined to one side of the diaphragm
Stage III - multiple lymph node groups either side of the diaphragm
Stage IV - extralymphatic involvement

203
Q

Why does oesophageal carcinoma have poor prognosis?

A

It isn’t normally caught until it’s metastasised.

204
Q

What are the symptoms of oesophageal carcinoma?

A

Difficulty swallowing, weight loss, persistent cough etc.

205
Q

What is chronic myeloid leukaemia?

A

Type of leukaemia where there is huge overproduction of all white blood cells and reduction in RBC and platelet counts.

206
Q

What is the presentation of chronic myeloid leukaemia?

A

Anaemia, inability to clot blood, vulnerable to fatal infections.

207
Q

What causes chronic myeloid leukaemia?

A

Formation of a philidelphia chromosome (from a t9:22) that creates a new oncogenic fusion protein.

208
Q

What is prognosis for chronic myeloid leukaemia and what affects this?

A

5 year survival 90%, high as imatnib can inhibit the oncogenic fusion protein.

209
Q

How is risk of endometrial cancer affected?

A

Increased by long-term use of tamoxifen (hormone therapy for breast cancer).
Decreased by long-term use of the contraceptive pill.

210
Q

What is the complication with bronchial squamous cell carcinomas?

A

Releases PTHrp (PTH related protein) so causes hypercalcaemia, and leads to osteoporosis as bone is broken down to release calcium.

Clinical Conditions (13 decks)

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