Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the laboratory diagnosis of excessive alcohol intake?

A

Isolated elevation of Gamma GT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the presentation of hepatitis B?

A
  • Jaundice
  • Fatigue
  • Abdominal pain
  • Anorexia
  • Nausea
  • Vomiting
  • Arthralgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the laboratory diagnosis for acute pancreatitis?

A

Elevated serum amylase and lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is hereditary haemochromatosis?

A

Genetic disorder resulting in increased intestinal absorption of dietary iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the presentation of hereditary haemochromatosis?

A
  • May be asymptomatic

- May present with multiple organ related symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are complications of hereditary haemochromatosis?

A
  • Liver damage
  • Heart dysfunction
  • Multiple endocrine failure especially pancreas, arthropathy, hypogonadism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the treatment of hereditary haemochromatosis?

A

Therapeutic phlebotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the presentation for alpha-1 antitrypsin deficiency?

A
  • Coughing
  • Wheezing
  • Sputum production
  • General respiratory work evident
  • Tachypnoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the complications of alpha-1 antitrypsin deficiency?

A
  • Emphysema
  • COPD
  • Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is coal workers’ pneumoconiosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the presentation of coal workers’ pneumoconiosis?

A

Usually asymptomatic but may have cough or sputum production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is complication of coal workers’ pneumoconiosis?

A

-Fibrosis
-Emphysema
If prolonged exposure or large quantities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the common causative organisms of pneumonia?

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Mycobacterium tuberculosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the complications of lobar pneumonia?

A
  • Death
  • Pleural effusion
  • Difficulty breathing
  • Abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the macroscopic appearance of acute appendicitis?

A
  • Swollen
  • Pus
  • Gangrene
  • Darker/Redder colour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the microscopic appearance of acute appendicitis?

A
  • Inflamed mucosa
  • Polymorphs
  • Macrophages present
  • Mucosal ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are possible causes acute appendicitis?

A
  • Pinworms
  • Faecal obstruction
  • Lymphoid hyperplasia
  • Adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the complications of acute pancreatitis?

A
  • Perforation leading to peritonitis
  • Bacteraemia
  • Sepsis
  • Fistulae
  • Abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is macroscopic appearance of bacterial meningitis?

A
  • Swollen

- Pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the microscopic appearance of bacterial meningitis?

A
  • Polymorph accumulation

- RBC accumulation adjacent to brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the complications of bacterial meningitis?

A
  • Sepsis

- Raised intracranial pressure leading to death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the complications Gallstones?

A
  • Hepatic abscess due to blocked duct allowing bacteria into liver
  • Pancreatitis
  • Fistulae
  • Perforation
  • Adult colic Carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the most common causative organisms of ascending cholangitis?

A
  • E.coli
  • Clepcilla
  • Streptococcus
  • Staphlycoccus
  • Enterobacter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the complication of ascending cholangitis?

A
  • Perforation
  • Cholecystitis
  • Peritonitis
  • Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the complication of hereditary angio-oedema?

A

Sudden death due to laryngeal involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the complications of chronic granulomatous disease?

A
  • Anaemia

- Malsorption syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the presentation of rheumatoid arthritis?

A
  • Painful, warm, stiff joints
  • Reduced range of movement
  • Deformity
  • Worse in the morning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the microscopic features of rheumatoid arthritis?

A
  • Plasma cells
  • Lymphocytes
  • Pannus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are rheumatoid nodules?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the presentation of ulcerative colitis?

A
  • Abdominal pain
  • Diarrhoea
  • Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is differential diagnosis of ulcerative colitis?

A
  • Crohns disease
  • Bowel cancer
  • Diverticulitis
  • Anorexia Nervosa
  • Inflammatory bowel disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the macroscopic appearance of ulcerative colitis?

A
  • Continuous distribution
  • Oedema
  • Mucopurulent exudate
  • Ulceration
  • Mucosal bleeding
  • Polyps
  • Mucosal scarring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the microscopic appearance of ulcerative colitis?

A
  • Superficial
  • Crypt abscesses
  • Distorted crypt architecture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the complications of ulcerative colitis?

A
  • Joint pain
  • Psoriases
  • Erythema nodosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the presentation of Crohn’s disease?

A
  • Abdominal pain
  • Diarrhoea
  • Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the differential diagnosis of Crohn’s disease?

A
  • Ulcerative colitis
  • Bowel cancer
  • Diverticulitis
  • Anorexia Nervosa
  • Inflammatory bowel disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the microscopic appearance of Crohn’s disease?

A
  • Transmural inflammation

- Granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the complications of Crohn’s disease?

A
  • Perforation
  • Fistulae
  • Intestinal bleeding
  • Malabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the macroscopic appearance of Chronic cholecystitis?

A
  • Strawberry-like appearance
  • Wall thickening
  • Gallstones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the microscopic appearance of Chronic cholecystitis?

A
  • Fibrosis
  • Muscular hypertrophy of wall
  • Lymphocytes
  • Entrapped epithelial crypts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the role of helicobacter in chronic gastritis?

A

Injures mucosa so cannot protect against stomach acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the microscopic appearance of chronic gastritis?

A
  • Granuloma
  • Mucosal atrophy
  • Goblet cell metaplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the complications of chronic gastritis?

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is cirrhosis?

A

Scarring of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is microscopic appearance of cirrhosis?

A
  • Nodules
  • Fibrous septa
  • Effacement of architecture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the causes of cirrhosis?

A
  • Alcohol excess
  • Hepatitis B
  • Hepatitis C
  • Non-acoholic fatty liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the complications of cirrhosis?

A
  • Cancer
  • Oedema
  • Ascites- (fluid accumulation in the peritoneal cavity)
  • Peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the microscopic appearance of tuberculosis?

A
  • Caseous necrosis

- Langhan’s cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the presentation of sarcoidosis?

A
  • Tiredness

- Cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the microscopic appearance of sarcoidosis?

A

Alveolar granuloma (non-caseating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the cause of scurvy?

A

Vitamin C deficiency causes weak collagen fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the pathophysiology of scurvy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the presentation of scurvy?

A
  • Fatigue
  • Poor healing
  • Tendency to bleed
  • Tooth loss
  • Old scars open
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is Ehler’s danlos syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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

A
  • Hyperextensible
  • Fragile skin
  • Hypermobile
  • Easily dislocated joints
  • Retinal detachement
  • Colon rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the macroscopic appearance of a keloid scar?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the microscopic appearance of keloid scars?

A

Excessive collagen network laid down beneath an otherwise relatively normal epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

\what is the clinical presentation of alport syndrome?

A
  • Haematuria in children progressing to renal failure
  • Eye defects
  • Deafness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is haemophilia A?

A

X-linked recessive deficiency in clotting factor VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the lab abnormalities of haemophilia A

A

Increased APTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is Haemophilia B?

A

X-linked recessive deficient of clotting factor IX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the lab abnormalities of Haemophilia B?

A

Increased APTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the presentation of Von-Willebrand disease?

A
  • Mucosal bleeding
  • Can be asymptomatic
  • Easy bruising
  • Prolonged bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are lab abnormalities for Von-Willebrand disease?

A
  • Low factor VIII and VWF

- Increased APTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is immune thrombocytopaenic purpura?

A

Autoimmune disease against platelets causing isolated low circulating platelet count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the presentation of immune thrombocytopaenic purpura?

A
  • Widespread petechiae
  • Headache
  • Easy bruising
  • Vision changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the lab abnormalities of Immune thrombocytopaenic purpura?

A

Bleeding time is long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the types of thrombophilias?

A
  • Factor V leidan
  • Prothrombin 20210 mutation
  • Protein C deficiency
  • Antithrombin deficiency
  • Antiphospholid syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the pathophysiology of thrombophilias?

A

Increased coagulability of blood due to clotting factor imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the presentation of thrombophilias?

A
  • Pain
  • Swelling
  • Tenderness of lower limbs (DVT)
  • Shortness of breath
  • Chest pain (PE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are the causes of Disseminated Intravascular Coagulation?

A

Sepsis, bacteraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is treatment for Disseminated Intravascular Coagulation?

A
  • Treat cause
  • Replacement therapy
  • Sometime heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the laboratory diagnosis for myocardial infarction?

A
  • Increased Troponin(I)

- Increased creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the complications of a myocardial infarction?

A
  • Death
  • Cardiac Tamponade
  • Arrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the pathophysiology of Deep Vein Thrombosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions