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Pathological Processes (Milly's) > Clincial Conditions > Flashcards

Clincial Conditions Flashcards

1
Q

What are the markers used to identify excessive alcohol intake? What are the results

A

GGT- liver enzyme that is increased by heavy alcohol intake
MCV- increased by prolonged heavy drinking
ALT and AST- increased levels indicate liver damage

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2
Q

What is the presentation of Hep B? (10)

A 
Fatigue 
General aches and pains
High temp (38+)
Nausea and vomiting
Decreased appetite 
Abdominal pain 
Diarrhoea 
Jaundice 
Dark urine
Pale-grey faeces
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3
Q

What are the diagnostic markers for acute Hep B?

A

Positive for:
HBsAg
IgM HBcAb

Negative for:
HBsAb (not protected against it)

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4
Q

What are the diagnostic markers for chronic hep B?

A

Positive for:
HBsAg
IgG HBcAb

Negative for:
HBsAb (not mounted a sufficient immune response)

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5
Q

What two enzymes would you measure to diagnose acute pancreatitis? What would be the results?

A

Serum amylase: increase

Serum lipase: increase

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6
Q

What is hereditary haemochromatosis?

A

A condition in which iron levels in the body slowly build up of the years

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7
Q

What are the earlier symptoms seen with hereditary haemochromatosis? (5)

A 
Fatigue,
Weight loss
Weakness 
Joint pain
Men: erectile dysfunction 
Women: irregular or absent periods
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8
Q

What are the later symptoms of hereditary haemochromatosis?

A 
Loss of libido and smaller testicles 
Abdominal pain and swelling
Chest pain
Darkening of skin/jaundice 
Severe pain and stiffness in joints
Swelling of hands and feets
Shortness of breathe 
Arrhythmias
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9
Q

What are the complications of hereditary haemochromatosis?

A

Liver damage
Diabetes (damage to pancreas)
Heart failure (damage to cardiac muscle)
Arthritis (damage to joints)

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10
Q

What is the current treatment for hereditary haemochromatosis?

A 
Phlebotomy (removing some blood) 
Chelation therapy (giving medication that causes iron to be excreted in urine and faeces)-done if phlebotomy is not an option
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11
Q

What is alpha-1 antitrypsin deficiency?

A

Deficiency in the AAT protein which controls enzymes that would otherwise damage healthy lung tissues

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12
Q

What is the pathophysiology of an alpha1 antitrypsin deficiency?

A

Caused by mutations to the SEPRINA1 gene, causing altered configuration of molecules, preventing their release
This results in the uncontrolled action of proteases (ie neutrophil elastase) which damage alveoli walls and can cause emphysema

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13
Q

What is the presentation of an alpha 1 antitrypsin deficiency?

A

Dyspnea (shortness of breathe)
Cough
Sputum production
Wheezing

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14
Q

What are the complications of an alpha 1 antitrypsin deficiency?

A 
Same as with COPD:
Pneumothorax
Pneumonia 
Acute exacerbation of air flow obstruction 
Respiratory failure
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15
Q

What is a coal-workers pneumoconiosis?

A

An industrial disease that is the result from breathing in carbon dust over a period of years. It can lead to inflammation, fibrosis and necrosis

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16
Q

Describe the symptoms associated with both simple and complicated coal-workers pneumoconiosis

A

Simple: shortness of breath (dyspnea) and chronic cough
Complicated: dyspnea, chronic cough and black sputum

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17
Q

What are the complications of coal-workers pneumoconiosis?

A

Lung dysfunction, pulmonary hypertension and heart problems

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18
Q

What is the difference betweenlobar pneumonia and bronchopneumonia?

A

LP: whole lobe affected
BP: only bronchioles and adjacent alveoli affected

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19
Q

What are commonest causative organisms of lobar pneumonia?

A

Strep. Pneumoniae
Haemophilus influenzae
Klebsiella pneumoniae

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20
Q

What are the complications of lobar pneumonia? (3)

A

Pleurisy (pleura become inflamed-can lead to resp failure)
Lung abscess (rare, usually seen in those with pre-existing illness or history of severe alcohol misuse)
Sepsis

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21
Q

What is the microscopic appearance of acute appendicitis? (Think about structure and cells present)

A

Structure:
No villi
No crypts
Ulcerated, complete loss of epithelium

Cells:
Polymorphs- neutrophils (most abundance acute inflammation cell)

*the epithelium is destroyed and replaces by inflammatory tissue that released proteases

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22
Q

What are the macroscopic features of acute pancreatitis?

A

Oedema due to fluid exudate

Swollen due to pus accumulation forming an abscess- fibrin mesh covering it

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23
Q

What type of necrosis occurs in the appendix?

A

Coagulative

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24
Q

What are the possible causes of acute pancreatitis?

A

Blockage to entrance of appendix by:

  1. Faecal matter
  2. Swollen lymph node (in wall of bowel due to infection elsewhere-upper resp tract)

These obstructions lead to inflammation and swelling, pressure can then cause the appendix to burst

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25
Q

What are the complications of an acute appendicitis? (2)

A

Peritonitis

Abscesses

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26
Q

What are the macroscopic features of bacterial meningitis?

A

Swelling,
Sulci filled with pus (giving cloudy appearance)
Gyri and sulci indistinguishable

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27
Q

What are microscopic features of bacterial meningitis?

A

Pus build up- made from neutrophils

It accumulates adjacent to the brain

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28
Q

What are commonest causative organisms of bacterial meningitis? (3)

A

Meningococcal bacteria
Pneumococcal bacteria
Haemophilus influenzae type B (Hib)

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29
Q

What are the complications of bacterial meningitis? (6)

A

Hearing and vision loss
Epilepsy
Problems with memory, concentration, co-ordination, movement and balance
Amputation and bone/joint problems (arthritis)
Kidney problems

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30
Q

What are the complications of gall stones? (5)

A

Acute cholecystitis (inflammation of gallbladder)
Jaundice
Acute cholangitis (infection of bile ducts)
Acute pancreatitis
Gallbladder cancer

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31
Q

What is ascending cholangitis?

A

Inflammation of the bile duct

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32
Q

What is the link between ascending cholangitis and gallstones?

A

Cholangitis is caused by a bacterial infection as a result of an obstruction of the biliary tree. A gall stone is the most common cause of the obstruction

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33
Q

What are the common causative organisms of ascending cholangitis? (3)

A

E.coli
Klebsiella species
Enterococcus species

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34
Q

What are the complication of acute cholangitis? (3)

A

Acute pancreatitis
Inadequate biliary drainage due to endoscopy, radiology or surgery
Hepatic abscesses

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35
Q

What is hereditary angio-oedema?

A 
Autosomal dominant inherited blood disorder causing episodic attacks of swelling which can affect the following:
Face
Extremities
Genitals
GI tract
Upper airways
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36
Q

What is the presentation of hereditary angio-oedema?

A

Recurrent swelling in face, extremities, GI, lips, larynx
Sensation of fullness but not pain or itching

*those who experiment abdominal swellings may experience acute pain in abdomen

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37
Q

What is chronic granulomatous disease?

A

A primary immunodeficiency disorder of phagocytes resulting from impaired killing of bacteria and fungi

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38
Q

What is the presentation of chronic granulomatous disease?

A

Early onset (first 2 years of life)
Severe recurrent bacterial and fungal infections
Dysregulated inflammatory response resulting in granuloma formation and other inflammatory disorders like colitis
Short stature

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39
Q

What is the presentation of rheumatoid arthritis?

A

Throbbing and aching pain in joints (often worse in the mornings and after periods of activity)
Stiffness in joints (lasting longer than 30 minutes-this would indicate osteoarthritis)
Swelling warmth and redness of joints

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40
Q

What are the microscopic features of rheumatoid arthritis?

A

[chronic inflammatory features:]

Pannus (layer of granulation tissue), Hyperplasia, fibrosis, errotion of articular cartilage, lymphocytes

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41
Q

What is a rheumatoid nodule?

A

A lump that appears subcutaneously in some patients with RA, usually not tender but occasionally painful

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42
Q

What is microscopic appearance of a rheumatoid nodule?

A

centre of fibrinoid necrosis

cellular palisade which is densely packed layer of macrophages and fibroblasts

Fibrous shell containing T cells and plasma cells in association with blood vessels

(Paler patchy middle, purple outline, then pink circle around that)

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43
Q

What is the presentation of ulcerative colitis?

A

Recurring diarrhoea which may contain blood, pus or mucus
Abdominal pain
Frequent need to empty bowels
Fatigue, loss of appetite and weight loss

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44
Q

What is the macroscopic appearance of ulcerative colitis?

A

Lumps (psuedopolyps)
Ulceration
Redness
Distal colon

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45
Q

What are the microscopic features of ulcerative colitis?

A 
Crypt distortion (loss of organisation)
Fibrosis (due to chronic inflammation)
Ulceration 
Limited to mucosa and submucosa 
Crypt abscesses
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46
Q

What are the complications of ulcerative colitis?

A

Osteroporisis (due to corticosteroid medication)
Poor growth and development (lack of absorption)
Primary sclerosing cholangitis
Toxic megacolon (dilated colon and other issues)

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47
Q

What is the presentation of Crohn’s disease?

A

Diarrhoea possibly containing blood and mucus
Abdominal pain
Fatigue and weight loss

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48
Q

What are the macroscopic features of Crohn’s disease?

A 
Cobblestone appearance
Thickening of wall
Thinning of lumen 
Bowel fistulae
Discontinuous distribution (but can be found throughout GI tract)
Anal lesions
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49
Q

What are the microscopic features of Crohn’s disease?

A

Granulomas

(Sometimes) cyrpt abscesses

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50
Q

What are the complications of Crohn’s disease? (2)

A 
Intestinal strictures (narrowing that causes problems by slowing or blocking the movement of food through an area)
Fistulas
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51
Q

What are the macroscopic features of chronic cholecystitis?

A

Thick walls-opaque grey/white appearance
Scarring (fibrosis)
Perforation of wall
Fistula formation

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52
Q

What is chronic cholecystitis?

A

repeated attacks of acute inflammation on the gallbladder, usually due to gallstones. The gallstones may block the opening of the gallbladder into the cystic duct or block the cystic duct itself.

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53
Q

What are the microscopic features of chronic cholecystitis?

A

Thickening of the gallbladder wall - due to fibrosis/muscular hypertrophy - key feature.
Chronic inflammatory cells - usu. “minimal”.
Lymphocytes - most common.
Rokitansky-Aschoff sinuses - common.[3]
Entrapped epithelial crypts – pockets of epithelium in the wall of the gallbladder.
+/-Foamy macrophages in the lamina propria (cholesterolosis of the gallbladder).

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54
Q

What is the role of helicobacter pylori in chronic gastric?

A

It is a gram negative bacilli that colonise and infect the stomach
Survive in mucous layer (covering gastric epithelium)
Can cause intense inflammatory responses in stomach and is associated with tissue damage

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55
Q

What changes can be seen microscopically in chronic gastritis caused by H.pylori?

A 
Helicobacter pylori organisms.
Chronic inflammation (and some acute inflammation) in the lamina propria and superficial epithelium.
Lamina propria fibrosis.
Mucosal atrophy.
Intestinal metaplasia.
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56
Q

How does helicobacter pylori cause gastritis?

A

By stimulating production of pro-inflammatory cytokines and by directly injuring epithelial cells and increasing acid secretion.

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57
Q

What are the complications of H.pylori associated chronic gastritis?

A

Stomach ulcers
Polyps in stomach
Tumours in the stomach (benign and malignant): ​Gastric adenocarcinoma or MALT (mucosa associated lymphoid tissue) lymphoma.

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58
Q

What is cirrhosis? What is process of this?

A

Scarring of the liver caused by continuous long term liver damage

Scar tissue replaces healthy tissue and prevents the liver working properly

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59
Q

What are some causes of liver cirrhosis? (3)

A

Alcohol consumption
Hepatitis
Non-alcoholic steatohepatitis (NASH)

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60
Q

What are some complications of cirrhosis? (4)

A 
Swollen varices
Ascites and peripheral oedema 
Encephalopathy (disease affecting the function of the brain) 
Sever bleeding (due to livers decreased ability to clot blood)
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61
Q

What is the macroscopic appearance of a cirrhotic liver?

A

Shrunken
Yellow-ish tan colour
(May be enlarged if alcohol was the cause)
Bumpy effect- micro/macronodular

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62
Q

What is the microscopic appearance of a cirrhotic liver?

A 
Scar tissue replacing normal parenchyma 
Dilated sinusoids 
No bile duct(?)
Fibrous septa 
Fatty cells 
Necrosis
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63
Q

What is the pathophysiology of Tuberculosis?

A

Infection with mycobacterium tuberculosis due to exposed of lungs/mucous membranes to infected aerosols
TB develops in the lungs for 2-12 weeks until there is a sufficient number of organisms to illicit an immune response

(Produces no toxins, causes disease by persistence and induction of cell mediated immunity)

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64
Q

What is the microscopic appearance of TB? (4)

A 
Granulomas made of:
Giant cells (langhans type)
Caseous necrosis centre 
Lymphocytes 
Epithelioid macrophages
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65
Q

How does TB differ to sarcoidosis?

A

TB has caseating granulomas (necrotic centres) whereas Sarcoidosis has non-caseating epithelioid cell granuloma

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66
Q

What is the presentation of sarcoidosis? (3)

A

Shortness of breath
Persistent dry cough
Tender red bumps or patches on the skin (shins) as well as rashes on upper body

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67
Q

What is the microscopic appearance of sarcoidosis?

A 
Granulomas:
Non-caseating 
Giant cells
Involves lymph nodes, lungs 
Lymphocytes
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68
Q

What causes scurvy?

A

Lack of Vit C

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69
Q

What is the pathophysiology of scurvy?

A

Without vitamin C, collagen cannot be replaced, the body’s tissues will begin to breakdown and deteriorate

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70
Q

What is the presentation of scurvy?

A 
Fatigue 
Irritability 
Pain in limbs (legs) + severe joint pain
Small red-blue dots on skin
Swollen gums
Shortness of breath
Easy bruising + redness and swelling in recently healed wounds
In infants: lack of appetite, irritability, poor weight gain, diarrhoea, temp >38
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71
Q

What is Ehlers-Danlos syndrome?

A

A group of rare inherited conditions that affect connective tissue

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72
Q

What is the clinical manifestation of Ehlers-Danlos syndrome?

A

Joint hyper-mobility
Stretchy skin
Fragile skin that breaks or bruises easy

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73
Q

What is osteogenesis imperfecta?

A

Brittle bone disease- genetic disorder that mainly affects the bones and results in the bones breaking easily

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74
Q

What is the clinical manifestation of Osteogenesis imperfecta?

A 
Malformed bones and short, small stature
Loose joints and muscle weakness 
Blue sclera
hearing loss (age 20/30)
Triangular face 
Curved spine
Brittle teeth
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75
Q

What is alport syndrome?

A

A genetic disorder causing a defect in type IV collagen

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76
Q

What is the clinical manifestation of alport syndrome?

A

Kidney disease: haematuria, proteinuria
Hearing loss (due to abnormalities in ear)
Eye abnormalities due to misshapen lenses in the eyes
Abnormal coloration of the retina
Vision loss (as a result of previous 2 points)

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77
Q

What is the macroscopic appearance of a keloid scar?

A 
Taller, more pronounced scar 
Smooth top
Pink/purple in colour 
Irregular shape 
Grow beyond boundaries of original wound

*wont regress over time like a normal scar

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78
Q

What is the microscopic appearance of a keloid scar?

A 
Type 3 (early) and type 1 (late) collage composition 
Lots of granulation tissue (scar tissue)
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79
Q

What is haemophilia A?

A

Deficiency in factor 8 affecting ones ability to clot

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80
Q

What is the presentation of haemophilia A?

A

Spontaneous haemorrhage
Easy bruising
Haemorrhage disproportionate to trauma

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81
Q 
What are the results of a lab test if someone has haemophilia A?
Consider the results of:
Platelet count
Bleeding time 
PT
APTT
Factor assays
A

PC: normal
BT:normal (measurement of platelet activity)
PT: normal (extrinsic pathway is fine)
APTT: prolonged APTT (factor 8 affecting intrinsic pathway)
Low factor 8 assay

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82
Q

What is haemophilia B? What is another name for it?

A

Christmas disease

Deficiency in factor 9, inherited conditions effecting ones ability to clot

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83
Q

What is the presentation of haemophilia B?

A

Spontaneous haemorrhage
Easy bruising
Haemorrhage disproportionate to trauma

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84
Q 
What are the results of a lab test if someone has haemophilia B?
Consider the results of:
Platelet count
Bleeding time 
PT
APTT
Factor assays
A 
PC: normal 
BT: normal 
PT: normal (extrinsic pathway fine)
APTT: prolonged (factor 9 is in this pathway)
Low factor 9 assay
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85
Q

What is Von-Willebrand disease?

A

Most common inherited bleeding disorder which affects the blood’s ability to clot
Deficiency in Von-Willebrand factor

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86
Q

What is the function of Von-Willebrand factor?

A

Assists in platelet plug formation by attracting circulating platelets
It stabilises factor 8, protecting it from premature destruction

*a lack of this will cause inadequate platelet function and adhesion

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87
Q

What is the presentation of Von-Willebrand disease?

A

Bruising easily
Bleeding from gums, nose and lining of the gut
Prolonged bleeding after cuts, excessive bleeding after tooth extraction and surgery
Menorrhagia (heavy periods)

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88
Q 
What are the results of a lab test if someone has Von-Willebrand disease?
Consider the results of:
Platelet count
Bleeding time 
PT
APTT
A

PC: normal
BT: increased (lowered platelet function)
PT: normal
APTT: prolonged (because Von-willebrand stabilises and protects factor 8 from destruction)

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89
Q

What is immune thrombocytopenic purpura?

A

Low platelet count with normal bone marrow

The low platelet count is due to reduced platelet survival

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90
Q

What is the presentation of thrombocytopenic purpura?

A

Purpuric rash

Increased tendency to bleed

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91
Q 
What are the results of a lab test if someone has thrombocytopenic purpura?
Consider the results of:
Platelet count
Bleeding time 
PT
APTT

What other tests might you want to do?

A

PC: low
BT: prolonged (due to low platelet activity)
PT: normal (assesses clotting cascade not platelet function)
APTT: normal (assesses clotting cascade not platelet function)

Bone marrow biopsy may be necessary to exclude other causes of low platelet counts

92
Q

What is a thrombophilia?

A

Inherited/acquired defect of haemostasis which results in a predisposition to thrombosis eg DVT/PE

93
Q

Name some types of thrombophilia? (5)

A 
Factor V leiden (no deactivation of factor V)
Antithrombin deficiency (natural anticoagulant)
Protein C deficiency (natural anticoagulant)
Protein S deficiency (natural anticoagulant) 
Antiphospholipid syndrome (autoimmune- attacks phospholipids which keep blood at correct consistency)
94
Q

What is the presentation of a thrombophilia resulting in DVTs?

A

Pain
Swelling
Tenderness and heavy ache in affected area (usually calve)

95
Q

What is the presentation of a thrombophilia resulting in PEs?

A

Chest and upper back pain
Shortness of breath (dyspnea)
Feeling lightheaded and fainting
Coughing (usually dry but can cough up blood)

96
Q

What is disseminated intravascular coagulation?

A

Thrombo-haemorrhagic disorder occuring as a secondary complication in a variety of conditions
(You bleed and clot at the same time)

97
Q

What are some possible causes of DIC?

A

Sepsis (gram negative bacteria as these have endotoxins that activate clotting)
Severe trauma (especially in the brain where there is a larger amount of thromboplastin)
Extensive burns
Complication in childbirth (amniotic fluid embolism, retained dead foetus)
Malignancy
Snake bites
Severe transfusion reactions

98
Q

What is the pathophysiology of DIC?

A

Systemic activation of blood coagulation leads to microthrombi
This consumes platelets and coagulation factors therefore activates fibrinolysis and patient experiences haemorrhages

99
Q

How is DIC diagnosed?

A

Diagnosis is made by combining clinical presentation with lab abnormalities

100
Q

Consider the following results of someone who has DIC?
Platelet count
FDP (fibrin degradation products) levels/D-dimer
Coagulation time
Peripheral smears (what do you see)

A

PC: low
FDP/D-dimer: increased (lots of fibrinolysis)
CT: prolonged (lack of clotting factors)
PS: see shistocytes (fragmented part of a RBC-typically irregularly in shaped, jagged, and have two pointed ends)

101
Q

What is the treatment of DIC?

A

Treat underlying cause (antibiotics if sepsis etc)
Platelet transfusion if thrombocytopenic and bleeding or at risk of bleeding (surgery)
*occasionally you may need to administer an anticoagulant like Heparin

102
Q

What is the role of thrombosis in MIs?

A

MI is caused by ischaemia often due to obstruction of a coronary artery by a thrombus
This occlusion starves the heart of oxygen and results in tissue death- infarction

103
Q

What are the markers used to confirm and measure the severity of a MI?

A

Troponin mainly
But can use creatine kinase (this is used less as it can be released by damaged skeletal muscle also)

{*take measurements over a 24 hr period as levels may not immediately be raised}

104
Q

What are the complications of MI?

A

Arrhythmias
Heart failure
Cardiogenic shock
Heart rupture

105
Q

What is the pathophysiology of a DVT? [think about Virchows triad]

A

Formation of a thrombus (due to slow or turbulent blood flow, increased coagulability of blood, damage to epithelium of vein) within a Deep vein has the potential to embolise and cause issues around the body (ie PE). The thrombus itself may occlude/narrow the lumen causing further issues

106
Q

Name some predisposing factors for DVT?

A

Anything that may disrupt Virchow’s triad
Changes in vascular wall [damage]: hypertension
Changes in blood flow [slow or turbulent]: sedentary life, being obese, major surgery/trauma
Changes in blood [hyper-coagulability]: DIC, old age, major surgery/trauma, pregnancy, oral contraceptives, thrombophilias (ie protein C deficiency)
Family history

107
Q

Wha is the presentation of PE?

A

Chest and upper back pain described as sharp (may be worsen upon inhalation)
Dyspnea
Coughing (dry but can cough up blood)
Feeling lightheaded, dizzy, fainting

108
Q

What is the pathophysiology of PE?

A

Usually arise from thrombi in deep veins of thigh and popliteal vein
Occlude/narrow lumens starving lungs-ischaemia- cell death

109
Q

What are the risk factors for PE?

A

Blood clot in deep vein of lower limb
Previous PE

Anything that causes DVT:
Alteration in blood flow: immobilisation, injury, pregnancy, obesity, cancer
Damage to walls: surgery, catheter causing direct injury
Factors affecting coagulation: contraceptive pill, thrombophilias, pregnancy, obesity, cancer

110
Q

What is the pathophysiology of an air embolism? When might it occur?

A

Occurs when one or more air bubbles enter a vein or artery and block it
This may occur during injections, surgical procedures, lung trauma and scuba diving

111
Q

What is the presentation of a fat embolism?

A

Breathlessness and vague pains in the chest
Fever and tachycardia
Petechial rash
CNS symptoms from mild headache to significant cerebral dysfunction
Haematuria

112
Q

What is the pathophysiology of an amniotic fluid embolism?

A

Amniotic fluid enters mother’s circulation through tear in membranes, this can cause sudden resp. Distress, hypotension, seizures, loss of consciousness, DIC-amniotic fluid contains prothrombotic substances

113
Q

What is heterozygous familial hypercholesterolaemia?

A

A defect in LDL receptors which means there is decreased haptic uptake of LDLs therefore more circulating LDLs

114
Q

What are the consequences of Heterozygous familial hypercholesterolaemia?

A

High levels of LDL cause an increased risk of atherosclerosis which can lead to ischaemic heart diseases and thus MI

115
Q

What is the role of atherosclerosis in ischaemic heart disease?

A

Lipid deposits build up in the coronary arteries and become hardened, stiffened and swollen to form a plaque
This leads to limitation of blood flow causing the myocardial cells to be starved of oxygen

116
Q

What is the role of atherosclerosis in transient ischaemia attack?

A

A dislodged atherosclerotic plaque in one of the carotid arteries can cause an embolus to occlude an artery in the brain

117
Q

What is the pathophysiology of a transient ischaemic attack?

A

A temporary reduction of cerebral blood flow in a specific neurovascular distribution as a result of partial or total occlude- no permanent damage

118
Q

What is the role of atherosclerosis in Cerebrovascular accident (stroke)?

A

A thrombus can form around an atherosclerotic plaque and break into an embolus and block a blood vessel in the brain

119
Q

What is the pathophysiology of a stroke?

A

Vascular occlusion secondary to thromboembolic disease, ischaemia causes hypoxia and depletion of ATP so ionic gradients cannot be maintained and passive inflow of Na+, Ca2+ and water leads to cytotoxic oedema

120
Q

What is the difference between an ischaemic stroke and a haemorrhagic stroke?

A

Ischaemic: obstruction within a blood vessel supply blood to the brain

Haemorrhagic: weakened blood vessels rupture (oftendue to uncontrolled hypertension)

121
Q

What is the roles of atherosclerosis in bowel ischaemia?

A

Atherosclerosis can cause thrombosis and cause impaired blood transfusion to the intestine which delivers bacterial to an otherwise sterile location. This induces an inflammatory response

122
Q

What is the role of atherosclerosis in peripheral vascular disease?

A

Atherosclerosis leads to blood vessels becoming narrowed and blood flow decreasing
Lacquers build up in the vessels and limit flow (and O2 delivery) to organs and limbs
Thrombi may develop and completely occlude artery which can lead to ischaemia- necrosis- loss of fingers, toes and limbs if untreated

123
Q

What is presentation of peripheral vascular disease?

A 
Intermittent claudication 
Hair loss on legs and feet
Numbness/weakness in legs and muscle wasting 
Brittle, slow growing toenails 
Ulcers which don't heal
Pale and shiny skins 
Erectile dysfunction 
Pain in both legs
124
Q

What is the role of atherosclerosis in abdominal aortic aneurysm?

A

The walls of an AAA often carry an atherosclerotic burden, but atherosclerosis cannot be used to explain the initial defect and cause of the occlusion

125
Q

What are the complications of an abdominal aortic aneurysm?

A
  1. Can leak and cause abdominal pain
  2. Rupture and cause death
  3. Associated with atherosclerosis and clot can embolise into smaller blood vessels
  4. (Rare) infection
126
Q

What are the causes of Left ventricular hypertrophy?

A

Aerobic exercise and strength training
Increased afterload due to aortic stenosis, aortic insufficiency and hypertension
Hypertrophic cardiomyopathy

127
Q

What are the complications of LV hypertrophy?

A
  1. Weakening of LV= heart failure
  2. Stiffening and loss of elasticity=heart failure
  3. Compression of coronary arteries= IHD
  4. Arrhythmias
  5. Aortic root dilation
  6. Stroke
  7. Sudden cardiac arrest
128
Q

What is barrett’s oesophagus?

A

An abnormal change (metaplasia) in the cells of the lower portion of the oesophagus characterised by the replacement of stratified squamous epithelial cells by simple columnar epithelium cell with goblet cells

129
Q

What causes Barrett’s oesophagus?

A

Gastroesophageal reflux (GERD) can cause it due to the exposure of oesophageal cells to stomach acid

130
Q

What are the complications of Barrett’s oesophagus?

A

Oesophageal cancer (1/20 within 10-20 years)

131
Q

What is traumatic myositis ossificans?

A

A benign process characterised by heterotrophic ossification within large muscles

132
Q

What is the macroscopic appearance of benign prostatic hyperplasia?

A

Swollen gland
Narrowing of urethra
Smooth
Symmetrical glands

133
Q

What are the complications of benign prostatic hyperplasia?

A

UTI

Acute urinary retention

134
Q

What is the presentation of psoriasis?

A

Patches of skin that are dry, red (plaques) and covered in silver scales
Itchiness and soreness
Plaques may be cracked or bleeding

135
Q

What is the macroscopic appearance of psoriasis?

A

Patches of red skin with plaques and covered in silver scales

136
Q

What is the microscopic appearance of psoriasis?

A

Inflammatory cells: dendritic cells, macrophages, T cells
Over abundance of skin cells (keratinocytes)

Clubbed epidermal projections that interdigitate with dermis
Epidermal thickening
Granula layer can sometimes be missing
Most superficial cells aren’t fully matured (still have nucleus)

137
Q

What is the pathophysiology of psoriasis?

A

Hyperproliferation of keratinocytes in the epidermis with an increase in the epidermal turnover rate
(Turnover very 3-5 days as opposed to 28-40)

138
Q

What is colorectal carcinoma?

A

A malignant epithelial neoplasm of the colon/rectum

139
Q

What are the predisposing factors for colorectal carcinoma?

A
  1. Old age
  2. Family history
  3. Diet high in red and processed meat
  4. Smoking and heavy drinking
  5. Obesity and inactivity
  6. Crohn’s disease and ulcerative colitis
140
Q

What is the presentation of colorectal carcinoma?

A
  1. Persistent change in bowel habit- more often with looser stall and abdominal pain
  2. Blood in the stool
  3. Abdominal pain,bloating and discomfort always due to eating
141
Q

What is the macroscopic appearance of colorectal carcinoma?

A

Ulcerated
Flat (sessile polyp)
Irregular margin

142
Q

What is the microscopic appearance of colorectal carcinoma?

A

Large pleomorphic cells, with dark nuclei
Poor differentiation
Mitotic figures

143
Q

What are the principals of staging a colorectal cancer?

A 
Dukes staging
A. Into but not through wall
B. Through wall
C. Lymph nodes
D. Metastases (distant)
144
Q

What is the screening programme for colorectal carcinoma?

A

M/F 60-74 screened every 2 years
74+ screened at request

Screen includes: bowel scope, testing for blood in stools

145
Q

What is the presentation of uterine leiomyoma?

A

Heavy or painful periods
Abdominal and lower back pain
A frequent need to urinate and constipation
Pain and discomfort during sex

146
Q

What is the macroscopic appearance of uterine leiomyoma?

A

Multiple tumours
Polyps (pedunculated)
Pushing the boundaries

147
Q

What are the microscopic features of uterine leiomyoma ?

A

Elongates cigar shaped Nuclei
Well differentiated
Pushing boundaries
Storiform structure (elongated cells radiating from centre)

148
Q

What is osteosarcoma?

A

Malignant neoplasm of the bone

149
Q

What is the presentation of osteosarcoma?

A
  1. Persistent bone pain that gets worse over times and continues into the night
  2. Inflammation over a bone which can make movement difficult, if affected bone is near a joint
  3. Noticeable lump on bone
  4. Weak bone that fractures easily
150
Q

What is the macroscopic effect of osteosarcoma?

A

Growth on bone, abnormal outlines

151
Q

What are the microscopic features of osteosarcoma?

A

Pleomorphic malignant cells (all look different)
Less osteoid
Poorly differentiated cells

152
Q

What is an ovarian teratoma?

A

Also called a dermoid cyst of the ovary, this is a bizarre tumor, usually benign, in the ovary that typically contains a diversity of tissues including hair, teeth, bone, thyroid, etc

153
Q

What is the presentation of ovarian teratoma?

A

Pelvic pain and pain during sex
Difficulty emptying bowels and a frequent need to urinate
Irregular/abnormal periods
Bloating, a swollen abdomen and feeling full after eating only a little

154
Q

What is the macroscopic appearance of an ovarian teratoma?

A

Cyst containing hair, sebum, teeth etc

155
Q

What is the microscopic appearance of a ovarian teratoma?

A

Serbacous glands
Epidermis
Etc

156
Q

What is the cell of origin for a dermoid cyst?

A

Germ cell

Growth of ectoderm, mesoderm and endoderm tissues (ie bone, hair, nerves)

157
Q

What is a strums ovarii?

A

A rare form of monodermal teratoma that contains mostly thyroid tissue which may cause hyperthyroidism

158
Q

What is chronic lymphocytic leukaemia?

A

A monoclonal disorder characterised by a progressive accumulation of functionally incompetent lymphocytes (B lymphocytes)

Common in adults over 50

159
Q

What is the presentation of a chronic lymphocytic leukaemia?

A
  • getting infections often
  • anaemia and bleeding and bruising
  • fever and night sweats
  • swollen glands in neck, armpits and groin
  • swelling and discomfort in the abdomen
  • unintentional weight gain
160
Q

What is chronic lymphocytic leukaemia a stage of?

A

Small lymphocytic lymphoma: the of B cell lymphoma which present primarily in the lymph nodes

161
Q

What is melanoma?

A

Cancer of the melanocytes (skin cancer)

162
Q

What are the predisposing factors for malignant melanoma?

A
  1. Repeated sunburn
  2. Radiotherapy treatment
  3. Lots of large moles/lots of freckles
  4. Family history
  5. Pale skin, fair hair, blue eyes
  6. HIV/immunosuppressants
  7. Previous diagnosis
163
Q

What is the presentation of malignant melanoma?

A

A new mole or a change in a mole: getting bigger, changing in shape or colour, bleeding or becoming crusty, itchiness and soreness

164
Q

What is the macroscopic appearance of malignant melanoma?

A

Mole on skin, large, variations in colour, asymmetrical shape, with irregular borders

165
Q

What is the microscopic appearance of malignant melanoma?

A

Proliferation of melanocytes
Inflammatory cells
Squamous epithelium
Melanocytes in dermis and epidermis

166
Q

What is pancreatic adenocarcinoma?

A

Malignant neoplasm of the pancreas (epithelium)

167
Q

What is the macroscopic features of a pancreatic adenocarcinoma?

A

Large growth

168
Q

What are the microscopic features of a pancreatic adenocarcinoma?

A

Rudimentary gland (the tumour is trying and failing to make glands)

169
Q

What are the complications/symptoms of a pancreatic adenocarcinoma?

A 
Weight loss
Jaundice 
Pain
Bowel obstruction 
Symptoms of diabetes
170
Q

What is a carcinoid tumour?

A

Slow growing well differentiated neuroendocrine tumour originating in the cells of the neuroendocrine system
They can be found in the bowel, lung and stomach as well as other places

171
Q

What is the presentation of a neuroendocrine tumour/carcinoid tumour that is found in the:
A) bowel
B) lung
C) stomach

A

A) bowel carcinoid tumour: abdominal pain, blocked bowel, rectal bleeding, diarrhoea and constipation
B) lung carcinoid tumour: cough which may include blood, wheezing, breathlessness, chest pain and tiredness
C) stomach carcinoid tumour: pain, weight loss, tiredness and weakness

172
Q

What are the complications of carcinoid tumours?

A

Carcinoid syndrome: skin flushing in face and neck, chronic diarrhoea and dyspnea
Carcinoid heart disease: may secrete hormones that thicken the heart chambers, valves and blood vessels=leads to heart failure
Cushing’s syndrome: lung carcinoid tumour can cause this by releasing ACTH/CRH

173
Q

What is Burkitt’s lymphoma?

A

Cancer of the lymphatic system, in particular the B cells found in the germinal centres.
Fasted growing human tumour
Associated with impaired immunity
Rapidly fatal if untreated

174
Q

Name some predisposing factors for Burkitt’s lymphoma?

A
  1. Immunocompromised (HIV or in immunosuppressants)
  2. Autoimmune condition
  3. Previous exposure to EBV, HTLV, H.pylori infections
  4. Previous chemo/radiotherapy
  5. Coeliac disease
175
Q

What is familial adenomatous polypsis?

A

Inherited condition in which numerous adenomatous polyps form mainly in the epithelium of the large intestine. While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated
Multiple benign growths in the colon may develop as early as teenage years

176
Q

What is an adenomatous polyp?

A

Polyps (abnormal growths) that grow on the lining of the colon and which carry a high risk of cancer, they are considered pre-malignant

177
Q

What is the genetic change that gives rise to familial adenomatous polyposis?

A

Mutations in APC gene which affects the ability of cells to maintain normal growth and function

178
Q

What is the macroscopic appearance of familial adenomatous polyposis?

A

Hundreds to thousands of colorectal polyps, small abnormalities in the intestinal tract

179
Q

What are the complications of familial adenomatous polyposis?

A

Colorectal carcinoma
Duodenal or periampullary adenocarcinoma
Desmond formation

180
Q

What is the treatment for familial adenomatous polyposis?

A

Surgery to prevent development of colon cancer

Sulindac and celecoxib can reduce the size and number of polyps in patients who have had surgery

181
Q

What is hereditary non-polyposis colorectal cancer?

A

Most common form of colorectal carcinoma

182
Q

What are the genetic changes that lead to the development of hereditary non-polyposis colorectal carcinoma?

A

Autosomal dominant syndrome due to defective mismatch repair protein (MMR)

183
Q

What is retinoblastoma?

A

Cancer of immature cells of a retinue (light detecting tissue of eye)

184
Q

What is the pathophysiology of a retinoblastoma?

A

Arises from a mulitpotential precursor cell that could develop into almost any type of inner or outer retinal cell

185
Q

What is the presentation of retinoblastoma?

A 
Normally occurs in those under 5
Unusually white reflection in the pupil
Squinting or poor vision
Colour change in iris
Red or inflamed eye
186
Q

What is xeroderma pigmentosum?

A

rare autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient

187
Q

What are the genetic changes that occur to result in xeroderma pigmentosum?

A

Mutation in the genes that are involved in DNA repair:
XPC
ERCC2
POLH

188
Q

What is the presentation of xeroderma pigmentosum?

A

Sever sunburn with only small amounts of exposure
Freckles at an early stage
Painfully sensitive eyes (to sun)
Rough surfaced growth/skin cancers
Blistering and freckles on minimum sun exposure

189
Q

What is malignant mesothelioma?

A

Cancer of the pleura or the peritoneum

190
Q

What is the predisposing factor for malignant mesothelioma?

A

Exposure to asbestos

191
Q

What is the macroscopic appearance of a malignant mesothelioma

A

Thickening of the mesothelium

192
Q

What are the predisposing factors for cervical cancer?

A 
HPV (human papilloma virus)
Smoking
Weakened immuno system
Taking the pill for more than 5 years
Having children
193
Q

What is the pathophysiology of HPV causing cervical cancer?

A

HPV expresses E6 and E7 proteins that inactive/inhibit tumour suppressor proteins: p53 and pRB (respectively)

Thus it:
Speeds cell through cell cycle
Inhibits apoptosis (because p53 is inhibited)
Combats cellular senescene

194
Q

What are the screening and prevention methods put into place to reduce the cervical cancer?

A

HPV test and vaccinations

195
Q

What are the predisposing factors for hepatocellular carcinoma?

A

Hep B/C
Alcoholism/liver cirrhosis
Aflatoxin
Haemochromatosis

196
Q

What is the tumour marker used for hepatocellular carcinoma?

A

Serum alpha fetoprotein which will increase

197
Q

What are the genetic changes seen in familial cases of breast cancer?

A

BRCA1 and BRCA2 abnormalities and mutations stop these genes from repairing cell damage

198
Q

What are the predisposing factors for breast cancer?

A 
Increased age
Genetic mutations (BRCA1/2 genes)
Early menstrual period (before age 12)
Late or no pregnancy 
Starting menopause after 55
Physical inactivity/being overweight after menopause
Having dense breasts
199
Q

What is the macroscopic appearance of breast cancer?

A 
Dimpling or puckering 
Rash crusting
Nipple discharge (clear/ bloody) 
Change in nipple appearance (being pulled in) 
Lump
200
Q

What two type of receptors can be identified within breast cancer tissue to establish the potential cause of the proliferation?

A 
Oestrogen receptors (cancer is called oestrogen-receptor-positive) 
Her2 receptors

*both these substances may have stimulate the cancer cells to divide and grow

201
Q

What are the two types of treatment for breast cancer?

A 
Hormone therapy (limited scope but non toxic)
Herceptin therapy (can have autoimmune side effects)
202
Q

Describe how hormone therapy is used to treat breast cancer?

A

Used to treat oestrogen receptor positive cancers.
They bind to the receptors and prevent oestrogen from binding
Eg tamoxifen

203
Q

Describe how herceptin therapy can be used to treat breast cancer

A

Used for cancers with large HER2 receptors, herceptin can block these and causes the cell to stop growing and death

204
Q

What are the predisposing factors for squamous cell carcinomas of the skin?

A

Fair skin
Xs sun exposure, use of tanning beds and history of sunburns
Personal history of precancerous skin lesions and of skin cancer

205
Q

What is the microscopic appearance of squamous cell carcinoma?

A

Islands of cells that look like epidermis, it will form keratin- pink fibrinolytic structures: looks like cabbage

206
Q

What is the macroscopic appearance of squamous cell carcinoma of the skin?

A

Ulcerated red patch

Hard raised edges

207
Q

What are the predisposing factors for a basal cell carcinoma?

A 
Chronic sun exposure
Radiation therapy for psoriasis or acne 
Fair skin
Male
Over 50 
Personal or family history of skin cancer
208
Q

What is the macroscopic appearance of basal cell carcinoma?

A

Red/brown abnormal lump/growths on skin

Raised (central ulceration)

209
Q

What is the microscopic appearance of a basal cell carcinoma?

A

Peripheral palisade

Islands of dark cells in epidermis and dermis of skin

210
Q

What is the behaviour of a basal cell carcinoma?

A

Rarely metastasises

Prognosis is excellent but if allowed to progress it can cause significant morbidly

211
Q

Name 5 types of lung cancer

A
  1. Adenocarcinoma (cells lining lungs, gland like properties)
  2. Squamous cell carcinoma (squamous cell lining of resp. tract)
  3. Large cell carcinoma (poorly differentiated)
  4. Large cell neuroendocrine tumour (fast growing type)
  5. Small cell lung cancer (type of neuroendocrine tumour, fast growing cancer that rapidly spreads/metastasises)
212
Q

What is the relationship between smoking and lung cancer?

A

Cigarette smoking is linked to 80-90% of lung cancer

At least 70 of the chemical in tobacco are known to be carcinogenic

213
Q

What are the predisposing factors for bladder cancer?

A

Smoking
Increasing age
Being white
Being male
Exposure to harmful chemicals (eg arsenic)
Previous cancer treatment aimed at the pelvis

214
Q

What is kaposi’s sacroma?

A

A cancer that causes patches of abnormal tissue grow under the skin/lining of mouth, nose and throat/ in lymph nodes etc

The patches are usually red or purple and are made of cancer cells, blood cells and blood vessels

215
Q

What are some causes of Kaposi’s sarcoma?

A

Human herpesvirus 8 (HHV-8)- spread during sex, by saliva or vertically
Particularly at risk if you have a weakened immune system or have a genetic vulnerability to the virus

216
Q

What are the two types of testicular cancer?

A

Seminoma and non-seminoma (teratoma, embryonal carcinoma, choricarcinoma, yolk sac tumours)

217
Q

What are the macroscopic appearances of testicular cancer?

A

Abnormal lumps

Changes in size, shape or weight (compared to other testicle)

218
Q

What are the tumour markers used for testicular cancer?

A 
Alpha fetoprotein (AFP)
Beta human chorionic gonadotropin 
Lactate dehydrogenase (LDH)
219
Q

What is the presentation of a Hodgkin’s lymphoma?

A 
Lymph node swelling in neck, armpits or groin
Night sweats and fever
Unintentional weight loss
Persistent cough or dyspnea 
Persistent itching all over body
220
Q

What is the microscopic appearance of Hodgkin’s lymphoma?

A

Multi-nucleated Reed-Sternberg cells in lymph nodes

Eosinophils (secreting IL5)

221
Q

What is the staging method used for lymphomas?

A

Ann Arbor:
Stage 1- 1 node region
Stage 2- 2 separate nodes on 1 side of diaphragm
Stage 3- 2 separate nodes on different sides of diaphragm
Stage 4- involvement of extra-lymph nodula structures involved ie bone marrow/lungs

222
Q

What is the macroscopic appearance of prostate cancer?

A

Enlarged prostate

Compressed urethra

223
Q

What are the microscopic features of prostate cancer?

A 
No glands 
Irregular cells
Large nuclei 
Pleomorphic 
Apoptotic debris 
Poorly differentiated
224
Q

How is prostate cancer graded?

A

Gleason grading system:
Stage 1. Cancer is small and only in prostate
2. Cancer is larger and may be in both lobes of prostate
3. Cancer had spread beyond prostate to nearby lump nodes/seminal vesicles
4. Cancer has spread to other organs like bone-metastatic

225
Q

What is the tumour marker used for Prostate cancer?

A

PSA - prostate specific antigen

Pathological Processes (Milly's) (21 decks)

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