Review of posters 25/04/2016 Flashcards Preview

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Flashcards in Review of posters 25/04/2016 Deck (51):
1

Treatment of angina (stable)

GTN spray for when the chest pain comes on.
Beta blockers/Calcium channel blockers
Aspirin

2

Treatment of unstable angina

Medical emergency- treat as you would heart attack (MONAC)

3

Describe the shapes abdominal aortic aneurysms can form.

Saccular- like a yolk sac
Fusiform
Mycotic (after infection)

4

Define a true aneurysm

One that has all three parts of the vessel wall intact.

5

Define a false (psuedo) aneurysm

Breach in the vessel wall

6

Describe the pathophysiology of an AAA

Decreased collagen and elastin in vessel walls.
Smooth muscle cell loss
Causing aortic dilatation

7

Lifestyle advice for angina

Encourage weight loss-eating healthily
Smoking cessation
Minimal alcohol intake
Exercise regularly

8

Describe the mechanism of an atrio-ventricular re-entrant tachycardia.

Accessory pathway exists. Due to the AV node holding the signal for a while and the accessory pathway not doing this, the signal from the accessory pathway passes into the ventricles before the signal down the normal route. This causes an abnormal contraction of the ventricles. Also, the signal can pass back up into the atria via the accessory pathway because it has finished its refractory period.
WOLF PARKINSON WHITE SYNDROME

9

Describe the mechanism of atrioventricular nodal re-entrant tachycardia

When the signal reaches the AV node- it is split into a fast pathway and a slow pathway. The fast pathway however has a long refractory period where as the slow pathway has a short refractory period. Normally, the signal would be split, the fast pathway would transfer the signal down to the Purkinje fibres and enter the refractory period. The slow pathway would then meet the fast pathway in it's refractory period and the signal would be terminated.
In AVNRT- a premature beat arrives when the slow track has recovered from its refractory period. This means it passes down this pathway however meets the fast pathway when it has just recovered from its refractory period. This means the signal can be transmitted back up into to atria and it bounces around.

10

Describe the process of atherosclerotic plaque RUPTURE.

Plaque rupture exposes sub-endothelial cells and von Willeband factors. The platelets notice this and start to respond as they would to injury. Initially they form a monolayer. However they become activated, and release factors such as thromboxane A2 and ADP which cause them to aggregate together with other platelets. Inflammation then occurs, blood clots form and the lumen of the vessel becomes occluded.

11

Describe the process of formation of an atherosclerotic plaque.

Toxins in the blood e.g. smoking, high levels of LDL cholesterol and high blood pressure can cause initial damage to the vascular endothelium.
When this occurs, LDL cholesterol migrates into the damaged endothelium and becomes oxidised. This is called a fatty streak and causes inflammation. The macrophages are then recruited into the site of injury where they digest some of the cholesterol, however they gorge on it (forming foam cells) and subsequently die (adding to the plaque). They release cytokines which attract other inflammatory cells which again aggregates the plaque. Smooth muscle cells start to notice this aggregation and migrate into the plaque to form a fibrous cap. They also release calcium which hardens the plaque.

12

Pathology of COPD

Toxins in cigarette smoke cause an inflammatory response by stimulating alveolar macrophages. Neutrophillic inflammation then occurs and proteases are released.

13

Pathology of emphysema

The proteases released from the neutrophillic inflammatory response digest the elastin in the alveolar cell walls. This causes impaired gas exchange and respiratory failure.

14

Pathology of chronic bronchitis

Goblet cells undergo hypertrophy and cause mucus hypersecretion. The mucocilliary escalator becomes paralysed. This means the mucus cannot be expelled. This along with smooth muscle spasm and hypertrophy leads to airway limitation.

15

Treatment of COPD.

SABA (salbutamol)
LABA/LAMA (salmeterol or ipatropium bromide)
Corticosteroids (Beclametasone)

16

Acute exacerbation of COPD

iSOAP
Ipatropium bromide IV
Salbutamol
Oxygen (24-28%)
Antibiotics (if infective)
P- prednisolone

17

What is streptococcal pneumonia also known as?

Pneumococcal pneumonia

18

What colour sputum does pneumococcal pneumonia produce?

Rusty coloured sputum.

19

Describe the symptoms of streptococcal pneumonia.

Acute in onset
Chest pain

20

What makes you more susceptible to streptococcus pneumoniae?

Female, HIV, alcohol.

21

Symptoms of mycoplasma pneumoniae

Headache, confusion, muscle pain. Generally mild.
Can cause haemolytic anaemia, skin rashes and hepatitis.

22

Symptoms of legionella pneumoniae?

Diarrhoea and vomiting
After travel
Neurological symptoms
Deranged liver enzymes and elevated creatine kinase.

23

Staphylococcus aureus

Past influenza involvement
Skin rashes

24

Chylamydophila psittaci

Mucoid sputum
Chest pain may develop
PET BIRD

25

Chlymydophila trachomitis

Common in pregnant women and infants.
Infants remain asymptomatic for three weeks.
Moderate illness

26

Describe the stages of sarcoidosis

Stage 1: Bilateral hilar lymphandenopathy
Stage 2: BHL with pulmonary infiltrates
Stage 3: Pulmonary infiltrates without BHL
Stage 4: fibrosis

27

What is bilateral hilar lymphadenopathy?

Bilateral enlargement of the lymph nodes of the pulmonary hilar
Detected on chest X-ray.
Nearly always involves lung parenchyma

28

What are the differential diagnosis' of BHL

Lymphoma, TB, carcinoma of the bronchus

29

What are pulmonary infiltrates?

Substances denser than air e.g. blood, pus, protein. May show as 'nodular shadows'

30

What are the differentials of pulmonary infiltrates?

Pulmonary fibrosis, pneumocoinosis and alveolar cell carcinoma.

31

Treatment of sarcoidosis

Corticosteroid therapy

32

Describe Churg Strauss syndrome?

Presents as a combination of what looks like asthma and rhinitis. Eosinophilic vasculitis and systemic vasculitis.
Patient may present with tender subcutaneous nodules on the skin. ANCA positive (anti-neutrophil cytoplasmic bodies).

33

Treatment of Churg Strauss syndrome

Corticosteroids.

34

What is Wegners Granulomatosis?

Single/multiple nodular masses with pneumonic infiltrates
symptoms include :
Rhinorhea- nasal cavity becomes blocked with mucus
nasal mucosal ulceration
cough
Haemoptysis
Pleuritic pain

35

Treatment of Wegners Granulomatosis?

Cyclophosphamide or ritixamab

36

Rheumatoid disease

Pleural adhesions, thickening and effusions
Often unilateral effusion
Decreased chronic glucose content

37

Microscopic vasculitis

recurrent haemoptysis
ANCA positive

38

GORD

gastro-oesophageal reflux disease- loss of tone of lower oesophageal sphincter.

39

Symptoms of GORD

Severe chest pain
Spasm of the oesophagus

40

Treatment of GORD

PPI e.g. omeprazole
Antacids

41

Achalasia

Birds beak appearance on CT.
Lower oesophageal sphincter has gone into spasm.

42

Treatment of achalasia

Surgical procedure.

43

Lower oesophageal rings

Two types- mucosal (shatzki or B rings)
Squamocolumnar mucosal junction- intermittent dysphagia.
Muscular (A rings)
Treatment- endoscopic dilatation.

44

Oesophageal webs

Thin membranous tissue covered in squamous epithelium that may cause dysphagia. Generally present in the anterior oesophagus just below the cricoid cartilage.

45

Peptic and oesophageal stricture

Narrowing of the vessel due to fibrous scar tissue forming. Primary cause is acid reflux.

46

Treatment of peptic and oesophageal strictures

Endoscopic dilatation
PPI therapy

47

Pathology of NSAIDs and peptic ulcers.

Inhibit COX2 causing an increase in acid production.
Also decreasing angiogenesis (formation of new blood vessels).
Inhibit COX1- impairs platelets
Decreases mucus secretion
Also cytotoxic to epithelial cells- disrupts barrier.

48

Symptoms of peptic ulcers

Epigastric pain
Relieved or aggravated by eating

49

Treatment of peptic ulcers

PPI
Stop NSAIDs immediately
All patients tested for H-pylori. If positive- eradication therapy. If negative- anti-secretary therapy.

50

H pylori eradication therapy

PPI and amoxicillin (1g twice a day)
Clarithromycin (500mg bd)

51

Anti-secretary therapy.

Citmetidine, raninidine, fomandine