Disease definitions

Question 1

Acute Myocardial infarction

Answer 1

A part of the coronary arteries gets blocked by a clot creating a necrosing area of the heart. Arythmia is seens and pain signals are sent to the brain. Because important backflow and high pressure there is a risk of pulmonary oedema.

Question 2

Unstable angina

Answer 2

Due to transiet formation of a non-occlusive thrombus

Question 3

Stable Angina

Answer 3

A loss of coronary blood flow reserve due to atherosclerosis of the coronary arteries. Precipitated by an increase in O2 demand (e.g. excercise). Tends to occurs when occlusion due to stenosis is more than 70%

Question 4

Vasospastic angina

Answer 4

Reduction in O2 supply due to spasm of the coronary artery. Occurs at rest, often at night.

Question 5

Mixed angina

Answer 5

unpredictable, occurs at different levels of exercise. Stenosis + spasm of arteries.

Question 6

Microvascular angina

Answer 6

Microvasculature is constricted

Question 7

Arrythmia

Answer 7

disturbance of the normal rythmic beating of the heart. The pacemaking is taken over by ‘latent pacemakers’ (AV node, bundle of his…) because they have ion channels required for phase 4 depolarisation. BUT it will beat more slowly than the SA node.

Question 8

Complete 3rd degree heart block

Answer 8

blocked electrical connection between atria and ventricle. Does not cause heart to stop but it beats more slowly. Heart beat is being kept alive by distal pacemaker (e.g. AV node instead of SA node).

Question 9

Tachyarrythmia

Answer 9

Occurs due to re-entry of conduction signal. One example is a wave of depolarisation going through purkinje fibres but because one of the branches has unidirectional block with slowed retrograde conduction (signal is able to travel back upwards), the signal will go back upwards and will cause a second depolarisation towards septum.

Question 10

Atrial Fibrillation

Answer 10

Chaotic atrial rythm with rapid and irregularly irregular ventricular rhythm. No beating in an organized way with small depolarizations.

Question 11

Ventricular tachycardia

Answer 11

A run of rapid successive ventricular beats caused by an ectopic site.

Question 12

Ventricular fibrillation

Answer 12

Choatic and disorganized activity of the heart

Question 13

Atherosclerosis

Answer 13

Progressive disease affecting tunica intima of elastic and muscular arteries. Lipid core covered by a fibrous cap

Question 14

Monckeber’s medial sclerosis

Answer 14

Calcification of the tunica media of muscular arteries.

Question 15

Arteriolosclerosis

Answer 15

Hyaline thickening of the walls of small arteries and arterioles

Question 16

Acute Heart failure

Answer 16

Cardiogenic shock

Question 17

Plural effusion

Answer 17

buildup of fluid in the lung pleura

Question 18

Pneumothorax

Answer 18

lung is deflated, away from the chest wall.

Question 19

Chest wall diseases

Answer 19

prevents lung expansion due to peural thickening.

Question 20

Interstital lung diseases

Answer 20

interstital inflammation, fibrosis. Impared gas exchange

Question 21

Pulmunary fibrosis

Answer 21

Proliferation of mesenchymal cells, collagen deposition. May be due to abnormal epithelial repair.

Question 22

Sarcoidosis

Answer 22

Multi-system granulomatous disease.

Question 23

Kyphoscoliosis

Answer 23

Combination of kyphosis (extensive curvature of spine) and scoliosis (excesive lateral curvature of spine)

Question 24

Asthma

Answer 24

Chronic inflammatory disease of the airways. Defined by an inflammatory response with tissue remodelling (epithelial damage, thickening, mucous gland hypertrophy…)Due to bronchial hyperresponsiveness to inhaled antigens. There is mucous cell metaplasia, thickening of bronchail wall.

Question 25

Acute asthma attack

Answer 25

Separated into different levels depending on percentage of normal peak flow, pa02

Question 26

Pneumonia

Answer 26

Infection from bacteria of the respiratory systems causing alveoli filling with pus. There is a leak of fluids from vascular into the lungs fmdue to inflammation. Usually leaves no residual damage. Causes impared gas exchange.

Question 27

Nocardia

Answer 27

pneumonia with cavitations and abscesses, empyema or inflammatory. nodules on skin

Question 28

Type I resp failure

Answer 28

Difined as an imparement of gas exchange within the lung causing hypoxia. VQ mismath, impared diffusion (e.g. pulmunary fibrosis), alveolar hypoventilation (e.g. guillaume barre), low oxygen partial pressure atmosphere (altitude), anatomical shunt (e.g. lobar pneumonia)

Question 29

Type II resp failure

Answer 29

Defined as an imparement of the pumping mechanism of the lung causing hypercapnia. It is an imbalance of the lung load, capacity and drive relationship (see slides for more)

Question 30

Chronic Obstructive Pulmunary disease

Answer 30

Narrowing of the airways and mucous hypersecretion. Inflammatory response increases proteolytic enzymes which destroy alveolar tissue -> emphysema. Loss of elastic recoil. This eventually causes lung hyperinflation -> patients breath very close to their TLC so cannot increase their ventilation (L/min). Breathlessness is caused by an increased resp load and reduced muscle pump capacity leading to increased neural drive for breaths.

Question 31

Acute COPD exacerbation

Answer 31

Acute worst ending of respiratory symptoms of COPD. increased airway inflammation, mucous production, increased gas trapping. Caused by an sudden increased in inflammatory response in airways. Can be emphysema, chronic bronchitis or both at the same time.

Question 32

Delirium tremens

Answer 32

Can carry on for 7 days. First 2 days are crucial. GABA-A receptor activity is increased by alcohol. In chronic consumption, these receptors become desensitized. glutamate transmission increases. when you remove alcohol, you get insufficient gaba and excessive glutamate.

Question 33

G overdose

Answer 33

G is a GABA analogue and binds to GABA-B receptors to decrease GABA release.

Question 34

Heroin overdose

Answer 34

Mu opioid receptors are overstimulated, which slows resp drive. Note this can happen at normal doses for that person (not an over dose). illicit opiates can change in potency, or some other condition can worsen reaction like COPD.

Question 35

Delirium

Answer 35

Acute brain failure. Very bad outcomes. Neurotransmitter related with cholinergic defficiency. Sometimes it is not fully curable and patients don't fully recover.

Question 36

Shift work disorder

Answer 36

Long term consequences of this is mood disorder, CV risk, cancer chances increase)

Question 37

REM Parasomnias

Answer 37

Puts you at risk of parkinson's and dementia

Question 38

Acute Kidney Injury (pre renal)

Answer 38

180L of filtrate produced everyday by kidneys. In AKI, something prevents the arteries leading to the kidney to be blocked or reduced blood flow causing lower volume to the kidneys

Question 39

Hyponatraemia

Answer 39

Loss of Na in system means that loss of osmotic gradient so water moves into the cells and raises intercranial pressures.

Question 40

Hypernatraemia

Answer 40

Results from water losses or hypertonic Na gain.

Question 41

Hypokalaemia

Answer 41

K is mostly stored in cells, used to generate conc gradients and action potentials.

Question 42

Pericarditis

Answer 42

Inflammation of the pericardium. Can be fibrin our (dry) or effusive (purulent)