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1 - PBLs > CR > Flashcards

CR Flashcards

1
Q

P wave

A

Atrial depolarisation

0.08-0.1s

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2
Q

QRS complex

A

Ventricular depolarisation

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3
Q

T wave

A

Ventricular repolarisation

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4
Q

PR interval

A

Delay at AVN

0.12-0.2s

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5
Q

QT interval

A

Time when all the ventricular muscle is contracting

0.35-0.43s

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6
Q

Physiology of AF

A

Atria experience chaotic signals and quiver

Only some APs pass through to ventricles giving irregular ventricular rhythm

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7
Q

Causes of AF

A 
Hypertension 
Heart attacks 
Abnormal valves
Hyperthyroid 
Sleep apnoea
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8
Q

Symptoms of AF

A 
Palpitations 
Reduced ability to exercise 
Fatigue 
Dizziness
Confusion 
Shortness of breath 
Chest pain
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9
Q

ECG evidence for AF

A

No distinct P wave

Irregular R-R intervals

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10
Q

Treatment for AF

A

Cardioversion to restore regular sinus rhythm
Thromboprophylaxis
Treatment of underlying cause if possible

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11
Q

Why is there an increased chance of clots with AF?

A

Pooling of blood in atria
Stagnant blood more likely to clot
Clots can dislodge and be pumped out of the heart
Can block arteries in the circulation
Can cause stroke if reach cerebral arteries

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12
Q

Rivaroxiban mode of action

A

Direct factor Xa inhibitor

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13
Q

Vitamin K antagonists

A

Warfarin

Prevent formation of some clotting factors

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14
Q

Heparins

A

Activate antithrombin III

Inhibits thrombin and factor Xa

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15
Q

Speed of action potential in different parts of the heart

A

Atria = 0.5m/s
AVN = 0.05m/s
Bundle of his and bundle branches = 2m/s
Purkinje fibres = 4m/s

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16
Q

Atrial contraction and exercise

A

10% of ventricular filling at rest
40% of ventricular filling in exercise
Less time for atrial filling in exercise
Atrial contractions needed to achieve maximum stroke volume

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17
Q

Normal cardiac output

A
  1. 9L/min for females

5. 6L/min for males

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18
Q

Normal stroke volume

A

70ml in 70kg male

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19
Q

Normal heart rate

A

60-100bpm

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20
Q

Normal MAP

A

65-110mmHg

21
Q

Local mediators controlling vasodilation of arterioles supplying muscles

A

CO2, H+, K+, AMP, adenosine, NO, bradykinin

22
Q

Blood distribution to muscles at rest and in exercise

A

21% at rest

85% in exercise

23
Q

Mutation in Liddle syndrome

A

Mutation in C terminus of the ENaC channel
Inability for Nedd4-2 to bind
Channel cannot be marked for degradation
Increased activation of ENaC
Increased sodium retention
Increased water retention
Increased blood volume and therefore pressure

24
Q

Symptoms of Liddle syndrome

A

Early onset hypertension
Metabolic alkalosis
Muscle wasting (low potassium)

25
Q

Diagnosis of Liddle syndrome

A

Hypokalemia
Elevated bicarbonate
Supressed renin and aldosterone
DNA probes

26
Q

Liddle syndrome inheritance pattern

A

Autosomal dominant

27
Q

Risk factors for hypertension

A 
Old age
Smoking 
Obesity 
Lack of exercise 
High salt intake 
Stress
Ethnicity - more common in ACs
Family history
28
Q

Treatment of hypertension

A 
ACEIs
Beta blockers
CCBs
Diuretics
Renin inhibitors 
Angiotensin II receptor antagonists 
Aldosterone antagonists
29
Q

Complications of hypertension

A 
Stroke 
Aneurysm 
Eye problems 
Ischaemic heart disease
Kidney damage 
Left ventricular hypertrophy
30
Q

Amiloride

A

Potassium sparing diuretic

Targets ENaC channels in distal convoluted tubule

31
Q

How can hypertension lead to left ventricular hypertrophy?

A

Leads to increased afterload
Heart has to pump harder to pump same volume of blood
Muscle thickens in response

32
Q

What does aldosterone target?

A

ENaC and Na/K ATPase

33
Q

Why does an increased blood volume lead to increased blood pressure?

A 
Increase in central venous pressure
Increased venous return to the heart 
Increased preload 
Increased stroke volume and cardiac output 
Increased BP
34
Q

How is intrapleural pressure maintained?

A

Elastic recoil properties of the lung and chest wall
Want to recoil against each other
Creates negative pressure
Surfaces stuck together by pleural fluid

35
Q

Types of pneumothorax

A

Primary spontaneous - rupture of bleb in absence of disease
Secondary spontaneous - due to lung disease - COPD
Traumatic - due to penetrating lung injury

36
Q

Pneumothorax risk factors

A 
Male 
Tall 
Marfan syndrome 
Thin 
Young 
Atmospheric changes 
Lung disease
Mechanical ventilation 
Scuba divers
37
Q

Pneumothorax symptoms

A 
Chest pain 
Shortness of breath 
Tachycardia 
Tachypnoea 
Repeated dry coughing 
Cyanosis
38
Q

Pneumothorax diagnosis

A 
Absent breath sounds on one side 
Tracheal deviation 
Unequal chest expansion
JVP distension 
X ray - lung borders in lung space 
CT - can show lung collapse
39
Q

Pneumothorax treatment

A

Left alone
Aspiration of air
Surgery to close hole in pleura

40
Q

Why can’t he fly

A

Cabin pressure reduced
May be lower than intraplerual pressure
Could cause lung to collapse again

41
Q

Asthma pathophysiology

A 
Hyperactive and hyper-responsive airways 
Increased IL-4 production 
IgE production 
Degranulation of mast cells 
Inflammatory cytokine release
Increased mucous secretion
Mucous plugging
42
Q

Asthma triggers

A 
Dust 
Pollen 
Animal hair 
Mould 
Smoke 
Asbestos 
Chemicals 
NSAIDs
Aspirin 
Exercise 
Chest infections
43
Q

Risk factors for asthma

A 
History of atopic disease
Family history 
Inner city environment
Obesity 
Viral infections in early childhood 
Smoking 
Early exposure to broad spectrum antibiotics
44
Q

Symptoms of asthma

A 
Shortness of breath 
Coughing 
Wheezing 
Chest tightness
Hypocapnia
45
Q

Symptoms of severe asthma attack?

A

SaO2 25bmp

Unable to complete sentences in one breath

46
Q

Diagnosis of asthma

A

Spirometry - reduced FEV1/FVC ratio

47
Q

Treatment of asthma

A

Beta2 agonists
Muscarinic antagonists
Inhaled corticosteroids

48
Q

Normal SaO2

A

> 95%

1 - PBLs (8 decks)

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