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Year 1 (PCS & Cases 1-6) > Case 4 > Flashcards

Case 4 Flashcards

1
Q

What G protein is linked to A2 receptors?

A

Gi

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2
Q

What G protein is linked to B1 and B2 receptors?

A

Gs

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3
Q

What G protein is linked to A1 receptors?

A

Gq

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4
Q

What is the difference between Propanolol and Atenolol

A

Both beta blockers.

P is non selective (so not good for people with asthma) A is b1 selective.

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5
Q

Name three Anticoagulants.

A

Warfarin

Heaprin

Ancrod

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6
Q

Name two Thrombolytic agents. What do they do?

A

Tissue plasminogen activator

Streptokinase

Action: Hydrolyse clots.

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7
Q

What is the action of warfarin?

A

Vitamin K antagonist.

Prevents synthesis of prothrombin and clotting factors.

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8
Q

What is the action of heparin?

A

Accelerates the activity of antithrombin which inhibits the action of thrombin.

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9
Q

What is the action of Ancrod?

A

It is a proteolytic enzyme.

It acts directly on fibrinogen to form an unstable form of fibrin which forms micro clots that are cleared from the blood by phagocytes.

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10
Q

How does sheer stress protect from atherosclerosis?

A

Stimulates the production of NO

Inhibits LDL oxidation

Inhibits leukocyte adhesion

Inhibits smooth muscle proliferation

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11
Q

Label the waves of this ECG trace (boxes in red)

A
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12
Q

What is represented by box A?

A

PR segment

Conduction from AVN –> Bundle of His

*AVN conduction delay*

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13
Q

What is represented by box B?

A

PR interval

Represents time from atrial depolarisation to ventricular depolarisation (0.12s - 0.20s)

*includes AVN conduction delay*

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14
Q

What is represented by box C?

A

QRS complex

Ventricular depolarisation (<0.12s)

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15
Q

What is represented by box D?

A

ST segement

All myocytes should now be depolarised (ST segment lies on the isoelectric line)

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16
Q

What is represented by box E?

A

QT interval (0.34s-.43s)

Represents the ventricular action potential

Includes depolarisation and repolarisation of the ventricles.

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17
Q

What makes up the 12 lead ECG?

A

1) UNIPOLAR leads –> 6 chest leads (V1-V6)
2) BIPOLAR leads –>

3 limb leads (I, II, III)

3 augmented leads (aVR, aVL, aVF)

10 ELECTRODES, 12 LEADS

18
Q

An ECG shows deviating waves in leads II, III, avF. What part of the heart is most likely affected?

A

Inferior part.

II, III and aVF view the heart inferiorly.

19
Q

How do you calculate heart rate from an ECG?

A

300 / number of big squares.

Use R R interval as reference for each square.

OR!

60 / (number of little squares x 0.04)

= 60 / (20 x 0.4) = 75bpm

20
Q

Where are the baroreceptors found?

What nerves are linked to the baroreceptors?

A

Carotid SINUS (joins carotid sinus nerve - links to glossopharyngeal)

AORTIC ARCH (joins aortic nerve - links to vagus nerve)

21
Q

Where are the chemoreceptors found?

A

Central - Brainstem, bathed in the CSF.

Peripheral - Carotid and Aortic BODIES

22
Q

What condition does this ECG show?

A

1st degree heart block.

Prolonged PR interval - prolonged AVN delay.

23
Q

What condition does this ECG show?

A

Second degree heart block.

Mobitz type 1.

PR interval gets progressively longer until an impulse fails to be conducted at all and the rhythm is reset.

24
Q

What condition does this ECG show?

A

Second degree heart block.

Mobitz type 2.

PR interval is fixed.

Not every P wave is followed by a QRS complex.

Either 2:1 (2 P waves for every QRS) or

4:1 (4 P waves for every QRS)

25
Q

What condition does this ECG show?

A

Third degree heart block.

No conduction of impulses through the AVN.

Atrial and Ventricular depolarisation occur independent of one another.

26
Q

What condition does this ECG show?

A

Atrial fibrillation.

NO P waves!

Disorganised, rapid, irregular contractions of the atria.

Ventricular rhythm is irregular due to the twitches of impulses recieved by the AVN from the atria.

27
Q

What condition do these ECGs show?

A

Atrial flutter.

Top is 2:1 block. Bottom is 4:1 block.

Appears “saw toothed”.

P waves are present.

Not as disorganised as atial fibrillation but contractions are rapid and abnormal.

28
Q

What condition does this ECG show?

A

Ventricular tachycardia.

Ventricles depolarise rapidly.

It may be ‘stable’ (monomorphic) or ‘unstable’ (polymorphic)

29
Q

What condition do these ECGs show?

A

Ventricular fibrillation (VF)

NO QRS complexes.

Very disorganised and uncoordinated.

Depolarisation from multiple areas in the centricular myocardium.

30
Q

How long is the cardiac cycle? (in seconds)

A

Total cycle = 0.8s

31
Q

Name the three cell junctions that are present in the Intercalcated discs that join cardiac myocytes.

A

Desmosomes

Adherens

Gap

32
Q

What are the BMI ranges for

underweight?

healthy?

overweight?

obese?

A

Underweight is under 18.5

Healthy is 18.5 to under 25

Overweight is 25 to 30

Obese is over 30

Morbidly obese is over 40.

33
Q

How can you distinguish between STEMI and NSTEMI on an ECG?

A

NSTEMI ST-depression, T-wave inversion.

STEMI ST-elevation, T wave inversion and pathological Q-waves

Both have raised Troponin T and I as well as CK-MB and Myoglobin (less specific markers)

34
Q

What are the four causes of systolic murmur?

A

aortic or pulmonary stenosis (narrowing)

tricuspid/ mitral regurgitation (leaky valves)

35
Q

What are the four causes of diastolic murmur?

A

aortic or pulmonary regurgitation

mitral/ tricuspid stenosis

36
Q

A peripheral artery is found to have 50% stenosis. Compared to a normal artery with no stenosis, by what factor has the flow of blood been decreased?

A

16

Flow = 1/r4.

Therefore, flow (aka. resistance) in this artery would be decreased by a factor of 16.

37
Q

What percentage of the coronary artery is filled with atherosclerotic plaque for it to be classed as a ‘fixed’ atherosclerotic plaque?

A

Fixed atherosclerotic plaques obstructing >75% of the coronary artery are associated with stable angina.

38
Q

Phases of SAN action potential?

A

3 phases

NO resting potential

Pre potential (Na+) - activated upon hyperpol

Dep (Ca2+)

Hyperpol (K+)

39
Q

What is the action of Fibrates?

A

Stimulate the activity of LPL so cells take up more triglycerides; by increasing HDL levels they promote the reverse cholesterol pathway which leads to more cholesterol being taken back to the liver for excretion in bile salts

40
Q

What is the action of Bile Acid Sequestrants?

A

Rarely used anymore but they work by binding to components of bile to prevent it from being reabsorbed from the gut.

Less bile reabsorbed means less cholesterol reabsorbed

41
Q

What happens to chylomicrons when they go through the blood stream?

(hint: receptors –> gaining and losing)

A

they gain apoC2 and apoE from HDLs.

*ApoC2 = receptor for LPL*

in adipose, ApoC2 binds to Lipoprotein Lipase on endothelial cells. TAGs –> fatty acids and glycerol.

As chylomicron’s triglyceride content reduces they lose apoC (donated back to HDL) so they only have ApoE left meaning they are a Chylomicron Remnant.

Chylomicron remnants (IDL) then travel to the liver where they bind with their apoE with the Chylomicron remnant receptor.

42
Q

What makes up the surface coat and core of a lipoprotein?

A

surface coat = Unesterified cholesterol, phospholipids, apolipoproteins

core = Triglycerides, cholesterol esters

Year 1 (PCS & Cases 1-6) (13 decks)

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