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MD > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Increased volume is likely to lead to which type of cardiac remodelling?

A

Eccentric hypertrophy > adaptation to more pre-load.

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2
Q

Increased pressure is likely to lead to which type of cardiac remodelling?

A

Concentric hypertrophy > adaptation to more afterload.

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3
Q

Describe the ECG findings of a first degree heart block:

A

Large PR Interval

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4
Q

Describe the ECG findings of a second degree heart block:

A

increasing PR then skip OR stable PR then skip.

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5
Q

Describe the ECG findings of a third degree heart block:

A

No pattern, P and QRS unrelated, HR around 30.

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6
Q

What medication shouldn’t you use for variant (spasm) angina?

A

Beta blocker

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7
Q

What are the suffixes of key cardiac drugs?

A

ACEpril, BETAlol, ALPHosin

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8
Q

Which diagnoses are likely for calf pain?

A

DVT, intermittent claudication due to atherosclerosis of leg arteries, trauma etc.

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9
Q

Fully describe the coagulation cascade.

A

Have the intrinsic path (12, 11, 9, 8) and the extrinsic pathway (7) they converge on factor 10 which turns prothrombin to thrombin, thrombin turns fibrinogen into fibrin.
Factor 13 breaks stabilises the clot.

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10
Q

Which two biochemical tests would confirm staph aureus?

A

Catalase + confirms any staph.
Coagulase + confirms staph aureus.

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11
Q

How does cooking chemically change fats?

A

Hydrogenation, raises LDL, lowers HDL.

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12
Q

The complement cascade converges on which molecule?

A

C3b - opsonin (C3a is inflammation)

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13
Q

Best drug to stop heart remodelling?

A

ACEi

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14
Q

What are the 3 areas of the heart that can stimulate heart pace and what are their heart rates?

A

SA node - 60-100 bpm
AV node - 50-60 bpm
Perkinje fibres - 30-40 bpm

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15
Q

Why is it important that AV node depolarization is delayed?

A

The AV node will cause ventricular contraction, it needs to be delayed to allow time for the ventricles to fill after the SA node causes atrial contraction.

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16
Q

If Perkinje’s are firing to cause ventricular contraction, what will be the ECG change?

A

The R wave will be upside down as the electricity is coming from opposite side of the heart.

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17
Q

What does a wide QRS mean on ECG?

A

Slow conduction

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18
Q

How to calculate HR on ECG?

A

300/no. of squares between peaks

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19
Q

What are the four types of cell injury adaptations?

A

Hypertrophy, Hyperplasia, Atrophy and Metaplasia.

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20
Q

What are 4 cellular irreversible occurrences due to injury:

A

mitochondrial damage, Ca2+ influx, membrane damage, DNA Damage.

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21
Q

3 main types of necrosis?

A

Coagulative, liquefactive, caseous.

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22
Q

What are pharmacokinetics and pharmacodynamics?

A

Kinetics: What does body do to drug.
Dynamics: what does drug do to body.

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23
Q

What type of bacterial toxins are resistant to IgG?

A

Endotoxins

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24
Q

What do B-lactams act on?

A

The transpeptidase enzyme responsible from cross linking in the peptidoglycan layer of the cell wall.

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25
Q

Give an example of a glycopeptide antibiotic and how it acts.

A

Vancomycin, targets D-Ala-D-Ala links of cell wall.

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26
Q

What is the target of macrolides?

A

50s unit of ribosome

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27
Q

What are the two phases of drug metabolism?

A

Phase 1 - cytochrome p450 to make it polar by adding functional group
Phase 2 - conjugation to make it soluble

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28
Q

What are the 3 layers of arteries and their functions?

A
  • tunica intima - gas/nutrient exchange
  • tunica media - blood flow control
  • tunica adventitia - incorporates
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29
Q

What vessel type determines arterial blood pressure?

A

Arterioles

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30
Q

What vessel type holds most of the blood?

A

Veins hold 80% of blood

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31
Q

What are the 3 mechanisms of venous return?

A

Vascular venous pump, musculovenous pump, thoracic venous pump (diaphragm).

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32
Q

What is the Warburg effect?

A

The anaerobic respiration of cancers.

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33
Q

Would a left ventricle hypertrophy following mitral stenosis?

A

No - mitral stenosis means that blood is not properly moving through the mitral valve into the left ventricle. This means blood will accumulate in the LA (will hypertrophy LA), not the LV. So not stretching = no hypertrophy.
The heart would hypertrophy under aortic stenosis.

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34
Q

When would you hear a mitral murmur?

A

Diastole

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35
Q

Why does Atrial fibrillation cause irregularly irregular heart beats?

A

AF is ectopic firing which can activate AV node, so SA and ectopics are controlling ventricular contraction - all over the fkn place ECG.

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36
Q

What are the risks with pig/mechanical replacement valves?

A

Pig - need immunesupressants
Mechanical - could form clot

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37
Q

Why may AF by a risk for coronary arteries?

A

More firing = less time in diastole = less time for coronary arteries to fill from aortic valve.

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38
Q

A loud S2 could mean what?

A

Either Pulmonary or Aortic valve is snapping shut due to pressure. Could be systemic HTN or pulmonary HTN.

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39
Q

Rheumatic heart disease typically affects which valve?

A

Mitral (often causes stenosis)

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40
Q

What anatomical features are present in the atria?

A

Pectinae muscles, auricle flaps (dog ear), fossa ovalis closed over.

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41
Q

What anatomical features are present in the ventricles?

A

Chordae tendinae attached to papillary muscles.
Trabeculae carnae ridges as well.

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42
Q

What is the order of conduction in the heart?

A

SA –> AV –> Bundle of His –> Bundle Branches –> Perkinjes

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43
Q

Which coronary artery supplies the SA and AV nodes?

A

The Right Coronary Artery - important if pace seems off following an MI.

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44
Q

Which coronary arteries cause the most MI’s?

A
  1. Left Anterior Descending
  2. Right Coronary Artery
  3. Circumflex Artery
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45
Q

What are the layers of the heart in order.

A

Heart Chamber –> Endocardium –> Myocardium –> Visceral serous layer –> pericardial sinus –> parietal serous layer –> Fibrous pericardium.

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46
Q

What is the order of isotype switching?

A

MDs Get Easy A’s.
Can’t go backwards.

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47
Q

Define true ribs, false ribs, typical ribs and atypical ribs.

A

true ribs attach directly to sternum - ribs 1-7.
False ribs don’t attach to the sternum: 8, 9 and usually 10.
Floating ribs - 11 and 12.

Typical:3-9
Atypical: 1,2,10-12.

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48
Q

What are the parts of the sternum?

A

Manubrium, body and xiphoid process.

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49
Q

What are the openings of the Diaphragm and where are they?

A

level 8- IVC
10- Esophagus
12- Aorta

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50
Q

Which vertebrae supply the phrenic nerve?

A

C3,4 and 5 keep the diaphragm alive.

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51
Q

Which lymph nodes are most likely to be involved in breast cancer?

A

Axilliary nodes, especially the pectoral node.

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52
Q

What is the imaginary line cut through the sternal angle called?

A

The Transverse Thoracic Plane (T4/5)

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53
Q

What are the branches of the aorta in order?

A

Braceocephalic, left carotid, left subclavian

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54
Q

Where does the azygous system rest?

A

On the right side of the thorax, posteriorly. It is the only vein system to sit posteriorly. Its left side counterpart is the hemiazygos.

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55
Q

What are the two types of anemia? Which is more serious?

A

Regenerative and Aregenerative.
Regenerative is more serious because it means their production is fine but they are still anemic = bleeding/haemolysis.

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56
Q

What are the two tests of the coagulation cascade and do they measure all the way to a clot?

A

The APTT (intrinsic) and INR (extrinsic) tests only measure amount of Fibrin, they do not take into account the Factor 13 conversion into an X-linked clot.

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57
Q

What is Virchow’s Triad and name two causes of each of the 3 points.

A
  1. Endothelial damage - smoking, HTN
  2. Hypercoagulability - OCP, pregnancy
  3. Blood stasis - Plane ride, AF
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58
Q

Best immediate treatment for shock?

A

FLUIDS

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59
Q

Platelet activation releases which molecules?

A

Thromboxane, ADP, Serotonin, Ca2+.
Allows them to form platelet (fibrinogen) plug.

60
Q

Which natural controls does our body have to clots?

A

Antithrombin III (inactivates parts of coagulation pathway) and plasmin (fibrinolysis).

61
Q

How does heparin work?

A

Injectable drug which allosterically stimulates antithrombin III - makes it so good you can’t form clots.

62
Q

What are the antidotes to Heparin and Warfarin?

A

Heparin = protamine
Warfarin = Vitamin K

63
Q

How does Warfarin work?

A

Antagonist of Vit K reductase - stops production of the Vit K dependant coagulation factors = 2, 7, 9, 10.

64
Q

Which tests are used to check heparin and warfarin efficacy?

A

APTT for Heparin .

INR for Warfarin - INR checks extrinsic which includes 7 which is one of the Vit K ones so it must be warfarin, that’s how you tell the difference.

65
Q

How does aspirin work?

A

inhibits COX. COX enzyme is responsible for thromboxane production, so platelets can’t activate.
Effects last around 8 days because platelets can’t make fresh COX.

66
Q

Name two thrombolytic drugs? Why are they dangerous?

A

Streptokinase and Alteplase.
Streptokinase can only be used once.
Both can cause bleeding and could reopen old wounds.

67
Q

Which conductive part of the heart conducts the fastest?

A

Purkinjes.

68
Q

What are the steps of atherosclerosis?

A
  • endothelial damage
  • LDL deposition
  • Macrophages
  • Inflammation
  • Foam cells
  • Smooth muscle forms fibrous cap
  • platelet activation for platelet plug
  • can occlude artery or cause embolus
69
Q

Which enzymes are released after an MI?

A

Troponin - fast to release but disappears quite quickly.
Creatinine Kinase sticks around for ages.

70
Q

Where is the Fc region of an antibody and what can bind here?

A

It is the non-varible region at the base, it can bind to immune cells and complement

71
Q

What type of T helper cell aids in isotype switching? Where are they?

A

T follicular helper cells (Tfh)
Germinal centres of lymph nodes

72
Q

Which antibodies are made without any T helper help?

A

IgM and also blood type antibodies

73
Q

Which T cell molecule interacts with B cells?

A

CD40L with CD40

74
Q

An immune response showing only IgM and blood antibodies alongside CD40L deficient cells is likely to be?

A

Hyper IgM Syndrome

75
Q

What do you suspect if small sicknesses are making granulomas all the time?

A

Suspect that phagocytes cannot kill properly so are forming granulomas. May be an issue with NADPH oxidase.
CHRONIC GRANULOMATOUS DISEASE

76
Q

What is CD18 used for?

A

Extravasiation into tissues, especially for neutrophils.

77
Q

How do cardiac cells rapidly polarise their neighbour?

A

Gap junctions - basically connected by their cytoplasm.

78
Q

Explain calcium movements in a heart beat?

A

Action potential travelling down a myocyte opens voltage gated calcium channels, calcium flows into cell from tubule, this then allows even more calcium to exit from the sarcoplasmic reticulum.
All that calcium binds to troponin causing actin/myosin cycling = contraction

79
Q

What pump facilitates repolarisation of the cardiomyocytes?

A

K+ pumps

80
Q

How does digoxin work and what is it used for?

A

Digoxin forces sodium to stay in the cell (Na/K ATPase blocker), which forces Calcium to stay in the cell longer too = more intense contraction.
It is used for congestive heart failure to increase contraction force and to regulate arrythmias.

81
Q

How does the nervous system control heart contractions?

A

Sympathetic NA - HR and SV up
Parasympathetic AchM - lowers HR - CANNOT IMPACT SV.

82
Q

What does an ECG measure?

A

The Sum of all heart electrical activity

83
Q

Can cardiac action potentials summate?

A

No they cannot build on top of each other due to the need for a repolarisation period.

84
Q

Which 3 ions are needed for heart contraction and what is the pattern?

A

Starts with sodium in and then its just a game of calcium and potassium, the calcium will follow the sodium (not directly but due to the movement of potassium in response to sodium).
Na in, K out, Ca in and K out, Ca stops, K is in and out, K comes in to repolarise.

85
Q

What is the starting cell channel in the cardiac pacemakers?

A

The Funny Channel - Na influx is caused by hyperpolarisation due to SNS activity. (NOT LEAKY CHANNELS).

86
Q

Which vessel type is the most compliant? Which is the most elastic?

A

Veins are the most compliant, arteries are the most elastic.

87
Q

Which type of capillary is associated with the kidney?

A

Fenestrated capillary

88
Q

How does vessel compliance relate to pressure?

A

if a vessel is very compliant, a change in volume will hardly cause any pressure change.

89
Q

Which vessel type has the lowest pressure?

A

Veins

90
Q

Which vessel type has the lowest blood velocity?

A

Capillaries

91
Q

What assumptions are made in terms of oncotic and hydrostatic pressure in a healthy person?

A

We assume that interstitial hydrostatic pressure and oncotic pressure are zero

92
Q

Which factor is most important in SV and which in TPR

A

SV - venous return
TPR - SNS activity

93
Q

How does greater volume in the ventricle impact the contraction?

A

More stretch = bigger contraction

94
Q

Describe the cardiac cycle.

A

Mitral/tricuspid open to allow blood into ventricle.
Atrial contraction to allow maximal filling.
Ventricle pressure is greater than atria, so S1 valves close.
All valves closed - diastole done.
Systole begins with isovolumetric contraction.
Ventricle pressure causes S2 valves to open.
Low ventricle pressure causes S2 closing.
Systole ends with isovolumetric relaxation.
Negative pressure in ventricles forces S1 valves open - repeat.

95
Q

What are EDV/ESV and how do they relate to isovolumetric contraction and relaxtion?

A

EDV is end diastolic volume, the volume in the ventricle at the end of diastole and before systole. This corresponds to isovolumetric contraction - the ventricle contracting at the start of systole whilst all the valves are closed.

ESV is end systolic volume, the volume in the ventricle at the end of systole and before diastole. This coincides with isovolumetric relaxation - the ventricle relaxing with all the valves closed, creating a low pressure to prepare for filling.

96
Q

What are afterload and preload, give a pathology of each.

A

afterload - the pressure exerted on the ventricle - can be due to hypertension, aortic stenosis etc.
preload - volume issue for ventricle, leading to stretch. eg. mitral stenosis decreased preload which will decrease SV.

97
Q

What does angiotensinogen do to the vessels?

A

Vasoconstriction

98
Q

Which receptors does the sympathetic system target in the periphery and which drugs are used for this?

A

alpha receptors of SNS NA, use -osin drugs.

99
Q

Beta blockers target which receptors and are contraindicated in who?

A

target B adrenergic receptors - B1 in heart and kidneys, B2 in airways.
don’t use for asthmatics or heart block

100
Q

Calcium channel blockers are contraindiacted in who?

A

HEART FAILURE - will cause bradycardia.

101
Q

What does dobutamine do?

A

Opposite of beta blocker - Beta adrenergic stimulant - used for heart failure.

102
Q

What does acetylcholinesterase do?

A

Breaks down Ach

103
Q

What is the MOA of salbutamol?

A

B2 selective agonist

104
Q

How to remember the functions of the muscarinic receptors?

A

Odds stimulate, evens inhibit.

105
Q

Which lymph node is the ‘final sentinel’ node?

A

Left supraclavicular

106
Q

What is HFrEF? Good treatments?

A

Heart Failure with reduced Ejection Fraction = systolic dysfunction.
Leads to hypertrophy.
Tx - virtually anything to reduce BP except calcium channel blockers.

107
Q

What are the broad steps in platelet activation and clot?

A
  1. Damage
  2. Platelet plug
  3. Vasospasm
  4. Coagulation cascade to fibrin clot
108
Q

What is the difference in location and on ECG for STEMIs and NSTEMIs

A

STEMI - ST elevation. Local impact.
NSTEMI - no ST elevation, may be depression. Tend to do circumference of heart.

109
Q

What histological feature indicates an MI is less than 24 hours old?

A

Contraction band necrosis

110
Q

What causes chest pain in an MI vs Angina

A

MI = lactic acid due to cell death
Angina = bradykinins

111
Q

What is an early diastolic murmur typical of?

A

Aortic regurgitation

112
Q

Which organisms tend to cause infective endocarditis and which valve is typically impacted?

A

Staph aureus for typical infective endocarditis, strep viridians for subacute.
Tricuspid valve gets vegetations.

113
Q

What histological feature is a red flag for rheumatic heart disease?

A

Aschoff bodies - nucleus looks like caterpillar

114
Q

Rheumatic heart disease typically causes what heart defect?

A

Mitral stenosis

115
Q

Systolic murmur is typical of what defect?

A

Aortic stenosis

116
Q

How to calculate stroke volume?

A

EDV-ESV

117
Q

What is the difference between Type 1 and II second degree heart block?

A

Type 1 has gradual lengthening of P distance until loss a QRS, type 2 has abrupt loss of a QRS

118
Q

What is a give away for A Fib and a giveaway for Third Degree heart block?

A

A Fib is irregularly irregular and Third degree heart block will only have a BPM of like 30.

119
Q

When is the troponin peak after an MI?

A

After about 24-48 hrs.

120
Q

How would a clot impact blood platelet levels?

A

They may be low as all the platelets are doing the clot.

121
Q

Broadly, what causes eccentric hypertrophy vs concentric hypertrophy of the heart?

A

Eccentric - due to preload - volume
Concentric - due to afterload - pressure

122
Q

Explain the thromboxane seesaw of aspirin.

A

Thromboxane and prostocylin are in a sort of balance and COX inhibitors will denigrate both but the PGE/PGI will bounce back faster because other cells will make those. So aspirin has a net push towards PGI.
IRREVERSIBLE.
Remember thromboxane vasoconstricts.

123
Q

Which enzyme makes cholesterol in the liver?

A

HMG-CoA reductase

124
Q

What is the mechanism of statins?

A

Competitive HMG-CoA reductase inhibitor - slow cholesterol creation

125
Q

What is the mechanism of resins?

A

Bile sequestrants - causes bile acids to be excreted. Causes liver to up LDL receptors to make more cholesterol for more bile acids.

126
Q

MOA of ezetimibe?

A

Stops cholesterol absorption from intestines.

127
Q

Which medications lower triglycerides?

A

Fibrates and fish oils

128
Q

What are the best physiological fixes for angina?

A

Dilate the coronary arteries OR increase diastole time to allow them to fill.

129
Q

MOA of nitrates and an example and side effects.

A

eg. GTN.
These vasodilate the vessels so they decrease pre-load.
Reflex tachycardia, hypotension.

130
Q

Name a drug that acts on funny channels.

A

Ivabradine.

131
Q

What drug would you not use for variant angina?

A

B blocker

132
Q

What two drug types would you use for unstable angina?

A

A HTN drug like a B blocker AND aspirin.

133
Q

fever + murmur = what (unless proved otherwise)

A

ENDOCARDITIS

134
Q

Two common effects of an MI?

A

Heart block, arrythmia, AF, heart failure.

135
Q

Explain the baroreflex?

A

If blood pressure is high, it will fire baroreceptors in the carotids and aortic arch MORE, causing SNS decrease and PNS increase.
Opposite is true for low pressure.

136
Q

What will hypertrophy do to an ECG?

A

The R wave will be taller because there are more cells to depolarise

137
Q

How do non-selective calcium channel blockers work?

A

Work on the heart and vessels.
- Decrease activity of L type calcium channels
- Decrease SV and HR in heart
- vasodilation in arteries

138
Q

Where do arterial/cardiac thrombi tend to originate vs venous?

A

Arterial/cardiac - sites of damage or turbulent flow such as bifurcation sites.

venous = stasis

139
Q

List the three complement paths and what triggers them.

A

Classical - antibody antigen complex
Alternative - hydrolysing
Lectin-mannose

140
Q

How do calcium channel blockers work in the heart and in the vessels?

A

target L-type calcium channels.
Decrease SV and HR in heart.
Vasodilation in blood vessels.

141
Q

Compare the causes of venous vs arterial thrombi

A

Venous - stasis
arterial - damage or turbulence

142
Q

Describe the Frank-Starling principle.

A

Don’t confuse with Starling principle of blood forces.
Frank Starling principle is that more pre-load = more EDV = more stretch = more contractility of heart

143
Q

What is a non-dihydropyridine calcium channel blocker and what other hypertension drug should not be used with it?

A

Non-selective calcium channel blocker.
Beta blockers.

144
Q

What impact does exercise have on VO2?

A

Should increase it

145
Q

What are the 3 functions of beta blockers?

A
  1. Act on SA node to lower CO
  2. Act on cardiomyocytes to lower CO
  3. Reduce renin release
146
Q

Which cytokine allows diapedesis?

A

IL-1

MD (14 decks)

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