CR EOYS6 Flashcards
Which factor, if in excess can cause of a hypercoagulable state
Factor X
Factor VII
Factor VIII
Factor IX
Which factor, if in excess can cause a of hypercoagulable state
Factor X
Factor VII
Factor VIII
Factor IX
Which one of the following is not a cause of a hypercoagulable state
Elevated factor VIII
Malignancy
Protein C deficiency
Antiphospholipid syndrome
Elevated factor Xa
Which one of the following is not a cause of a hypercoagulable state
Elevated factor VIII
Malignancy
Protein C deficiency
Antiphospholipid syndrome
Elevated factor Xa
Which of the following would you prescribe alongside aspirin for NSTEMI treatment
Clopidogrel
Prasugrel
Ticagrelor
Abciximab
Which of the following would you prescribe alongside aspirin for NSTEMI treatment
Clopidogrel - (clopidogrel 300mg is an alternative if higher bleeding risk)
Prasugrel
Ticagrelor
Abciximab
Name the receptor on platelets that is activated by ADP
P2Y12
COX-1
TXA2
Glycoprotein IIb/IIIa
Name the receptor on platelets that is activated by ADP
P2Y12
COX-1
TXA2
Glycoprotein IIb/IIIa
Which of the following acts a receptor for von Willebrand Factor (vWF)
P2Y12
COX-1
TXA2
Glycoprotein Ib
Which of the following acts a receptor for von Willebrand Factor (vWF)
P2Y12
COX-1
TXA2
Glycoprotein Ib
This diagram depicts platelet adhesion to endothelium
Which of the following is VWF
A
B
C
D
This diagram depicts platelet adhesion to endothelium
Which of the following is VWF
A
B
C
D
glycoprotein IIb/IIIa (GPIIb/IIIa) an integrin complex found on platelets. It is a receptor for fibrinogen[1] and von Willebrand factor and aids platelet activation. The complex is formed via calcium-dependent association of gpIIb and gpIIIa, a required step in normal platelet aggregation and endothelial adherence
This diagram depicts platelet adhesion to endothelium
Which of the following is fibrinogen
A
B
C
D
This diagram depicts platelet adhesion to endothelium
Which of the following is fibrinogen
A
B
C
D
This diagram depicts platelet adhesion to endothelium
Which of the following is GpIIb/IIIa
A
B
C
D
This diagram depicts platelet adhesion to endothelium
Which of the following is GpIIb/IIIa
A
B
C
D
This diagram depicts platelet adhesion to endothelium
Which of the following is GpIb
A
B
C
D
This diagram depicts platelet adhesion to endothelium
Which of the following is GpIb
A
B
C
D
Bleeding from mucosal surfaces (epistaxis, gum bleeding, menorrhagia) would indicate
VWD
Factor deficiency
Bleeding from mucosal surfaces (epistaxis, gum bleeding, menorrhagia) would indicate
VWD
Factor deficiency - rate
This brusing would indicate
VWD
Factor deficiency
This brusing would indicate
VWD - small / multiple
Factor deficiency - one large bruise
What underlying pathologies might cause angina if the problem is occuring from a reduced o2 supply? [2]
Reduced O2 demand:
-
CAD:
- Atherosclerosis
- Post radiation therapy
- Spasm: normal coronary arteries which spasm causing temporary occlusion - Anaemia
What underlying pathologies might cause angina if the problem is occuring from an increased myocardial demand? [3]
- Left ventricular hypertrophy (from: HTN, aortic stenosis, aortic regurgiation, hypertrophic cardiomyopathy)
- Right ventricular hypertophy (from: pulmonary HTN, pulmnonary stenosis)
- Rapid tachycardiarythmias
Describe the pathway you would undertake to diagnose stable angina
Clinical assesment:
How many of the following do they have?
- General chest discomfort lasting 5/10 mins?
- Is this provoked by exercise?
- Is this relieved by rest or nitrates?
- Answer = <1, No diagnostic testing, no medication
- Answer = 2 characteristics = atypical angina
- Answer = 3 characteristics = typical angina
If Atypical angina or typical angina: initial management and investigations:
- CTCA
- Functional imaging if CTCA inconclusive
Describe the managment pathway for someone with angina
How do different drugs / therapies target different physiological areas to relieve angina symptoms?
Increasing O2 delivery
Increase coronary blood flow:
- Nitrates
- CCBs
- Revasc.
- Nicorandil (Combination of K+ blocker and nitrate)
Reducing myocardial demand:
1. Reduce HR:
- BB
- ivabradine (funny current (If) inhibitor)
2. Decrease LV wall tension:
- BB
- Nitrates
- Nicorandil
- CCBs
- Ranolazine (Na+ pump inhibitor)
3. Reduce contractility:
- BB
- CCBs
4. Modify energy metabolism
- Trimetazidine
How can you pharmacologically reduce risk of MI for patients who are at risk of angina? [4]
- Aspirin: this produces an antithrombotic effect that helps to reduce the risk of heart attacks and strokes.
- Statins: reduces cholesterol (HMG Reductase inhibitor)
- Ace Inhibitor: If there is hypertension or diabetes or other comorbidities
-
P2Y12 receptor
antagonist: After PCI or if allergic to statins (P2Y12 receptor blockers are another group of antiplatelet drugs. This group of drugs includes: clopidogrel, ticlopidine, ticagrelor, prasugrel, and cangrelor)
What drug is initially used to treat stable angina? [1]
glyceryl trinitrate (GTN).
What are 3 risk factors for thromboembolism - what is the name for these factors combined? [4]
Virchow’s Triad
Endothelial injury
Stasis or turbulence of blood flow
Blood hypercoagulability
Inflammation: causes procaogulant state - acts in combination with one of the above
Why does vein wall pathology increase chance of DVT / PE?
How can vein wall pathology / damage occur? [3]
Heparan sulfate projects out of the endothelial wall. These projections prevent platelet adhesion to intact endothelial membrane. If damaged - less heparan sulfate:
- increases risk of clot formation, especially if combined with reduced blood flow
Vein wall pathology can occur from:
a) smoking / alchohol
b) diabetes
c) chronic inflam disease (RA)
How do you diagnose DVT?
Use Wells’ Score:
- Add up points on the score: 2 points or more is likely. 1 is unlikely
- If 2 or more score: have proximal leg vein ultrasound
i) have positive scan - give treatment
iI) have negative scan, repeat in 6-8 days - do a D Dimer test
a) if D-dimer is positive: repeat scan in 6-8 days
b) if second sacan D-dimer is negative - consider alternative disease, but discuss symptoms with patient so they can look out for it - Venography - gold standard
* o D-dimer is fibrin degradation product
o Is a marker of fibrin formation
o Raised in VTE and other pathologies
D dimer: fibrin degradation product released when thrombus is degraded by by fibrinolysis low D dimer = low DVT risk.
Why might someone have hypercoaguable blood? [3]
When would you consider hypercoagulable states for DVT?
Why might someone have hypercoaguable blood?
- Antithrombin deficiency
- Protein C or S defiency (anti-coagulant proteins)
- Factor V Leiden mutation :causes resistance to activated protein C
Consider when no obvious signs for VTE/ PE
How would you investigate for PE?
Classification system? [1]
ECG? [3]
CXR? [1]
ABG [1]
o Wells Score greater than 4
ECG - sinus tachycardia, right heart strain. T-wave inversion on anterior leads (V1-V3). Classic finding: S (deep S wave in lead I), Q ( present in lead III) and T (inverted T in lead III).
o CXR- possible small pleural effusion, peripheral wedge shaped density above diaphragm, focal oligemia. Most common finding with PE patients is a normal CXR, but used to excludes other diagnoses
o ABG - often hypoxic, low CO2 (due to hyperventilation)
Explain how PE can cause cardiac failure xx
- Right ventricle has thin muscle (pulmonary vasculature is a low pressure system)
- Increased pressure in the pulmonary vasculature due to PE
- Thin right ventricle has to work harder / dilates and is understrain
- Dilatation of right ventricle gets in the way of the left ventricle (pushes through interventricular septum) – less filling of the LV: fall in BP / decreased CO
- This causes release of adrenaline / noradrenaline: causes PE to vasoconstrict.
- Repeats cycle – can lead to MI / arrthymia
- So main cause of death is right sided heart failure leading to left sided heart failure cardiac arrest
- ALSO get patent foramen ovale in 1/3 patients: severe hypoxaemia & increased risk of stroke
-
Which artery is occluded here? Explain what type of ACS is causing this ECG [1]
a) LAD
b) RCA
c) LCA
d) circumflex artery
Which artery is occluded here? Explain what type of ACS is causing this ECG [1]
a) LAD
b) RCA
c) LCA
d) circumflex artery: ST depression in V5 & V6
What does this ECG indicate? [2]
T wave depression in V1-V3
Occlusion in LAD
Explain the basic overview from vessel injury –> stable haemostatitc plug
- Vasoconstriction occurs to reduce blood loss
- Collagen released is also. This causes platelet released, which in turn causes release of serotonin, TXA ADP & platelet phospholipids.
- Serotonin then helps with vasoconstriction, whilst TXAADP helps with platelet aggregation.
- Together they help to make a primary plug
- Through vasoconstriction, shear stress is increased. This cause various molecules to be release, including VWF (important in platelets adhering to vessel walls)
- Simultaneously to vasoconstriction: tissues factor is exposed. This causes coagulation cascade.
- Platelet Phospholipid is the surface for many of the coagulation cascade that occurs.
- Thrombin is created fibrin
- together makes stable hameostatic plug
Give brief overview on how primary haemostasis occurs to make platelet plug
- Vessel injury causes collagen to be exposed
- VWF binds to collagen one side, and the otherside to platelets via glycoprotein 1b receptor
- Platelets become activated, start clump other platelets. Through glycoprotein IIb, IIIa and fibrin, form stable haemostatic plug.
Fill in the differences
Describe how the kidney reabsorbs bicarbonate if there is respiratory alkalosis
- Decreased carbonic anhydrase activity within the cell: less CO2 converted to bicarbonate and protons. Less protons in cell means less protons excreted by sodium-proton exchange ATPase in luminal wall into urine to be excreted.
- This results in less bicarbonate is converted to CO2 in tubule and filtered bicarbonate is excreted in urine
- Leads to decreased excretion protons and decreased bicarbonate reabsorption
Explain the MoA behind HACE
In hypoxaemia ATP supply in nerve cells decreases and sodium pumps run down
Sodium leaks into nerve cellpulling water with it brain cells swell.
Raises intracranial pressure (icp) and blocks cerebral veins
Cerebral circulation fails, hypoxia worsens, neurons, starved of oxygen and squashed together, start to die.
Dead neurons release ions and fluids – worsen cerebral oedema
Explain the mechansim of action of an ADP receptor antagonist [2]
Name three of the most common [3]
The ADP receptor antagonists bind to the P2Y12 receptor to prevent ADP-induced platelet activation
Clopidogrel
Prasugrel
Ticagrelor
Which of the following prevents the conversion of arachidonic acid to thromboxane A2
Heparin
Warfarin
Aspirin
Dabigatran
Edoxaban
Which of the following prevents the conversion of arachidonic acid to thromboxane A2
Heparin
Warfarin
Aspirin
Dabigatran
Edoxaban
Explain the mechanism of action of aspirin [3]
Non-selective for COX-1 and COX 2 enzymes (prevent aggregation)
COX 2 inhibition prevents arachidonic acid conversion to Thromboxane A2
Thus preventing Thromboxane A2 formation, preventing platelet aggregation.
Describe MoA of the DOACs:
Rivaroxaban
Apixaban
Edoxaban
Direct factor Xa inhibitor (more modern version of heparin)
