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Human diseases stage 3 > CVS part 2 > Flashcards

CVS part 2 Flashcards

1
Q

What are Korotkow sounds. Apparatus used

A

-Systolic when sounds appear (top pressure)
-Diastolic when they disappear (bottom pressure)

Pump cuff around arm so brachial pulse disappears. When deflates, pressure can be measured. Take average of 2 readings [Unobstructed and healthy blood flow is silent]
-be aware of white coat effect= higher when see doctor

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2
Q

What level of blood pressure constitutes hypertension. Values when they need meds. What value is severe hypertension

A

-120/80 is normal
>140/90 mmHg, consistently
>160/100 mmHg, in clinic
>180/110 mmHg, in clinic

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3
Q

Causes of essential hypertension. What % of hypertension is this

A

-90%
-no definitive cause
-Poly-causal = obesity, salt, lack of exercise, alcohol

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4
Q

Causes of secondary hypertension. What % of hypertension cases this is

A

-10%. A secondary cause of disease
-Renal artery stenosis
-Conn’s syndrome
-Adrenal adenoma
-Cushing’s syndrome
-Glomerulonephritis
-Fibromuscular disease
-medications

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5
Q

How Conn’s syndrome, adrenal adenoma and Cushing’s syndrome, kidney ischamia cause hypertension

A

-Conn’s and adrenal adenoma increase aldosterone (hyperaldosteronism) - increases sodium and fluid retention so increases BP. Also activates sympathetic system
-Cushing’s - too much cortisol causing vasoconstriction
-Ischamia of kidney - inappropriate activation of renin-angiotensin system, increasing aldosterone

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6
Q

List complications of hypertension

A

-Coronary heart disease- left ventricular dysfunction, MI, heart failure
-Peripheral vascular disease, Malignant hypertension, Dissection aneurysms, Renal failure, Aortic aneurysms
-Cerebral infarction and haemorrhage = Stroke. hypertensive encephalopathy - coma and seizures

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7
Q

What eye changes can occur in hypertension

A

-blood vessels weaken and cause haemorrhage areas in eye
-can be sight threatening

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8
Q

How to manage hypertension

A

-Lifestyle changes: weight reduction, exercise, decrease salt intake, alcohol reduction
-[reducing fat and smoking don’t reduce BP but reduce CVD risk]
-Meds = ACEI, ARBS, Beta blockers, Ca blockers, thiazide diuretics

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9
Q

General symptoms of a stroke

A

Symptoms depend on part of brain damaged
-unilateral face paralysis (opposite side to damaged brain)
-unilateral weak/ numb arms
-double vision
-slurred speech
-difficulty swallowing
-loss of sensation
-unsteady on feet
-Loss of ability to use and understand language (knows what something is but cannot name it)

FAST (Facial drooping, Arm weakness, Speech difficulties and Time)

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10
Q

Area of brain involved in speech, sight, understanding language,

A

-Speech = Broca’s area in frontal lobe
-Sight = Visual area, at the back
-Understanding = Wernicke’s area

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11
Q

Name some arteries involved in the circle of Willis

A

-Anterior, middle and posterior cerebral arteries
-Vertebral arteries and internal carotids supply the circle of willis
-Basilar arteries with pontine arteries
-Anterior and posterior communicating arteries

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12
Q

Risk factors for stokes. which is most common

A

-Hypertension - 52% = largest risk factor
-Vascular disease elsewhere - 38%
-Smoking - 45%
-Diabetes - 10%
-TIA - 14%
-Atrial fibrillation - 5% - Can cause a mural thrombus on the wall of the atria due to microstasis, which can then embolise and cause a stroke

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13
Q

Stroke prevention

A

-antihypertensives, lose weight, exercise, decrease salt intake, alcohol reduction
-Anti-platelet drugs (aspirin)
-Lipid lowering (statins)
-Anti-coagulants: Warfarin to reduce risk of thrombi-embolism
-Stop smoking
-Surgery

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14
Q

What drugs can cause hypertension

A

-Amphetamines -stimulant drugs
-Cocaine
-Oestrogens (e.g. oral contraceptive pill)
-Cyclosporin – (immunosuppressant)
-Sympathomimetic amines
-Erythropoetin

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15
Q

List drug classes used to reduce hypertension. Which are 4th line

A

-ACE inhibators
-Angiotensin receptor blockers
-Calcium channel blockers
-Diuretics (thiazide-like)

4th line:
-Beta blockers
-Anti-aldosterone
-Alpha blockers

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16
Q

Describe the renin angiotensin system - how its activated, hormone involved, what it causes

A

-low blood volume increases renin from kidney
-renin converts Ang to Ang I
-Ang I converts to Ang II (by ACE)
-Ang II causes vasoconstriction and stimulates aldosterone release from adrenal cortex
-This increases Na reabsorption, increased K secretion, increased fluid retention, increased blood volume = increased BP

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17
Q

Action of ACE inhibitors. Uses. Name drugs

A

-Inhibits ACE so inhibits conversion of Ang I to Ang II so reduced aldosterone (reducing water retention) Reduces BP. Renal vasodilation
-Inhibits breakdown of bradykinin, a vasodilator (releases nitric oxide and prostaglandins)

-1st line for hypertension. Used in heart failure
-Lisinopril, captopril, enalapril

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18
Q

Action of angiotensin receptor blockers. Uses. Name drugs

A

-Inhibit binding of Ang II at receptors, causing vasodilation
-very selective so not many adverse effects
-treats heart failure and hypertension
-Losartan, Irbesartan

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19
Q

Action of B blockers, atenolol, propranolol, bisoprolol. Uses Which is best for asthmatics

A

-Beta-adrenoceptor antagonist. Reduces sympathetic activity by blocking adrenaline on B1/B2.

-atenolol and bisoprolol = cardio-selective, only acting on B1, causing reduced HR, CO, BP. Also Inhibits RAS. No B2 bronchoconstriction so fine for asthmatics.
-Used for 4th line in hypertension, tremors, rate control in AF, heart failure

-propranolol = non-selective, acting on B1 and B2 so not used in asthmatics. Mainly used for anxiety and stress related hypertension, migraine prophylaxis

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20
Q

Action of calcium channel blockers. Uses. Name drugs

A

Act on L-type voltage calcium channels.
-Reduces Peripheral resistance: slows Ca entry into smooth muscle cells, causing vasodilation.
-Reduced coronary resistance: Slow Ca reduces SA node firing so reduces rate and force of contraction of myocardium, decreasing HR, BP

-used for hypertension. Sometime arrhythmias. Not used in heart failure

-amlodipine, nifedipine, diltiazem, verapamil

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21
Q

Action of diuretics (thiazide-like and loop) Name drugs

A

-Inhibit ADH, decrease blood sodium, decreased fluid retention and blood volume, increase urine

-This lowers BP to treat hypertension (weaker, thiazide-like) = indapamide
-Removes oedema to treat heart failure (more powerful loop diuretics) = furosemide

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22
Q

Action of aldosterone antagonists. Use. Name drugs

A

-Inhibit aldosterone, which is involved in increasing Na and fluid retention. Therefore less fluid retention and reduced BP
-4th line for hypertension
-spironalactone, eplerenone

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23
Q

Action of alpha blockers. Use. Name drugs

A

-Blocks a1 adrenoreceptors, sympatholytic.
-causing vasodilation, reducing BP
-4th line for hypertension
- Doxazosin

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24
Q

For step 1, which hypertensives to give <55 years. Which to give if >55 of African/ carribean. Then which ones to add (step 2, 3, 4)

A

<55= ACEI or ARBs
>55 or black= Ca blocker or Diuretics
Step 2 = A+C, or A+ thiazide D
Step 3 = A+C+thiazide D
Step 4= add extra thiazide D, or B blocker

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25
Q

Propranolol use. Side effects

A

-Blocks B1 and B2 adrenoreceptors, causing blocking sympathetic activity on heart (and lungs)
-used for anxiety and stress related hypertension, migraine prophylaxis, tremors
-not used for heart failure

-side effects: bronchoconstriction, heart failure, bradyarrhythmias, fatigue, dry mouth, blunting of recognising hypoglycaemia in diabetes, lichenoid eruptions, increased tooth demineralisation

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26
Q

Uses of Ca channel blockers. Name dihydroyridine and non-dihydropyridines. Which vasodilator, which slow heart contraction.

A

-used for treating hypertension, sometimes arrhythmias. Not used in heart failure

  1. Dihydropyridine – peripheral vessel dilation, lowering BP
    -Amlodipine and Nifedipine

2.Non – slows HR, slows contraction force
-Verapamil

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27
Q

Side effects of calcium channel blockers for hypertension, and in particular verapamil

A

In general: flushing (vasodilation), headache, oedema (increased capillary permeability), bradycardia, heart block
-verapamil: hypotension, heart failure, constipation

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28
Q

Side effects of thiazide-like diuretics for hypertension

A
  • Gout flare
  • Impaired glucose tolerance
  • Increased LDL cholesterol
  • Hypercalcemia
  • Lichenoid reactions
  • Steven Johns syndrome
  • Thrombocytopenia
  • Hyponatraemia (low Na)
  • Pancreatitis
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29
Q

Adverse effects of ACE inhibitors for hypertension

A
  • Renal failure, Hyperkalaemia
  • Dry cough - due to increased tissue bradykinin levels
  • Angioedema – increased bradykinin. Glossitis, anaphylaxis
  • Urticaria - hives
  • Burning mouth syndrome
  • Fetal injury - congenital malformations so AVOID IN PREGNANCY
  • Erythema multiforme
  • Lichenoid reactions
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30
Q

Adverse effects of alpha blockers for hypertension

A

-Not first choice for hypertension as causes deterioration in heart failure (baroreceptor mediated increased heart rate), peripheral oedema, postural hypotension (so avoided in elderly)

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31
Q

Which combination of anti-hypertensives to avoid

A

Avoid combination Beta blockers and Diuretics – ↑ risk of developing new-onset diabetes

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32
Q

Name long-acting and short-acting nitrates for angina

A

-Short-acting: GTN spray
-Long-acting: Isosorbide, mononitrate, dinitrate

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33
Q

Action of nitrates. use

A

-Nitric oxide causes vasodilation by increasing cGMP, reducing BP and CO. Dilates coronary arteries so increases blood flow to heart. Redistribution of coronary blood flow to ischamic myocardium. Reduce oxygen demand.
-Used for stable angina

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34
Q

what is nitrate tolerance

A

nitrate tolerance: Decreased effect after repeated doses. May be due to depletion of sulfhydryl groups necessary to produce active intermediate metabolite of nitrates

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35
Q

What ion channels in the SA node affect SA node firing

A

calcium channels, IF channels, potassium channels, sodium channels

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36
Q

What type of drug is Nicorandil and what does it treat. Side effects

A

-It is a potassium channel activator (in SA node), with a nitrate component
-anti-anginal
-causes vasodilation
-adverse effects= dizzy, headache, flushing, oral ulceration, myalgia, angioedema

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37
Q

What drugs are used for heart failure and their general functions

A

-Inotropes = increase force of contraction
-Diuretics = increase urine out – try to remove oedema
-Beta blockers- stabilise heart beat
-ACE inhibitors, ARBS – block RAS, reduce BP

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38
Q

What are inotropes. Uses. Name examples of drugs

A

-Increase force of contraction of the heart by stimulating cardiac B1 receptors
-for cardiac arrest, heart failure, arrhythmia, bradycardia
eg. atropine, digoxin

39
Q

What do the adrenoreceptors a1, B1 and B2 do

A

A1 – vasoconstriction to increase BP
B1 – inotropic = increases cardiac contraction and rate
B2 – vasodilation in smooth muscle
-bind adrenaline

40
Q

What drug classes are used to treat (ventricular and supra-ventricular) arrhythmias and why they are used

A

-want rhythm and rate control

Class I: Lidocaine (inhibit depolarisation)
Class II: Reduce HR (B blockers)
Class III: Potassium channel blockers (amiodarone, prolongs AP duration and refractory period so unable to repolarise)
Class IV: Calcium channel blockers (Verapamil, inhibit depolarisation, reduce HR)

Also cardiac glycosides (digoxin), adenosine

41
Q

How Digoxin works and adverse effects, for chronic atrial fibrillation and supraventricualr arrhythmia

A

-Antiarrhythmic: enhances action of vagus nerve effect (parasympathetic), reducing rate and conduction velocity in sinus and AV nodes
-Inotropic - increases intracellular Ca = increases heart force of contraction (blocks a Na/K ATPase so Na increases in cell so more Ca exchange into cell)
-adverse effects= nausea, vomitting, constipation, confusion, yellowing vision.

42
Q

Difference between K losing and K sparing diuretics. Which are loop and thiazide-like diuretics

A
  1. Losing: Lose water and potassium
  2. Sparing: Lose water and retain potassium

Loop and thiazide diuretics are K losing

43
Q

Name diuretics used for heart failure and hypertension.

A

-Loop diuretics used for heart failure as they are stronger and remove oedema. Work at loop of henle. Furosemide
-Thiazide-like are used for hypertension to reduce BP. Work at distal tubule. Indapamide

44
Q

Side effects of loop diuretics

A

-stronger so more side effects than thiazide-like
- Renal dysfunction
- Ototoxicity
- Hypomagnesemia
- Urinary retention
- Precipitation of hepatic encephalopathy

  • Hyponatraemia (low Na)
  • Thrombocytopenia
  • Pancreatitis
45
Q

What is sinus bradycardia, nodal bradycardia and heart block. What drugs may induce heart block

A
  1. Sinus bradycardia – sinus node is depolarising slowly
  2. Nodal/Junctional bradycardia – sinus node not doing anything
  3. Heart block = delay in/ no impulse being conducted through AV node. May cause blackouts or dizzy spells. (can be induced by Ca channel and beta blockers)
46
Q

How atropine is used to treat cardiac arrest. Adverse effects

A

-muscarinic Ach antagonist - parasympatholytic, increasing HR - inotropic
-Anticholinergic adverse effects:
- dry mouth
- mydriasis – pupil dilation
- postural hypotension

47
Q

What is supraventricular tachycardia. What it looks like on ECG

A

-tachycardia arising in SA or AV node
-narrow QRS
-symptomatic but benign

48
Q

What is ventricular tachycardia. What it looks like on ECG

A

-tachycardia that arises in ventricles or Purkinje fibres
-Wide QRS complex as takes time for impulse to conduct (looks upside down kinda)
-can cause cardiac arrest due to instability, patient may need shock

49
Q

Side effects of anti-arrhythmia drugs

A

-they are often negatively inotropic so this causes hypotension and may make heart failure worse
-constipation, Vasodilatation, oedema, flushing
-only used when benefits outweigh the risks

50
Q

Drugs used in cardiac arrest with 1) no heart beat, and 2) with chaotic rhythm (ventricular fibrillation)

A
  1. Adrenaline
  2. DC shock.
    If doesn’t work, then adrenaline + amiodarone.
    Lidocaine
    Atropine
51
Q

What does verapamil do. Side effects

A

-Calcium channel blocker, decreasing HR
-for supraventricular arrhythmias, hypertension
-heart failure, hypotension, constipation. And with B blockers produces heart block.
-common Ca blocker side effects: flushing, headache, oedema, bradycardia

52
Q

Drugs that cause gingival hyperplasia

A

-Calcium channel blockers – Nifedipine, amlodipine
-Immunosuppressants – Cyclosporin
-Anti-convulsants (anti-epileptic) – Phenytoin

53
Q

What is cardiopulmonary bypass surgery

A

-Drain venous blood from heart
-Oxygenate it to make arterial blood
-Cool it down to a defined temperature
-Pump it back into the aorta

54
Q

Ways of managing coronary artery disease

A

-medication: for vasodilation or thrombolysis
-PCI: angioplasty and stenting
-Coronary bypass surgery

55
Q

What is angioplasty. when it is used

A

– opens up narrowed or blocked arteries
-insert catheter, open up with balloon, and put in stent if re-collapse
-minimally invasive, simple, no LA needed. But doesn’t last as long as surgery
-for MI

56
Q

What is coronary artery bypass surgery. when it is done. What are the risks involved

A

-making alternate pathway for blood, to bypass around blocked coronary arteries
- done if many arteries affecting in angina and MI, and if stent didn’t work
-very successful with hospital mortality <1%.
-Risks: Stroke (1-2%), Infection (2%), MI (5%), Arrhythmia (25%), Bleeding (5%). Recurrent angina - usually after 15 years

57
Q

What is cardioplegia

A

-stopping the heart for surgical means
-high K solution mixed with blood to stop the heart. Cross clamp aorta

58
Q

List medications used for treating stable angina

A

-vasodilators: nitrates
-antihypertensives: ACEI, Ca blocker,
-lower cholesterol: statins
-antiplatelets: aspirin, clopidogrel

59
Q

Symptoms of peripheral critical ischameia (gangrene)

A

-pain at rest (claudication is just waking)
-worse at night as poor gravity makes ischaemia worse
-tissue necrosis = purple/red/black skin
-felt in toes and feet

60
Q

Causes of acute ischaemia

A

-thrombosis or embolisms, causing stoke, MI, PE (accounts for 50%)
-trauma
-extrinsic compression
-severe venous obstruction
-vasoconstrictor drugs

61
Q

How long it take for acute ischamia to cause irreversible damage. What are the 5 critical symptoms of acute ischamia in peripheral vascular disease (6 Ps)

A

-irreversible changes after 4-6 hours
Pain in leg
Pale
Perishing- cold
Pulseless
Paralysis - can’t stand or walk
Paraesthesia/ numbness - nerves die off

62
Q

How big an aortic aneurysm is. when and how it is treated

A

-50% of its normal size
-if <5.5cm it is managed via observation with ultrasound
-if >5.5cm it is treated by open surgery or stenting

63
Q

complications of carotid disease. surgery

A

-TIA or stroke due to embolism or occasionally CA stenosis
-carotid endarterectomy or carotid stenting to prevent stroke

carotid endarterectomy= artery opened, plaque removed, then patched up. During procedure insert shunt from common carotid into internal carotid so no cerebral ischaemia during procedure

64
Q

What systems are activated due to reduced CO in heart failure. long term consequences they have

A

-renin-angiotensin-aldosterone system: low BP causes renin then aldosterone to increase fluid volume and BP
-sympathetic activation: adrenaline stimulates heart contractility and vasoconstriction to maintain CO and BP

-long term, fluid retention and oedema. Vasoconstriction increases resistance so heat has to work harder. Sympathetic stimulation damaged heart muscle

65
Q

What is ANP and BNP and how are they increased in heart failure

A

-increased intracranial pressure detected by stretch receptors. Atria and ventricle release ANP and BNP to stimulate sodium excretion to reduce fluid volume and BP
-ANP=atrial natriuretic peptides. released by atrium
-BNP=brain natriuretic peptides. released by brain

66
Q

Which drugs and surgery used for heart failure

A

-Loop diuretics= reduce oedema
-Anti RAS: ACE inhibitors, ARBs
-nitrates -vasodilators

Pacemaker, valve replacement, repair, transplantation

67
Q

Why ARBs used instead of ACEI

A

ACEI cause dry cough and rash

68
Q

Distinctive symptoms of RHS and LHS heart failure

A

-RHS: peripheral oedema and raised JVP (congested systemic veins)
-LHS: pulmonary oedema (blood dams back into pulmonary veins, increases venous pressure, alveoli fill with fluid = SOB lying down, cough)

69
Q

What is left ventricular systolic dysfunction (LVSD)

A

-left ventricle, which pumps most of the blood, becomes weak, perhaps because it’s got bigger so can’t contract the way it should
-the two sides of the heart beat at different times

70
Q

What is a pacemaker used for

A

generates electrical pulses delivered by electrodes to the chambers of the heart. Used whenever have had a problem with conduction of heart
-bradycardia, AF, heart block if cardiac arrest, heart failure

wire threaded into vein under clavicle. Through SVC and LV

71
Q

what are ectopic heart beats or extrasystole

A

-common, non-sustained arrhythmia, usually harmless
-extra heart beat, beating too soon, feels like a skipped beat
-due to stress, caffeine, alcohol or certain cold medications

72
Q

What is atrial fibrillation

A

-commonest sustained arrhythmia
-an irregular supra ventricular tachycardia
-irregular heart beat due to chaotic SA signalling, causing uncoordinated contractions
-usually too fast. but sometimes slow

73
Q

Causes of sinus and ventricular tachycardia

A

-sinus= normal response to exercise, emotion. Or due to hyperthyroidism, hypovolaemia, fever, heart failure, loss of blood
-ventricular= associated with ischaemic heart disease, or drugs. Can cause cardiac arrest

74
Q

What is ventricular fibrillation. causes

A

-Uncoordinated & ineffective electrical activity of the ventricles
-can cause MI
-can cause cardiac arrest (but still heart beat) So need Direct Shock Cardioversion
-Cocaine, digitalis overdose, cardiomyopathy

75
Q

What is asystole

A

-Absence of electrical activity and contraction
-Cardiac arrest
-There may be evidence of atrial activity
-Causes sudden loss of consciousness and death

typically occurs as a deterioration of ventricular fibrillation or pulseless ventricular tachycardia

76
Q

Name 3 anti platelet drugs used and their different mechanisms

A
  1. Aspirin: COX inhibitor, inhibits platelet thromboxane
  2. Clopidogrel: ADP receptor antagonists
  3. Dipyridamole: Adenosine re-uptake inhibitor
77
Q

Do you stop someone’s aspirin before dental treatment

A

no. it would take 7-10 days for its effects to stop anyway. only stop if doctor who prescribed it gives permission. Use local measures to reduce risk of haemorrhage

78
Q

Uses of aspirin

A

-preventing thrombi-embolism events, so used for AF, previous stroke or TIA, MI
-for claudication, acute MI, acute stroke, stable angina
-for fever, migraines

79
Q

What are contraindications for aspirin

A

-Allergy
-Age <12 years (risk of Reye’s Syndrome – encephalopathy secondary to renal problems)
-Active peptic ulceration
-Recent GI or intracranial bleeding
-Bleeding disorders
-Severe liver disease

80
Q

Clopidegrol: action, why better than aspirin in some ways, do you need to stop it if using with aspirin, what drug it interacts with

A

-ADP receptor antagonist, prevents platelet aggregation - anti-platelet
-less GI bleeding and haematological toxicity than aspirin
-May be given in combination with aspirin if need heavy anticoagulation, however, need to stop 1 (NOT BOTH) before doing treatment that would make them bleed
-reacts with proton pump inhibitors - omeprazole

81
Q

Dipyramidole use, action, contraindication

A

-adenosine re-uptake inhibitor
-anti-platelet
-for prothetic valves to prevent thromboembolism
-contraindicated in uncontrolled angina as may exacerbate it

82
Q

Heparin: action, administration, metabolisation site, half life, antidote

A

-anticoagulant by inhibiting prothrombin (II)
-IM (low dose) or IV (high dose) due to poor GI absorption
-immediate onset to cover warfarin 1-2 day lag period
-metabolised in liver
-protamine sulphate antidote for overdose
-Short half life of 1-5 hours. So wears off quickly

83
Q

Advantage of low molecular weight heparin. disadvantage

A

-no need to monitor APTT, smaller bleeding risk, reduced risk of thrombocytopenia, less likely for allergy
-subcutaneous administration so outpatient use
-BUT less reversible than heparin so no antidote

84
Q

Heparin unwanted effects

A

haemorrhage (especially GI), transient thrombocytopenia, allergy, osteoporosis, impaired liver function

85
Q

Warfarin: action, administration, protein bound %, half life, antidote

A

-vitamin K antagonist so inhibits clotting factors 2,7,9,10
-oral
-98% protein binding
-long 35-37 hour half life
-vitamin K antidote
-1-2 day lag period so given heparin

86
Q

How is heparin and warfarin monitored

A

heparin= APTT
warfarin= INR and PT

87
Q

Drugs that increase and decrease effect of warfarin

A

Effects increased by: [competes for protein binding, increasing hameorrgae]
- Aspirin (AVOID)
- Fluconazole (lower dose) and miconazole (AVOID)
- Erythromycin (AVOID)
- Metronidazole (AVOID) can get INR 17
- Penicillin, amoxicillin (AVOID)
- Cephalosporine (AVOID)
Effects decreased by: rifampicin (AVOID)

88
Q

Do you stop warfarin for dental procedures

A

-don’t need to stop for low risk: simple extractions (1-3 teeth), incision and drainage, Detailed perio examination, RSI, Restorations with sub-gingival margins, provided INR<4
-for high risk (surgical flap, biopsy, ginigval re contouring) miss morning dose.
-But never interrupt it if DVT or PE in last 3 months, or on it for cardioversion, stent, have heart valve)

89
Q

Warfarin uses

A

-anticoagulant, less likely for blood to clot
-prevent DVT, treat PE
-for AF and prosthetic heart valve to prevent thrombi-embolism
-For previous stroke, MI, DVT

90
Q

Action of the DOACs: dabigatran, rivaroxaban, apixaban, edoxaban

A

-Dabigatran: thrombin IIa inhibitor
-Rivaroxaban etc.: inhibits clotting factor Xa

91
Q

Do you need to stop DOACs before dental treatment

A

-For low risk procedure (Simple extractions (1-3 teeth), incision and drainage, Detailed perio examination, RSI, Restorations with sub-gingival margins)=Don’t need to alter dose if INR<4
-High risk (biopsies, surgical flap, gingival re contouring) miss morning dose of dabigatran and give evening dose >4 hours after haemostasis. For rivaroxaban delay morning dose and give it >4 hours after haemostasis

92
Q

Link between periodontal disease and CVD

A

-bacteraemia can potentially cause oral bacteria associated with perio disease to infect heart and may contribute to atherosclerosis formation
-both inflammatory so bi-directional relationship
-but share co-founding factors (smoking) so difficult to say if directly linked

93
Q

most common cause of hemianopia (vision loss). and bitemporal hemianopia

A

-stroke
-lesions of optic tract, pituitary tumor

94
Q

Causes of hypovolemia

A

septic or anaphylactic shock
No volume loss, however increased vessel permeability causes blood to leave circulating system and into the extravascular compartments

Human diseases stage 3 (9 decks)

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