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Human Disease > Cardiovascular Diseases > Flashcards

Cardiovascular Diseases Flashcards

1
Q

When taking a history and examination of a patient, what should you look for when looking for CV disease

A

History:

  • Generally fit and well?
  • Heart problems
  • High BP?
  • Medications
  • More specific qs if necessary
  • Pt exercise tolerance (how far can you walk unaided without stopping, can you climb stairs, what prevents you from going further)

Examination:

  • General appearance
  • Breathlessness at rest
  • Apprehensive, sweaty expression

Hands:

  • finger clubbing
  • Pale nail bed may suggest anaemia
  • Splinter haemorrages typical of endocarditis

Face and Oral Cavity:
-Cyanosis
Blue discolouration of the lips or palate
Poor oxygenation of blood and they may have a cardiac cause
-Gingival overgrowth
Antihypertensives
-Xanthelasma (yellow patches around the eyes) indicate high cholestrol

Pulse:

  • Palpation of radial pulse with index and middle fingers
  • Atrial fibriation
  • Rate>100/min then tachycardia
  • Rate<60/min then bradycardia

Blood pressure

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2
Q

Definition of Hypertension

A
  • long term medical condition in which the blood pressure in the arteries is persistently elevated
  • 20-30% of adult population
  • Persistently high blood pressure
  • 140/90 mmHg persistantly raised
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3
Q

Normal blood pressure readings v hypertension v hypotension

A

Normal:
Between 90/60mmHg and 120/80mmHg

High BP:
140/90mmHg or higher

Low BP:
90/60 of lower

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4
Q

Complications of hypertension

A 
-Long-term blood pressure is a major risk for 
coronary artery disease, MI
stroke
heart failure
vision loss
chronic kidney disease and renal failure
peripheral vascular disease
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5
Q

Normal cardiac rate v brachycarida v tachycardia

A
  • Between 80-90/min considered normal
  • Athletes can be as low as 50-60/min
  • Brachycardia is <60b/min
  • Tachycardia is >100b/min
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6
Q

Types of hypertension and explanation

A

Primary (Essential) Hypertension

  • 90%
  • No identifiable cause
  • Prevalence increases with age
  • Tends to be familial and is likely to be the consequence of an interaction between genetic and environmental factors
Multifactoral aetiology:
Genetic factors
Environmental (obesity, alcohol, salt intake, stress)
Humoral mechanisms
Insulin Resistance

Secondary Hypertension

  • Underlying primary cause
  • Renal Disease eg diabetic nephropathy, chronic glomerulonephritis, adult polycystic disease
  • Pregnancy
  • Endocrine Disease eg Conn’s syndrome, Adrenal hyperplasia, Cushing’s syndrome, acromegaly
  • Drugs eg. corticosteroids, oral contraceptive pill
  • Coarctation of the aorta
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7
Q

Diagnosis of hypertension

A
  • Measurement of blood pressure on at least 3 occasions over a 3 month period
  • Usualyl >140/90mmHg
  • Often require a 24h monitor
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8
Q

Treatment of hypertension

A
  • If secondary hypertension, treat the cause if possible
  • If primary hypertension then give genera advice about weight loss, exercise, reducing alcohol, stopping smoking, reducing salt intake, increasing fruit and vegetables

-or medical treatment:
ACE Inhibitors eg captopril, ramipril
Angiotensin II receptor blockers eg candesartan, losartan
B blockers eg atenolol, propranolol
Ca channel blockers eg nifedipine, amlodipine
Diuretics eg bendroflumethiazide

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9
Q

Dental Relevance of hypertension

A
  • Minimise stress and pain to minimise further increase in BP which may precipitate cerebrovascular accident (stroke), MI
  • No problem with adrenaline in LA, as long as the intravacular injection is avoided
  • Controlled hypertensive-treat as normotensive
  • Uncontrolled hypertensive (>140/90mmHg)- delay elective treatment. Refer to GP
  • Severe hypertension (>180/110mmHg)- refer urgently to GP or hospital
  • Post operative bleeding more likely
  • Patient likely to be taking aspirin

-Oral manifestations due to the use of ACE inhibitors include:
Loss of taste
Angiodema
Lichenoid Reaction

-Oral manifestations due to B blockers include
Lichenoid reactions

-Oral manifestations due to calcium channel blockers include
Gingival overgrowth

-Oral manifestations due to diuretics include
Xerostomia

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10
Q

Atherosclerosis definition

A
  • Disease in which the inside of the artery narrows due to the build up of plaque
  • Associated with the radio between LDL:HDL
  • Initially there are no symptoms
  • Narrowing of arteries limits flow of oxygen rich blood to the parts of the body
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11
Q

Atherosclerosis complications

A 
-If severe, 
Coronary heart disease
Stroke
Peripheral artery disease 
Kidney problems

Dependent on which arteries are affected

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12
Q

Risk factors for atherosclerosis

A
  • Abnormal cholesterol levels
  • High blood pressure
  • Diabetes
  • Smoking
  • Obesity
  • Family history
  • Unhealthy diet
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13
Q

What is a plaque made up of

A
  • Fat
  • Cholesterol
  • Calcium
  • Other substances from the blood
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14
Q

Treatment of atheroschlerosis

A

-Modifiable factors such as exercise, diet, smoking etc

  • Statins decrease cholesterol
  • Blood pressure meds
  • Aspirin decreases clotting

-Regression includes antioxidants and HDL

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15
Q

Difference between arteriosclerosis, arteriolosclerosis, and artherosclerosis

A
  • Arteriosclerosis general term for describing any hardening of M or L arteries
  • Arteriolosclerosis is the hardening of arterioles
  • Artherosclerosis is the hardening of an artery specifically due to atheromatous plaque
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16
Q

Clinical features of atherosclerosis

A

-Asymptomatic for decades as arteries enlarge at all plaque locations causing no effect on blood flow

  • S/s only occur after severe narrowing impeding blood flows to different organisms enough to induce symptoms
  • Depends on which arteries have been narrowed
-Coronary arteries 
Chest pain 
SOB
Nausea
Dizziness
Palpatations 
-Carotid artery 
Cant think straight 
Difficulty speaking 
Dizziness
Blurred vision

-Peripheral arteries
Numbness in extremities

-Renal arteries
Decreased kidney blood flow and chronic kidney disease

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17
Q

Different layers of artery from inner to out

A
  • Tunica intima (endothelial layer on top)
  • Tunica media
  • Tunica adventitia

Same for vein

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18
Q

Are fatty streaks present in infants

A
  • Present in 45% of infants dying in first y of life

- Reversible at this stage

19
Q

PDAY study on atherosclerosis

A

-Smoking caused 3 times more likely

  • Females: more plaques in abdominal aorta
  • Males: more plaques in coronary arteries
20
Q

Stages of Atherosclerosis

A

1) LDL particles from bloodstream bind to the LDL receptors on the surface of endothelial cells
2) Receptor:LDL Complex internalised by endocytosis of the endothelial cell
If plasma LDL concentrations exceed the endocytic capacity then LDL may pass the endothelial barrier without receptor and gets trapped in the subendothelial space above the internal elastic lamina
3) Oxygen free radicles are sent to the LDL particles from the endothelial cells
4) Monocytes migrate through the endothelium into the subendothelial space
5) Transormation into macrophage
6) Oxidised LDL is taken up by the macrophage, leading to intracellular accumulation of cholestrol
7) Macrophage becomes a foam cell
8) Macrophage also activates T cells
9) Cytokines are released from macrophages foam cells and endothelial cells which further amplifies the immune reaponse
10) Endothelial cells secrete growth factors that attract smooth muscle cells and stimulate cell migration and proliferation from the tunica media into the subendothelial space
11) Foam cells release free cholestrol into the intima
12) Cytokines released from the macrophages continue to stimulate the proliferation of smooth muscle cells in the subendothelial space
13) Smooth muscle cells synthesize collagen leading to formation of a fibrous cap
14) Blood vessels grow into the plaque

21
Q

Key ratio of LDL:HDL and the role of HDL

A
  • Ratio of >3:1 indicates a high risk of atherosclerosis
  • HDL should be >1mmol/l
  • LDL should be <3mmol/l

-Role of HDL is protective

22
Q

Complications of the pathogenesis of atherosclerosis

A

Fatty Streak
Fibrous Plaque

  • Rupture
  • Ulceration
  • Thrombosis
  • Haemorrhage
  • Calcification
  • Aneurysm
  • Embolus
23
Q

Hyperlipidaemia and LDL:HDL balance

A
  • Familial hypercholesterolaemia
  • Decreased receptors for LDL cholesterol
  • Increased levels of LDL
  • Heterozygotes: 50% reduction in receptors: disease development in 40s
  • Homozygotes: disease development in 20s
24
Q

Relation between hypertension and atherosclerosis

A
  • Positive correlation with hypertension
  • Hypertensive patients are more vulnerable to build-up
  • Haemodynamic forces- dynamics of blood flow
  • Damage to endothelial cells and facilitating passage of LDL into the intima
  • Coarctation of aorta findings (aortic narrowing, left venticle has to work harder)
25
Q

Risk factors for advanced atherosclerosis

A
  • Sex: primarily a disease of men until 70s when protective effect of female sex hormones are lost
  • Cigarette smoking as it damages the endothelial cells
  • Diabetes leads to increased incidence of hyperlipidaemia and microvascular damage
26
Q

Calcification of an atheroma

A
  • Forms against vascular smooth muscle cells
  • Especially those adjacent to the atheromas and on the surface of atheroma plaque and tissue
  • In time, as cells die, this leads to extracellular calcium deposits between the muscular wall and the outer portion of the atheromatous plaques
  • Plaque interferes with the regulation of calcium deposition so it accumulates and crystalises
27
Q

Stages of development from the initial lesion

A
  • Initial lesion is just isolated foam cells
  • Fatty streak is mainly intracellular lipid accumulation
  • Intermediate lesion is small extracellular lipid pools/intracellular lipid accumulation
  • Atheroma
  • Fibroatheroma
  • Complicated lesion, often calcified and fibrosed
28
Q

What happens after an atheroma is formed

A

-Interference with blood flow to a target organ (ischaemia/infarction)
Ischaemia is the restriction in supply of blood to the tissues causing a shortage of oxygen and glucose necessary for cellular metabolism
Infarction is tissue death caused by a lack of oxygen due to obstruction in blood flow

  • Thrombosis
  • Embolisation
29
Q

Interference with blood flow can develop onto and clinical features of this

A

-Ischaemia: restriction in supply of blood to tissues leading to a shortage of ocygen and glucose necessary for cellular metabolism
Angina, TIA, peripheral vascular disease

-Infarction: tissue death caused by a lack of oxygen due to obstruction in blood flow
Myocardial infarction
Stroke
Gangrene

30
Q

The likelihood of blood flow being effected by an atheroma depends on…

A
  • Collateral blood supply?
  • Speed of artial occlusion
  • Metabolic needs of the tissue
  • Degree of arterial blocking
31
Q

Definition and aetiology of ischaemic heart disease

A
  • aka coronary heart disease
  • Inadequate O2 supply to meet the demands of the heart
  • Most common cause of death in Western world
  • Caused by atheromatous plzque within coronary arteries causing constriction of blood flow
  • Risk of plaque rupturing leading to an acute thrombus and MI

-Angina, unstable angina, myocaridal infarction and sudden cardiac death

32
Q

Angina definition and subsequent result

A
  • Chest pain caused by a lack of blood flow to the heart muscle
  • Angina pectoris- reduced o2 perfusion of the cardiac muscle
  • Feels like strangling feeling in the chest
  • Breathlessness
  • Pain radiates to the jaw and left arm
33
Q

Myocardial Infarction and signs/symptoms

A
  • Blood flow decreases or stops to a part of the heart
  • Causes damage to the heart muscle

-Symptoms:
Central strangling pain that lasts longer than 15 mins
Pain radiates to neck, jaw and left arm
Nausea and vomiting

-Sign
Grey tinge
Sweating
Tachycardia

34
Q

IHD risk factors

A

-Unmodifiable
Age
Gender
Fam History

-Modifiable 
Hyperlipidaemia 
Smoking 
Alcohol
Hypertension 
Obesity 
Diabetes 
Exercise 
Stress
35
Q

Angina management in dental clinic and dental relevance

A
  • Pain resolves in minutes following rest and GTN
  • Jaw involvement
  • Reassurance

-Polypharmacy due to medications:
Aspirin - bleeding tendency
Nicorandil- oral ulcerations. Potassium channel activator that relaxes and widens blood vessels
Beta Blockers/Ca channel blockers- lichenoid reactions and gingival hyperplasia respectively

36
Q

Management of MI and Dental Relevance

A
  • Sit pt up
  • Calm and relaxed approach
  • Dial for ambulance
  • Administer O2 and GTN
  • Repeat every 10 minutes
  • Aspirin 300mg PO crushed or chewed
  • Entonox if available
  • Monitor pulse and oxygen saturation
  • Dental tx may precipitate angina/MI- need to minimise stress and pain
  • Presents as jaw pain
  • GTN may be used prophylactically
  • If unstable angina delay elective tx until controlled
  • Likely to be taking aspirin (clotting issues)
  • Ca channel blockers (gingival hyperplasia)
  • B blockers (lichenoid reactions)
  • Nicorandil (ulcerations)
37
Q

Clotting v Thrombosis

A
  • Clotting is the essential, physiological and beneficial activation of the clotting cascade when there has been tissue injury
  • Activation of protein cascade leading to formation of fibrin
  • Thrombosis involves activation of both platelets and the clotting cascade
  • Haemostasis occuring in the wrong place and at the wrong time
  • Harmful
38
Q

Factors that promote thrombosis and how these factors affect it

A

-VIRCHOWS TRIAD

-Changes in the surface of the vessel
Atheromatous plaque
Splitting/fraying/loss of surface endothelial layer
Exposure of subendothelial tissues leads to platelet activation
Burning/freezing
Vasculitis

-Changes in the blood flow 
Patients with congestive cardiac failure (venous stagnation)
Post myocardial infarction 
Atrial Fibrillation
Heart valve disease 
Arterial v venous thrombosis 
Turbulence v speed

-Changes in the constituents of the blood
Hypercoaguable state: haemostatic equilibrium is tilted in the favour of thrombosis
Due to increased pro-coagulant factors, decrease in anti-coagulant factors, increased viscosity of blood, and increased platelet count and adhesiveness

39
Q

Fate of a thrombus

A

-Lysis
-Organisation/recanalization
-Embolisation
Thrombi detach and travel at high speed into the circulation until a vessel is reached whose lumen is smaller than the size of that thrombus

40
Q

Embolisation and types of emboli

A

Thrombi detach and travel at high speed into the circulation until a vessel is reached whose lumen is smaller than the size of that thrombus

Mainly thrombus 
Infective (vegetations of infective endocarditis)
Gaseous 
Fat
Foreign material
41
Q

Heart Failure definition

A
  • When the heart is not able to pump blood at a rate that the body requires
  • Heart can not fill quickly enough to match demand or where it can not pump the blood out
  • Can be left sided right sided or both
42
Q

Causes of heart failure

A

-Pump failure
Heart muscle disease, restricted filling, inadequate heart rate

-Excessive preload
Mitral regurgitation, fluid overload

-Chronic excessive afterload
Aortic stenosis
Hypertension

43
Q

Difference between left sided failure and right sided failure in terms of signs and symptoms

A

Left Sided Failure:

  • Orthopnoea and paroxysmal nocturnal dyspnoea
  • Pulmonary congestion (cough, wheeze, crackle, blood tinged sputum)
  • Restlessness
  • Confusion
  • Tachcardia
  • Fatigue
  • Cyanosis

Right sided failure or Cor Pulmonale

  • Fatigue
  • Increased peripheral venous pressure
  • Ascites
  • Enlarged liver and spleen
  • Distended jugular veins
  • Weight gain
  • Dependent edema
  • Anorexia and complaints of GI distress

Human Disease (19 decks)

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