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Cardiovascular > Disease > Flashcards

Disease Flashcards

1
Q

Angina Pectoralis

A

Myocardial workload increases using all ATP, supply of blood and O2 falls. Switches to anaerobic metabolism that creates increased cell permeability- releasing histamine:kinin/enzymes that stimulate pain.
If blood flow not restored within 20mins then progress to MI

Chest pain from reduced coronary blood flow, temporary imbalance between supply and demand. Ischaemia caused by coronary artery spasm , partial obstruction, thrombus
O2 demand increased by exercise, thyrotoxicosis, stimulants, hyperthyroidism, emotional stress, anaemia, heart failure, ventricular hypertrophy, pulmonary disease

Three types
Stable- caused by predictable increase in work of heart (exercise)
Prinzmetal- atypical that is unpredictable often at night, caused by artery spasm

Unstable- increased frequency, severity and duration, pain unpredictable and occurs with decreased level of activity

Treat- GTN, beta blockers, calcium Channel blockers, aspirin

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2
Q

Atherosclerosis

A

Plaque formation that affects intimacy and medial layers of large and midsized arteries. Lipoproteins and fibrous tissue accumulate in arterial wall.
Attracts platelets and lipoproteins to bind to extra cellular portion of the vessel, stimulating proliferation of the vessel wall and restricts ability of vessel to dilate.
Fibrous tissue can rupture causing thrombus

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3
Q

Myocardial Ischemia

A

Type of acute coronary syndrome-Myocardial cells become ischaemic when oxygen supply is inadequate to meet metabolic demands

Can be STEMI, or NSTEMI or unstable angina

Causes-
T1- atherothrombic coronary artery disease usually precipitated by atherosclerotic plaque

T2- oxygen supply and demand mismatch (coronary dissection, emboli, vasospasm, microvascular dysfunction

T3- typical MI symptoms but death occurs before blood bio markers (troponin) can be taken

T4a- associated with percutaneous coronary intervention. Must have elevated troponin and evidence of myocardial Ischaemia

T4b- due to stent thrombosis

T5- CABG associated MI

S&S- chest pain radiating to left arm or jaw, SOB, diaphoretic, weakness, anxiety

Women, elderly and diabetics may present like reflux, dyspnoea, nausea and vomiting, palpitations, syncope

Check- heart and lungs, BP on both arms, ECG, pulses on all limbs, bloods,

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4
Q

Electrical disturbances

A 
Damage to heart tissue
Anaemia
Exercise
HT
Smoking
Fever
Medication 
Hyperthyroidism
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5
Q

Murmur

A

Diastolic (between S2&S1)

systolic (between S1&S2)

Over aortic, pulmonary, tricuspid or mitral valve

Midsystolic-aortic stenosis, pulmonary stenosis, atrial septal defect, semilunar valve disease/ hypertrophic cardiomyopathy

Holosystolic- mitral valve regurgitation, tricuspid valve regurgitation, VSD

Panstolic- AV valve disease

Late Systolic- MItral valve prolapse

Early diastolic- aortic regurgitation, pulmonary regurgitation, Austin flint

Mid/late diastolic- mitral stenosis, tricuspid stenosis

pre-systolic- mitral stenosis

Continuous- PDA

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6
Q

Systolic heart failure

A

Ventricle fails to contract adequately to eject blood

Ischaemia, infarction, cardiomyopathy, inflammation

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7
Q

Diastolic heart failure

A

Heart can’t completely relax in diastole, disrupts normal filling

Hypertrophic and cellular changes

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8
Q

Left sided heart failure

A

Increased pressure in atria/ventricle causes pulmonary congestion/decreased CO

S&S -Dizziness, syncope, dyspnoea, cough, orthopnoea, cyanosis, inspiration crackles and wheeze, S3 gallop, decreased exercise tolerance (due to increased CO and hearts reduced ability to cope with increase in blood returning to heart, afterload and tachycardia)

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9
Q

Right sided heart failure

A

Causes acute- pulmonary emboli, right ventricle MI, myocarditis, cardiac tamponade, LVAD insertion (heart not used to increased venous return to right atria and septal bowing from left ventricle remains), superior or inferior vena cava obstruction, pulmonary hypertension, ARDS, chronic lung disease

Causes chronic- myocarditis, cardiomyopathy, chronic thromboembolic pulmonary hypertension, congenital heart disease

Increased pulmonary pressure or right ventricle/atrial/tricuspid damage or impaired vena cava flow impair blood pumped to pulmonary system and can’t per fuse the lungs. Blood accumulated in systemic venous system and causes abdominal organs to congest and peripheral tissue oedema

S&S -Anorexia, nausea (GI congestion), RUQ pain due to liver enlargement, neck vein distention, dyspnoea,

Management- maintain O2 delivery to tissues (supplimental O2), monitor volume status- sodium and fluid restriction, daily wt, arrhythmia support, activity restriction, advanced therapies for refractory HF, palliative care, diuretics

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10
Q

Low output failure

A

Cardiomyopathy, CHD, HT

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11
Q

High output failure

A

Increased blood flow can’t meet O2 requirements, compensation mechanisms increase CO which increases O2 requirement that can’t be met

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12
Q

Cardiogenic pulmonary oedema

A

Causes-systolic dysfunction, diastolic dysfunction, mitral stenosis, renovascular hypertension

Left ventricle failure causes pulmonary hydrostatic pressure to rise, fluid leaks from pulmonary capillaries into interstitial tissues decreasing lung compliance and gas exchange.

As pressure increases junctions of alveoli walls are disrupted and fluid (RBC and protein molecules)enters alveoli

Treat= Morphine- anxiety and vasodilator
O2 via positive pressure
Loop diureticGTN- vasodilation

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13
Q

Rheumatic fever/RHD

A

Abnormal immune response to pharyngeal infection by group A beta haemolytic streptococci

Antigens bind to cells in heart, brain, muscle and synovial joints creating immune response. Inflammatory lesions develop on heart,joints and skin.

Can lead to carditis in myocardium, pericardium or endocardium.

Endocarditis affects valves and leaves fibrous scarring causing deformities.

Repeated attacks cause stenosis and regurgitation of valves- mostly mitral

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14
Q

Infective endocarditis

A

Inflammation of endocardium- lesions on deformed valves and tissue damages sites. Usually left side and mitral valve, IV drug users affects right side and tricuspid

Lesions create platelet/fibrin that cause bacteria to colonise, enlarge then covered by more platelets which protects bacteria from immune system defences
Scar tissue obstructs blood flow

Treat- antibiotics/ surgery

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15
Q

Myocarditis

A

Inflammation of heart muscle

Myocardial cells damaged in inflammatory response cause local swelling, infectious agents infiltrate interstitial tissue forming abscess

Treat- antibiotics, antiviral immunosuppressants, bed rest, activity restriction

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16
Q

Pericarditis

A

Inflammation caused by infectious agent or non-infectious agent (myocardial injury, uraemia, neoplasms, radiation, trauma, surgery, myxoedema, autoimmune disorders, rheumatic fever, connective tissue disease, drugs, .

Damage creates inflammatory response, mediators released cause vasodilation, hyperaemia, oedema, capillary permeability Increases allowing plasma to escape into pericardial space. WBC destroy causative factor which turns into exudate and scarring restricts cardiac function.

Complications- pericardial effusion, cardiac tamponade, chronic constrictive pericarditis

Treat- aspirin, NSAIDs, pericardiocentesis, surgery

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17
Q

Stenosis

A

Valve narrow impeding forward blood flow, atria enlarge, reduced CO and high pressures into ventricles can damage ventricles ( risk endocarditis), increases myocardial O2 requirement, workload exceeds O2, Ischaemia, chest pain

High pressures push backward and cause pulmonary oedema, pulmonary HT, ventricle failure

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18
Q

Mitral stenosis

A

Narrowing of mitral valve, obstructs blood flow in left atria.
Caused by RHD or bacterial endocarditis

Complications- atrial arrhythmia (AF), thrombi

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19
Q

Mitral regurgitation

A

Blood flows back into atria during systole, left atrium dilates to accomodate increased blood, pulling valve more open making it worse. Left ventricle dilates to accomodate increased preload and low CO

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20
Q

Mitral prolapse

A

One or more aerial valve cusps billow I to atrium during systole

Associated with marfans/ connective tissue disorders

Complications - bacterial endocarditis, heart failure, thrombi

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21
Q

Aortic stenosis

A

Obstructs blood flow from left ventricle to aorta during systole

Can be idiopathic/congenital/RHD/ degenerative

Valve decreases in size, increasing workload of left ventricle to eject blood through narrowing, ventricle hypertrophies and compliance decreases. Increased myocardial workload and O2 consumption cause myocardial Ischaemia.
Left ventricle pressure increases causing increased left atrium pressure and pulmonary oedema.

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22
Q

Aortic regurgitation

A

Allows blood to backflow into left ventricle.
Caused by RHD, congenital, infective endocarditis, chest trauma, aortic aneurysms, syphilis, marfans, chronic HT.
Impedes complete valve closure and adds blood volume to left ventricle. Increased left ventricle pressure, increases preload causing more forceful contractions and high SV. Muscle cells hypertrophy to compensate-compromises CO and increases regurgitation.
High left ventricle pressure causes high left atrial pressure leading to pulmonary congestion and eventually right heart failure

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23
Q

Tricuspid stenosis

A

Obstructs blood from right atrium to ventricle. Increase in atrial pressure enlarges atrium, ventricle SV decreases, reducing volume going to pulmonary system and left heart causing reduction in SV, tissue perfusion and CO

Usually from RHD

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24
Q

Tricuspid regurgitation

A

Stretching distorts valve, prevents closure. Right atrium enlarges causing systemic venous congestion and low CO, atrial fibrillation

Caused by left ventricle failure/pulmonary HT leading to right atrial overload

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25
Q

Pulmonary stenosis

A

Obstructs blood flow from right ventricle to pulmonary system. Right atrium and ventricle hypertrophy to compensate and heart fails when it can no longer generate adequate pressure to force blood into pulmonary vein

Usually congenital

26
Q

Pulmonary regurgitation

A

Stretch and dilated pulmonary valve cannot close causing blood flow back into ventricle. Decreased blood flow to pulmonary system.

Complication of pulmonary HT

27
Q

Cardiomyopathy

A

Dilated- heart chambers dilated and ventricle contraction is impaired, end diastolic and end systolic volumes increase and left ventricular ejection fraction is reduced decreasing CO.

Hypertrophic- decreases compliance of left ventricle and hypertrophy of ventricular muscle mass impairs ventricle filling creating small end diastolic volumes and low CO- autosomal dominant

Restrictive- rigid ventricular walls that impair filling cause decreased ventricular size elevated end diastolic pressure and decrease CO-

Caused by=Primary-idiopathic, secondary- Ischaemia, infectious disease, exposure to toxins, connective tissue disorder, metabolic disorder, nutritional deficiencies

28
Q

Coronary heart disease

A

Impaired blood flow to myocardium, accumulation of atherosclerotic plaque

Asymptomatic or leads to angina or MI, acute coronary syndrome, arrhythmia, heart failure, death

Left (anterior descending-left ventricle and septum, circumflex-lateral wall ventricle)
Right (right ventricle and posterior descending artery-posterior of heart)

29
Q

Atherosclerosis

A

Lipoprotein (cholesterol) and fibrous tissue accumulate, vessels can’t dilate properly.

Caused by inflammation, endothelial dysfunction, abnormal lipid metabolism, injury

30
Q

Acute coronary syndrome

A

Unstable cardiac Ischaemia- includes unstable angina and MI.
Blood flow acutely reduced by not fully occluded- cells get injured but acute Ischaemia.

Partial occlusion, clot formation, O2 demand mismatch, changes in patency of vessels

Treat- thrombolytics, nitrates, beta blockers, aspirin, revascularisation procedures

31
Q

Myocardial infarction

A

Necrosis of myocardial cells due to demand higher than metabolic needs.
Atherosclerotic plaque forms lesions. Stable lesions gradually occlude vessel (angina), unstable prone to rupture/ thrombus formation leads to MI. Anaerobic metabolism leads to cellular acidosis, electrolyte imbalance, hormones released that affect impulse conduction and myocardial contractility causing arrhythmias, myocardial contractility decreases, reduced SV, CO, BP and tissue perfusion
Blood to cells completely blocked leads to prolonged Ischaemia (25-40min) =irreversible
Starts in subendocardium, then epicardium 1-6hrs, when all myocardium involved = transmural infarction (significant Qwave)

Described by damage area of heart ( anterior, lateral, right ventricular, inferior, posterior

Metabolic demands affected by

  1. Coronary perfusion (plaque, narrowed vessels, hypotension, vessel spasm)
  2. Myocardial workload ( HR, preload, afterload, contractility)

Treat- code blue, aspirin, defibrillation, thrombolytics, antiarrhythmic, analgesia/morphine, GTN, beta blockers, ACE inhibitors, high flow O2, revascular procedures

32
Q

Sinus node arrhythmia

A

Sinus arrhythmia- rate varies with respiration- irregular, increases with inspiration, descreases with expiration- digoxin toxicity, increases vagal tone, morphine

Sinus tachycardia- rate >100, SNS stimulation or blocked vagal activity- anything that increases O2 demand (hypoxia, exercise, hyperthyroidism, anxiety, fear, hypovolaemia, MI, cardiogenic shock, PE, caffeine, adrenaline.

Sinus bradycardia- rate <60. Increased vagal activity or depressed automaticity due to injury/ ischaemia to SA node, pain, increases intracranial pressure, sinus node disease, AMI, hypothermia, acidosis.

Sick sinus syndrome- sinus node disease or dysfunction. Caused by injury to sinus tissue, fibrosis of conduction fibres with age, digoxin/beta blockers/calcium channel blockers. ECG changes are- sinus Brady, sinus pauses, atrial tachy, atrial fibrillation, atrial flutter

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

33
Q

Supraventricular arrythmmias

A

Premature atrial contraction- atrial ectopic beat that occurs earlier than the next expected beat- caused by strong emotion, excessive alcohol, tobacco, stimulants, MI, heart failure, hypoxaemia, PE, digoxin toxicity, electrolyte imbalance. P wave is abnormal, QRS is narrow, occasional miss or QRS

Paroxysmal superventricular tachycardia- sudden onset and termination. Impulse re-enters AV node Over and over. Affects ventricle filling and CO decreases affecting coronary artery perfusion. Caused by SNS stressors, fever, sepsis, hyperthyroid, MI, RHD, myocarditis, acute pericarditis, wolf parkinson white.

Atrial flutter- intra-atrial reentry. Caused by SNS stimulation- anxiety, caffeine, alcohol, thyrotoxicosis, CHD, MI, PE, WPW, RHD. Two types:
Type 1- rate 240-340 right atrium
Type 2- rate 350.
Picket fence P wave, ventricle rate rarely greater than 150-175. 2:1/4:1/6:1 ratio atria-ventricle. T wave usually hidden by overriding F wave, inverted QRS

Atrial fibrillation- multiple small re-entry circuits in atria, atrial cells can’t repolarise in time to respond to next stimuli. Irregular ventricle response, associated with heart failure, RHD, CHD, HT, hyperthyroid. P waves to fast to see, irregular QRS

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

34
Q

Junctional arrhythmia

A

AV node/ bundle branches

Response to failure of higher pacemaker, retrograde conduction where impulse goes back up to atria. ECG=inverted P wave, marrow QRS, potentially no P wave.
Caused by drug toxicity, hypoxemia, hyperkalaemia, increased vagal tone, damage to AV node, MI, heart failure

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

35
Q

Ventricular arrhythmia

A

Premature ventricular contractions- ectopic ventricle beats, don’t reset atrial rhythm and followed by full compensatory pause.results from enhanced autonomicity, or re-entry phenomenon.
Caused by anxiety, stress, Tobacco, alcohol, caffeine, hypoxia, acidosis, electrolyte imbalance, sympathomimetic drugs, CHd, heart failure, mechanical stimulation of the heart (catheterisation), reperfusion after thrombolytics therapy.
ECG- isolates/coupled/ triplet/ bigwmany/ trigeminal, high QRS and inverted T with Premature ventricular contraction (PVC).

Warning signs for person with acute heart disease:
PVC develops within 4 hours of MI
Frequent PVC (>6/min)
Couplets/triplets
Multi focal PVC
R on T phenomenon

In people without heart disease presents a skipping a beat, with heart disease indicates drug toxicity.

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

36
Q

Ventricular tachycardia

A

Rapid ventricle rhythm defined as three or more PVC. Rate >100 and regular.
Associated with valve disease, RHD, cardiomyopathy, anorexia, metabolic disorder, drug toxicity.

Torsades de pointes- type of VT associated with long QT, may be genetic or acquired (electrolyte imbalance, MI, cocaine use, liquid protein diets, medications).

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

37
Q

Ventricular fibrillation

A

Extremely rapid, chaotic ventricular depolarisation. Ventricles quiver and cease contracting- cardiac arrest.
Triggered by severe MI, digoxin toxicity, metabolic acidosis, repercussions. Therapy, antiarrhythmic drugs, hypokalaemia, hyperkalaemia, hypothermia, mechanical stimulation, electrical shock.

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

38
Q

Atrioventricular conduction blocks

A

First degree- benign conduction delay. Injury to AV node. ECG PR interval >0.20

Second degree- failure to conduct one or more impulses from atria to ventricle
Type 1- (mobitz/wenckenach phenomenon)- increased AV conduction until one fails to conduct to ventricles. ECG PR interval progressively lengthens toll drops QRS.
Type 2- (mobitz 2)- intermittent failure of AV node to conduct to ventricle. ECG p waves consistent then QRS is dropped, HIS purkinje delayed so widened QRS

Third degree- atrial impulses are completely blocked. Atria and ventricles are controlled by independent pacemakers. ECG- QRS depends on where location of pacemaker- QRS wide and rare slow if from distal you bundle of HIS.
Associated with inferior/ante rose petal MI, congenital conditions, acute/degenerative cardiac disease, drugs, electrolyte imbalance.

AV dissociation- complete dissociation of atrial and ventricle rhythm. Primary factors leading to this are severe sinus Brady and lower pacemaker (junctional or ventricular) that competes with normal sinus rhythm.
Associated with MI, cardiac surgery, drugs

Treat- antiarrhythmic, sympathomometics (adrenaline), anticholinergics (atropine), counter shock, synchronised cardioversion (direct electrical current synchronised with heart rhythm), defibrillation, pacemaker therapy, implantable cardioverter-defibrillator, cardiac mapping and catheter ablation

39
Q

Sudden cardiac death

A

Cardiac causes- reperfusion, CHD, myocardial hypertrophy, cardiomyopathy, inflammatory myocardial disorders, valve disorders, primary electrical disorders, dissecting or ruptured aortic/ventricular aneurysm, cardiac drug toxicity

Non cardiac causes- PE, cerebral haemorrhage, autonomic dysfunction, chocking, electric shock, electrolyte: acid-base imbalance

40
Q

Hypertension

A

Caused by excess SNS overstimulation of A&B adrenergic receptors, altered function of renin-angiotensin system, other chemical mediators of vasomotor tone (ANP), interaction between insulin resistance- excess insulin creates sodium retention, increases SNS activity, hypertrophy of vascular muscle, changes on ion transport across cell membrane

Complications- heart failure, MI, CHD, renal failure, neurological conditions, accelerated atherosclerosis, micro aneurysm, stroke.

41
Q

Secondary hypertension

A

Elevated BP with identifiable underlying process- kidney disease, coarctation of the aorta, endocrine disorders (adrenal), neurological disorders (intracranial pressure), drug use, pregnancy

42
Q

Aortic aneurysms

A

Abnormal dilation of a blood vessel, commonly at a site of weakness or tear in the vessel wall. Mostly caused by atherosclerosis, HT, arteriosclerosis, trauma.
Loss of elasticity results in dilation, loss of collagen results in rupture

Thoracic- due to arteriosclerosis, HT, trauma, syphillis, fungal infections and marfans

Abdominal- arteriosclerosis, HT, age, smoking

Popliteal/femoral- arteriosclerosis

Aortic dissection- life threatening tear in intima leaking into media.
Type A- ascending aorta
Type B- descending aorta
Due to HT, male, age, pregnancy, congenital defects
Dissection along length of vessel, can prevent valves from closing, occlude branches of aorta

Treat- beta blockers, sodium nitroprusside (IV antihypertensive), anticoagulant, surgery (endovascular aneurysm repair)

43
Q

Peripheral vascular disease

A

Impaired blood supply to peripheral tissues.
Arteriosclerosis is the most common chronic arterial disorder (thickening, loss of elasticity and calcification of arterial walls

Complications- gangrene, rupture of aneurysm, infection, sepsis, extremity amputation

Treat- aspirin (reduce risk of thrombosis), cilostazol (platelet inhibitor/vasodilator), pentoxifylline (decreases blood viscosity and RBC flexibility), revascularisation- PTA stent, atherectomy

44
Q

Acute arterial occlusion

A

Development of thrombus or embolism, blood flow to tissues is impaired resulting in acute tissue Ischaemia and risk of necrosis/gangrene

Arterial thrombus- blood clot adhered to vessel wall
Arterial emboli- sudden obstruction of debris ( part of clot, plaque, bacteria, cancer cells, amniotic fluid, air bubbles, bone marrow fat)
Often from left side of heart and lodge in carotid artery causing neurological deficits.

Treatment- anticoagulant, intra-arterial finrinolytic therapy using streptokinase, urokinase, tissue plasminogen activator (t-PA), surgery (embolectomy).

45
Q

Thromboangiitis obliterans (burrgers disease)

A

Occlusive vascular disease where small and midsized arteries become inflamed and spastic causing clots to form.
Inflammatory cells infiltrate wall of artery in hands and feet, thrombus forms and vasospasms of arterial segments impair blood flow, as disease progresses arteries become scarred and fibrotic

Caused by smoking, more relevant in asians and Eastern Europeans

46
Q

Raynauds

A

Intense vasospasm in small arteries and arterioles of fingers and toes.

No identifiable cause, Raynaud’s phenomenon occurs secondary to other disease, other known causes of vasospasm or long term exposure to cold or machinery. Mainly affects women 20-40

Treat- vasodilator, calcium Channel blockers, a-adrenergic blocker prasozin, GTN, keep hands warm, stop smoking, stress reduction measures

47
Q

Venous thrombosis

A

Blood clot forms on wall of vein, accompanied by inflammation and some degree of obstruction
Trauma stimulates platelet aggregation, clot forms and fibrin mesh covers, grows and tenderness and swelling start at site. Fibroblasts eventually invade thrombus scarring vein wall and destroying venous valves

Superficial or deep
Associated with immobilisation, surgery, trauma, cancer, pregnancy, hormone therapy, coagulation disorders
Three factors influence: stasis of blood, vessel damage, increased blood coagulopathy
Superficial- due to venous catheters/infusions, May develop in conjunction with thromboangiitis obliterans, various veins, DVT.
Complications- PE

Treatment- prophylaxis-anticoagulant, elevate foot of bed with knees bent, early mobilisation.
Finrinolytic drugs, NSAIDS, warm compress, extremity rest, TEDS, surgery (venous thromboectomy), insertion of filter to catch thrombi

48
Q

Chronic venous insufficiency

A

Post DVT large veins may remain occluded increasing pressure on other veins. Increased pressure distends veins, separating valves and impairing ability to close. Results in impaired unidirectional blood flow and deep vein emptying. Venous blood pools in lower limbs, pressure increases and starts to impair arterial circulation to lower extremities. Ability to provide O2 and nutrients and remove waste diminished, eventually cells die, skin atrophies, and fat deposits necrose-forming ulcers
Cause- DVT, leg trauma, various veins

Treat- wet compress of boric acid, buffered aluminium acetate, isotonic saline, topical corticosteroids, bed rest, anti fungal, topical antibiotics

49
Q

Varigous veins

A

Irregular tortuous veins with incomplete valves.
Long standing increases pressure and stretches venous walls which inhibit valves from closing and they become incompetent

Cause- genetic, white race, standing jobs, obesity, venous thrombosis, pregnancy

Complications- venous insufficiency, stasis ulcers, stasis dermatitis, SVT

Treat- TEDS, daily walking, leg elevation, compression sclerotherapy, surgery

50
Q

Lymphadenopathy/ lymphangitis

A

Enlarged lymph nodes, usually from inflammatory process

Inflammation of lymph vessels draining an infected area of body

51
Q

Lymphoedema

A

Primary or secondary disorder from inflammation, obstruction, or removal of lymphatic vessels.
Obstruction of lymph drainage prevents fluid and protein molecules from interstitial tissues from returning to the circulation. Protein molecules increase osmotic pressure in interstitial tissues, drawing in additional fluid that causes oedema in soft tissues.

Begins distally then progresses upward, starts as soft and putting oedema then becomes fibrotic, thick, rough and woody texture.

Treat- skin and foot care, exercise, leg elevation, TEDS, antibiotics, diuretics, surgery

52
Q

Blood transfusion

A

Side effects-

  • ABO incompatibility- agglutination (clumping) or RBC blocks capillaries resulting in Ischaemia and macrophages engulf RBC leading to increased free haemoglobin circulating that travels to kidneys to remove and may block renal tubules leading to renal failure
  • febrile reaction- antibodies attack WBC causing febrile and chills
  • hypersensitivity- antibodies react against protein (immunoglobulin A)
53
Q

Shock

A

Causes- insufficient CO, insufficient blood volume, compromised vascular system not allowing blood to flow, tissues that are unable to extract and use O2

Stages-
1- early- baroreceptors and chemoreceptors detect sustained drop in MAP of less than 10mmHg from normal levels (can be blood loss <500mls). SNS compensates with pulse rate slightly elevated and increased force of contraction, peripheral vasoconstriction (increasing SVR)
- compensatory mechanisms start after a MAP fall of 10-15 or 25-35% blood loss
- stimulation of SNS to release adrenaline/nor-adrenaline that stimulate alpha and beta adrenergic fibres. Alpha causes vasodilation in heart, skeletal, respiratory (increases resp rate)
- renin angiotensin released as blood flow to kidneys reduced and stimulates uptake of water and sodium and to release potassium- increasing BP and volume
-hypothalamus releases adrenocorticotrophic hormone causing aldosterone release
- posterior pituitary release ADH to conserve water
-decreased capillary hydrostatic pressure causes a fluid shift from interstitial space to capillaries
-compensation can only continue for a short time. If treated- no permanent damage

Stage 2- (intermediate)- MAP decreases 20mmHg and fluid loss of 35-50% (1800-2500mls)

  • compensation continues but not able to maintain MAP at a level sufficient to maintain organ perfusion
  • vasoconstriction now limits blood flow to tissues and cells become oxygen deficient
  • cells switch to anaerobic metabolism which produces lactic acid
  • lack of energy forces potassium out of cell and sodium and water move in
  • cells swell and cell membrane integrity is lost and damage occurs which releases enzymes that damage remaining cells
  • lactic acid dilates precapillary arterioles and constricts post capillary venules which causes increased hydrostatic pressure within capillary and fluid shifts back to interstitial space
  • capillaries become permeable to proteins allowing them to move into interstitial space and more fluid moves out of capillaries
  • cells in the heart and brain become hypoxic while other body cells become Ischaemic
  • state of acidosis and hyperkalaemia ensues
  • if not treated chances of survival are poor

Stage 3- (refractory)- tissue anoxia and cellular death so widespread that damage is irreversible and death occurs

System effects of shock:

Cardio- early-tachycardia, increased BP, weak/thready pulse. Late- MAP <60, hypotension, non-palpable peripheral pulses, cardiac arrhythmias (from acidosis, hypoxia and hyperkalaemia damaging electrical system and contractility)
Respiratory- increased resp rate, decreased O2, increased CO2, respiratory acidosis, ARDS (damage from hypoxia creates water into cells and pulmonary oedema)
GI- reduces blood flow constricts splenic artery and redirects blood to brain/heart so no blood goes to GI. Paralytic ileus, ulceration of GI, permeability allows bacteria to travel into abdomen and may cause sepsis
Hepatic- early- glucogeneisis (forming glucose from no -carbs) and glycogenolysis (converting glycogen-glucose) increases= hyperglycaemia. Late= hypoglycaemia, metabolism of fat/protein impaired so liver cannot remove lactic acid and causes metabolic acidosis
Neurological- altered LOC, restless, cerebral oedema, decreased sympathetic activity (systemic vasodilation and pooling of blood in peripheries)
Renal- decreased GFR, oliguria, renal failure
Skin- cool/pale/clammy, temperature-decreased, thirst- increased

Diagnosis- FBE, BUN, ABG, electrolytes, blood cultures, WBC, serum cardiac enzymes

Treat- fluids (crystalloids-goes into interstitial and vein =hartmanns/N-Saline/CSL
Colloid-keeps in vein=albumin, gelofusion, plasma protein), vasoactive drugs (adrenaline-constrict/GTN-dilate), inotropic- dopamine (improve cardiac contractility), sodium bicarb, antihistamines, antibiotics, steroids, morphine (dilates vein/decrease anxiety), O2

54
Q

Hypovolaemic shock

A

Decrease in volume by >15%

S&S-
initial- decrease in BP, tachycardia, normal resp rate, cool/pale (periphery), alert, urine slightly decreased, thirst
Compensatory stage- hypotension, pulse rapid/thready, increased resp rate, cool/pale (trunk), poor turgor, restless/anxious/confused, oliguria, thirst, acidosis, hyperkalaemia
Irreversible- severe hypotension, weak/rapid/thready pulse, resp rapid/shallow/crackles, disorientated, anuria, loss of reflexes and peripheral pulses

55
Q

Cardiogenic shock (pumping failure)

A

Hearts pumping ability is compromised (MI, cardiac tamponade, restrictive pericarditis, cardiac arrest, arrhythmias, cardiomyopathy, electrolyte imbalances, drugs, head injury)

S&S- hypotension, rapid/thready pulse, distension of veins on hands/neck, resp rate increased, crackles, pulmonary oedema, pale/cyanotic/cold, oliguria, restless, anxious, dependant oedema

56
Q

Distributive shock (septic)

A

Begins with septicaemia and as pathogens are destroyed their ruptured cell membranes allow endotoxins to leak into plasma and trigger immune and inflammatory response. Endotoxins damage blood vessels and stimulate activation of vasoactive proteins and coagulation factors. This causes clots and peripheral vasodilation. Increased permeability causes a fluid shift into interstitial space and hypovolaemia results

S&S-
Early- hypotension, rapid/thready pulse, rapid/deep resps, warm/flushed skin, alert, urine normal, fever/chills
Late- hypotension, tachycardia, arrhythmias, rapid/shallow resps, cool/pale/oedematous skin, lethargic/coma, oliguria, normal to decrease temp, DIC

57
Q

Obstructive shock

A

Cardiac tamponade, PE , tension pneumothorax

58
Q

Distributive shock- neurogenic

A

Imbalance of PNS and SNS (head injury, trauma to spinal cord, insulin reactions, CNS depressant drugs, anaesthesia, severe pain, prolonged exposure to heat)

S&S- bradycardia then tachycardia, MAP falls, hypotension, pulse slow and bounding, skin warm/dry then cool, anxious, restless, oliguria, low temp

59
Q

Distributive shock- anaphylaxis

A

Widespread hypersensitive reaction in the body produces immunoglobulin E antibodies. Large amounts of histamine and vasoactive substances released causing vasodilation and increased cell permeability, construction of smooth muscle

S&S- hypotension, tachycardia, arrhythmias, dyspnoea, stridor, wheeze, pulmonary oedema, warm/oedematous skin, restless, anxious, oliguria, parasthesia, pruritus, abdominal cramps

60
Q

Decompensating heart failure

A

Causes- coronary artery disease (coronary syndrome, MI, ventricle septal rupture), myocarditis, acute valve syndromes (mitral/aortic regurgitation, thrombosed mitral/aortic valve, tear or perforation mitral/aortic valve), progressive valve disease, cardiomyopathy, poorly controlled HT

S&S -
Mild-moderate ADHF- progressive dyspnoea, abdominal/peripheral congestion (leg swelling, epigastric tenderness from hepatic congestion), nocturia, confusion, headaches, insomnia, anxiety, disorientation, impaired memory, elevated JVP, diminished air entry at bases of lung (usually from pleural effusion), murmur, cardiomegaly

Hypertensive ADHF- BP>140, minimal weight gain

ADHF with severe pulmonary oedema- sudden overwhelming sense of suffocation, extreme anxiety, cough, expectorate pink frothy liquid, sits bolt upright, not speaking in full sentences, tachypnoeic, nasal flaring, use of accessory muscles, sweating, cool skin, cyanotic, tachycardia (increased adrenergic drive), O2 less than 90%, course airway sounds, 3rd or 4th heart sound, cardiomegaly

ADHF Cardiogenic shock- BP <90, fatigue, altered mental state, tachypnoeic at rest, tachycardia, cool cyanotic peripheries with poor cap refill, diminished pulse pressure

ADHF high output- warm extremities, pulmonary congestion, tachycardia, wide pulse pressure

Diagnosis- ECG, chest X-ray, cardiac enzymes (troponin), BNP/ANP, echo, ABG, electrolytes, BUN, serum creatinine, bicarb, FBE

61
Q

Transcatheter aortic valve implantation (TAVI)

A

Complications- emboli, AKI (contrast use), MI, coronary artery blockage, valve displacement, aortic dissection/perforation, valve perforation, arrhythmias, bleeding, annular rupture, stroke, AF, tamponade, hypotension and cardiogenic shock

Long term complications- valve regurgitation, valve obstruction, infective endocarditis, thrombus, death, bleeding

62
Q

Chest pain

A

Causes-

Cardiac- MI, pericarditis, myocarditis, cardiac tamponade, aortic dissection, arrhythmias, heart failure, cardiomyopathy, angina

Pulmonary- PE, tension pneumothorax, pneumonia, lung cancer, COPD, pleural effusion, pulmonary sarcoidosis, pulmonary hypertension

Other- esophageal rupture, heart burn, sickle cell anaemia, esophagitis, hiatal hernia, pancreatitis, cholecystitis, biliary colic, musculoskeletal, rib fractures, trauma, anxiety/panic attacks

Cardiovascular (6 decks)

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