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Clinical Therapeutics 2 > Week 6 - Cardiovascular > Flashcards

Week 6 - Cardiovascular Flashcards

1
Q

Acute Pericarditis

A
  • Pericardium (inflammation of the outer layer of the heart) roughened, possible exudate
  • Sudden chest pain
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2
Q

Pericardial Effusion

A
  • Accumulation of fluid in pericardial cavity
  • Compression of heart may cause cardiac tamponade
  • Treated by pericardiocentesis (aspiration of fluid from the pericardial space)
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3
Q

Constrictive Pericarditis

A
  • Chronic inflammation of the pericardium with thickening, scarring, and muscle tightening.
  • Visceral and parietal layers adhere obliterating the pericardial cavity
  • Compress the heart CO (down)
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4
Q

Aortic stenosis

A
  • Diminishes blood from LV into aorta

* Result in ischemia, arrhythmias and heart failure

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5
Q

Mitral stenosis

A
  • Impaired blood flow from the LEFT atrium to the LEFT ventricle
  • Valve leaflets become and fibrous and fuse, chordae tendineae shorten
  • Atrial arrhythmias and thromboemboli
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6
Q

Aortic regurgitation

A
  • Inability of the aortic valve leaflets to close properly during diastole
  • Backflow of blood into LV causes it to dilate and hypertrophy
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7
Q

Mitral regurgitation

A
  • Backflow of blood into LA causes atrium to dilate, LA pressure
  • LV dilate and hypertrophy to maintain CO
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8
Q

Mitral valve prolapse syndrome

A
  • Valve cusps billow upward into atrium

* Replace with porcine or mechanical valve

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9
Q

Infective Endocarditis

A
  • Inflammation of the endocardium
  • Agents; Bacteria (staph or strep), viruses, fungi, and parasites in blood
  • Endothelium damaged (valves)
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10
Q

Disorders of the Arteries: Arteriosclerosis

A
  • Chronic disease with abnormal thickening and hardening of arterial walls
  • Smooth muscle cells and collagen migrate into Tunica intimata
  • Decreased elasticity
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11
Q

Disorders of the Arteries: Atherosclerosis

A

 Form of arteriosclerosis caused by accumulation of lipid-laden macrophages
 Results in plaque formation
 Is the main cause of CAD and CVA
 ½ deaths of western world
 Inflammatory disease initiated by injury to endothelium
 Injury from smoking, hypertension, diabetes,  LDL,  HDL, chronic infection

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12
Q

Atherosclerosis

A

 Clinical Manifestations
 Symptoms associated with inadequate perfusion of tissue
 Transient (intermittent claudication) or permanent
 Diffuse atherosclerosis will elevate systemic resistance and cause hypertension
 Major cause of MI and CVA

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13
Q

Evaluation and treatment of Atherosclerosis

A

 Reduction of risks
 Diet (most important contributor)
 Drugs can stabilise plaque before rupture (i.e. Aspirin: antithrombotic)

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14
Q

Aneurysm

A

 Localised dilation or out pocketing of a vessel wall or cardiac chamber
 Once initiated aneurysm grows bigger as tension in the vessel wall increases
 Can exert pressure on surrounding organs, rupture or dissect

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15
Q

Causes of an Aneurysm

A

 Atherosclerotic plaque erode and weakens tunica media
 Syphilis and other infections
 Chronic hypertension (50% of AAA)
 Marfans – inherited collagen vascular disease causes thoracic aortic aneurysm

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16
Q

True Aneurysm

A

* Involves all 3 tunica layers

Fusiform – entire circumference of vessel
Saccular – part of circumference, saclike

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17
Q

False Aneurysm

A
  • Initiated by break in tunica intima only
  • Extravascular haematoma as a result of graft leakage
  • Dissecting, saccular – blood entry causes longitudinal separation of vessel wall to form a blood-filled channel
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18
Q

Common sites of aneurysms

A
  • Aorta particularly susceptible

* Post infarct – stretching of non contractile muscle in heart

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19
Q

Clinical Manifestations

A

 Related to pressure on surrounding organs
 Most AAA asymptomatic
 Pulsating mass, calcified mass
 Pain is mild to severe mid-abdominal, lumbar or back region
 Stasis of blood favors thrombus and peripheral emboli

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20
Q

Dissecting Aneurysm

A

 Abrupt excruciating tearing pain
 Chest pain suggests ascending aorta; back pain descending aorta
 Dissection can be a life-threatening situation upon rupture

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21
Q

Dissecting Aneurysm Treatment

A

Risk of death depends on site of dissection
 Ascending aorta (type A) usually requires surgical repair with Dacron graft
 Descending thoracic aorta (type B) may be medically managed by aggressive control of BP and HR while aorta heals
 Once healed surgery may not be required

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22
Q

Intermittent claudication

A 
	Leg pain on ambulation due to atherosclerosis of iliofemoral arteries
	Dopplers to determine blood flow
	Vasodilators and antithrombotics
	Exercise rehabilitation
	Surgery
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23
Q

Thromboangiitis obliterans (Buerger Disease)

A
  • Inflammatory disease in male heavy smokers
  • Obliteration of arteries in hands and feet
     Pain, tenderness, Reynaud’s Phenomenon, cyanosis, redness and ulcers
     Gangrene
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24
Q

Reynaud’s Phenomenon and Disease

A

 Bilateral spasm in arteries and arterioles of hands
 Skin color and sensation changes
 Prolonged attacks affect cell metabolism in hands
 May be secondary to systemic disease i.e. scleroderma (excessive collagen deposition), smoking, exposure to cold or vibrating machinery
 Triggered by brief exposure to cold
 Common in young females
 Cause unknown

25
Q

Varicose veins

A

* A vein in which blood has pooled
 Distended, tortuous, and palpable veins
 Caused by incompetent vein valve(s) and/or weakening of leg vein wall (collagen level)
 Effects saphenous veins and perforating veins

26
Q

Risk factors for Varicose Veins

A

* Genetics, age, gender, race, pregnancy (any hormone changes), obesity, diet, prolonged standing or sitting

27
Q

Signs and symptoms of Varicose Veins

A

* Enlarged veins, leg swelling, painful legs, itchy legs, skin discolouration, thrombophlebitis

28
Q

Treatment for Varicose Veins

A
  • Self-care measures – leg exercises, support stockings, avoid high heels, avoid long periods of sitting or standing, elevate legs
  • Medical or surgical – remove or close off varicose vein i.e. sclerotherpy, laser, ambulatory phlebectomy, vein ligation and stripping
29
Q

DVT

A
  • Accumulation of clotting factors and platelets in deep leg vein

 Promoting factors
 Venous stasis (immobility, age, CHF)
 Venous endothelial damage (trauma)
 Hypercoagulable states (pregnancy, hormone replacement)

30
Q

Thrombus

A
  • Blood clot that remains attached to vessel wall
     Develops where conditions promote activation of platelets and coagulation cascade
     Intimal irritation and roughening (atherosclerosis)
     Inflammation
     Infection
     Blood stasis (economy flights, aneurysms, phlebitis)
     Trauma
     Calcified areas or bacterial vegetations on heart valves
31
Q

Treatment for Thrombus

A
  • Anticoagulants to stop further growth of thrombus (Heparin or Warfarin)
     Aspirin (antiprostaglandin) blocks platelet aggregation and platelet plug formation
     IV and Intra-arterial Streptokinase to dissolve clot
     Balloon-tipped catheter can pull thrombus out
32
Q

Embolus

A 
	A bolus of matter circulating in blood
	Thromboemboli
	Air bubble (IV line or chest trauma)
	Aggregate of amniotic fluid
	Foreign substance (IV line or trauma)
	Aggregate of fat (long bone trauma)
	Bacteria (SBE)
	Cancer cells
33
Q

Hypertension

A
  • Sustained elevation of systemic arterial BP;
     Systolic > 120 mmHg Diastolic > 90 mmHg
     Sustained diastolic pressure can lead to CHF, infarction, end-organ damage
34
Q

Types of Hypertension

A
  • Primary – 90-95 % are of unknown origin
  • Secondary – due to a primary disease
  • Isolated systolic – elevated systolic and normal diastolic
35
Q

Factors associated with Primary Hypertension

A

 Family History
 Gender and Age
 Black race
 High sodium intake
 Low intake of potassium, calcium, or magnesium,
 Diabetes mellitus
 Smoking and obesity
 Heavy alcohol consumption
 Pathophysiology
 Genetic susceptibility and environmental factors cause neurohumoral dysfunction, inflammation and insulin resistance
 Causes  peripheral resistance and  blood volume

36
Q

Secondary Hypertension

A
  • Systemic disease process which CO and PR
- Renal
- Endocrine
- Vascular
- Pregnancy 
- Drugs 
	
Fix or remove disease and BP resolves
37
Q

Complicated Hypertension

A
  • Chronic damage to systemic blood vessels
  • Hypertrophy and hyperplasia of smooth muscle cells in arterial walls with associated fibrosis leads to ‘vascular remodeling’
  • Results in reduced blood flow and organ dysfunction
38
Q

Malignant Hypertension

A

* Hypertensive emergency where diastolic > 140 mmHg.

* Can cause encephalopathy (cerebral oedema)

39
Q

Preeclampsia or toxemia

A

 After 24th week of pregnancy
 Occurs in 6% of pregnancies, risk ^ age
 Acute hypertension, proteinuria and oedema
 Affects metabolism, renal function, CNS, fluid, electrolyte imbalance and may result in eclampsia (convulsions/coma)
 Cause unknown
 Resolves with birth of baby

40
Q

Antihypertensive drugs

A

 Beta blockers
 Atenolol, Metoprolol

 Diuretics
 Hydrochlorothiazide, Spironolactone

 ACE inhibitors
 Captopril

 Calcium channel blockers
 Nifedipine, etc

 Centrally-acting drugs
 Clonidine

 Vasodilators
 Hydralazine

41
Q

ACE Inhibitors

A

 Angiotensinogen is produced constantly by the liver
 Low renal blood flow (low BP), low sodium and/or potassium levels and β-adrenergic stimulation (adrenaline type stimulation) all cause renin release from juxtaglomerular cells in the kidneys
 Renin converts Angiotensinogen to Angiotensin I
 ACE, produced constantly in the lungs, converts Angiotensin I to Angiotensin II
 Angiotensin II effects aldosterone secretion, smooth muscle constriction, Na+ and water retention
 ACE inhibitors prevent conversion of Angiotensin I to Angiotensin II
 End Results:
 Decrease fluid retention, afterload
 Example: Captopril

42
Q

Captopril

A 
Indication
	Hypertension, heart failure
Adverse Effects 
	Hypotension, angioedema (head, neck, intestinal), hyperkalaemia, proteinuria, cough; GI upset
Practice points
	Give small test dose
	Monitor serum electrolytes
43
Q

Postural/Orthostatic Hypotension

A

 Drop of 20 mmHg systolic BP or 10 mmHg diastolic BP within 3 minutes of standing
 Vasodilation and blood pooling in muscles, spleen and kidneys
 Results in dizziness and blurred vision

44
Q

Acute Hypotension

A

 Sympathetic vasoconstriction mechanisms sluggish
 30 to 50% of elderly, pregnancy and immobility (venous pooling)
 Circulatory shock

45
Q

Chronic Hypotension

A

Secondary to disease or poor nutrition

46
Q

Treatment for Idiopathic Hypotension

A 
	Liberalization of salt intake
	Raise head of bed
	Slower position changes
	Support stockings
	Volume expansion 
	Vasoconstrictors
47
Q

Dyslipidaemia

A

The Problem:

  • High serum levels of cholesterol- and/or triacylglycerol molecules
  • Thought to contribute to atherosclerotic disease

 Solutions:
 Decrease lipoprotein synthesis (bile acid binders)
 Increase lipoprotein catabolism (fibrates)
 Increase cholesterol removal (statins)

48
Q

Niacin

A

Inhibits lipolysis in fat cells

49
Q

Acute Rheumatic Fever and Rheumatic heart disease

A
  • Inflammation of joints, skin, nervous system and heart

* Treatment - antibiotics - 9 days

50
Q

Infective Endocarditis

A
  • inflammation of the endocardium (inside lining of the heart)
  • Treatment - 4-6 weeks antibiotics/ repair or replacement surgery
51
Q

Dissecting Aneurysm

A
  • Abrupt excruciating tearing pain
52
Q

Dyslipidaemia

A
  • high levels of cholesterol/ triacylglycerol molecules
53
Q

Simvastatin

A

Inhibit liver enzymes

54
Q

Colestipol

A

Binds to bile salts

55
Q

Statins

A
  • Lower the rate of cholesterol production

Adverse E: Stomach cramps, muscle/joint pain, rash, nausea and vomiting and constipation
* Hepatitis

  • More effective at night
  • Short half lives, once daily admin
56
Q

Heparin

A

Occurs naturally in the body

Prevents fibrin clot

57
Q

Warfarin

A

Antagonist to Vit K

Reversed with Vit K

58
Q

Thrombolytics

A
  • Given to dissolve thrombi
59
Q

Abdominal Aortic Aneurism

A

Enlarged area of the lower part of the aorta

Types:
o Ascending: present with chest pain and require surgical correction
o Descending aorta: presents with back pain. Can be managed by medication to stabilise BP and HR.

Clinical Therapeutics 2 (9 decks)

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