Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVS > Pathology > Flashcards

Pathology Flashcards

1
Q

Hypertension

A

Primary hypertension is a clinical syndrome characterized by increase in systemic arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors of hypertension

A

Non-modifiable
1. ethnic-genetic risk
2. age
3. gender

Modifiable
1. diabetes
2. overweight
3. alcohol
4. salt intake
5. combination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Classification of Hypertension & etiology

A

Primary / essential hypertension
1. genetic, familial (uncontrollable)
2. environmental (controllable)
- stress
- obesity
- smoking
- physical activity
- NaCl intake

Secondary hypertension
1. Renal: acute glomerulonephritis, chronic renal disease, renin-producing tumors, polycystic disease
2. Endocrine: Cushing syndrome, primary aldosteronism, acromegaly, pheochromocytoma
3. CVS: coarctation of aorta, increased intravascular volume
4. MISC: increased cardiac output, increased intracranial pressure, acute stress, sleep apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathogenesis of Hypertension

A

the pathogenesis of primary hypertension is still unclear

  1. genetic factors: offspring of hypertensive parents are prone to suffering from essential hypertension compared with that wihout hypertensive family
  2. sodium intake: the mechanisms leading to hypertension due to increased blood volume and the content of sodium in the smooth muscle cells enhance following subsequent calcium increase
  3. RAAS: renin - angiotensinogen - angiotensin I - angiotensin II - increase systemic arterial pressure
  4. sympathetic nervous activation: activation of sympathetic nervous can increase periphery resistance which increase systemic arterial pressure
  5. endothelial dysfunction: NO, prostacyclin, kinins ; endothelin-I, platelets, serotonin, thromboxane, angiotensin-II
  6. insulin resistance: increased absorbability to sodium, increased sympathetic nervous activation, increased cellular contents in sodium and calcium causes vascular wall hypertrophy
  7. others: obesity, alcohol, smoking, low Ca Mg K
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

malignant hypertension

A

not a type of hypertension, can complicate from both primary & secondary hypertension
BP > 200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

symptoms of hypertension

A
  1. headache: classic hypertensive headache is present on walking in the morning, situated in the occipital region of the head, radiating to the frontal area, throbbing in quality, and wears off during the course of the day
  2. epistaxis: whilst epistaxis is not associated with mild hypertension, it is much more common in moderate to severe hypertension
  3. nocturia: this is one of the most frequent clinically apparent consequences of blood pressure elevation resulting from reduction in urine-concentrating capacity
  4. others: dizziness, flushed face, fatigue, palpitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Symptoms associated with target organ damage

A
  1. CVS: dyspnea, orthopnea, LV hypertrophy, hypertensive cardiomyopathy
  2. CNS: pseudobulbar plasy, dementia, intracerebral haemorrhage, cerebral infarction, splinter haemorrhages, lacunar infarcts
  3. Renal: hematuria (malignant HTN), benign nephrosclerosis (grain-leathery kidney, hyaline arteriolosclerosis)
  4. Retinopathy: papilloedema, hypertensive retinopathy
  5. Large blood vessels: Macroangiopathy
  6. Small blood vessels: Microangiopathy
    - Hyaline arteriosclerosis
    - Hyperplastic arteriosclerosis (malignant hypertension, onion skin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypertensive retinopathy

A

Grade I: thickening of arterioles
Grade II: focal arteriolar spasms. Vein constriction
Grade III:
- Haemorrhages (flame shape)
- cotton wool spots (retinal ischemia)
- yellow hard exudates (lipid deposition)

Grade IV: papilloedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complications of HTN

A
  1. hypertensive emergencies
  2. hypertensive encephalopathy
  3. cerebrovascular disease
  4. heart failure
  5. chronic kidney disease
  6. dissection of aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Dyslipidemia

A

consequence of abnormal lipoprotein metabolism
* Elevated total cholesterol (TC) - hypercholesterolemia
* Elevated triglycerides (TG) - hypertriglyceridemia
* Elevated low-density lipoproteins (LDL)
* Decrease high-density lipoproteins (HDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Classification of hyperlipidemia

A
  1. Familial (primary): caused by genetic abnormalities
  2. Acquired (secondary): when resulting from another underlying disorder that leads to alterations in plasma lipid and lipoprotein metabolism.
  3. Hyperlipidemia may be idiopathic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Primary Hyperlipidemia etiology

A
  • single or multiple gene mutation - resulting in disturbance of LDL, HDL, triglyceride production or clearance
  • should be suspected in patients with
    1. premature heart disease
    2. family hisotry of atherosclerosis diagnosis
    3. serum cholesterol >240 mg/dl
    4. physical signs of hyperlipidemia
  • Familial hypercholesterolimia
  • Familial combined hyperlipidemia
  • Dysbetalipoproteinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Secondary hyperlipidemia causes

A
  1. Diet
  2. Hypothyroidism
  3. Nephrotic syndrome
  4. Anorexia nervosa
  5. Obstructive liver disease
  6. Obesity
  7. Diabetes mellitus
  8. Pregnancy
  9. Acute hepatitis
  10. Systemic lupus erythematousus (SLE)
  11. AIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of high LDL

A
  1. Diabetes mellitus
  2. Hypothyroidism
  3. Nephrotic syndrome
  4. Obstructive liver disease
  5. Drugs
  6. Anabolic steroids
  7. Progestins
  8. Beta-adrenergic blockers (without intrinsic sympathomimetic action)
  9. thiazides

Genetic disorders
- Monogenic familial hypercholesterolemia
- Familial defective apolipoprotein B-100 (Apo B)
- Polygenic hypercholesterolemia

Family testing to detect affected relatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of high triglyceride

A
  1. Alcoholism
  2. Diabetes mellitus
  3. Hypothyroidism
  4. Obesity
  5. Renal insufficiency
  6. Drugs
  7. Beta-adrenergic blockers (without intrinsic sympathomimetic action)
  8. Bile acid binding resins
  9. Estrogens
  10. Ticlopidine
  11. Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of low HDL

A
  1. Smoking
  2. Diabetes mellitus
  3. Hypertriglyceridemia
  4. Menopause
  5. Obesity
  6. Puberty (males)
  7. Uremia
  8. Drugs
  9. Anabolic steroids
  10. Beta-adrenergic blockers (without sympathomimetic action)
  11. Progestins
  12. Physical inactivity
17
Q

Clinical presentation of hyperlipidemia

A
  1. Premature arcus senilis: white or gray opaque ring in the corneal margin
  2. Tendon xanthomata: these are hard, nontender nodular enlargment of tendons. They are most commonly found on the knuckels and Achilles tendons
  3. Xanthelasma
18
Q

Drugs causing mild to moderate hyperlipidemia

A
  1. Beta-blockers
  2. thiazide diuretics
  3. antiretroviral drugs
  4. hormonal agents
19
Q

Investigations of hyperlipidemia

A
  1. Lipid profile
    -Total cholesterol
    -Triglyceride
    -LDL-c
    -HDL-c
    -Apolipoprotein measurement: Apo A-I, apo B-100 and Lp(a)
  2. Fasting blood glucose: exclude hyperlipidemia secondary to diabetes mellitus
  3. Renal function test: to exclude chronic kidney disease
  4. Liver function test: (transaminase) to rule out liver disease in the event of a statin having to be initiated
  5. Thyroid stimulating hormone (TSH): should be done if dyslipidemia is present, to exclude myxodema
20
Q

Complications of hyperlipidemia

A
  1. heterozygous familial hypercholesterolemia: 4 fold increased risk of CAD
  2. familial combined hyperlipidemia: increased risk of CAD, but CAD usually only presents after age of 60
  3. severe hypertriglyceridemia: pancreatitis
  4. decreased levels of serum HDL-C are also an independent risk factor for CAD
21
Q

Atherosclerosis

A

It is a specific form of arteriosclerosis affecting primarily the intima of large and medium sized muscular arteries and is characterized by fibro fatty plaque or atheromas

22
Q

Most commonly affected arteries of atherosclerosis

A

Aorta
Coronary
Cerebral arterial systems

23
Q

Risk Factors of atherosclerosis

A

Major constitutional
1. Age: fully developed lesions appear in 4th decade & beyond
2. Gender: 3 times more in men
3. Genetic Factors: hereditary genetic derangements of lipoprotein metabolism predispose individual to high blood lipid level & familial hypercholesterolemia
4. Familial-racial factors:
- Familal predisposition related to other risk factors like diabetes, hypertension & hypercholesterolemia.
- Racial differences: Blacks have generally less severe atherosclerosis than whites

**Major Acquired: **
1. Hyperlipidemia: The atherosclerotic plaque contains cholesterol and cholesterol esters largely derived from lipoproteins in the blood
2. Hypertension: mechanical injury to the arterial wall
3. Diabetes: risk of developing IHD, CVD is increased, gangrene 100 times increased
4. Smoking: reduced LDL, increased CO produces carboxy Hb & eventually hypoxia in arterial wall favouring atherosclerosis

Minor:
1. Environmental influences: developed countries higher incidence, underdeveloped countries lower prevalence
2. Obesity: increased risk
3. Hormones (oestrogen deficiency, oral contraceptives): increased developing MI & stroke
4. Physical inactivity: increased risk
5. Stressful life style: increased risk
6. Infections (herpes, pneumonia, CMV): found in atherosclerotic lesions. Infections acts in combination with some other factor
7. Homocystinuria: early atherosclerosis & CAD
8. Alcohol: controversial

24
Q

Pathogenesis of atherosclerosis

A

Reaction to injury hypothesis

  1. Endothelial injury: haemodynamic stress from hypertension, chronic hyperlipideamia
  2. Initimal smooth muscle cell proliferation: endothelial injury causes adherence, aggregation & platelet release reaction at the site of exposed subendothelial connective tissue
  3. Role of monocytes: mechanism of foam cell formation. Plasma LDL entry into intima - oxidiation (oxidized LDL - cytotoxic) - activation, attraction, imobilisation, scavenger receptor of monocytes - phagocytose LDL - foam cell
  4. Role of hyperlipidaemia: causes endothelial injury and increased endothelial permeability, increased endothelial concentration of LDL, VLDL - promotes foam cell formation
  5. Thrombosis: atheromatous lesions enlarge by attaching fibrin & cells from the blood so that thrombus becomes a part of atheromatous plaque
25
Q

Morphology of atherosclerosis

A
  1. Fatty streaks and dots: precursor lesions of atheromatous plaque
    -Gross: lesions flat / slightly elevated & yellow, form of small multiple dots or elongated beaded streaks
    -Microscopically: foam cells, lipid containing elongated smooth muscle cells, lymphoid cells, lipid, collagen, proteoglycans
  2. Gelatinous lesions: precursor lesions of atheromatous plaque, round or oval, circumscibed grey elevations
  3. Atheromatous plaques
    -Gross: white to yellowish white lesions
    -Microscopically: cholesterol cleft, fibrin, necrotic debris & lipid laden foam cells in deeper central core
  4. Complicated plaques:
    - Calcification: common in aorta & coronaries, calcium saltes are deposited around the necrotic area
    - Ulceration: layers covering the soft material of an atheroma may ulcerate as a result of haemodynamic forces or mechanical trauma. Results in discharge of emboli
    - Thrombosis: ulcerated plaques & the endothelial damage are vulnerable areas for foramtion of superimposed thrombi
    - Haemorrhage: intimal haemorrhage occur (1) blood in vascular lumen through an ulcerated plaque (2) rupture of thin walled capillaries that vascularise the atheroma from adventitial vasa vasorum
    - Aneurysmal dilatation: advanced lesions may be associated with secondar changes in media & adventitia
26
Q

What is ischaemia heart disease

A

**Acute or chronic form of cardiac disability arising from imbalance between the myocardial supply and demand for oxygenated blood. **

  • Group of closely related syndromes all due to myocardial ischaemia
  • 90% cases - Atherosclerotic Coronary Artery Disease (CAD)
  • Risk factors are same as Atherosclerosis
  • 90% of IHD patients have atherosclerosis
27
Q

Pathogenesis of IHD

A

Coronary Atherosclerosis

  • One or more than one branches may have atherosclerosis: Anterior descending left coronary is the most common branch, Right coronary, least is Circumflex branch to get affected by atherosclerosis
  • 75% or more blockage of coronary lumen usually causes chronic myocardial ischaemia.
  • Mostly the severe blockage is about 3-4 cm away from opening (coronary ostia) and near bifurcation of coronary.
  • Fixed atherosclerotic plaque in coronary are eccenteric and buldges in lumen of coronary

Superadded changes in atherosclerosis of coronary

  • Acute changes in plaque: Haemorrhage in plaque, Fissuring in plaque and Ulceration of plaque leading to thrombosis & embolism of debris of plaque or thrombus. Such acute changes occurs due to spasm of coronary, tachycardia, haemorrhage inside plaque and hypercholesterolemia.
  • Coronary thrombosis: thrombus develops on ulcerated atherpmatous plaque, lipid content of plaque is thrombogenic, and small fragment of thrombus may get dislodged and embolised and block blood supply
  • Local platelet aggregation and coronary spasm: Sometimes local aggregation of platelets on plaque may form like thrombus and block coronary. And platelets releases vasospasmodic mediators cause spasm of coronary.

Non-atherosclerotic causes
* Vasospasm (without atherosclerosis)
* Stenosis of coronary ostia (extension of syphilitic aortitis)
* Arteritis (rheumatic vasculitis, polyarteritis nodosa)
* Embolism (embolus from anywhere in body)
* Thrombotic diseases (shock, polycythemia vera, sickle cell anaemia, thrombotic thrombocytopenia purpura)
* Trauma (penetrating injury)
* Aneurysm (dissecting aneurysm of aorta)
* Compression (primary / secondary tumor)

28
Q

General pathology of myocardial ischemia

A

Functional:
- ischemic muscle ceases to contract within a few minutes. Necrosis is inhibited if flow is restored within 20-40mins

Biochemical:
- oxygen tension falls, mitochrondrial respiration declines - ceases
- fatty fuels cannot be used - anaerobic glycolysis - increased concentration of lactic acid
- limited glycogen stores - reduced intracellular ATP - concentrations reach zero in 40-60 mins
- creatinine phosphate concentration - zero in 15mins. Myosin ATPase inhibited - cessation of contraction

29
Q

IHD clinical syndrome

A
  1. Angina pectoris
  2. Myocadial infarction
  3. Chronic ischaemic heart disease & heart failure
  4. Sudden cardiac death
30
Q

Angina pectoris

A

It is clinical syndrome of ischemic heart disease resulting from transient myocardial ischemia
Angina is caused by
- paroxysmal and recurrent pain in the substernal or precardial region of chest aggravated by increased in demand of heart and relieved by decreased work load of heart
- constricting, chocking, squeezing, knifelike feeling
- transient - 15 sec to 15 mins
- No cardiac muscle cell death
- falls short of infarction

31
Q

Patterns of Angina Pectoris

A
  1. Stable (typical) angina
    -most common form
    -reduction of coronary perfusion due to chronic stenosing atherosclerosis
    -seen at times of increased demand
    -attack comes after physical or emotional stress and strain
    -relieved by rest, nitroglycerin, or other vasodilators
    -ECG shows ST segment depression
    -no elevation of enzymes (no myocardial damage)
  2. Prinzmetal or variant angina
    -caused by pain at rest
    -cause: not known may be due to sudden vasospams due to coronary atherosclerosis
    -ECG: ST segment elevation
    -respond to nitroglycerin
  3. Unstable or cresendo angina
    -pattern of pain that is progressive with increasing frequency
    -most serious pattern
    -precipitated by less effort
    -often occurs at rest
    -tends to be long duration
    -induced by disruption of atherosclerotic plaques, with superficial thrombosis, embolisation and vasospasm
    -pre infarction angina
    -ECG: non ST segment elevation
32
Q

Myocardial infarction

A

Infarction of myocardial muscle due to ischemia due coronary artery diseases

Acute coronary syndromes
1. myocardial infarction
2. unstable angina
3. sudden cardiac death

33
Q

Major risk factors for MI & coronary atherosclerosis

A
  1. DM
  2. Hypertension
  3. Dyslipidemia (familial hypercholesterolemia)
  4. Smoking
  5. Obesity
  6. Lack of adequate exercise
  7. Stress & strain
  8. Family history
34
Q

Pathogenesis of MI

A

Myocardial ischaemia
* diminished blood supply due to blockage or shock, increased myocardial demand in exercise, hypertrophy of cardiac muscles without increase in blood supply
* due to reduced or inadequate blood supply by blocked coronary. Oxygen tension in myocardium falls which causes disturbances in electrical, mechanical, and biochemical functions of myocardium, ventricular contractility is affected in ischemia area leading to disturbance in myocardial pumping action
* When ischaemia is transient it usually cause angina pectoris
* but when it remain for longer time it causes myocardial necrosis and scarring with or without clinical picture

Platelets
- rupture of plaque exposes subendocardial collagen and platelets are attached to damaged area and get activated cause aggregation and mass which leads to thrombosis or embolism.

Plaque
- acute rupture of plaque and haemorrhage usually cause acute MI

Non atherosclerotic cause
- block the blood supply in vasospasm, stenosis, arteritis, embolism, vegetative endocarditis, trauma, compression

Unexplained

35
Q

Location of myocardial infarct

A
  • Left ventricle more affected > than right ventricle
  • Left atrium is relatively protected due to oxygenated blood supply from left atrium
  • Blockage of coronary decides the region of heart involve
    • Left anterior descending artery
    • Right coronary artery
    • Left circumflex artery

CVS (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions