Brainscape's Knowledge GenomeTM

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


See full index

Pathology > CVS ll > Flashcards

CVS ll Flashcards

1
Q

Dyslipidemia is aka?

A

Hyperlipidaemia

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

causes of Primary Dylipideaemia

A

1) Primary (Genetic): Single or multiple gene
mutations that result in:
* Either overproduction or defective clearance
of Triglycerides and LDL Cholesterol
* Or underproduction or excessive clearance of
HDL

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

causes of Secondary Dyslipidaemia

A
  • A sedentary lifestyle in conjunction with
    excessive dietary intake of saturated fat,
    Cholesterol, and trans fats
  • Diabetes Mellitus (DM) type 2
  • Alcohol overuse
  • Chronic kidney disease
  • Hypothyroidism
  • Drugs, such as thiazides, beta-blockers,
    oestrogen and progestins and glucocorticoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are 3 types of Primary Dyslipidaemia

A

1) FAMILIAL HYPERCHOLESTEROLAEMIA
2) FAMILIAL COMBINED HYPERLIPIDAEMIA
3) FAMILIAL TYPE III HYPERLIPIDAEMIA

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

which Fredrickson phenotype has elevated Chylomicrons (Lipoprotein) and elevated Triglycerides

A

Phenotype I (primary chylomicronaemia)

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

which Fredrickson phenotype has elevated LDL (Lipoprotein) and elevated Cholesterol

A

IIA (Familial Hypercholesterolaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

which Fredrickson phenotype has elevated LDL &VLDL (Lipoprotein) and elevated Cholesterol & Triglycerides

A

IIB (Familial Combined Hyperlipoproteinaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which Fredrickson phenotype has elevated Chylomicron remnants &VLDL (Lipoprotein) and elevated Cholesterol & Triglycerides

A

III (Familial Dysbetalipoproteinaemia)

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

which Fredrickson phenotype has elevated VLDL (Lipoprotein) and elevated Triglycerides

A

IV (Familial Hypertriglyceridaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which Fredrickson phenotype has elevated Chylomicron &VLDL (Lipoprotein) and elevated Cholesterol & Triglycerides

A

V (Familial Mixed Hypertriglyceridaemia)

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

Macrovascular complications for Dyslipidaemia

A
  • Unstable Angina (Chest Pain)
  • Myocardial Infarction (Heart Attack)
  • Ischaemic Cerebrovascular Disease (Stroke)
  • Coronary Artery Disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Microvascular complications of Dyslipidaemia

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cause of ischaemic heart disease

A

Atheroma formation within coronary
arteries, aggravated by thrombosis or vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors of ischaemic heart disease

A
  • Central obesity
  • Atherogenic lipid patterns
  • Hypertension
  • Insulin resistance (overt DM)
  • Elevated C-reactive protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is Ischaemic heart disease clinically identified as ?

A

Clinically silent or manifested as angina pectoris, myocardial infarction or chronic IHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

complications of Ischaemic heart disease

A

1) Atherosclerosis
2) Angina pectoris (stable, unstable)
3) MI (STEMI, NSTEMI)
6) Chronic ischaemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of atheroscelrosis

A

A.
➢ Gradual occlusion of coronary vessel(s) →
➢ Gradual reduction in blood flow →
➢ Mismatch btw. demand and supply of
O2/nutrients to the myocardium →
➢ Ischaemia = Reversible process that is associated with tissue dysfunction, due to interference with blood flow to a tissue

B.
❖ Complete occlusion of coronary vessel(s) →
❖ Sudden reduction in blood flow →
❖ Infarction = Irreversible process that is related to tissue death (necrosis) , because of disturbances in the blood flow to a tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cause of Stable Angina

A

Stable, but gradually enlarging plaque
→ Severe narrowing of atherosclerotic coronary vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

clinical manifestaions of Stable Angina

A

Predictable cardiac-type
pain, which shows following characteristics:
1) Precipitation by exertion
2) Duration of 1-2 min
3) Relief of pain by rest or intake of Glyceryl
trinitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

causes of Unstable (“Crescendo”)Angina

A
  • Disruption of atherosclerotic plaque with
    superimposed thrombosis
  • Embolisation
  • Vasospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

clinical features of Unstable Angina

A

(at least one of the following
three, present):
1. Occurs at rest (or with minimal exertion),
usually lasting 3–5 minutes
2. Is severe and of new onset (i.e. within the
prior 4–6 weeks)
3. Occurs with a crescendo pattern (i.e.
distinctly more severe, prolonged, or
frequent than before)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cause of MI

A

Coagulative necrosis of myocardium, due to
coronary artery occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cellular components of MI

A

Neutrophils, macrophages
and fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the 2 patterns of MI necrosis

A
  • Transmural infarction: Whole thickness of
    myocardium
  • Subendocardial infarction: Inner 1/3 of left
    ventricular wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

cause of STEMI

A

Occurs when a coronary artery is totally
occluded → Trans-mural myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ECG findings of STEMI

A
  • ST-segment elevation with pathological Q-waveformation
  • Sometimes, T-wave inversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Blood test findings of STEMI

A

Cardiac markers:
1) ↑ of Troponin T, Troponin I, and CK-MB (Creatine Kinase Myocardial Band)
–> Troponin T and Troponin I start to rise at 4-6 hours and remain high for up to 2 weeks
–> CK-MB starts to rise at 4-6 hours and falls to
normal within 48-72 hours

Full blood count:
* ↑ of White Blood Cell (WBC) count
* ESR and CRP may elevate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cause of NSTEMI

A

Occurs when a coronary artery is partially
occluded → Sub-endocardial MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Clinical feature of NSTEMI

A

Ischaemic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ECG findings of NSTEMI

A

ST depression and/or T wave inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Laboratory findings of NSTEMI

A

Delay in rise of troponin levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

State the difference between NSTEMI and Unstable Angina

A
  • Difference in severity of myocardial ischaemia;
    NSTEMI > Unstable Angina
  • NSTEMI: Elevation of cardiac enzymes; Unstable
    Angina: No or only very minimal elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are 4 sequence of events of MI?

A
  1. Myocyte necrosis
  2. Induction of an inflammatory response
    (Infiltration of neutrophils)
  3. Organisation (Replacement of dead cells by
    granulation tissue; First step of the repairprocess)
    4.Scar formation (Progressive scar tissue
    deposition; Second step of the repair-process)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Microscopic features:
* Contraction band necrosis
* Loss of cross striations
* Irregular darker pink wavy contraction bands
* Not clearly visible nuclei
* Many neutrophil infiltrates
with karyorrhexis
* Many macrophages
* Numerous capillaries
* Fibroblast proliferation

Are the features of which heart disease?

A

MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

complications of MI

A

1) Arrhythmia → Death, within first hours
2) Myocardial failure → Congestive heart failure
or shock
3) Myocardial rupture → Cardiac tamponade
(4-7 days)
4) Ruptured papillary muscle
5) Mural thrombosis → Left sided embolism
6) Ventricular aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

pathogenetic mechanism of Chronic ischaemic heart disease

A
  • Gradual enlargement of stable plaque→
  • Gradual stenosis of the lumen →
  • Low grade chronic myocardial ischaemia →
  • Progressive fine diffuse myocardial fibrosis →
  • Reduction in contractile function but also enough time for compensatory changes → LV hypertrophy →
    → Maintenance of cardiac output [No
    symptomatology] BUT
  • … → Finally, myocardium decompensates →Onset of progressive Chronic Heart Failure →↓ Cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

casue of Cardiomyopathy

A

unexplained ventricular dysfunction:
* Heart failure unresponsive to digitalis (drug
causing increase in cardiac contractility)
* Ventricular enlargement
* Ventricular arrhythmias

38
Q

classifications of Cardiomyopathies

A

1) Congestive or Dilated Cardiomyopathy
2) Restrictive Cardiomyopathy
3) Hypertrophic Cardiomyopathy
4) Arrhythmogenic Right Ventricular Cardiomyopathy

39
Q

mechanism (of heart failure) of congestive/Dilated cardiomyopathies

A

Impairment of contractility (systolic dysfunction)

40
Q

Epidemiology of congestive/dilated cardiomyopathies

A

Most common form;M > F

41
Q

Etiology of congestive/dilated cardiomyopathies

A
  • Unknown (most often)
  • Alcohol
  • Thiamine (Vitamin B1) deficiency (beri-beri)
  • Myocarditis
  • Mutations of cytoskeletal proteins [dystrophin, desmin] or sarcomeric proteins [cardiac myosin heavy chain or actin]
  • Mutations in mitochondrial genes
42
Q

pathogensis of congestive/dilated cardiomyopathies

A
  • Damage of the muscle tissue → Weakening of the myocardium → Insufficient pumping action of the heart
  • Increase in fluid retention (↑ blood volume) → Expansion (dilatation) of heart ventricles
  • Stretching of the heart muscle → Enlargement of the heart (Cardiomegaly)
  • Long term effect: Development of both right and left-sided intractable heart failure
43
Q

Macroscopic findings:
* Globular-shaped heart
* Increased heart weight
* Biventricular/Four-chamber dilatation
* Normal or diminished LV thickness
* Mural thrombi
* Prominent LV endocardial trabeculations
* Annular dilatation of atrio-ventricular valves
* Endocardial fibrous thickening of septal portion of left ventricle

are the features of which heart condition?

A

CONGESTIVE OR DILATED CARDIOMYOPATHY

44
Q

Microscopic findings:
* Myocyte hypertrophy (nuclear size/shape)
* Interstitial/perivascular fibrosis
* Interstitial lymphocytes and macrophages
* Reduced number of myocytes (myofibrillar loss)

are the features of which heart malformation?

A

CONGESTIVE OR DILATED CARDIOMYOPATHY

45
Q

complications of congestive or dilated cardiomyopathy

A

1) Heart failure
2) Heart valve disease
3) Irregular heart rate (arrhythmias)
4) Formation of blood clots in the heart that leads to:
* Pulmonary embolism
* Stroke or myocardial infarction

46
Q

Restrictive cardiomyopathy is aka?

A

Infiltrative Cardiomyopathy

47
Q

mechanism (of heart failure) of Restrictive cardiomyopathy

A

Impairment of compliance (diastolic dysfunction)

48
Q

cause of restrictive cardiomyopathy

A
  • Idiopathic
  • Cardiac amyloidosis (“stiff heart syndrome”)
  • Haemochromatosis (build-up of iron in the body)
  • Sarcoidosis
  • Radiation fibrosis
  • Metastatic tumours
49
Q

pathogensis of restrictive cardiomyopathy

A
  • Infiltrative processes within heart muscle →
  • → Stiffening of myocardium →
  • → Restriction of the heart to stretch properly →
  • → Affects the filling capacity of the
    heart ventricles →
  • → Reduction in blood flow →
  • → Blood backs up in the circulation →
  • → Heart Failure
50
Q

Mechanism (of heart failure) of hypertrophic cardiomyopathy

A

: Impairment of
compliance (diastolic dysfunction)

51
Q

Cause of hypertrophic cardiomyopathy

A

100% Genetic; Autosomal dominant
characteristic

52
Q

pathogensis of Hypertrophic cardiomyopathy

A

Myocardial hypertrophy → Poorly compliant left ventricular myocardium → Abnormal diastolic filling → and intermittent ventricular outflow obstruction → Danger of syncope and sudden death (unexpectedly, in athletes)

53
Q

Macroscopic findings:
* Markedly thick-walled left ventricle (asymmetric [septal hypertrophy]/symmetric)
* Whorled appearance of septal musculature
* Normal or reduced left ventricular cavity
* Endocardial thickening or mural plaque
formation in the left ventricular outflow tract
* Thickening of the anterior mitral leaflet
* Increase in the right ventricular wall thickness

are the features of which cardiac malformation?

A

Hypertrophic cardiomyopathy

54
Q

Microscopic findings:
*Marked myocyte hypertrophy
* Myocyte disarray pattern (irregularly arranged, interwoven myocyte fibers)
* Interstitial and perivascular fibrosis
* Endocardial fibrosis
* Fibrous mural changes in intra-myocardial
arteries

Are the features of which heart disease ?

A

Hypertrophic Cardiomyopathy

55
Q

cause of Arrhythmogenic right ventricular cardiomyopathy

A

Defective cell adhesion proteins in desmosomes of adjacent cardiac myocytes

56
Q

pathogenetic mechanism of Arrhythmogenic right ventricular cardiomyopathy

A
  • Gradual replacement of right ventricular muscle by adipose and fibrous tissue
  • The right ventricle inflow tract, apex, and outflow tract are involved → Dilatation of right ventricle and attenuation of the free wall
  • The left ventricle can also be affected, but usually in conjunction with right ventricle disease
57
Q

Naxos syndrome?

A

–> Associated with mutations in genes desmoplakin and plakoglobin
–> includes Arrhythmogenic Right Ventricular Cardiomyopathy
–> Palmo-plantar keratoderma

58
Q

Clinical features of Arrythmogenic right ventricular cardiomyopathy

A

1) Palpitations and fainting after physical activity
2) Dizziness and lightheadedness
3) Ventricular arrhythmias → Sudden cardiac death

59
Q

Macroscopic findings:
* Replacement of myocardial tissue by adipous and fibrous tissue
* Dilatation of the right ventricle and attenuation of the free wall ventricle

are the features of what heart condition

A

ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY

60
Q

Microscopic findings:
* Markedly decreased numbers of myocytes
* Extensive fatty infiltration and fibrosis
* In some cases, collections of mononuclear inflammatory cells are found within the adipose tissue

Are the features of what heart condition

A

ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY

61
Q

Clinical features of Myocarditis

A

Manifests as biventricular heart failure in young persons, without valvular, rheumatic or congenital heart disease

62
Q
  • scalloped of myocytes
  • inflammatory cells infiltrates
  • Fragmentation of myocytes with remnants of cytoplasm or “bare nuclei”

are the Histopathological features of what heart condition?

A

Myocarditis

63
Q

causes of Lymphocytic myocarditis

A

Coxsackie B (Enterovirus), Echovirus,
Adenovirus

64
Q

pathogensis of Lymphocytic myocarditis

A
  • Post-viral autoimmunity mechanisms
  • Direct viral cytopathic injury
  • Induction of viral-specific immune response
    through mediators (ILs, TNF, IFN, NO)
  • Viral mediated endothelial injury → Intima
    proliferation → Ischaemic sequelae
65
Q

Macroscopic findings:
* Range from normal cardiac configurations to
four-chamber dilatation and cardiac enlargement
* Flattening of the papillary muscles and
trabeculae
* Pale and flaccid appearance of the myocardium
* Myocardium’s cut surface: Usually pale with foci of haemorrhage or haemorrhagic necrosis
* Many cases have fibrinous pericarditis and
exudative effusions

Are the features of which heart condition?

A

Lymphocytic myocarditis

66
Q

Microscopic findings:
* Architectural patterns include focal, multifocal
and diffuse interstitial infiltrates
* Interstitial widening caused by tissue oedema
and inflammation
* Majority of lymphocytes: CD3(+), both helper
and suppressor subtypes
* Presence of macrophages and natural killer cells
* Infrequent or absent B lymphocytes

Are the features of which heart condition?

A

Lymphocytic myocarditis

67
Q

causative agents of infectious myocarditis

A

Bacteria, fungi, protozoa, rickettsiae

68
Q

Epidemiology of infectious myocarditis

A

Affects mainly individuals with:
1) AIDS
2) Advanced stages of malignancy
3) Transplantation-associated immunosuppression

69
Q

Causative drugs of Hypersenisitvity myocarditis

A

Antibiotics, diuretics, and antihypertensive drugs, prolonged infusion (7% of patients undergoing cardiac transplantation)

70
Q

clincial signs of Hypersensitivity Myocarditis

A

1)Rash
2)Fever
3)Peripheral eosinophilia
4)Arrhythmias, sudden death, and congestive
heart failure (occasionally)

71
Q
  • Temporally uniform lesions; distributed in the subendocardial, perivascular, and interstitial tissues between bundles of myocytes
  • Eosinophils (predominant inflammatory cell), but also variable numbers of histiocytes and
    scattered lymphocytes (T cell phenotype) present
  • Oft, infiltration of vessel walls by eosinophils
  • Collections of histiocytes centered on degenerated collagen bundles form ill-defined granulomas in up to 25% of cases
  • Myocyte necrosis usually absent or very focal,
    except in severe cases
  • Hypersensitivity vs. Drug induced Giant-cell
    Myocarditis: Absence of diffuse myocardial
    necrosis and giant cells
  • Hypersensitivity vs. Acute Necrotising Eosinophilic Myocarditis: Absence of extensive necrosis, dense interstitial inflammatory cell infiltrates and systemic allergic symptoms

Are the histopathlogical features of what cardiac malformation?

A

HYPERSENSITIVITY MYOCARDITIS

72
Q

mechanism of Toxic Myocarditis

A

Direct myocyte cytotoxicity

73
Q

causative agents of Toxic Myocarditis

A

Cyclophoshamide, *Doxorubicin, Catecholamines, Cocaine, Fluorouracil, Lithium
compounds

74
Q

Histopathology:
* Lymphocytes
* Neutrophils
* Pyknotic debris, associated with myocyte damage

Are the features of what heart condition?

A

Toxic Myocarditis

75
Q

Causes of Hydropericardium

A

Congestive heart failure, Hypoproteinaemia (Nephrotic syndrome), Chronic liver disease

76
Q

Causes of Haemopericardium

A

Traumatic perforation of heart or aorta,
myocardial rupture after acute myocardial
infarction

77
Q

Haemopericardium vs Hydropericardium:

A

Hydropericardium: Accumulation of serous transudate in pericardium

Haemopericardium: Accumulation of blood in pericardium

78
Q

Causes of Acute Pericarditis

A

1) Infectious
➢ Bacterial [Gram (+), Gram (-) bacteria, Mycobacteria, Spirochetes]
➢ Fungal, Viral, Parasitic
2) idiopathic
3) Post-myocardial infarction
4) Iatrogenic (postsurgical, radiation therapy, drug reaction)
5) Metastatic neoplasm
6) Systemic disease (autoimmune, renal failure, endocrine)
7) Traumatic

79
Q

causes of Serous Pericarditis:

A

SLE, Rheumatic Fever and Viral infections

80
Q

Macro-/Microscopic picture:
Clear, straw-colored, protein-rich exudate with a few inflammatory cells

are the features of what cardiac defect?

A

ACUTE PERICARDITIS

81
Q

causes of Fibrinous or Sero-Fibrinous Pericarditis:

A

: Uraemia, Myocardial infarction, Acute
Rheumatic Fever

82
Q
  • Macro-/Microscopic picture:
    Fibrin-rich exudate

are the features of what cardiac defect?

A

Fibrinous or Sero-Fibrinous Pericarditis

83
Q

causes of Purulent or Suppurative Pericarditis:

A

Bacterial infection

84
Q

Macro-/Microscopic picture:
Cloudy or frankly purulent inflammatory exudate

are the features of what cardiac disease?

A

Purulent or Suppurative Pericarditis

85
Q

causes of Haemorrhagic Pericarditis

A

Tumour invasion of the pericardium, Tbc
or other bacterial infections

86
Q

Macro-/Microscopic picture:
Bloody inflammatory exudate

are the features of what cardiac malformation?

A

Haemorrhagic Pericarditis

87
Q

Causes of Chronic/Constrictive Pericarditis

A

1) Idiopathic
2) Following episode of acute pericarditis
3) Infectious (Mycobacteria [e.g. Tbc], fungal)
4) Post-surgical (including transplantation)
5) Systemic disease (autoimmune, renal failure)
6) Radiation therapy
7) Neoplasms (usually metastatic tumours)

88
Q

pathogenesis of chronic (constrictive) pericarditis

A
  • Organisation of an acute pericarditis and healing with dense fibrosis and calcifications →
    Results in a thickened, scarred pericardium →
    Loss of elasticity → Inability of pericardium to stretch → Interference with cardiac action and venous return (mimics right-sided heart failure)
89
Q

Macro-/Microscopic picture:
proliferation of fibrous tissue and focal calcification

Are the features of what heart condition

A

Chronic (Constructive) Pericarditis

90
Q

what heart malformation has the follwing characteristics :
“scintillating (sparkling) gold paint appearance”, due to the cholesterol crystals in the fluid

A

Idiopathic cholestrol pericarditis

91
Q

Idiopathic Cholesterol pericarditis has been associated with?

A

1) Hypothyroidism,
2) Rheumatoid Arthritis, and
3) Tuberculosis
4) recurrent pericardial effusions

Pathology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions