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Cardiovascular System > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the most common acquired heart disease in children and young adults?

A

Acute Rheumatic fever

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2
Q

What is the causative agent for Acute rheumatic fever?

A

Group A β-hemolytic Streptococcus.

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3
Q

What is the criteria used in diagnosing acute rheumatic fever?

A

Jones criteria

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4
Q

What is the Jones criteria for Acute Rheumatic fever?

A

Evidence of Group A streptococcus infection
- elevated or rising ASO titer
- Throat culture
- Rapid antigen test

AND

Two major manifestations OR one major and two minor manifestations.

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5
Q

What are the MAJOR manifestations of Acute Rheumatic fever?

A

P- Polyarthritis
E - Erythema marginatum (type of skin rash)
C - Carditis
S - Sydenham’s chorea (uncontrollable movements)
S - Subcutaneous nodules

” PECSS Major”

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6
Q

What are the MINOR manifestations of Acute rheumatic fever?

A

P - Prolonged PR interval on ECG.
E - Elevated ESR or CRP
A - Arthralgia
F - Fever

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7
Q

What is the most important protein in the causation of ARF and where is it located?

A

M protein in Group A strep

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8
Q

What is the term given to the inflammation of all layers of the heart?

A

Pancarditis

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9
Q

What is the main histological feature for ARF carditis?

A

Aschoff nodule which contains the pathognomonic cell called the Anitschkow cell

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10
Q

What is the most common valve associated with Chronic rheumatic heart disease?

A

Mitral valve

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11
Q

What is Infective endocarditis?

A

A microbial infection of heart valves or endocardium covering wall of heart

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12
Q

What are Congenital Heart Diseases?

A

Congenital heart diseases are abnormalities of the heart or great vessels that are present at birth.

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13
Q

What are the most common Congenital Heart diseases?

A

Ventricular septal defect
Atrial septal defect

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14
Q

Which genetic abnormalities are associated with Congenital Heart diseases?

A

Trysomy 21
Trisomy 13&18
Turner’s syndrome
22q11.2 deletion syndrome ( DiGeorge syndrome )

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15
Q

What are other causes of Congenital Heart diseases?

A
  • Congenital rubella infection
  • Teratogens
  • Maternal diabetes, and genetic factors
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16
Q

When do most congenital heart abnormalities occur ?

A

First 8 weeks of Pregnancy ( Embryogenesis)

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17
Q

When does the formation of the heart structure and great vessels occur?

A

Weeks 1-4

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18
Q

When does the formation of valves and completion of septa dividing right from left heart occur?

A

Weeks 4-8

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19
Q

True or False? A left to right Arteriovenous shunt can result in left ventricular hypertrophy.

A

FALSE!! Left to right shunt results in RIGHT ventricular hypertrophy .

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20
Q

What are the disorders associated with Left to Right AV shunts?

A

*Atrial septal defects (ASDs),
* Ventricular septal defects (VSDs),
*Patent ductus arteriosus (PDA)
* Atrioventricular septal defect (AVSD)

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21
Q

What is the name given to the late onset of cyanosis seen in Left to right shunts?

A

Eisenmenger syndrome

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22
Q

What is an Atrial Spetal Defect?

A

This is a defect in the interatrial septum ( septum separating right and left atria)

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23
Q

At what age does 50% of Atrial septal defect close?

A

By age 5.

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24
Q

What is Ventricular Septal Defect ( Hole in the heart)?

A

This is a defect in the ventricular septum.

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25
Q

What are the main types of Ventricular septal defects?

A
  • Perimembranous - most common type
  • Muscular
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26
Q

What is Atrioventricular Septal defects?

A
  • This is a defect of the septum at the atrioventricular junction.
    It involves the lower atrial septum and upper ventricular membranous septum
  • Disrupts the tricuspid and mitral valves.
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27
Q

Which diseases is associated with hearing” Machinery- like murmurs”?

A

Patent Ductus Arteriosus

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28
Q

What is the most common cause of Patent Ductus Arteriosus?

A

PDA occurs when there is a failure of the ductus arteriosus to close and may be as a result of HYPOXIA.

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29
Q

What are the most common causes of Right to Left venous shunts?

A

Tetralogy of Fallot ( TOF )
Transposition of the Great Arteries (TGA)

To the lefTT to the lefTT.

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30
Q

What are the four cardinal features associated with Tetralogy of Fallot?

A
  • Pulmonary Stenosis - Obstruction of the outflow from the right ventricle.
  • Ventricular Septal Defect (VSD)
  • Aorta that overrides the VSD
  • Right ventricular hypertrophy.
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31
Q

What is Dextrocardia?

A

This is an abnormality of position , opposite rotation of the heart with apex pointing to the right side.

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32
Q

What is the term given to an abnormal morphology usually with thickening and modularity of leaflets or cusps of valves?

A

Dysplasia

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33
Q

What is the term given to a reduction in the circumference of a valve orifice and may occur with an otherwise normal valve with a dysplastic valve?

A

Stenosis

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34
Q

What is Atresia?

A

This is complete occlusion of valve orifice due to poor or no development of valve apparatus.

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35
Q

Fill in th blanks. “ In 95% of cases, Primary hypertension is ______ or ________.”

A

Essential or Idiopathic

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36
Q

What are the causes of Secondary Hypertension?

A
  • primary renal disease, renal artery narrowing (renovascular hypertension), or adrenal disorders
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37
Q

What are examples of accelerated hypertension?

A

Severe hypertension
Renal failure
Retinal haemorrhage / exudates.

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38
Q

Which hypertensive vascular disease is associated with small arteries and arterioles?

A

Hyaline arteriosclerosis( Benign)
Hyperplastic arteriosclerosis ( Malignant)

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39
Q

What are the morphological features found in Benign nephrosclerosis?

A

Bilateral changes
Mild decrease in size
Diffuse, fine granularity of cortical surface area

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40
Q

What are the clinical features of Left-sided heart failure?

A

Increased Dyspnoea on exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea
Pulmonary oedema
Cough
haemoptysis
Respiratory tract infections.

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41
Q

What are the clinical features of Right sided heart failure?

A

Elevated venous pressure
Tender hepatomegaly
Oedema

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42
Q

What is shock?

A

A state of generalized inadequate tissue perfusion or a state in which there is severe circulatory impairment such that the metabolic needs of the tissues/organs of the body are not met.

note: it’s systemic hypoperfusion (basic definition)

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43
Q

True or False? Shock is normally accompanied with Hypertension.

A

FALSE!! It is usually accompanied by HYPOTENSION.

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44
Q

What are the types of shock?

A
  • Cardiogenic shock
  • Obstructive shock
  • Hypovolemic shock
  • Distributive shock: septic shock, anaphylactic shock, neurogenic shock
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45
Q

What is the most common type of shock?

A

Hypovolaemic Shock

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46
Q

What is HYpovalemic shock?

A

Hypovolemic shock results from low cardiac output due to loss of blood or plasma volume (e.g., resulting from hemorrhage or fluid loss from severe burns).

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47
Q

What are the clinical manifestations of Hypovalemic shock?

A
  • Pallor (especially in cases of haemorrhage)
  • cyanosis
  • Sweating (in the early stage)
  • Tachycardia
  • Hypotension
  • Cardiac dysrrhythmias
  • Tachypnea
  • Oliguria ( urinary output less than 400 ml per day or less than 20 ml per hour)
  • Circulatory collapse/shock
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48
Q

True or False? Cardio-vascular collapse/shock occurs with blood/fluid loss >40%

A

TRUE!!

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49
Q

What is the management for a Hypovalemic shock?

A

Fluid (crystalloid +/- blood) & correction deranged electrolytes - important in the resuscitation of patients .

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50
Q

What are the three types of Distributive shock ?

A

Anaphylactic shock
Neurogenic shock
Septic shock

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51
Q

What is the main pathophysiology in Distributive shock?

A

The problem is not loss of blood , but excessive dilation of blood vessels or decreased vascular resistance causing the blood to be improperly distributed.

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52
Q

What is the cause of Septic shock?

A

Gram -negative bacteria or endotoxic release. May also be due to Gram -positive bacteria.

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53
Q

Fill in the blanks. “ _________ are an important component of atherosclerotic plaques.

A

Lipids

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54
Q

What are the other components in the formation of atherosclerotic plaques?

A

Macrophages, Cytotoxic factors and inflammatory agents

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55
Q

Fill in the blanks. “ Atheroscelorosis in peripheral arteries gives rise to _______ and in the carotid or cerebral arteries gives rise to _________which may cause a __________.”

A

Atherosclerosis in peripheral arteries gives rise to PERIPHERAL VASCULAR DISEASES and in the carotid or cerebral arteries to CEREBROVASCULAR disease which may cause a STROKE.

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56
Q

What are the risk factors for Ischaemic heart diseases?

A

Smoking
Hypertension
Serum LDL
Diabetes Mellitus (DM)
Obesity
Fibrinogen
Lipoprotein a
Homocysteine

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57
Q

True or False? Lipids are classified as sterols.

A

TRUE!!

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58
Q

What are Eicosanoids?

A

These are multiple lipid based signaling molecules that has effects on blood coagulation bronchial and vascular contractility , reproduction .

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59
Q

Where are Sphingolipids used?

A

In the Central nervous system and blood group substances.

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60
Q

Vitamin E is mainly used for?

A

Neural function and as an antioxidant .

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61
Q

Vitamin K is used for?

A

Activation of clotting factors

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62
Q

Fill in the blanks. “ Cholesterol serves as precursors for the synthesis for ________, _______ & __________.”

A

Steroid hormones, Vitamin D and Bile acids

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63
Q

What maintains the cholesterol balance?

A

The liver- where in excess it is secreted by the liver directly , into bile or by conversion into bile acids.

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64
Q

What is the name given to small surface invaginations that serve as binding sites for receptors and signalling molecules?

A

Caveolae

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65
Q

What are the two substances that form a Caveolae or lipid raft?

A

Cholesterol and Sphingomyelin

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66
Q

How is a constant concentration of cholesterol in plasma membrane maintained?

A

This is achieved by the transcription of genes encoding enzymes involved in cholesterol synthesis

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67
Q

What are phytosterols?

A

These are Plant sterols that act in the intestines to lower cholesterol absorption.

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68
Q

What are the two types of Phytosterols?

A
  • Delta5-phytosterols ( eg beta-sitosterol )
  • 5 alpha-reduced phytosterols (stanols)
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69
Q

What is the basic structure of Fatty acids?

A

RCOOH

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70
Q

True or False? Saturated Fatty acids are mostly ANIMAL derived while UNSATURATED fatty acids are mainly PLANT derived.

A

TRUE!!

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71
Q

What is the main dietary fat?

A

Triglycerides - a concentrated form of metabolic energy.

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72
Q

What is the name of the enzyme which hydrolyses triglycerides in the gut?

A

Lipoprotein lipase.

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73
Q

True orFalse? Monoglycerides undergo re-esterification in enterocytes and subsequent incorporation into chylomicrons.

A

TRUE!!

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74
Q

Where are the major sites of endogenous triglyceride synthesis?

A

The liver and Adipose tissue

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75
Q

Fill in the blanks. “ Fatty acids are mobilised from adipose tissue by the action of__________.”

A

Hormone sensitive lipase (HSL)

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76
Q

Hormone sensitive lipase (HSL) is activated by ?

A

Glucagon and Adrenaline

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77
Q

Hormone sensitive lipase (HSL) is inhibited by?

A

Insulin

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78
Q

True or False? Phospholipids contain a Hydrophilic (phosphate group ) and a hydrophobic (fatty acid ) domains

A

TRUE!!

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79
Q

What is the shape of HDL?

A

Discoidal

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80
Q

What is the shape of Lipoproteins?

A

They are Generally spherical

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81
Q

Which Chylomicron remnant is anti-atherogenic?

A

HDL

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82
Q

Majority of chylomicron remnants is said to be?

A

Pro-atherogenic - VLDL, IDL, LDL, Lp(a)

83
Q

What are the functions of apolipoproteins?

A
  1. Serving a structural role
  2. Acting as ligands for lipoprotein receptors
  3. Guiding the formation of lipoproteins
  4. Serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins.
84
Q

Chylomicrons are made by?

A

The intestines

85
Q

What is the largest and most buoyant class of Lipoproteins?

A

Chylomicrons

86
Q

What is the major chylomicron protein?

A

APO B-48

87
Q

True or False? Chylomicron remnants are enriched with cholesterol and are pro-atherogenic.

A

TRUE!!

88
Q

What are Chylomicron remnants?

A

These are smaller particles caused by the removal of triglycerides from chylomicrons by peripheral tissues.

89
Q

What is the major protein of Very low density lipoproteins (VLDL)?

A

Apo B-100

90
Q

What are the proteins found in VLDL?

A

apo B-100
apo C-1
apo c-II
apo c- III
apo E
apo-A

91
Q

True or False? VLDL particles are LARGER than Chylomicrons.

A

FALSE!!! VLDL particles are SMALLER than chylomicrons

92
Q

How are Intermediate density lipoproteins (IDL) produced?

A

They are produced during the conversion of VLDL to LDL .

  • they are VLDL remnants
93
Q

What are the structural component of IDL?

A

Cholesteryl esters
apo B-100
apo - E

94
Q

Fill in the blanks. “ __________ represents the end products of VLDL catabolism .”

A

Low density lipoproteins (LDL)

95
Q

What is the major cholesterol - containing lipoprotein?

A

Low - density lipoprotein( LDL)

96
Q

What is the main component in LDL?

A

Apo B-100

97
Q

True or False? Small dense LDL are more pro-atherogenic than large LDL.

A

TRUE!!

98
Q

True or False? Large LDL particles have a decreased affinity for the LDL receptor resulting in a prolonged retention time in the circulation .

A

FALSE!! Small dense LDL
have a decreased affinity for the LDL receptor.

99
Q

Fill in the blanks. “Small Dense LDL are more susceptible to _______ which could result I an enhanced uptake by macrophages.”

A

Oxidation

100
Q

Which lipoprotein is the smallest and most dense?

A

HDL

101
Q

Which lipoprotein has anti-oxidant , anti-inflammatory , anti- apoptotic properties which also contribute to its ability to inhibit atherosclerosis?

A

HDL

102
Q

Which lipoprotein is considered a risk factor for Cardiovascular diseases?

A

High Lp(a) - cut off 300 mg/dL

103
Q

What is the major structural protein of HDL?

A

Apolipoprotein A- I

104
Q

Where is Apolipoprotein A- I synthesised?

A

In the liver

105
Q

What is the name of the enzyme that converts free cholesterol into cholesteryl ester ?

A

Lecithin cholesterol acyltransferase(LCAT)

106
Q

What is an activator of the enzyme,e Lecithin cholesterol acyltransferase(LCAT)?

A

Apolipoprotein A-1

107
Q

Which apolipoprotein may play a role in regulating food intake?

A

Apolipoprotein A -IV

108
Q

Which apolipoprotein is an activator of LPL mediated lipolysis and thereby plays an important role in the metabolism of triglyceride rich lipoproteins?

A

Apolipoprotein A- V

109
Q

Which Apolipoprotein is the major structural proton of chylomicrons and chylomicron remnants?

A

Apo B-48

110
Q

Apolipoprotein B-100 is the major structural component in what lipoproteins?

A

VLDL
IDL
LDL

111
Q

Where is Apolipoprotein C synthesised?

A

In the liver

112
Q

Fill in the blanks. “ __________ is a co-factor for lipoprotein lipase (LPL) and thus stimulates triglyceride hydrolysis.”

A

Apo C-II

113
Q

What is the most common isoform of Apolipoprotein E?

A

Apo E- 3

114
Q

Patients who are homozygous for Apo- E2 can develop what disease?

A

Familial Dysbetalipoproteinemia

115
Q

Which Apolipoprotein is associated with an increased risk of Alzheimer’s disease and an increased risk of atherosclerosis?

A

Apo E4

116
Q

What is the process by which the LDL receptor uptakes LDL, Chylomicron remnants and IDL?

A

Endocytosis

117
Q

True or False? Ischaemic Heart diseases are a collection of Syndromes.

A

TRUE!!

118
Q

What are the cardiac syndromes which can cause clinical presentations associated with IScahemic Heart disease?

A
  • Angina Pectoris (stable/unstable)
    *Chronic IHD with heart failure
    *Myocardial infarction
    *Sudden cardiac death
119
Q

What are the causes of Ischaemic Heart Disease?

A
  • Atherosclerotic coronary artery disease (~90%)
  • Vasospasm

*Vasculitis

*Embolism (plaque, thrombus, tissue, foreign body)

*Coronary artery dissection

120
Q

What are the aggravating factors of Ischaemic Heart Disease?

A
  • Increased cardiac demand.
  • Hypertrophy (e.g. hypertensive heart disease)
  • Decreased perfusion e.g. low systemic blood pressure
  • Hypoxaemia e.g. COPD, anaemia

*Increased heart rate: Increased demand and decreased diastolic filling

121
Q

Fill in the blanks. “ Ischaemic heart disease is a late manifestation of ___________.”

A

Atherosclerotic coronary artery disease.

122
Q

True or False? Clinically, acute plaque change manifests as Acute Coronary Syndrome (ACS).

A

TRUE!!

123
Q

What are the intrinsic factors of the atheromatous plaque
?

A
  • Thin fibrous cap
  • ↑ lipid and foam cells
  • Few smooth muscle cells
  • ↑ inflammatory cells increased MMPs 🡪 ↓ collagen
124
Q

What are factors extrinsic to plaque?

A
  • Adrenergic stimulation
  • Blood pressure control
  • Vasospasm
  • Platelet reactivity
  • Emotional stress
125
Q

What are the symptoms of a Myocardial Infarction?

A
  • Central crushing chest pain, prolonged
  • Weak, rapid pulse
  • Diaphoresis / sweating
  • Shortness of breath
  • Asymptomatic
126
Q

What are the biochemical abnormalities associated with a MI?

A

Increase in Tropinin- I and T

127
Q

What are the ECG abnormalities associated with a Myocardial infarction?

A

ST segment elevation

128
Q

If there is an infarction present on the Right ventricle, posterior wall of left ventricle or in the posterior septum. Which artery is occluded?

A

Right coronary artery

129
Q

If the Left Anterior Descending coronary artery is occluded if there is an infarction present where on the heart?

A

In the Anterior wall of left ventricle OR anterior septum

130
Q

If there is an infarction in the Lateral wall of left ventricle which artery is occluded?

A

Left Circumflex coronary artery

131
Q

If there is occlusion of the artery for less than two minutes (<2) what is the outcome/ impact on myocardium ?

A

Loss of cell function

132
Q

If there is occlusion of the artery for less than two minutes (<20)what is the outcome/ impact on myocardium ?

A

Reversible cell injury

133
Q

If there is occlusion of the artery for 20-40 minutes what is the outcome/ impact on myocardium ?

A

Irreversible cell injury

134
Q

What are the impacts on the myocardium after a myocardial infarction?

A
  • Electrical instability
  • Electrolyte disturbances
  • Damage to conduction system
  • Tissue necrosis
135
Q

What is the most common pattern of a Myocardial Infarction?

A

Transmural (Full thickness)

136
Q

What are the features of a sub-endocardial infarction?

A
  • Inner 1/3 of ventricular wall (furthest away from source).
  • May extend outside arterial distribution pattern.
137
Q

When does a sub-nedocardial MI occur?

A
  • Acute plaque change with subtotoal occlusion
    OR
  • Low perfusion pressure with non-critical stenosis
138
Q

Which pattern of a Myocardial infarction involves small intramural vessels?

A

Multifocal microinfarction

139
Q

Fill in the blanks. “ A multifocal micro infarction can be caused by ______ or ________.”

A
  • Endogenous catecholoamines- ex from a pheochromocytoma
  • Drugs such as cocaine, ephedrine
140
Q

What is the major primary prevention of a MI?

A

Risk factor modification: Atherosclerosis

141
Q

Which drugs can help the treatment myocardial infarction?

A
  • Aspirin prophylaxis; anti-platelet agents
  • Anticoagulation
  • Beta blockers
  • ACE inhibitors
  • Statins
142
Q

What are surgical treatments of a Myocardial infarction?

A

*Thrombolysis:
- Fibrinolytic therapy
- Percutaneaous transluminal coronary angioplasty (stents)

*Coronary artery by-pass grafting (CABG)

*Left ventricular assist devices

  • Implantable defibrillators and pacemakers
143
Q

Which pattern of a myocardial infarction Begins approximately 30 minutes after complete occlusion?

A

Transmural

144
Q

True or False? The right ventricle is MORE common in a Transmural MI than the left ventricle.

A

FALSE!!Left ventricle involvement more common than right.

145
Q

True or False? Diabetes Mellitus is a major risk factor for Periperl vascular diseases?

A

FALSE!! It is a MINOR factor.

146
Q

What are the major risk factors for Peripheral Vascular Disease?

A

Hypertension
Hypercholesterolemia
Cigarette Smoking

147
Q

What are the minor risk factors for Peripheral vascular diseases?

A

Obesity
Diabetes Mellitus *
Hypertriglyceridemia
Sedentary lifestyle
Stress
Family history

148
Q

What are the surgical treatments for Critical limb ischaemia?

A
  • Angiography indicated
  • Percutaneous Transluminal
  • Angioplasty (PTA)
  • Bypass Surgery
  • Amputation
149
Q

What is the most common bypass to be used in Peripheral Vascular diseases?

A

The most common bypass is the Fem-Pop bypass

150
Q

What are the clinical features of Chronic occlusion seen in Peripheral Vascular diseases?

A

*Claudication
*Rest pain
*Blistering/ulceration
*Gangrene

151
Q

What is Leriche Syndrome?

A

Leriche Syndrome also commonly referred to as aortoiliac occlusive disease, is caused by severe atherosclerosis affecting the distal abdominal aorta, iliac arteries, and femoro-popliteal vessels.

152
Q

What are the examinations to be done in suspected Peripheral diseases?

A
  • Cardiac Examination
  • Pulses
  • Trophic changes
  • Ankle brachial indices
153
Q

What is the treatment for Claudication?

A
  • Control of risk factors
  • Burger’s exercises
  • Careful follow-up
154
Q

Where is the LDL receptor located?

A

It is present in the liver.

155
Q

True or False? A LOW number of LDL receptors is associated with HIGH plasma LDL levels BUT a HIGH number of LDL receptors in the liver is associated with LOW plasma LDL levels.

A

TRUE!!

156
Q

True or False? Lipoproteinlipase (LPL) is synthesised in the liver.

A

FALSE!! It is synthesised in the heart, muscle and adipose tissue.

157
Q

Fill in the blanks. “ The enzyme lipoprotein lipase requires __________ as a co-factor.”

A

APO C-II

158
Q

What is the function of lipoprotein lipase(LPL)?

A

It hydrolyses triglycerides carried in the chylomicrons and VLDL to fatty acids.

159
Q

Which apoproteins inhibit the activity of LPL?

A

Apo C-III and Apo A-II

160
Q

What hormone stimulates LPL expression?

A

Insulin

161
Q

Where is the enzyme Hepatic lipase located?

A

On the sinusoidal surface of liver cells

162
Q

What is the function of Hepatic Lipase?

A
  • It mediates the hydrolysis of triglycerides and phospholipids in IDL and LDL leading to smaller particles of LDL.
  • It also mediates the hydrolysis of triglycerides and phospholipids in HDL resulting in smaller HDL particles.
163
Q

What is the function of the Lecithin cholesterol acyltransferase (LCAT) ?

A

LCAT catalyses the synthesis of cholesterol esters in HDL by facilitating the transfer of a fatty acid from position 2 of lecithin to cholesterol.

164
Q

Cholesterol in the intestinal lumen is primarily derived from ______.?

A

Bile

165
Q

Fill in the blanks. “ Chylomicrons are secreted into the lymph and delivered via the __________ to the circulation.”

A

Thoracic duct

166
Q

What is the primary determinant of the rate of VLDL synthesis?

A

The availability of triglycerides

167
Q

In Type IIa dyslipidaemia what is the elevated lipoprotein?

A

LDL

168
Q

What is the Gene involved in Type IIa dyslipidaemia (Familial Hypercholesterolemia )?

A

Auto-dom - defects in LDL receptor ApoB or PCSK9

169
Q

What is the serum lipid pattern and electrophoretic change in Type IIa dyslipidaemia (Familial l Hypercholesterolemia)?

A

Serum lipid pattern - elevated cholesterol

Electrophoretic change - Incr beta band

170
Q

The gene Auto recess -two mutant alleles of LPL etc is associated with which dyslipidaemias?

A

Type 1 ( Familial hyperchylomicronemia)

171
Q

What is the serum lipid pattern in Diabetes and Obesity?

A

Increased triglycerides , Decreased HDL

172
Q

What is the Serum lipid pattern in Alcohol excess ?

A

Increased triglycerides and HDL

173
Q

What is the serum lipid pattern for Cholestasis?

A

Increased LDL , Increased total cholesterol

174
Q

What is the serum lipid pattern of Hypothyroidism?

A

Increased LDL, Increased total cholesterol , increased triglycerides.

175
Q

In nephrotic syndrome, what lipoprotein is lost in urines?

A

HDL

176
Q

What is the cause of Nephrotic syndrome?

A

Due to a hepatic overproduction of apo B-100 as part of increased hepatic protein synthesis typical of the condition.

  • Most likely hypercholesterolaemia or mixed hyoerlipidaemia
177
Q

Which enzyme activity is reduced in Nephrotic syndrome?

A

HMG COA

178
Q

True or False? Alcohol causes Hypertriglyceridaemia.

A

TRUE!!

179
Q

Which drugs can raise plasma Tryglicerides. and lower HDL ?

A

Non-selective beta blockers ex propanolol & beta -1 selective beta blockers

180
Q

Which drugs increases LDL , Triglycerides and HDL?

A

Glucocorticoids

181
Q

How is HDL investigated?

A

It is measured by assessing cholesterol content after precipitation of APO b containing lipoproteins

182
Q

Fill in the blanks. “ LDL is mostly derived by ______.”

A

Friedewald Formula

183
Q

True or False? The lipoprotein electrophoresis on cellulose acetate paper, agarose and polyacrylamide assessment is QUANTITATIVE.

A

FALSE!! IT IS QUALITATIVE .

184
Q

What is Backward failure?

A

Heart unable to accommodate venous return resulting in vascular congestion-pulmonary/hepatic

185
Q

What is Forward failure?

A
  • Heart unable to maintain adequate cardiac output.
  • Low output failure-cool peripheries
186
Q

What is the clinical features of a systolic dysfunction?

A
  • Impaired myocardial contractile function.
  • MI, myocarditis, Dilated Cardiomyopathy.
  • Impaired stroke volume(EF)
  • Symptoms of decreased cardiac function.
  • Usually leads to low output heart failure.
187
Q

What are the clinical features of Diastolic disfunction?

A
  • Normal systolic function
  • Impaired relaxation or compliance (increased stiffness and impaired filling)
  • May be due to ischaemia of myocardium
    ( relaxation is an active process) or hypertrophy
  • Increased filling pressures
  • Leads to venous congestion
188
Q

What are the causes of High output heart failure?

A

Thyrotoxicosis
Anaemia
Beri-beri
A-V fistula
Paget’s disease of bone

189
Q

True or False? Heart failure is a diagnosis.

A

FALSE!! Heart failure is a SYNDROME

190
Q

What are clinical features of Cardiac dysfunction?

A
  • Decreased cardiac output
  • Increased preload (LV dilatation)
  • Activation of SNS-tachycardia
  • Activation of RAAS-salt and water retention
191
Q

What are the compensatory mechanism for Cardiac dysfunction?

A

Frank-Starling mechanism
Activation of Sympathetic system
Activation of RAAS system
Ventricular dilation and hypertrophy
Tahycardia
Reduced vagal activity
Vasopressin
Circulating catecholamines
Natriuretic peptides

192
Q

What are the causes of Cardiac Dysfunction?

A
  • Coronary artery disease (60-70%)
  • Idiopathic (20%)(often DCM)
  • Valvular
  • HTN
  • Alcohol
193
Q

What are the symptoms of Low cardiac output?

A
  • Fatigue, tiredness, mental cloudiness.
194
Q

What are venous congestion symptoms of cardiac failure?

A
  • Dyspnea, orthopnea, PND
  • Cough
  • Hemoptysis
  • Peripheral oedema
  • Tender liver
195
Q

What are Investigations to be done to identify cardiac failure?

A
  • Identify and treat precipitating causes.
  • Blood work-U&E,CBC,Thyroid test,BNP,cardiac enzymes,ferritin
  • ECG
  • CXR
  • Echocardiogram
  • Nuclear imaging tests
196
Q

What are. the functions of BNP- B type natriuretic peptide?

A

▪ Increases in the presence of LV dilatation and dysfunction.
▪ May be used as a screening test in patients with non-specific dyspnea.
▪ May be used as a prognostic marker.

197
Q

What are the surgical procedures for treatment of cardiac failure?

A
  • CABG(coronary artery bypass grafting) and angioplasties
  • Valve surgeries
  • Resynchronization therapy-
  • Biventricular pacing to improve synchronicity of
    contraction (MIRACLE) * ICD
  • Primary and secondary prevention of sudden death(MADIT-1,MUST,MADIT-2)
  • LVAD
  • Cardiac Transplantation
198
Q

What is Cardiomyopathy?

A

This is a cardiac condition with disorder in the myocardium not as a result of causes such as ischaemia, congenital,valvular ,pericardial and hypertension.

Primary- no known cause
Secondary- known cause

199
Q

What are the types of Cardiac myopathy?

A
  • Dilated
  • Hypertrophic
  • Restrictive
200
Q

What is Dilated cardiomyopathy?

A

Dilated usually generalised hypokinesia of the Left ventricle

201
Q

What is Hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy- familial,genetic.

202
Q

In which cardiomyopathy will the ECG present with giant T waves?

A

Hypertrophic cardiomyopathy

203
Q

Which cardiomyopathy is caused by amyloid,haemochromatosis,eosinophili as,Fabry’s disease,glycogen deposition?

A

Restrictive cardiomyopathy

204
Q
A

Cardiovascular System (10 decks)

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