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medicine year 1 and 2 > case 2 > Flashcards

case 2 Flashcards

1
Q

what happens microscopically in coagulative necrosis?

A

initially no change then progressive loss of nuclear staining accompanied by loss of cytoplasmic detail.

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2
Q

what happens to the texture of the tissue in coagulative necrosis?

A

Initially normal/firm texture then softens as tissue is digested by macrophages.

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3
Q

what is dry gangrene?

A

reduced blood supply due to vascular problems.

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4
Q

what is wet gangrene?

A

infection, swelling from infection occludes blood vessels, superimposed liquefactive necrosis.

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5
Q

what is gas gangrene?

A

muscle necrosis causing sepsis and gas production, commonly clostridium perfringens (type of bacteria)

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6
Q

what is paroxysmal nocturnal dyspnoea?

A

when patients wake up in the middle of the night gasping for breath

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7
Q

what heart condition is paroxysmal nocturnal dyspnoea seen in?

A

pulmonary oedema.

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8
Q

what type of heart failure is paroxysmal nocturnal dyspnoea related to?

A

left sided

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9
Q

what is syncope?

A

medical term for fainting or passing out

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10
Q

what does idiopathic mean?

A

any disease or condition which arises spontaneously or for which the cause is unknown.

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11
Q

what is kussmaul’s sign?

A

paradoxical rise in JVP with inspiration.

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12
Q

what is gastrulation?

A

the formation of the germ layers.

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13
Q

in which weeks is it a pre-embryo?

A

weeks 1-2

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14
Q

in which weeks is it an embryo?

A

weeks 2-8

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15
Q

what is a blastocyst?

A

pre-embryo with cavity.

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16
Q

what does congenital heart disease involve?

A

ASDs (atrial septal defects) and VSDs (ventricular septal defects)-commonly known as holes in the heart.

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17
Q

what are progenitor cells?

A

populations of specific cell types that contribute to the development of specific anatomical structures.

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18
Q

what can defects in cardiac progenitor cells lead to?

A

VSD (ventricular septal defect)

tetralogy of fallot

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19
Q

what is tetralogy of fallot?

A

combination of 4 congenital abnormalities:

  • VSD
  • pulmonary valve stenosis
  • misplaced/overriding aorta
  • right ventricular hypertrophy
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20
Q

what happens in congenital pulmonary valve stenosis?

A

deformity on or near pulmonary valve narrows valve opening and slows blood flow

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21
Q

what happens in right ventricular hypertrophy?

A

right ventricular wall gets thickened

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22
Q

what is the first visceral organ to develop in the embryo?

A

heart

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23
Q

around how many weeks does the heart develop?

A

3 weeks

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24
Q

what is phospholamban?

A

protein that regulates Ca2+ ATPase pump in the cardiac myocytes.

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25
Q

what does phospholamban do?

A

when not phosphorylated inhibits Ca2+ ATPase pump

when phosphorylated loses its ability to inhibit pump-increases contraction.

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26
Q

what is atrophy?

A

decrease in both size and number of cells resulting in a decrease in tissue or organ size.

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27
Q

what pathway is atrophy related to?

A

ubiquitin-proteasome pathway

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28
Q

what are the 2 types of atrophy?

A

physiological (normal) and pathological (abnormal)

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29
Q

what is an example of physiological atrophy?

A

right ventricle of heart visibly decreases in size after birth.

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30
Q

what is an example of pathological atrophy?

A

if you break your leg and can’t use your muscles and they experience atrophy.

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31
Q

what type of atrophy happens in Alzhiemer’s?

A

cortical atrophy-cortical matter shrinks.

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32
Q

what is hypertrophy?

A

increase in cell SIZE (NOT number) which results in an increase in tissue and muscle size.

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33
Q

what is an example of physiological hypertrophy?

A

muscular growth attained by doing weights

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34
Q

what is an example of pathological hypertrophy?

A

cardiac hypertrophy-when in heart failure heart muscle is chronically overloaded + cardiac muscle tries to adapt with hypertrophy.

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35
Q

what is hyperplasia?

A

increase in the NUMBER of cells, usually resulting in an increase of mass of organ or tissue.

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36
Q

what causes hyperplasia?

A

1) growth-driven proliferation of mature cells

2) increased output of new cells from tissue stem cells.

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37
Q

what is the relationship between hyperplasia and cancer?

A

hyperplasia doesn’t equal cancer but it can produce a more dangerous environment for cancer to develop.

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38
Q

what is metaplasia?

A

reversible change in which 1 differential cell type (mesenchymal or epithelial) is replaced by another.
to clarify: the epithelial or mesenchymal cells are the ones being replaced.

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39
Q

what are mesenchymal cells?

A

multipotent stem cells found in bone marrow.

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40
Q

in metaplasia, what is differentiation brought on by?

A
  • cytokines
  • growth factors
  • extracellular matrix components
  • transcription factors
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41
Q

how do extracellular matrix components cause differentiation?

A

promote expression of genes that drive cells towards a specific pathway of differentiation.

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42
Q

when does cellular injury occur?

A

when stress exceeds ability of cell to adapt.

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43
Q

what does the cell response to stress depend on?

A

1) severity of injury

2) type of cell-eg neurone can survive hypoxia for 3-5 mins but skeletal muscle can survive it for a long time.

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44
Q

what can chronic blood shortage lead to?

A

atrophy

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45
Q

what can acute severe blood shortage lead to?

A

parenchyma death

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46
Q

what is the parenchyma?

A

functional tissue of an organ as distinguished from the connective and supporting tissue.

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47
Q

what are the causative agents of cell injury?

A 
hypoxia
free radicals
physical agents-eg hot and cold, blast injuries
chemical-poisons or drugs
biological-infectious organisms
ionising radiation
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48
Q

what cell types are the most vulnerable to ionising radiation?

A 
rapidly dividing ones:
lymphoid tissue
bone marrow
mucosa of GI tract
germinal tissue
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49
Q

what is germinal tissue?

A

tissue made of germ cells-that will go on to form sperm and eggs. found in ovaries and testes.

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50
Q

what happens to water on ionisation?

A

forms highly reactive radicals.

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51
Q

what is vasculitis?

A

inflammation of the blood vessels.

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52
Q

what colour does fibrinoid necrosis stain?

A

bright red/pink.

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53
Q

how does pancreatitis cause fat necrosis?

A

release of lipases causes enzymatic lysis of fats around the pancreas.

54
Q

what is the usual flow of blood?

A

laminar.

55
Q

describe laminar blood flow.

A

concentric layers of blood moving parallel down the length of a blood vessel-the highest velocity of blood in the centre of the blood vessel. (remember ur physics)

56
Q

what are heart murmurs caused by?

A

turbulent (abnormal) blood flow through the heart.

57
Q

what is pericarditis?

A

inflammation of the pericardium, often caused by viral infections.

58
Q

what is cardiomyopathy?

A

a myocardial disorder in which the heart muscle is structurally and functionally abnormal with no underlying heart condition to explain it. (no coronary artery disease, hypertension, valvular, or congenital diseases.)

59
Q

what is the most common cause of cardiomyopathy?

A

genetic

60
Q

what can cardiomyopathy cause?

A

heart failure, arrhythmias, sudden cardiac death

61
Q

what are the 4 main types of cardiomyopathy?

A

dilated
hypertrophic
restrictive
arrhythmogenic right ventricular

62
Q

what is myocarditis?

A

inflammation of the myocardium-heart muscle

63
Q

what is systemic lupus erythrematosus?

A

most common form of lupus-when the immune system attacks its own tissues.

64
Q

what is thyrotoxicosis?

A

excess of thyroid hormone in the body.

65
Q

what does a rhythm strip do in an ECG?

A

allows you to look at a more prolonged period of time.

66
Q

what is normal sinus dysrhythmia/arrhythmia?

A

heart rate changes with your breathing.

67
Q

what is an ectopic beat caused by?

A

ventricular muscle cell randomly fires-send wave in wrong direction around ventricles and they contract earlier than usual.

68
Q

what happens to the QRS complex in an ectopic beat?

A

is wider-because the electricity is travelling abnormally through the ventricles.

69
Q

what is a side effect of digoxin?

A

more ectopic beats.

70
Q

if the P wave isn’t followed by a QRS, where is the problem?

A

the AVN-cos contraction has happened in atria but hasn’t been able to reach ventricles.

71
Q

what does ST elevation usually happen in?

A

acute MI

72
Q

what happens if the QT interval is too long?

A

risk of adverse CV effect being triggered.

73
Q

how do CT scans work?

A

take a series of x rays at different levels and feed into processor to create 3D image.

74
Q

what are some benefits of CT scans?

A

quick
less resource heavy
more accessible-hospitals usually have several Ct scanners running 24/7

75
Q

what are some negatives of CT scans?

A

difficult in certain areas eg soft tissue-muscles, ligaments, tendons
exposure to ionising radiation.

76
Q

about how much ionising radiation does 1 CT scan expose you to?

A

several years of background radiation.

77
Q

what is precession?

A

change in orientation of rotational axis of a spinning body.

78
Q

what is radiopaque dye?

A

dense liquid which dilutes in blood but doesn’t allow x rays to penetrate it.

79
Q

what is orthopnea?

A

difficulty breathing when lying down.

80
Q

what is pro-BNP?

A

hormone secreted by cardiomyocytes in the heart ventricles in response to stretching or fluid overload.

81
Q

what is a key test for heart failure?

A

pro-BNP-if they don’t have elevated pro-BNP it’s highly unlikely they have heart failure.

82
Q

what is a key part of heart failure management?

A

healthy lifestyle changes-balanced diet, exercise, no smoking.

83
Q

what are most heart failure drugs aimed at?

A

reducing the compensatory effects of the body due to the decreased cardiac output.

84
Q

how does the body compensate for decreased cardiac output in heart failure and what are the effects of this?

A

stimulates RAAS-increased heart rate, vasoconstriction, body retains more fluid-these all ultimately increase afterload so make the heart failure worse.

85
Q

what do some heart failure patients require and why?

A

pacemaker or implantable defibrillator- severe heart failure can cause disorganised contractions or rhythms.

86
Q

what is shock?

A

a critical condition brought on by a sudden drop in blood flow through the body.

87
Q

what are the 4 types of shock?

A

cardiogenic
septic
anaphylactic
hypovolaemic

88
Q

what is cardiogenic shock?

A

mechanical or electrical failure of the ventricles, eg due to cardiac tamponade or post MI.

89
Q

what is septic shock?

A

vasodilation due to bacterial toxins leading to a drop in blood pressure.

90
Q

what is anaphylactic shock?

A

exaggerated immune response.

91
Q

what can hypovolaemic shock be caused by?

A

haemorrhage
blood plasma loss due to severe burns
severe loss of fluid eg vomiting, diarrhea.

92
Q

in a young fit healthy person, how much of their blood can be lost before their blood pressure starts to drop?

A

about 30%.

93
Q

when does ability to compensate for blood loss drop?

A

old age
myocardial or respiratory diseases
drugs eg beta blockers

94
Q

draw out a flow chart of CV response to haemorrhage-answer’s in ur notebook.

A

go do it

95
Q

what are the 5 risk factors that present the greatest risk of developing heart disease?

A

1) smoking
2) diabetes mellitus
3) hypertension
4) hypercholesterolaemia
5) physical inactivity

96
Q

what is an inferior MI?

A

infarction of right coronary artery - supplies inferior aspects of the heart.

97
Q

what ECG leads can you see an inferior MI on?

A

II, III, aVF

98
Q

how does smoking increase risk of thrombus formation?

A

chemicals on tobacco smoke damage the vascular endothelium of the blood vessel, increasing development of atheroma.

99
Q

how is a blood clot formed from an atheroma?

A

turbulent blood flow -cap of atheroma breaks off-softer material exposed-platelets aggregate.

100
Q

what is compliance?

A

property of a chamber that describes how easy it is to fill- how much of a change in pressure causes a change in volume. high compliance=easier.

101
Q

what are the 2 types of ischaemic heart disease?

A

chronic

acute

102
Q

what is the 6 month mortality rate of infective endocarditis with treatment?

A

20-25%

103
Q

what are the 2 features of infective endocarditis?

A

endocardial damage

bacteria

104
Q

what is the endocardium?

A

inner lining of the heart. includes heart valves.

105
Q

what is infective endocarditis?

A

infection of the endocardial surface.

106
Q

what types of phenomena can features of endocarditis be caused by?

A

1) vascular phenomena (septic emboli)

2) immunological phenomena

107
Q

what is an infarct?

A

small localised area of dead tissue that has died from lack of blood supply.

108
Q

what is the conjunctiva?

A

clear, thin membrane that covers part of the front surface of the eye and the inner surface of the eyelids.

109
Q

what is dyspnoea?

A

difficult or laboured breathing.

110
Q

what is a dermatome?

A

area of skin that’s supplied by a single spinal nerve.

111
Q

what toxic substance does paracetamol overdose create in the body?

A

(acetaminophen) free radicals.

112
Q

when can you call the pre-embryo the embryo?

A

after implantation.

113
Q

when does the embryo become the fetus?

A

around 8 weeks.

114
Q

what is the difference between the embryo and fetus stage?

A

fetus characterised by growth, embryo characterised by development of body systems.

115
Q

what is the 1st organ to form in the embryo?

A

heart

116
Q

what are positional words that in embryo terms all mean the head of the embryo?

A

cranial
rostral
anterior

117
Q

what does rostral mean?

A

(from the Latin rostrum, to mean towards the nose/beak). therefore refers to the anterior (front) aspect of the head.

118
Q

what does caudal mean?

A

comes from the word tail, means at the tail end.

119
Q

what forms the trilaminar disc?

A

the 3 germ layers.

120
Q

around how many days does heart development start to happen?

A

20 days.

121
Q

what structure forms the flexible membranous component of the septum in atrial septation?

A

Septum primum

122
Q

what is morbidity?

A

the condition of having a disease/the rate of disease in a population.

123
Q

DEFINE rheumatic fever.

A

systemic, POST-STREPTOCOCCAL non-suppurative INFLAMMATORY DISEASE affecting the heart and extra- cardiac sites (eg joints, brain, skin)

124
Q

what is a suppurative infection?

A

one that produces pus.

125
Q

what are the 2 cardiac valves most commonly affected in rheumatic valvular disease?

A

mitral and aortic

126
Q

what is haemoptysis?

A

the coughing of blood.

127
Q

what are the typical clinical manifestations of mitral stenosis?

A 
Dyspnoea
Fatigue
Dizziness/syncope
Palpitations
Oedema
Haemoptysis
Bibasilar crepitation or Crackles
Abnormal heart sounds:
             o   opening snap
             o   first heart sound (S1) is loud
             o   Diastolic murmur
128
Q

how does mitral valve stenosis cause dyspnoea?

A

1) usually results from the elevation in left atrial pressure and pulmonary venous hypertension which leads to reduced compliance of the lungs and a decrease in vital capacity.
2) also may be related to an inability to increase the cardiac output with increased metabolic demands

129
Q

what may result from abnormal reabsorption of the septum primum?

A

patent foramen ovale-cos of the remaining short septum primum not closing the foramen ovale.

130
Q

why might inspiration ‘split’ the second heart sound?

A

the aortic valve closing before the pulmonary valve-the pulmonary valve may stay open longer due to an increased venous return to the right side of the heart, leading to a slightly longer ventricular emptying time on the right.

medicine year 1 and 2 (29 decks)

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