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HDT 2.2 > physiology/pathology of heart disease > Flashcards

physiology/pathology of heart disease Flashcards

1
Q

what is the haemorrhage, haemostasis, thrombosis?

A

haemorrhage; bleed from ruptured blood vessel

heamostasis; stopping bleeding

thrombosis; formation of a clot inside a blood vessel

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2
Q

what are the types of haemorrhage and what are the causes of it?

A

Internal - leaky blood vessels inside body
external - natural opening or break in skin

causes:
trauma - different types of injury 
medical condition - IV; defects in the blood 
intramural; defects in the vessel walls 
EV; defects outside blood vessels
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3
Q

what are the risk factors for haemorrhage?

A
  • medication
  • age
  • trauma
  • disease
  • infection
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4
Q

what are the classifications of haemorrhage?

A

Class I; loss of 15% BV and no change in vital signs
Class II; loss of 15-30% BV
Class III; loss of 30-40% BV and decrease in BP and higher HR
Class IV; loss of >40% BV and possible death

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5
Q

what is the grading scale of haemorrhage?

A 
Grade 0; no bleeding 
Grade 1; petechial bleeding 
Grade 2; mild blood loss
Grade 3; gross blood loss
Grade 4; debilitating blood loss, maybe death
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6
Q

what happens when you have a haemorrhage shock?

A

decreased BV
decreased CO
decreased organ perfusion

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7
Q

what are the clinical and physiological reponses you can have to a haemorrhage?

A
  1. stop further blood loss
    - vasoconstriction
    - haemostasis
    - fibrinolysis
    - surgery
  2. replace lost blood volume
    - volume expanders; crystalloids are aqueous solutions of mineral salts or other water soluble molecules
    - blood transfusion
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8
Q

what is a thrombus made up of?

A

coagulation (fibrin clot) + platelets (haemostatic plug) n

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9
Q

how does tissue damage affect fibrin clot being formed?

A

it amplifies thrombin so more fibrinogen is turned into fibrin clot and this integrates clot to stabilise it

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10
Q

what is the steps of coagulation initiation and amplification?

A

tissue damage causes inactive XII to turn into XIIa and this causes XI to form XIa.
XIa is responsible for causing IX to turn into IXa and IXa causes Factor X to become active Xa
Factor Xa causes prothrombin to form thrombin and this thrombin will convert fibrinogen into fibrin and this fibrin causes a fibrin clot

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11
Q

what is thrombin used for?

A
  1. coagulation amplification
  2. vasoconstriction
  3. platelet activation
  4. fibrin clot
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12
Q

what are some positive and negative inhibitors that allow platelet activation/inhibition?

A 
activators; increase thrombosis 
- collagen
- thrombin
- fibrinogen 
- VWF 
inhibitors; increase anti-thrombotic 
- PGI2
- nitric oxide 
- ITIM receptors 
-
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13
Q

what do platelets secrete when activated?

A

they secrete ADP which is involved in a autocrine pathway to allow platelets to bind together
they secrete TxA2 to allow a loop of platelet activation to occur

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14
Q

how does platelet aggregation occur?

A

so fibrinogen and integrin is released and they can bind to together to then bind platelets together for them to aggregate

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15
Q

what is the difference between a resting and activated platelet?

A 
resting has 
- discoid shape 
- granular 
- active integrins
activated has
- shape change to lamellipedia 
- degranulation 
- aggregation 
- adhesion to sub endothelium 
- spreading
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16
Q

what are some anti-platelet drugs?

A
  • ticagrelor
  • clopidogrel
  • prasugrel
  • tirofiban
  • abciximab
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17
Q

what other roles do platelets have apart form thrombosis and haemostasis?

A
  • wound repair
  • infection
  • immunity
  • cancer
  • inflammation
  • tissue regeneration
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18
Q

what is fibrinolysis?

A

degradation of a fibrin clot

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19
Q

what degrades fibrin clots?

A

plasmin; a serine protease which causes fibrin degradation

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20
Q

what can stop fibrin clot degradation?

A

TAFIa reduced fibrin clot degradation

so there’s an increase clot stability

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21
Q

what are the compensatory mechanism I for a haemorrhage?

A

when you have blood less -> decrease ABP and altered blood gases
lower ABP causes baroreceptor reflex and gases change causes chemoreceptor reflex to both be activated
so more cardiac stimulation and systemic vasoconstriction; allows flow and volume redistribution so increased CO

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22
Q

what are the compensatory mechanism II for a haemorrhage?

A

you have activation of RAAS, vasopressin release, and catecholamine release
these all allow vasoconstriction to occur so more blood volume and increased cardiac stimulation

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23
Q

signs and symptoms of hypovolemia?

A
  • tachycardia
  • rapid breathing
  • decrease systolic pressure, confusion
  • loss of peripheral pulses so less urine
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24
Q

what are the 3 peaks of death for prognosis of hypovolemia?

A

minutes - exsanguination
hours - decompensation
days/weeks - sepsis and organ fialure

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25
Q

what can be the treatment for hypovolemia?

A
  • maximise oxygen delivery
  • stop bleeding
  • replace fluids
  • can use pressor agents
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26
Q

what are some haemostatic agents you can use to reduce bleeding?

A
  1. recombinant factor VIIa; increases formation of IXa and Xa and so fibrin formation
  2. desmopressin; stimulates VWF release and increases VIII levels so more fibrin formation
  3. fibrinogen; causes more fibrin clot formation
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27
Q

what are some antifibrinolytic agents?

A
  • tranexamic acid; stops plasminogen being converted to plasmin so less fibrinolysis so more clot stability
  • aprotinin; inhibits plasmin
  • epsilon aminocaproic acid; inhibits conversion of plasminogen to plasmin
28
Q

why does sympathetic activity increase in essential hypertension?

A

it is due to the increase in descending excitatory activation from spinal cord from pre-motor sympathetic neurones in medulla

29
Q

when is SN activity increased?

A

in hypertension, obesity, heart failure, renal failure, metabolic syndrome, sleep apnea

30
Q

how can you compensate for mild to moderate haemorrhage?

A

increase heart rate and ventricular contractility

allow vasoconstriction to occur and so retention of water and sodium by kidney

31
Q

what happens when you have a more severe haemorrhage?

A

need a blood tranfusion
if ABP falls below cerebral auto regulatory range so less brain blood flow
you can have multiple organ failure so irreversible shock
neutrophils are activated, inflammatory mediators are released so myocardium is depressed as smooth muscle doesn’t constrict so lower ABP so death

32
Q

how does inspiration effect SV?

A

inspiration leads to increased venous return to right ventricle so increased right SV so increased left EDV and SV
it also increases heart rate

33
Q

what neurones and receptors inhibit cardiac vagal neurones? what does this explain as well?

A

the central respiratory neurones and the pulmonary stretch receptors
this causes heart rate to increase and airways widen and this inhibits vagal activity as well

  • they explain respiratory sinus arrhythmia
34
Q

what mechanisms can cause heart rate to increase when reparation increases?

A
  1. voluntary hyperventilation
  2. mental stress/anxiety
  3. systemic hypoxia
  4. exercise
35
Q

what is the effect of exercise in healthy person?

A

increase in respiration and increase in heart rate
- vasoconstriction in splanchnic circulation + kidney
- but vasodilation in the exercising muscle
so increased oxygen to working muscles and ABP is maintained and so is cerebral blood flow ( by auto regulation)
there’s an increase in SV and the CO
SV is increased due to sympathetic activity to ventricular muscle increase
EDV increases due to respiratory and muscle pump

36
Q

where do the pre-motor sympathetic neurones enter?

A

goes in through afferent fibres and up the spinal chord

increased heart rate

37
Q

what are the two types of heart failures?

A

you can have reduced ejection fraction <30%
- systolic dysfunction so dilated ventricle and so impaired contraction
you can have preserved ejection fraction >50%
diastolic dysfunction so stiff ventricular wall and limited filling

38
Q

what is reduced ejection fraction associated with? what is its characteristics?

A

with renal failure and atrial fibrillation

  • smoking
  • MI
  • obesity and age
39
Q

what is preserved ejection fraction associated with? what is its characteristics?

A
  • obesity and ageing
  • AF
  • women
  • renal dysfunction
40
Q

what is the classification of congestive heart failure?

A

I; no limitation of physical activity
II; slight limitation of activity. dyspnoea and fatigue
III; marked limitation of activity. dyspnoea with minimal activity
Iv; severe limitation of activity

41
Q

how can drugs affect heart function?

A
  • directly
  • > force of contraction and rate/rhythm
  • indirectly
  • > vasculature
42
Q

what is stroke volume determined by?

A
  • preload - left ventricular end diastolic pressure
  • afterload; pressure in left ventricle wall during ejection
  • inotropy = contractility
43
Q

what determines contractility?

A

the contractile machinery of myocardial striated muscle is basically the same as that of voluntary striated muscle
need calcium

44
Q

what does inotropic mean?

A

force of heart contraction increase
+ve drugs - increase calcium levels and heart rate
-ve drugs - decrease heart rate e.g. verapamil

45
Q

what is the MoA for digoxin?

A
  • inhibits cell membrane for sodium and potassium ATPase which means reversal of Na+/Ca2+ exchange
    more Ca exchange level means higher level intracellularly so stronger contraction; +ve inotropism

affects electrical physiology of the heart blocking AV conduction and reducing heart rate

46
Q

what is digoxin used for?

A

used for AF with a fast ventricular rate

should be used for first line treatment for AF and heart failure patients

47
Q

what is digoxins toxicity and what are signs and symptoms of it?

A

has a low therapeutic index
patients should be reviewed for clinical signs

signs are bradycardia and arrhythmia and nausea with vomiting

48
Q

what should digoxins dose be?

A

for AF patients a high initial loading dose should be given
dose of 15mcg/kg of lean body weight should be given
maintenance dose is a fraction of the effective dose; changed for renal function looking at creatinine clearance

49
Q

what monitoring is needed for digoxin?

A

monitor for toxicity and monitor creatinine clearance

U&Es should be monitored; annually if stable but more if not

50
Q

what are some examples of sympathomimetics?

A 
dopamine 
- increased force of contraction 
- has alpha effects causing peripheral vasoconstriction 
dobutamine 
- acts on B1
- causes less tachycardia
- increased force of contraction
51
Q

what does adrenaline do?

A

acts on alpha and B1 and B2
causes peripheral vasoconstriction and strong positive chronotropia
e.g noradrenaline is an alpha adrenoreceptor that has a vasoconstrictor action

52
Q

why are phsophodiesterase inhibitors used rarely?

A

used rarely due to increased risk of mortality and used only in severe heart failure
e.g. enoximone

53
Q

what is heart failure?

A

a condition caused by heart failing to pump enough blood around body at right pressure

54
Q

What are the types of heart failure?

A
  • heart failure caused by ventricular systolic dysfunction (LVSD)
  • heart failure with preserved ejection fraction (HFPEF)
  • heart failure caused by damaged heart valves
55
Q

what are symptoms of HF?

A
  • rapid weight gain
  • shortness of breath
  • increased swelling in lower body
  • trouble sleeping
  • loss of appetite
56
Q

what are the general principles for treatment for heart failure?

A
  • medicines adherence
  • multidisciplinary approach to care
  • comorbidities
57
Q

first line treatment for HF and reduced ejection fraction?

A

ACE inhibitors for patients with HF and reduced ejection fraction
start at a low dose and titrate upwards in short intervals until max dose is reached
- measure serum Na and K and assess renal function

58
Q

what’s the counselling for ACE inhibitors?

A

take first dose at night to avoid dizziness caused low BP

report if you have a persistent cough

59
Q

what is first line treatment for HF patients with left ventricular systolic dysfunction?

A

can have beta blockers which are licensed for heart failure with heart failure due to left ventricular systolic dysfunction
start at low dose and increase slowly
assess HR and BP and clinical status after each titration

60
Q

what’s the counselling for beta blockers?

A

dont stop taking unless advised

  • you may experience side effects such as fatigue, dizziness
  • must have regular check ups
61
Q

what’s an alternative to ACE inhibitors for HF patients due to left ventricular systolic dysfunction?

A

can have an ARB as an alternative

seek specialist advice for considering hydralazine in combination with nitrate

62
Q

what treatment should be given to patients with reduced ejection failure and HF?

A

add a mineralocorticoid receptor antagonist with there ACE inhibitor or ARB

63
Q

what counselling points are needed for ivabradine?

A
  • avoid grapefruit juice
  • may cause temporary luminous visual phenomena
  • be careful when driving or using machines
  • might get effects like fatigue, irregular heartbeat
64
Q

what is ivabradine?

A
  • drug that inhibit the If channel in the sinus node
  • slows HR with patients in sinus rhythm
  • less contraction
  • reduces CV death
  • improves left ventricular function
65
Q

if toxicity is suspected what should you do with digoxin?

A

measure serum digoxin every 8-12 of last dose

66
Q

what is sacubitril valsartan?

A

used for treating symptomatic chronic heart failure with reduced ejection fraction
- must be started by a specialist
only in people
- with class II to IV symptoms
- with left ventricular ejection fraction of <35%

HDT 2.2 (10 decks)

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