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Cardiovascular > Pathology 1 + 2 > Flashcards

Pathology 1 + 2 Flashcards

1
Q

What percentage of population are hypertensive?

A

25% - 1 in 4

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2
Q

Why are repeat measurements for hypertension important?

A

Normal variation in individuals at different times of day

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3
Q

What is white coat hypertension?

A

Raised blood pressure due to fear when visiting doctor

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4
Q

Complications of hypertension? (5)

A
  • Cardiac failure
  • cerebral haemorrhage
  • atheroma
  • renal failure
  • sudden cardiac death
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5
Q

Epidemiology of hypertension?

A
  • Incidence varies between countries
  • Higher in black populations
  • Lower in South Pacific
  • Runs in families
  • Rises with age
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6
Q

What are 2 ways to classify hypertension?

A
  • Aetiological (according to cause)

* Clinicopathilogical (according to consequences)

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7
Q

What are aetiological classifications of hypertension? Clinicopathological?

A
  • Primary (no known cause) and secondary (known cause)

* Benign (often primary) and malignant (often secondary)

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8
Q

What happens to blood velocity at arterioles? Why? What happens when arterioles are damaged?

A
  • Decreases
  • Due to resistance
  • BP will rise
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9
Q

What is an example of a drug used to treat hypertension?

A

ACE-Inhibitors

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10
Q

What is primary hypertension? Incidence?

A
  • No obvious cause

* 90% of cases

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11
Q

What are possible causes of primary hypertension? (5)

A
  • Genetic factors (twin studies)
  • Salt intake -25% salt sensitive hypertension
  • Protein intake
  • Renin - Angiotensin system
  • Sympathetic activity (as BP = CO x SVR)
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12
Q

What is salt sensitive hypertension? What can put you more at risk of salt sensitive hypertension? How is it controlled?

A
  • Increase in dietary salt leads to increase in BP
  • Genetic polymorphisms
  • Controlled by reduced salt diet
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13
Q

In renal disease, what is the hypertension?

A

Salt sensitive

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14
Q

What is secondary hypertension? Causes? (5)

A
  • Underlying disease (cause) is implicated
  • Renal disease
  • Endocrine disease
  • Aortic disease
  • Renal artery stenosis
  • Drug therapy - steroids
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15
Q

What are renal causes of secondary hypertension?

A
  • Any renal disease (renal artery stenosis, acute or chronic glomerulonephritis, chronic pyelonephritis, cystic diseases, interstitial nephritis)
  • reduced renal blood flow
  • excess renin release
  • salt and water overload
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16
Q

What is chronic pyelonephritis?

A

Dysfunction of ureters, leading to disruption to renal blood flow and hypertension

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17
Q

What are endocrine causes of secondary hypertension? Examples? (3)

A

Adrenal gland hyperfunction / tumours

  • Conn’s syndrome - excess Aldosterone
  • Cushing’s syndrome - excess corticosteroid
  • Phaeochromocytoma - excess noradrenaline (due to tumour in adrenal gland
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18
Q

Other causes of secondary hypertension?

A
  • Coarctation of the aorta - congenital narrowing of segments of the aorta
  • Drugs - including corticosteroids
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19
Q

What is benign hypertension? How is it diagnosed?

A
  • Cause of serious life threatening morbidity

* Asypmtomatic, incidental finding often health checks

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20
Q

What are complications of benign hypertension? (5)

A
  • Left ventricular hypertrophy
  • Congestive cardiac failure
  • Increases atheroma
  • Increases aneurysm rupture - aortic dissection, Berry aneurysms (catastrophic brain haemorrhages)
  • Renal disease
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21
Q

What are the effects of hypertension on the heart? (8)

A
  • Left ventricular hypertrophy
  • Increased LV load
  • Poor perfusion
  • Interstitial fibrosis
  • Micro-infarcts
  • Diastolic dysfunction
  • Arrhythmias
  • Cardiac failure
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22
Q

What are the effects of left ventricular hypertrophy? (3)

A
  • Sudden cardiac death (due to arrhythmia and poor perfusion)
  • Cardiac failure
  • Affects outcome of other disease
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23
Q

What are the effects of atherosclerosis in the aorta?

A

Can become rigid due to calcification so unable to stretch to receive systolic impulse

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24
Q

What is aortic dissection?

A
  • Hypertension damages tunica intima

* Endothelial tear – blood enters and can split layers apart

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25
Q

What is a subarachnoid haemorrhage? Caused by?

A
  • Uncommon type of stroke caused by bleeding on the surface of the brain
  • Rupture of berry aneurysm caused by benign hypertension
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26
Q

What is the risk of MI with benign hypertension? Stroke?

A
  • Every 10mmHg of diastolic pressure above 85 doubles risk of MI
  • Every 8mmHg of diastolic pressure above 85 doubles risk of stroke
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27
Q

Does hypertension only affect large vessels? What is this?

A
  • No, can cause microvascular injury

* Blood vessel wall changes in small arteries and arterioles

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28
Q

What vessels are usually affected in microvascular injury? Effects of microvascular injury? (2)

A
  • Retina and kidney
  • Thickening of media (smooth muscle)
  • Hyaline atherosclerosis (plasma proteins forced into vessel wall making vessels rigid)
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29
Q

What sign can be looked for in the kidney to diagnose hypertension?

A

Hypertensive arteriosclerosis

30
Q

What is malignant hypertension? What does it develop from? Why is malignant hypertension so urgent?

A
  • Serious life-threatening condition where diastolic pressure >130
  • Can develop from either benign primary or secondary hypertension ( ‘accelerated’ hypertension), or arise de-novo
  • Needs urgent treatment to prevent death from stroke etc
31
Q

Complications of malignant hypertension? (5)

A
  • Cerebral oedema - seen as papilloedema (swelling of optic disc)
  • Acute renal failure
  • Acute heart failure
  • Headache and cerebral haemorrhage
  • Fibrinoid necrosis and endarteritis proliferans of blood vessel walls
32
Q

What can be seen in microscopy when viewing afferent arteriole of kidney in patient with malignant hypertension? (4)

A
  • Onion-skinning (swirling mass of endothelial cells)
  • No lumen
  • Haemorrhage
  • Fibrin deposition in vessel wall
33
Q

What is pregnancy-associated hypertension? Complications?

A
  • Common - up to 10% of pregnancies
  • Increased maternal and foetal morbidity and mortality
  • Pre-eclampsia
  • Eclampsia (resolve following birth/surgical removal)
34
Q

What is the treatment for pre-eclampsia? Eclampsia? What can cause hypertension associated with pregnancy?

A
  • C-section (resolve following deliver)

* Hypertension in pregnancy can occur secondary to silent renal or systemic disease

35
Q

What is a thrombus? An embolism?

A
  • Abnormal mass of coagulant formed from flowing constituents within circulation
  • Abnormal mass of coagulant (in solid, liquid or gaseous state) that travels within circulation and can impact vessels
36
Q

What is ischaemia? Infarction?

A
  • Ischaemia - reduction in tissue/organ perfusion

* Infarction - ischaemic necrosis

37
Q

What is a clot? What is the difference between a clot and thrombosis? (2)

A
  • A coagulum of blood
  • Clot occurs from bleeding outside circulation and is not an active process
  • Thrombosis occurs within blood vessels and is an active, controlled process
38
Q

Where can thrombosis occur? (3) What is this known as?

A

Anywhere but is favoured locations with the following:-

  • Sites of endothelial injury
  • Turbulent blood flow
  • Hypercoagulable blood

Virchow’s Triad

39
Q

What is thrombosis? What 2 things are required to form a thrombus? (2)

A

Intravascular coagulation

  • Platelet activation
  • Fibrin production via coagulation cascade
40
Q

What is the effect of platelet activation? (2)

A
  • Attract and aggregate with other platelets

* Aggregate with fibrin

41
Q

What is the end point of the coagulation cascade?

A

Fibrin

42
Q

Explain the platelet activation pathway (6)

A
  • Endothelium lost (e.g. due to damage) so underlying collagen exposed
  • Collagen binds to glycoprotein Ia/IIb on platelets
  • Von Willebrands Factor (vWF) also binds to glycoprotein Ia/IIb
  • Increases integrin expression on platelets allowing aggregation
  • Glycoprotein IIa/IIb binds fibrinogen
  • Activated platelets release granules to attract other platelets e.g. vWF, platelet activating factor (PAF), thromboxane A2 (TXA2) and ADP
43
Q

What granules are released by activated platelets? (4) What is their purpose?

A
  • vWF, platelet activating factor (PAF), Thromboxane A2 (TXA2), ADP
  • To attract other platelets
44
Q

What are the 2 pathways of the coagulation cascade? What does the intrinsic pathway start with? Extrinsic?

A
  • Intrinsic and extrinsic
  • Hageman factor (FXII) and kalikrien
  • Tissue factor
45
Q

What happens in the extrinsic pathway of coagulation cascade? How is intrinsic pathway measured? Extrinsic?

A
  • Tissue factor joins factor VII (commonest pathway)
  • Prothrombin Time (PT)
  • Activated Partial Thromboplastin Time (APTT)
46
Q

What is the common pathway of both the intrinsic and extrinsic pathways in coagulation cascade? (2)

A
  • Factor Va and Xa activate factor IIa (thrombin)

* Factor IIa and XIII then convert fibrinogen into insoluble fibrin (end point of coagulation cascade)

47
Q

What is vitamin K required for with regards to coagulation pathway? What is vitamin K? Therefore, what happens in liver disease?

A
  • Required to make factors II, VII, IX and X
  • Fat soluble vitamin stored in the liver
  • Liver disease stops production of factor II, VII, IX and X
48
Q

What is the effect of Warfarin with regards to the coagulation pathway?

A

Stops production of II, VII, IX and X

49
Q

What can cause endothelial injury? (6)

A
  • Hypertension (turbulence)
  • Toxins
  • Infectious agents
  • Smoking
  • Autoimmune disease (primary vasculitis)
  • Previous DVT
50
Q

When will thrombosis occur in arterial system? Why will thrombosis not occur in arterial system normally?

A
  • When there is underlying atherosclerosis

* Arterial system is high flow so pro-coagulant materials are washed along before being able to do anything

51
Q

What is atherosclerosis? What sites on an artery are more predisposed to endothelial damage?

A
  • Formation of plaques at sites of endothelial damage

* Sites where arteries branch as there is turbulent flow and hence increased endothelial damage

52
Q

How can atherosclerosis lead to thrombus formation?

A

Surfaces of atheromatous plaque very thin so can rupture and cause thrombus formation

53
Q

What are sites commonly affected by atherosclerosis/thrombosis/emboli? (5)

A
  • Brain (cerebral infarction i.e. stroke)
  • Carotid arteries (TIAs and strokes)
  • Heart (MI, cardiac failure)
  • Aorta (aneurysms -rupture causes sudden death)
  • Legs (peripheral vascular disease with intermittent claudication)
  • Feet etc (gangrene)
54
Q

What are complications of atherosclerosis?

A
  • Thrombosis

* Narrowed coronary artery (stable angina)

55
Q

What is stable (exercise-induced) angina? Unstable?

A
  • Stable - coronary artery narrowed by atherosclerosis

* Unstable angina - plaque ruptures causing thrombosis and large occlusion of coronary artery

56
Q

What is primary vasculitis? What is it causative of?

A
  • Autoimmune disease charactersied by inflammation directed at vessel walls (body attacks own blood vessels)
  • Endothelial injury
57
Q

What does turbulence cause? (2)

A
  • Endothelial injury

* Stasis

58
Q

What is stasis? (2)

A
  • Blood flow normally laminar with constituents in centre of vessel and slow plasma flowing peripherally
  • Stasis is increased contact of platelets etc with vessel walls (no washing out) due to slow flow
59
Q

Where does blood slow down? What does stasis normally occur as a result of?

A
  • Deep venous system

* Faulty valves and venous insufficiency (walls, etc) produce stasis

60
Q

What are causes of hypercoaguability? Examples? (3)

A

Anything that causes increased viscosity

  • Dehydration
  • Polycythemia (increase in number of cells)
  • Leukaemia
61
Q

What is an example of a clot buster?

A

Plasmin

62
Q

What are examples of anti-clotting proteins? (3) How do they work? (2)

A
  • Protein C, protein S and antithrombin III
  • Protein C and S - degrade factor V and VIII
  • Antithrombin III - degrade II, IX and X
63
Q

What is an example of an inherited disorder that causes hypercoaguability? What is this?

A
  • Factor V Lieden

* Mutation at point in factor V targeted by C and S protein

64
Q

What are other inherited hypercoaguability disorders other than factor V Lieden?

A
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin III deficiency
65
Q

What are secondary causes of thrombosis? (8)

A
  • Prolonged immobility
  • Significant tissue injury (burns etc)
  • Antiphospholipid syndrome (autoimmune)
  • MI
  • Atrial fibrillation
  • Cancer
  • Chemotherapy
  • Marantic endocarditis
66
Q

What are low risk secondary causes of thrombosis? (4)

A
  • Contracetpive pill
  • Smoking
  • Renal disease (nephrotic syndrome)
  • Cardiomyopathy
67
Q

How does cancer cause thrombosis? Chemotherapy? Marantic endocarditis?

A
  • Activate coagulation cascade through tumour produced TF, mucin, inflammatory cytokines
  • Chemotherapeutic agents injure endothelium and increase risk of thrombosis
  • Aseptic thrombotic endocarditis (thrombi form on heart valves)
68
Q

What are other forms of embolism other than thromboembolism?

A
  • Air (IV lines, etc)
  • Septic (injecting drugs, abscess rupture)
  • Amniotic fluid
  • Tumour
  • Fat (from bone marrow, gets into blood vessels usually from fractures)
69
Q

What are the effects of lack of ATP? (2) What does this lead to? (5)

A
  • Blocks Na/K/ATPase
  • Ca channels (NCX1 blocked?) so increased intracellular calcium
  • ATPase (makes things worse)
  • Phospholipase (membrane damage)
  • Proteases (membrane and cytoskeleton damage)
  • Endonuclease (DNA damage and breakdown)
  • Mitochondrial permeability (release pro death factors)
70
Q

What are branching vessels that are at risk of endothelial injury (thus atherosclerosis)? What are organs distal to these branches at risk of? (2)

A
  • Coronary vessels
  • Above bifurcation of Aorta
  • Origin and division of carotid arteries
  • Renal arteries
  • Superior Mesenteric Artery

Organs susceptible to embolism and infarction e.g. stroke, small bowel infarction

71
Q

Why should caution be taken with drugs that lower blood pressure?

A

Do not want to lower DBP too much, as heart perfused during diastole

Cardiovascular (28 decks)

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