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CVS Flashcards

1
Q

Hypertension management- what is the 1st drug go to offer if <55 or T2DM

A

ACE inhibitor or angiotensin 2 receptor blocker

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2
Q

Hypertension management- what is the 2nd step to offer if <55 or T2DM

A

ACEI or ARB + calcium channel blocker
Or
ACEi or ARB + thiazide like diuretic

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3
Q

Hypertension management- what is the 3rd step to offer if <55 or T2DM

A

ACEi or ARB + Calcium channel blocker + thiazide like diuretic

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4
Q

Hypertension management- what is the 4th step to offer if <55 or T2DM

A

Look at K

If < 4.5 add spironolactone

If > 4.5 add alpha or beta blocker

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5
Q

Hypertension management changes in > 55 and no T2DM or black ethnicity

A

Start on calcium channel blockers

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6
Q

What is the 2nd stage of hypertension management for black patient

A

Already on calcium channel blocker therefore add ARB not ACEi

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7
Q

what is acute limb ischaemia and how is it caused

A

sudden decrease in limb perfusion which threatens viability of limb = surgical emergency

caused by embolism (thrombus which breaks off), thrombus in situ (atheromatous plaque rupture), trauma (compartment syndrome)

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8
Q

what is the clinical presentation of acute limb ischaemia

A

6 Ps

painful
pallor 
perishingly cold 
pulseless 
paraesthesiae 
paralysis
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9
Q

what happens in acute limb ischaemia

A

occlusion of blood vessel → ischaemia and infarction → death of limb

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10
Q

investigations for acute limb ischaemia

A
  • bedside - vitals, ECG
  • bloods
    • lactate - anaerobic respiration
    • thrombophilia screen (if <50)
    • group and save - transfusion
  • imaging - Doppler US (reduced blood flow through limb), contrast angiography (visualisations of blood vessels - occlusion and narrowing)
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11
Q

management of acute limb ischaemia

A
  • SURGICAL EMERGENCY
  • revascularisation required within 4-6 hours
    • embloectomy - removal of clot
    • angioplasty - balloon catheter and stent
    • by pass surgery
  • heparin infusion after surgery
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12
Q

what conditions does chronic limb ischaemia include

A

peripheral artery disease
critical limb ischaemia
intermittent cluadication

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13
Q

what is peripheral artery disease, critical limb ischaemia and intermittent claudication

A

Peripheral Arterial Disease results in symptomatic reduced blood supply to the limbs. This often occurs as a result of atherosclerosis causing narrowing of the arteries supplying the limbs and periphery.

Critical Limb Ischaemia is the end stage of peripheral arterial disease where there is an inadequate supply of blood to a limb and it cannot function normally at rest.

Intermittent Claudication is the symptom of having ischemia in a limb during exertion that is relieved by rest. This pain is typically a crampy, achy pain in the clad muscles associated with muscle fatigue when walking beyond a certain intensity.

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14
Q

risk factors for acute limb ischaemia and peripheral vascular disease

A

acute - smoking, diabetes, AF

PVD - smoking, coronary or cerebral artery disease, diabetes, hypertension, hyperlipidaemia

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15
Q

what is the cause of peripheral artery disease

A

atherosclerosis which narrows the arteries -> reduced blood flow to downstream organs -> ischaemia

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16
Q

how would someone present with peripheral vascular disease

A

claudication
night pain

ulcers and gangrene 
skin changes 
weak pulses 
pallor 
coldness 
increased CR 
peripheral bruits
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17
Q

what is vascular claudication

A

intermittent crampy pain in the limb during exertion
relieved by rest
occurs after walking in the heart and thigh or buttock

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18
Q

what beside tests can we measure in someone with chronic limb ischaemia

A

ankle brachial index
ECG
bloods - FBC, U&Es, lipids, blood glucose

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19
Q

what is the ABPI and what is the severity classification

A

ankle brachial pressure index - compares BP of upper and lower limb

<0.9 = peripheral vascular disease

> 0.9 normal
0.8-0.9 mild
0.5-0.8 moderate
<0.5 severe

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20
Q

what imaging techniques can be used for chronic limb ischaemia

A

doppler US

angiography

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21
Q

what is the management for asymptomatic and intermittent claudication in chronic limb ischaemia

A

conservative management

  • lifestyle advice
  • statin therapy
  • anti-platelets (clopidogrel)
  • diabetes and BP control
  • encourage exercise
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22
Q

what is the surgical management for chronic limb ischaemia

A
  • angioplasty - with or without stenting (opens up narrowed vessels
  • bypass grafting - younger patients
  • amputations - if gangrene → sepsis (attempt to preserve knee)
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23
Q

what drug should be prescribed to patients with PVD?

A

clopidogrel and atorvastatin

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24
Q

what is shock?

A

reduction of effective blood flow and inadequate tissue perfusion with decreased delivery of oxygen to the capillary exchange bed

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25
Q

what are the 2 causes of shock

A

reduction in CO (cardiogenic, hypovolaemic)

loss in systemic vascular resistance (septic, anaphylactic, neurogenic)

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26
Q

what are the different types of shock

A

cardiogenic
hypovolaemic
neurogenic
distributive - septic, anaphylactic

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27
Q

signs of cardiogenic shock

A 
low BP
increased systemic vascular resistance 
increased HR 
decreased CO
cold and clammy
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28
Q

signs of hypovolaemic shock

A 
increased systemic vascular resistance 
increased HR
decreased BP
decreased CO
cold and clammy
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29
Q

signs of septic shock

A 
reduced systemic vascular resistance 
increased HR 
normal/increased CO
decreased BP
warm and well perfused
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30
Q

signs of neurogenic shock

A 
damage to spinal cord (unopposed parasympathetic innervation)
reduced BO
reduced systemic vascular resistance 
low BP
warm (then goes cool)
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31
Q

what is the significance of tachypnoea in shock?

A

increased lactate - metabolic problem

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32
Q

bedside investigations for shock

A

ECG

bloods - troponin, cardiac enzymes, U&Es, ABG

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33
Q

management of hypovolaemic shock

A

raise legs

fluids

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34
Q

management of cardiogenic shock

A
  • O2
  • analgesia - diamorphine
  • investigations - CVP, BP, ABG, ECG, urine
  • fluid status - plasma expanders of inotropic support
  • reverse causes - MI, PE
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35
Q

what is cardioresp arrest

A

patient who is unresponsive and not breathing properly is in cardiorespiratory arrest and requires CPR

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36
Q

causes of cardioresp arrest

A

Reversible causes for Cardiorespiratory Arrest are (4H’s, 4T’s):

4H’s:

Hypoxia

Hypovolemia

Hyper/Hypokalaemia

Hypothermia

4T’s:

Thrombosis

Tension Pneumothorax

Tamponade

Toxins

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37
Q

basic life support management for cardioresp arrest

A
  • call arrest team and bring fibrillator
  • ABC approach
    • airway - chin lift
    • breathing -Look, listen and feel for breathing for no more than 10 seconds
    • circulation and chest compressions
      • heel of one hand on the centre of the chest
      • second hand on top and interlock fingers
      • ratio of 30 compressions to 2 rescue breaths until a defibrillator becomes available
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38
Q

advanced life support for cardioresp arrest

A
  • Chest compressions should be stopped for less than 5 seconds to assess the rhythm and determine if it is shockable or non-shockable
    • shockable = VF [irregular] or pulseless VT [regular] (wide QRS complex tachy)
    • non-shockable - asystole
  • shockable rhythm
    • defibrillate then continue CPR
    • repeat defibrillation
    • give adrenaline and amiodarone after 3 shocks
  • non-shockable
    • continue CPR
    • obtain IV access and secure airway
    • give adrenaline
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39
Q

what is an arterial aneurysm?

A

localized dilatation of an artery, involving all three layers of the blood vessel, by at least 50% of its original size

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40
Q

what is a triple A?

A

abdominal aortic aneurysm - dilatation of abdominal aorta by more than 50% of its original size

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41
Q

where is the most common site for a triple A?

A

between the renal arteries (L1) and the bifurcation of aorta (L4)

because abdo aorta lacks vasa vasorum so it is weaker

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42
Q

what is an unruptured AAA classed as?

A

abdo aorta larger than 3cm across

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43
Q

risk factors for AAA

A 
Smoking 
Age
Atherosclerosis
Gender (Male)
Ethnicity 
Connective Tissue Disorders - Marfan's Syndrome or Ehlers-Danlos
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44
Q

differentials for AAA

A

Kidney Stones

Back/Muscle Strain

Thoracic Aortic Aneurysm

Myocardial Infarction

Perforated Bowel

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45
Q

which gender is a AAA more common in?

A

3 times more common in men

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46
Q

what are the different types of aneurysms?

A

true - all 3 layers of blood vessels are involved in the aneurysm

pseudoaneurysm - hole in artery allowing blood to spill out and pool around the artery

fusiform - symmetrical bulging of the aneurysm

saccular/berry - asymmetrical bulging of aneurysm (one side of blood vessel dilates, resulting in turbulent flow or weakness)

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47
Q

what law increases the risk of aneurysm rupture

A

Laplace

48
Q

what are the clinical features of an unruptured AAA

A

asymptomatic
can present with abdo/back pain
pulsatile and expansile abdo mass (in time with heartbeat)

49
Q

what are the clinical features of a ruptured AAA

A

severe and acute onset abdo pain - radiates to back
hypotension
pulsatile and expansile abdo mass

50
Q

signs of shock from ruptured AAA

A

pale, cold, clammy, mottled skin

tachycardia

hypovolaemia

oliguria (decreased urine output)

decreased GCS

tachypnoea

51
Q

what does a ruptured AAA present as in an elderly patient

A

renal colic - kidney stones

suspect this in the elderly

52
Q

what are the 3 layers of a blood vessel

A

tunica intima - in direct contact with flowing blood, endothelial cells

tunica media - smooth muscle cells, maintain vascular tone

tunica adventitia - fibroblasts, collagen, macrophages involved in cell trafficking, signalling and repairing injured vessels = contains vasa vasorum

53
Q

what is the pathophys of an arterial aneurysm

A

Trigger - genetic predisposition, local haemodynamic stress

Cellular migration - macrophages, neutrophils, T and B cells

Inflammatory infiltrate - increased chemokines, free radicals, increased MMP activity

Collagen degradation - weakening of tunica media, aneurysmal dilatation, degradation of the collagen through small damages to the vessel wall. Aorta is weakened dilatates over time

Once aneurysm is formed there is progressive enlargement

54
Q

bedside investigations for arterial aneurysm

A

vital signs - tachycardic, tachypnoeic, hypotensive

55
Q

what blood tests would be organised for an arterial aneurysm

A

FBC - anaemia

U&Es - renal function

56
Q

what imaging can be ordered for arterial aneurysm?

A

US or CT (if suspected rupture)

57
Q

what is the national screening programme for unruptured AAA?

A

for all men aged 65+ offered US scan

negative test <3cm

positive test >3cm

58
Q

if positive result on screening for AAA - when will the scan be repeated?

A

small AAA (3-4.4cm) - repeat in 1 year

medium AAA (4.5-5.4cm) - repeat in 3 months

> 5.5cm - urgent referral to vascular surgeons for elective surgery

59
Q

what is the management of a ruptured AAA?

A

ABC

supplemental O2
large bore IV access
urinary catheter
bloods - cross match

patient needs URGENT surgery

60
Q

what are the 2 methods of repair for ruptured AAA?

A

endovascular anuerysm repair (EVAR)

open surgical repair - midine laparotomy

61
Q

what is an EVAR and which patient group is it used on

A

enter through iliac artery - insert stent guided by X-ray

has long term complications - require life long surveillance (ensure functioning)

preferred in patients with co-morbidities (physiologically deranged) - not young and healthy patients

62
Q

what is an open surgical repair for a ruptured AAA - which patient group is it used in

A

midline laparotomy
move duodenum and small bowel out of the way
clamp above and below aneurysm (open aneurysm and stitch in graft)
sow in tube or trouser stent

associated with high mortality - clamping -> end organ ischaemia also large blood loss

for young and healthy patients

63
Q

which type pf AAA rupture has the best prognosis

A

retroperitoneal rupture (tamponade -> limit blood loss)

anterior rupture = high mortality

64
Q

what are the complications of a AA?

A

rupture - haemorrhage
thrombosis and embolism - occlusion of downstream blood vessels -> limb ischaemia

fistula formation

pressing on other structures

haemorrhagic stroke - if rupture in cerebral circulation

65
Q

what is an aortic dissection

A

tearing in wall of aorta

tunica intima splits from tunica media and externa/adventitia

media splits which creates a new channel for blood flow = false lumen

66
Q

what are the layers of the blood vessel wall

A

LIMA

lumen
intima
media
adventitia/externa

67
Q

how would someone with aortic dissection present

A

tearing pain between shoulder blades

hypertension

asymmetrical pulses (different in each arm)

68
Q

risk factors for aortic dissection

A

hypertension
connective tissue disorder - marfans
pregnancy
bicuspid aortic valve

69
Q

what are the 5 killer chest pains

A 
aortic dissection 
MI
oesophageal rupture 
tension pneumothorax 
PE
70
Q

what are the 2 ways aortic dissection creates pathology?

A

reduces blood flow through true lumen = reduces blood flow to other tissues -> ischaemia and infarction

external rupture of aortic dissection leading to cardiac tamponade (compression of great vessels) -> reduced preload and decreased CO

71
Q

bedside tests for aortic dissection

A

vital signs - symmetrical radial pulses, asymmetrical brachial BP

72
Q

imaging for aortic dissection

A

CT - see false lumen

X-ray - see wide mediastinum

73
Q

what are the 2 classes of aortic dissection

A

type A - involves ascending aorta = most serious requires surgical repair

type B - does not involve ascending aorta = less serious, medical management strict BP control

74
Q

what are the complications of a type A aortic dissection

A

compromise blood flow:
carotid dissection -> stroke
coronary dissection -> MI

rupture into pericardium -> tamponade

stretching of aortic valve -> aortic regurgitation

external rupture into thoracic cavity -> exsanguination

75
Q

what are the complications of type B aortic dissection

A

occlusion of coeliac or mesenteric a = gut ischaemia

occlusion of renal arteries = renal failure

extension to iliac arteries = lower limb ischaemia

76
Q

what is haemostasis

A

physiological response that involves the formation of a solid plug due to damage at a blood vessel
prevents loss of blood from circulation

77
Q

what is inflammation

A

body’s response to any form of cellular injury (infection, heat, trauma, hypoxia, radiation)

78
Q

what is the aim of inflammation

A

to remove injurious agents, clear away any dead tissue and trigger healing of damaged tissue

79
Q

what are the harmful effects of inappropriate activation of inflammation

A

anaphylactic shock

autoimmune disease

80
Q

what are the effects of inappropriately activated haemostasis

A

thrombosis

81
Q

what are the 2 types of inflammation

A

acute inflammation - transient (involves vascular changes and neutrophil accumulation)
chronic inflammation - persistent (on-going tissue destruction and repair)

82
Q

what are the cardinal signs of acute inflammation

A 
redness
heat 
pain 
swelling 
loss of function
83
Q

what is the inflammatory cell of acute inflammation

what are the 2 major events of acute inflammation

A

neutrophils

vascular changes = blood vessels dilate to increase blood flow to injury site
endothelial cell activation =increased permeability of capillaries so fluid and small proteins (fibrinogen) leak into the area of damage
coagulation cascade is activated (thrombin produced to convert fibrinogen to fibrin)

neutrophil leukocytsis and accumulation in area of damage
BM increases neutrophil production
endothelial cells are activated which leads to up-regulation of adhesion molecules on endothelial cells (CAM) = neutrophils migrate here

overall both stages lead to formation of acute inflammatory exudate in area of damage

84
Q

what accounts for the warmth and redness in acute inflammation

A

cells damage and die -> activation of endothelial cells

endothelial cells become separated -> capillary bed becomes leaky

therefore fluids and protein leak out into the tissue space -> swelling

85
Q

what are the 2 types of leak

A

transudate (watery) = oedema

exudate (protein + water) = get this in acute inflammation which contains fluid, fibrin and neutrophils

86
Q

what are the 3 parts to acute inflammation

A 
cell injury (triggering factor) 
neutrophils 
vascular changes
87
Q

what role does fibrin have in acute inflammation

A

acts as a solid scaffold which neutrophils can use to move around areas of inflammation

neutrophils phagocytose and kill microorganisms and release enzymes to break down damaged tissue - necrotic material can be cleared away

88
Q

if there is severe injury, what systemic effects occur in response to inflammatory mediators (IL-1, IL-6, TNF-a)

A

fever
CRP secreted by liver
hormone production (ADH, cortisol, adrenaline) = malaise, weakness, appetite loss

89
Q

what does bacteria induce macrophages to produce

A

IL-6 which acts on hepatocytes (liver) to induce synthesis of acute phase protein (CRP)

CRP activates complement cascade and is an opsonin

therefore, CRP facilitates phagocytosis of bacteria

CRP is not specific to bacterial infections - can be high in other inflammatory conditions

90
Q

what are the 3 outcomes of acute inflammation

A

1 - regeneration with resolution
2 - repair with scarring
3 - chronic inflammation - ongoing injury and tissue response

91
Q

what happens in split thickness skin graft

A

zimmer powered dermatome is used to harvest skin

graft contains all epidermis and variable amount of dermis

92
Q

what cells are unable to regenerate

A

permanent - post mitotic cells

brain, cardiomyocytes

93
Q

what does tissue repair result in and what are the 2 steps of reapir

A

fibrous scar formation

organisation and scar formation

94
Q

what happens in the organisation process of fibrous scar formation

A

acute inflammatory exudate is replaced by granulation tissue (healing tissue) = red colour

95
Q

what does granulation tissue consist of

A

fragile complex of proliferating interconnecting capillaries, fibroblasts and macrophages

96
Q

what happens during scar formation

A

granulation tissue is replaced by scar tissue - laid down by fibroblasts
fibrous tissue contains collagen fibres hence white colour

97
Q

what is the disadvantage of scar tissue

A

lacks specialised function of original tissue but it is mechanically strong

98
Q

what is an abscess and what infection initiates it

A

localised collection of pus within a newly formed cavity on a tissue

staph aureus - inflammatory response causes emigration of neutrophils which after phagocytosis release lysosomal enzymes -> damage to tissues and cavity

99
Q

what are the zones of an abscess

A

cavity containing pus (necrotic tissue with dead neutrophils, fibrin, oedema)

periphery = layer of living neutrophils and fibrin

wall/membrane has 2 zones (repair process by body)

  • inner layer of granulation tissue
  • outer layer of fibroblastic tissue (scar tissue)
100
Q

what is the difference between empyema and abscess

A

empyemas are accumulations of pus in pre-existing cavity

whereas abscess is a newly formed cavity

101
Q

what are the advantages and disadvantages of abscess wall/membrane

A

advantage = prevents further spread of infection

disadvantage = prevents release of abscess contents - healing cannot occur therefore requires incision and drainage

102
Q

what is chronic inflammation and list some examples

A

inflammation persists for weeks-months

due to persistent injury

there is an ongoing attempt to heal by fibrosis

persistent infection = H.pylori, TB, hep C
autoimmune disease
non living material = asbestosis, pneumonoconiosis

103
Q

what are the 3 inflammatory cells of chronic inflammation

A

lymphocytes
macrophages
plasma cells (B cells make ab)

104
Q

what 3 processes occur during a chronic gastric ulcer

A

persistent tissue injury and destruction at surface
ongoing inflammatory response to limit damage
fibrosis at base of ulcer

105
Q

consequences of chronic inflammation

A

scarring - obstruction
tissue destruction - perforation or haemorrhage
development of cancer h.pylori, gastric carcinoma)
diversion of nutrients
amyloidosis

106
Q

what type of inflammation is granulomatous

A

chronic

107
Q

what is a granuloma

A

aggregate of activated/epitheloid macrophages

108
Q

common causes of granulomatous inflammation

A

TB
sarcoidosis
crohns disease

109
Q

what type of granuloma is seen in mycobacterium infection

A

caseous necrosis - surrounded by activated macrophages

protective

110
Q

what is the purpose of granulomatous structure in TB

A

contains the mycobacterium to stop progression of infection

can be reactivated if immune system suppressed

111
Q

where does atherosclerosis occur

A

in arteries

112
Q

which layer of the arterial wall does atherosclerosis affect

A

intima

113
Q

what are the modifiable risk factors for atherosclerosis

A

smoking
hypertension
DM
dyslipidaemia

114
Q

what is the bodys response to cell injury in the arteries

A

smoking, hypertension = increases arterial pressure

leads to endothelial dysfunction and inflammatory response = increased permeability, adhesion of macrophages and T lymphocytes to endothelium
leads to migration of inflammatory cells to the intima

macrophages are activated -> production of free radicals which drives LDL oxidation
growth factors are produced and stimulate migration of smooth muscle cells from media

oxidised LDL accumulates within macrophages beneath endothelial cells = foam cells

smooth muscle cells proliferate and produce collagen and other ECM proteins = forms a cap which stabilises the cap

115
Q

what happens when the endothelium is damaged (atherosclerosis)?

A
  • damaged endothelial cells become dysfunctional - increased permeability
  • endothelial cells produce adhesion molecules and cytokines which attract inflammatory cells
  • VCAM1 binds to monocytes of T cells

this leads to recruitment of inflammatory cells to site of injury
-monocytes and T cells adhere to endothelium and migrate into the intima = monocytes become macrophages

116
Q

what is the role of macrophages once inside the initima?

A
  • produce free radicals to drive LDL oxidation = oxidised LDL = atherogenic
  • engulf oxidised LDL and cholesterol crystals = foam cells
  • foam cells produce GFs to stimulate migration of smooth muscle cells from media to intima
117
Q

what happens after oxidised LDL accumulates under endothelial cells

A

lipid laden macrophages sit in the intima layer can progress to atherosclerotic plaque

as the foam cells die, their lipid cytoplasm is released

smooth muscle cells secrete collagen and other ECM proteins -> formation of fibrous cap (scarring)

Revision (20 decks)

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