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Block 31 Cardio-respiratory > high risk of cardiovascular problem > Flashcards

high risk of cardiovascular problem Flashcards

1
Q

What are the non modifiable risk factors for cardiovascular disease?

A

age
sex
family history

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2
Q

what are the modifiable risk factors for cardiovascular disease?

A 
hypertension
diabetes mellitus
obesity
smoking
physical inactivity
dyslipidemia
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3
Q

what are the female specific/ predominant factors for cardiovascular disease?

A
  • pregnancy induced hypertension, preeclampsia, eclampsia
  • gestational diabetes
  • PCOS
  • menopause
  • systemic inflammatory rheumatolgic diseases
  • mental stress/depression
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4
Q

what are the methods of primary prevention of CVD?

A 
ABCDE
Assess risk/aspirin
Blood pressure
Cholesterol
Cigarettes
Diet/weight/diabtes
Exercise
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5
Q

describe tertiary prevention of CVD?

A
  • reduce complications of disease
  • reverse course of disease
  • eg treat heart attack
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6
Q

describe secondary prevention of CVD?

A

Prevent further events in patients with clinical evidence of CVD

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7
Q

describe primary prevention of CVD?

A

prevent cardiovascular events in patient without evidence of CVD

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8
Q

Describe the role of the CVD risk prevention chart?

A
  • used for estimating CVD risk for patients without coronary heart disease or other major atherosclerotic disease
  • they help in making clinical decisions
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9
Q

in what patients should the CVD risk prevention chart not be used in?

A

patients with CHD or atherosclerotic disease, inherited dyslipidaemias, chronic renal dysfunction, diabetics

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10
Q

what clinical decisions should the CVD risk prevention chart not be used for?

A
  • whether to introduce BP mediation when it is above 160/100 or when target organ failure due to hypertension-should be given regardless of chart
  • whether to introduce lipid lowering medication when ratio exceeds 7
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11
Q

on the CVD risk prevention charts what does the red area indicate?

A

10 year CVD risk greater than 20%

those with a risk greater than 30% (line in red area) should be treated immediately

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12
Q

in what situations is the risk of CVD greater than that shown in the CVD risk prevention chart?

A
  • family history of premature CVD or stroke
  • raised triglycerides
  • premature menopause
  • impaired fasting glucose
  • ethnic minorities
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13
Q

what class of drug is aspirin?

A

COX inhibitor

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14
Q

what affect do low doses of aspirin (75-81mg/day) have?

A

irreversibly acetylate serine 530 of cyclooxygenase (COX)-1. This effect inhibits platelet generation of thromboxane A2, resulting in an antithrombotic effect.

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15
Q

what affect do intermediate doses of aspirin (650mg-4g/day) have?

A

inhibit COX-1 and COX-2, blocking prostaglandin (PG) production, and have analgesic and antipyretic effects.

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16
Q

what affect do high doses of aspirin (4-8g/day) have?

A

effective as anti-inflammatory agents in rheumatic disorders; the mechanism(s) of action at these high doses may include both PG-dependent (particularly COX-2-dependent PGE2) and independent effects.

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17
Q

what is the issue with using aspirin at high doses?

A

toxicity, including tinnitus, hearing loss, gastric intolerance

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18
Q

why can aspirin cause GI side effects?

A

it isn’t a specific blocker of prostaglandin synthesis so binding to PG2 can cause GI side effects

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19
Q

what patients should aspirin be avoided in?

A
  • avoid in patients on warfarin

- shouldn’t be given in children as it can cause Reye’s syndrome unless in Kawasaki disease

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20
Q

what is the mechanism of action of statins?

A
  • inhibit HMG CoA reductase
  • reduces intracellular cholesterol levels
  • activates protease which then cleaves SREBPs from endoplasmic reticulum
  • SREBPs translocate to nucleus where they upregulate expression of LDL receptor gene
  • lowers serum LDL
  • also reduces levels of isoprenoids which are intermediates in cholesterol biosynthesis
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21
Q

give examples of lipid lowering drugs?

A

statins
fibrates
specific cholesterol absorption inhibitors

22
Q

what is the mechanism of action of fibrates?

A

decrease serum triglycerides.
variable effect on LDL cholesterol
-inhibit triglyceride synthesis, reduces vLDL release into circulation
-increase lipoprotein lipase activity which catabolises chyclomicrons and vLDL
-increase HDL through improved Apo A-I and APO-II synthesis

23
Q

give examples of fibrates

A

clofibrate (atromid-S)
gemfibrozil (lopid)
Fenofibrate (antara, lofibra, triglide)

24
Q

give examples of specific cholesterol absorption inhibitors?

A

ezetimibe (zetia)

vytorin

25
Q

what is the mechanism of ezetimibe?

A

lowers LDL by inhibiting absorption of cholesterol in intestines
no evidence to suggest it reduces risk of heart disease

26
Q

what is the mechanism of vytorin?

A

combines ezetimibe and a statin

decreases total LDL cholesterol and raises HDL levels

27
Q

what is the purpose of the national CVD prevention programme?

A

set up to develop targeted interventions to optimise care by maximising diagnosis and treatment to minimise both individual risk factors and population risk
aims to deliver commitments set out in long term plan

28
Q

how is the national CVD prevention programme implemented?

A
  • improve early detection and treatment
  • improve effectiveness of NHS health checks
  • expand access to genetic testing
  • support pharmacists and nurses in primary care
  • commisioning CVD prevention audit for primary care
  • improve response of public to somebody having cardiac arrest
  • work with partner organisations to increase number of people who know ABCs
  • increasing proportion of patients that have completed course of cardiac rehabilitation
29
Q

what is the basis of many features of metabolic syndrome?

A

overweight and insulin resistance (that can cause NAFLD)
metabolic syndrome is a combination of risk factors and its role of predicting CVD risk is questionable as the sum of the combined risk factors involved in the syndrome does not offer more than each individual factor added together

30
Q

what are the 2 classification systems for metabolic syndrome?

A
  • IDF (international diabetes federation)

- ATP III NCEP (adult treatment panel 3 national cholesterol education programme)

31
Q

what are the similarities between the ATP III NCEP and the IDF classification of metabolic syndrome?

A
  • triglycerides >1.7mmol/L (150mg/dL)
  • HDL cholesterol <1.03mmol/L-men or <1.29mmol/L-women
  • blood pressure >130/85
32
Q

how are the metabolic syndrome classification systems calculated?

A
  • ATP III NCEP (any 3 of 5 features)

- IDF (large waist + 2 other features)

33
Q

what are the differences between the ATP III NCEP and IDF classification of metabolic syndrome?

A
  • waist circumference (ATP III NCEP - men >102cm/ women >88cm vs IDF - men >94cm / women >80cm)
  • fasting glucose - ATP IIINCEP - >6.1mmol/L vs IDS ->5.6 mmol/l
34
Q

what is metabolic syndrome?

A

group of metabolic abnormalities that confer increased risk of CVD and diabetes mellitus

35
Q

what are the major feature of metabolic syndrome?

A 
central obesity
hypertriglyceridemia
low levels of HDL
hyperglycaemia
hypertension
36
Q

describe the epidemiology of metabolic syndrome?

A
  • worldwide variance due to age/ethnicity etc
  • prevelance increases with age
  • native americans have increased prevelance
  • greater levels of obesity due to global industrialisation so increased prevelance in younger populations
37
Q

what are the risk factors for metabolic syndrome?

A
  • overweight/obesity
  • sedentary lifestyle
  • ageing
  • diabetes mellitus
  • CVD
  • lipodystrophy
38
Q

what is the aetiology of metabolic syndrome?

A
  • insulin resistance
  • increased weight circumference
  • dyslipidaemia
  • glucose intolerance
  • hypertension
  • proinflammatory cytokines
  • adiponectin
39
Q

what is the most accepted hypothesis to describe the pathophysiology of metabolic syndrome?

A

insulin resistance

high circulating fatty acids is major contributor

40
Q

describe the role of increased weight circumference in causing metabolic syndrome?

A

Doesn’t reliably distinguish increases in SC adipose tissue from those in visceral fat (this requires CT or MRI)
Visceral fat could be a marker of excess postprandial free fatty acids in obesity

41
Q

describe the role of dyslipidaemia in aetiology of metabolic syndrome?

A

Patients with metabolic syndrome have high levels of ApoCIII carried on VLDLs and other lipoproteins
This is inhibitory to lipoprotein lipase leading to further hypertriglyceridemia and associated with atherosclerotic CVD
Reduction in HDL-in presence of hypertriglyceridemia a decrease in HDL is due to reduced cholesteryl ester content of lipoprotein core

42
Q

describe the role of glucose intolerance in aetiology of metabolic syndrome?

A

Impaired suppression of glucose production by liver and kidney and reduced uptake and metbaolism in insulin sensitive tissues
The mechanism to compensate for the defects in insulin action fails.

43
Q

describe the role of hypertension in aetiology of metabolic syndrome?

A

In insulin resistance the vasodilatory effects of insulin is lost but still has effects on sodium absorption in kidneys
Insulin increases activity of sympathetic nervous system
Decreased blood flow due to imbalance in production of NO and secretion of endothelin 1
Vasoactive role of perivascular adipose tissue. Reactive oxygen species released by NADPH oxidase impair endothelial function causing vasoconstriction
Hyperuricaemia is a consequence of insulin resistance

44
Q

describe the role of proinflammatory cytokines in aetiology of metabolic syndrome?

A

Increase in IL-1, IL-6 and IL-18, resistin, TNF-alpha and CRP reflect over production by expanded adipose tissue mass
Adipose tissue derived macrophages may be primary source

45
Q

describe the role of adiponectin in aetiology of metabolic syndrome?

A

Anti-inflammatory cytokine produced by adipocytes
Enhances insulin sensitivity and inhibits steps in the inflammatory process
It inhibits gluconeogenic enzymes in the liver
In the muscle in increases glucose transport and fatty acid oxidation
Levels are reduced in metabolic syndrome

46
Q

what is the pathophysiology of metabolic syndrome?

A
  • FFA released from expanded adipose tissue
  • in liver FFA cause increased production of glucose, triglycerides and vLDL secretion
  • reduction in HDL and increase LDL
  • FFA reduces insulin sensitivity in muscle by inhibiting insulin mediated glucose uptake (reduction in glucose to glycogen, and can also increase pancreatic insulin secretion leading to hyperinsulinemia to sodium reabsorption and hypertension)
  • proinflammatory state and contributory to insulin resistance
  • secretion of IL-6 and INF alpha by adipocytes and macrophages leading to insulin resistance and lipolysis of adipose tissue triglyceride stores
  • enhanced hepatic glucose, vLDL production, hypertension and muscle insulin resistance
  • cytokines and FFA increase hepatic fibrinogen and adipocyte production of PAI-1 causing prothrombotic state
  • cytokine stimulate hepatic CRP production
  • reduced adiponectin production
47
Q

what are the clinical features of metabolic syndrome?

A

Typically no symptoms but on examination; waist circumference expanded and BP elevated. Less frequently lipoatrophy or acanthosis nigricans is found on examination

48
Q

what diseases are associated with metabolic syndrome?

A

CVD

type 2 diabetes

49
Q

what are the metabolic alterations seen in metabolic syndrome?

A

Insulin resistance
Increase in ApoB and ApoCIII, uric acid, prothrombotic factors, serum viacoaity, asymmetric dimethylarginine, homocysteine, white blood cell count, proinflammatory cytokines, CRP, microalbuminuria, NAFLD, polycystic ovary, obstructive sleep apnoea

50
Q

how is a diagnosis of metabolic syndrome made?

A
  • criteria fulfilment
  • laboratory tests (fasting lipids, glucose, ApoB, CRP, fibrinoge, uric acid, urinary microalbumin, liver function, sleep study)
51
Q

what is the treatment for metabolic syndrome?

A 
lifestyle
Obesity is the driving force of metabolic syndrome so weight reduction important
Physical activity
Behaviour modification
LDL cholesterol reduction
metformin

Block 31 Cardio-respiratory (15 decks)

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