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Bio > Biology Test 2 > Flashcards

Biology Test 2 Flashcards

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1
Q

Discuss the importance of healthcare associated infections:

A

1) 200,000 cases per year in Australia
2) Unecessary pain and suffering
3) prolonged hospital stay
4) Economic burden/ lost productivity

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2
Q

Differentiate between prevention and the control of infection:

A

Preventions: are precautions you take to stop the micro organisms breaking barrier

Control: managing the spread infection, implementing strategies to control the infection and reduce spread

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3
Q

Explain the different ways in which microbes can enter the body:

A

Portal of entry:

Mouth
Cuts in the skin
Eyes

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4
Q

Describe the defences that prevent this and explain how they work:

A

First line:

Physical barriers:
Skin
Mucous membrane
Secretions

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5
Q

Identify potential risks for transmission of infection:

A

Modes of transmission:

Contact transmission

  • direct contact
  • indirect contact
  • droplet transmission

Common vehicle transmission

  • airborne transmission
  • water-brone transmission
  • food-borne transmission

Transmission via vectors

  • mechanical transmission (one host to another without being infected itself)
  • biological transmission (animal that carries a disease from one host to another)
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6
Q

Discuss ways in which health professionals can act to prevent infection including immunisation:

A

Personal protective equipment:
Correct shoes, mask, apron

Keeping sterile field

Hand hygiene

Education

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7
Q

Definition of obesity:

A

Abnormally high % of body fat generalised or localised

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8
Q

Define the diagnostic criteria of obesity:

A

Body mass index of 30 or higher

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9
Q

What is anthropometry:

A

Is the science of measuring the human body as to height, weight and size of component parts to study and compare the relative proportions under normal and abnormal conditions.

Anthropo = human

Merton= measurement

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10
Q

Describe the types of obesity:

A

Apple /android

  • excess fat on the abdomen
  • Common in men
  • significant correlation with metabolic syndrome
  • deposited around abdominal organs

Pear/ Gynoid

  • excess fat on the things and buttocks
  • common in women
  • non significant correlation with metabolic syndrome
  • deposited under the skin (bum and thighs)
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11
Q

What is the prevalence of obesity in Australia:

A

In Australia 36 percent of adults are overweight and 28 % are obese (64% percent of Australians adults in total)

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12
Q

How do you work out your BMI?

A

weight (kilogram)
Divided by:
Height (meters squared)

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13
Q

Describe the physiological factors contributing to obesity:

A

1) Stress which leads to increased stress hormones and eating as a response to emotions such as boredom, sadness, anger eating
2) Using food as a rewards for comfort or attention

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14
Q

Describe the environmental factors contributing to obesity:

A

Said

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15
Q

What is waist circumference:

A

Waist circumference (WC) provides a simple and practical diagnosis of intra abdominal adiposity (IAA) in patients with an elevated CV risk.

Women
Equal to or above 80cm is considered risk
Equal to or above 88cm is considered high risk

Men
Equal to or above 94 is considered risk
Equal to or above 102 is considered high risk

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16
Q

How do you work out waist to hip ratio?

A

Waist in cm
Divided by
Hip in cm

WHR
Normal men= 1.0
Normal women= 0.9

Obesity and related diseases over
Men =over 1.0
Women= over 0.9

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17
Q

Why is abdominal obesity more harmful?

A

It is more metabolically active

18
Q

What is bioelectrical impedance? (BI)

A

BI is the measurement based on the electrical conductivity of fat and fat free mass. The instrument will allow the calculation of body volumes i.e fat, bone and water.

19
Q

What are environmental factors that contribute to obesity?

A
  • lifestyle behaviours
  • family dietary patterns
  • physical activity patterns
20
Q

What is metabolic syndrome (MetS)

A
  • Cluster of interrelated cardiovascular disease risk factors
  • Upper-body (central) obesity
    • elevated waist circumference
  • High blood sugar
    • BGL > 5.5 mmol/L
  • Hypertriglyceridema
    • Triglyceride equal to or greater than 1.7 mmol/L
    • HDL -C < 1.0mmol/L in men <1.3 mmol/L in women

-Hypertension
Equal to or greater than 130 systolic
Or
Equal to or greater than 85 diastolic

21
Q

What are the complications and comorbidities of obesity?

A

Sex hormone imbalance:
- Hormone dependent tumors

Increased free fatty acids:

Metabolic syndrome: insulin resistance, hypertension, dyslipidemia —>

  • Type 2 diabetes mellitus
  • Cardiovascular disease

Mechanical stress:

  • sleep apnea
  • osteoarthritis
  • low back pain
  • shortness of breath
22
Q

What are prevention and therapeutic strategies for obesity:

A

Lifestyle modification:

  • low calorie, low fat diet
  • Increased physical activity
  • Dealing with any underlying causes e.g counselling for emotional issues

Pharmacological approach:
- an adjunct to lifestyle modification ONLY after 6 months of trial

Bariatric surgery only for patients with:

  • extreme obesity (BMI > 40)
  • BMI 35-40 have heart disease or type 2 diabetes and drug therapy has failed
23
Q

What is atherosclerosis?

A

During atherosclerosis is a disorder of the capillaries:

fatty deposits accumulate in arterial walls over time arteries become thickened and hardened due to excessive build up of plaque.

Artery hardening—> excess build up of plaque—> obstruct blood flow through the vessel causing more resistance

24
Q

What is the pathogenesis of atherosclerosis?

A

1) damage to endothelial cells (i.e hypertension, they become more permeable)
2) lipoproteins enter the intima
3) monocytes turn into macrophages, engulf lipoproteins & turn into “foam cells”
4) macrophages release chemicals, causing smooth muscle cells to enter intima
5) smooth muscle cells also engulf lipoproteins
6) formation of fatty streak
7) smooth muscle cells proliferate (make more of)
8) smooth muscle cells form fibrous cap
9) fibrous cap hardens
10) growth of atheroma (a hard plaque)

25
Q

What are the consequences including blockages and aneurysm? :

A

Rupture & thrombus formation
Weaken vessel wall (aneurysm)
Break off and travel (embolus/ a travelling clot)

Consequences: 
Myocardial infarction (heart attack)

Cerebral infarction (stroke in the cerebral artery suppling the brain)

Aortic aneurysms (commonly in the aorta)

Peripheral vascular disease (gangrene of the legs)

26
Q

What are the pharmacodynamics of statins:

A

Pharmacodynamics (what the drug does to the body)
_____________________

Inhibit enzyme HMG-CoA reductase

Decreased production of cholesterol in liver

Decreased blood cholesterol levels

Statins are a drug class that lower levels of LDL cholesterol (bad cholesterol that causes heart disease)

27
Q

What are the pharmacokinetics of statins:

A

Taken orally, so undergoes h-panic first pass

28
Q

What are the pharmacological effects of statins:

A
  • lower total cholesterol
  • increased expression of hepatic LDL receptors (by decreasing amount of receptors in the liver)
  • Increased HDL
29
Q

What are the adverse effects of statins:

A
  • gastrointestinal discomfort
  • Headaches
  • insomnia
  • dizziness
30
Q

What is arterial blood pressure?

A

Arterial pressure is the volume of blood entering the arteries (both stroke volume and heart rate), the volume exiting the arteries (determined by peripheral resistance) and the compliance of the arterial vessels.

31
Q

What is systolic pressure?

A

Peak arterial pressure during ventricular systole/ contraction

32
Q

What is diastolic pressure?

A

Minimum arterial pressure during diastole/ relaxation

When ventricles stop contracting

33
Q

What is the pulse pressure?

A

The difference between systolic pressure and diastolic pressure

34
Q

What is the mean arterial pressure? (MAP)

A

The average pressure in arteries during one cardiac cycle.

I.e the average driving pressure made up of systolic and diastolic.

35
Q

What are the determinants of MAP?

A

Cardiac output

-the amount of blood ejected by ventricle into artery each minute
Beats per minute (HR)
Blood per minute (SV)

Total peripheral resistance

-diameter of arterioles
(Vasoconstriction the resistance increases)

36
Q

What controls the MAP?

A

Cardiac output—> so the rate of your heart and the volume of your stroke
These are controlled by the autonomic nervous system

The SNS = increases blood pressure (sympathetic)
The PNS = decreases blood pressure (parasympathetic)

Another control of the MAP:
The total peripheral resistance (major factor of resistance is the size of your vessel)
Vessel diameter- controlled by the SNS

37
Q

What is hypertension as defined by WHO?

A

Hypertension is a condition in which the blood vessels have persistently raised pressure (WHO)

The systolic at or above 140mmHg
The diastolic at or above 90mmHg

38
Q

Explain why ‘statins’ are prescribed for people at risk of coronary artery disease?

A

To lower and prevent the spread of high cholesterol and reduce plaque formation in blood vessels as it inhibits the enzymes that produce LDL’s.

39
Q

What are the different types of hypertension?

A

Primary (idiopathic)
- no identifiable underlying cause

Secondary
- underlying cause i.e renal disease, diseases of the arteries etc they have a condition that eventuates to hypertension

Pre-eclampsia
- associated with pregnancy i.e genetics, diets with fats, disease in arteries, stress (?)-is this pre-eclampsia

40
Q

What are the primary risk factors of hypertension?

A
  • cultural background/ race
  • age (blood vessels lose elasticity with age —> high blood pressure
  • gender
  • smoking
  • alcohol
  • stress
  • lack of exercise
  • sodium —> increased fat means increased vessels and blood
  • obesity
  • diabetes mellitus (increased glucose levels)
41
Q

What is the aetiology/pathogenesis of hypertension?

  1. Excess sympathetic activity
A
  1. Excess sympathetic activity
    - increased TPR (total peripheral resistance) through vasoconstriction
    - adrenaline binds to muscle cells, and contract more forcefully because we have stretched the chambers
    - increased CO (cardiac output) because adrenaline binds to smooth muscle cells to constrict the blood vessels
    - stroke volume
  2. Overactive RAAS
  3. Altered neurohumoral control
  4. Metabolic disturbances

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