Test 4 Study Guide Part 4 Flashcards

1
Q

Average blood pressure in systemic circulation:

Average blood pressure in respiratory circulation:

A

120 / 80 mmHg

22 / 8 mmHg

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2
Q

Pulse pressure:

  • Define:
  • Relates to:
A
- Define:
systolic - diastolic = pulse pressure
E.G. 120 - 80 = 40
- Relates to:
stroke volume
strength ventricular contraction
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3
Q

Hypertension:

  • Defined at:
  • Primary (essential):
  • Secondary:
A
- Defined at:
> 130 mmHg systolic
> 90 mmHg diastolic
- Primary (essential):
No known cause
90% of causes
- Secondary:
known cause
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4
Q

When does risk begin for high blood pressure?

- What is the medical goal?

A

> 115 mmHg systolic
75 mmHg diastolic
- What is the medical goal?
no more than 120 mmHg systolic, and 80 mmHg diastolic

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5
Q

Causes of secondary hypertension:

A

Diseases of kidney and arteriosclerosis of the renal arteries.
reduction of renal blood flow can cause hypertension do to renin release

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6
Q

What must be associated with essential hypertension?

A

Cardiac output could have increased (increased blood volume is associated with this)
Peripheral resistance could have increased

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7
Q

High salt diets can cause increased blood pressure because:

A

higher blood osmolality -> more ADH -> more retained water (plasma) -> higher blood pressure

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8
Q

Inappropriately high levels of aldosterone secretion are correlated with:

A

age (old people often have this)
higher blood osmolality and hypertension (retained salt -> higher blood osmolality -> more ADH -> more retained water (plasma) -> higher blood pressure)

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9
Q

Glomerular Filtration Rate:

- Relation to hypertension:

A

How much plasma is filtered out by the kidney
- Relation to hypertension:
The more inefficient the kidney’s the higher the salt conc. the higher blood pressure

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10
Q

Potassium’s effect on salt’s effect on blood pressure:

A

Increased levels of K+ can reduce NaCl’s ability to cause hypertension.

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11
Q

Issues associated with hypertension:

A

Organ failure
Enlargement of the heart
Stroke
Atherosclerosis

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12
Q

How is higher blood pressure treated?

A

1st:
- lifestyle: exercise, weight loss, stop smoking, reduce alcohol intake
2nd:
diuretics:
3rd:
B1 adrenergic antagonists (atenolol)
4th
angiotensin converting enzyme inhibitors (ACEIs) and Angiotensin-II Receptor Blockers (ARBs)
- Act to decrease salt levels, decreased osmolality, increased

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13
Q

Angiotensin Converting Enzyme inhitors (ACE inhibitors) and Angiotensin 2 receptor blocker (ARB) act to do what?

A

Decrease release of aldosterone (which increases salt retention)
- This will lower blood pressure
Reduce vasoconstriction caused by angiotensin II
Reduce ADH secretion slightly

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14
Q

What is the most common drugs to treat hypertension?

A

Angiotensin Converting Enzyme inhitors (ACE inhibitors) and Angiotensin 2 receptor blocker (ARB)

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15
Q

Shock:

A

Inadequate perfusion of the tissue

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16
Q

Hypovolemic Shock:

  • Define:
  • Causes:
A
  • Define:
    Inadequate perfusion of tissues do to inadequate blood supply
  • Causes:
    burn, wound
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17
Q

Hypovolemic Shock:

- Body response:

A

Baroreceptors: increase vasoconstriction and heart rate

Activate renin angiotensin system: (increased salt, pulls fluid into the plasma, vasoconstriction

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18
Q

Hypovolemic Shock:

- Symptoms:

A
Low blood pressure
Cold skin (blood diverted to brain and heart)
Decreased urine production (ADH and Aldosterone, increased production)
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19
Q

Septic shock:

A

Endotoxin activates nitric oxide synthase within macrophages.
Causes vasodilation and sever hypotension (shock)

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20
Q

Anaphylactic shock:

A

Widespread release of histamine causes vasodilation and hypotension

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21
Q

Damage to brain or spinal cord, results in loss of sympathetic tone (which will cause vasodilation)

  • Medula could be damaged
  • Spinal cord injury
A

Neurogenic shock:

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22
Q

Cardiac failure, cardiac output has dropped low enough that perfusion cannot be maintained.

  • myocardial infarction
  • Severe valve damage or cardiac arrhythmia
A

Cardiogenic Shock:

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23
Q

Cardiac output of a ventricle is insufficient

A

Congestive Heart Failure:

24
Q

Left Ventricular failure is usually caused by:

A

Myocardial infarction
aortic valve stenosis
incompetence of aortic or mitral valve

25
Q

Heart failure can also be caused by changes in K+ and Ca2+ balance

A

True

26
Q

Congestive is applied to heart failure because:

A

Usually left ventricle fails -> right ventricle pushes harder to counteract it -> increased pulmonary pressure causes fluid build up in lungs

27
Q

If the right ventricle fails where will we see congestion?

A

The systemic circulation will have edema, not congestion

28
Q

Chronically low cardiac output: is associated with:

- Causes:

A

elevated blood volume and dilation and hyptertophy of ventricles.
- Causes:
Less ventricular volume due to ventricular hypertrophy
Body has to overwork to compensate
Vasoconstriction compensates for low stroke volume (due to smaller end diastolic volume)

29
Q

Treatment for chronically low cardiac output:

A

Drugs that…

  • Strengthen contractility (digitalis)
  • vasodilators (nitroglycerin)
  • Beta adrenergic receptor blockers (atenolol), compensate for overactive sympathoadrenal system
  • Diuretics (lower blood volume)
  • ACE inhibitors ARBs
30
Q

Endotoxin is a portion of lipolysaccharide, as it is shared by many pathogens, it is likely targeted by ____ immunity.

A

Innate

31
Q

Ortho define:

A

straight upright

32
Q

Lowering of blood pressure upon standing.

A

Orthostatic hypotension:

33
Q

Hypotension after eating

A

Postprandial hypotension:

34
Q

Normally baroreceptor reflexes stop orthostatic hypotension.

What causes it to happen anways?

A

Postprandial hypotension
Low blood pressure from dehydration
Medications (beta-adrenergic receptor blocks)
Postprandial hypotension (common among elderly)

35
Q

Innate (nonspecific) Immunity:

Adaptive (specific ) immunity:

A

All mechanisms, intracellular, and extracellular, including barriers like the skin and mucous membranes, which act to hinder large groups of pathogens.
Taylor made responses for specific pathogens. Lymphocytes.

36
Q

Pathogen-Associated Molecular Patterns (PAMPs):

  • Define:
  • Two common PAMPs:
A
- Define:
Molecular domains or molecules which are  commonly associated with pathogens which innate immune cells have hard programed receptors to recognize.
- Two common PAMPs:
Lipopolysaccharide
Peptidoglycan
37
Q

What are the receptors that recognize PAMPs called?

A

Pathogen Recognition Receptors (PRRs)

38
Q

Toll-like receptors:

  • class of:
  • how many identified?
  • purpose:
A
- class of:
Pathogen Recognition Receptors
- how many identified?
10
- purpose:
recognize non-human (non-self) pathogen associated domains
39
Q

NOD-like receptors:

  • What are they?
  • What do they do?
A
  • What are they?
    Intracellular receptors, which detect bacterial metabolic products (PAMPs and DAMPs).
  • What do they do?
    Activate intracellular host defense mechanisms like autophagy
40
Q

Chemokine:

A

Cell attractant molecules

41
Q

Cytokine:

A

Cell growth and regulator molecules

42
Q

Activation of a pathogen recognition receptor by a innate immune cell usually results in?

A

Cytokine and chemokine release

43
Q

Mutated NOD-genes contributes to what disease?

A

Chrohn’s disease

44
Q

Complement system:

  • How many protein:
  • How it the complement system activated?
  • What does it do?
A
  • How many protein:
    9 proteins
  • How it the complement system activated?
    Recognition of an antigen antibody complex
  • What does it do?
    Promote phagocytosis, lysis, and other issues
45
Q

Danger-Associated Molecular Patterns:

  • Define:
  • What do they do:
A
  • Define:
    Products of cell death (necrosis), which are produced when cells do not die form apoptosis.
  • What do they do:
    similar to PAMPs, but activated by mass tissue damage. Promote inflammation (proinflammatory)
46
Q

Three groups of phagocytic cells:

A
  • Neutrophils:
  • Mononuclear phagocytes:
  • Organ specific phagocytes:
47
Q

Neutrophils:

A

Phagocytic cells

48
Q

Mononuclear phagocytes include:

A

Monocytes (in the blood)
Macrophages (in the tissue), derived from monocytes
Dendritic cells (in the tissue), derived from monocytes

49
Q

Where do we have a high conc. of dendritic cells?

What are dendrites descended from (hint: same as macrophages)

A

In the skin.

Monocytes which leave the bloodstream

50
Q

Organ specific phagocytes:

  • Located in:
  • Examples:
A
- Located in:
Liver, brain, lungs, spleen, lymph nodes
- Examples:
Microglia
Kuppfer cells
51
Q

Kuppfer Cells:

A

Cells fixed in the hepatic sinusoids of the liver, which help eliminate pathogens from the blood

52
Q

NOD in NOD-like receptor stands for:

A

nucleotide-binding oligomerization domain-like receptors

53
Q

Alpha-1 andronergic receptors effect:

A
Vasoconstriction of smooth muscles in the veins of:
- Skin
- Gastrointestinal tract
- Kidney
- Brain
Also glycolysis and gluconeogenesis
54
Q

Alpha-2 andronergic receptors effect:

A

Negative feedback receptors on presynaptic cells

55
Q

Beta-1 andronergic receptors effect:

A

Increase heart rate, causes renin release from juxtaglomerular cells

56
Q

Beta-2 andronergic receptors effect:

A
Lungs dilate (relax smooth muscle of bronchioles)
juxtaglomerular apparatus release renin
Inhibit insulin release
Glycolysis
gluconeogenesis
lipolysis