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1st Semester Nursing > Pathophysiology - 1st exam > Flashcards

Pathophysiology - 1st exam Flashcards

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1
Q

What are the three levels of protection (immunity)

A

Physical/Chemical
(Innate, nonspecific)

Inflammatory
(Innate, nonspecific)

Acquired Immunity
(Adaptive: Specific antibodies)

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2
Q

T/F

Inflammatory response varies based on tissue type

A

False

response to an injury/antigen is the same in all tissues

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3
Q

Hallmark signs of inflammation

A 
Swelling
Heat
Impaired Function
Pain 
Redness

SHIPR

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4
Q

Goal of Inflammatory Response

A

To remove the causal agent and limit tissue damage

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5
Q

How long does an acute inflammatory response usually last?

A

8-10 days

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6
Q

Danger of chronic inflammation

A

Can lead to permanent cellular damage:

  • fibrosis of affected tissue/organs
    • narrowing of airways in asthma
  • cancer
    • chronic acid exposure (due to inflammatory response) mutates the DNA in chronic HPV infections of the throat and cervix.
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7
Q

What happens in chronic reactive airway disease?

A

Due to chronic inflammatory response:

Fibrotic scarring and narrowing of upper airways

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8
Q

What is the most important cell type in the inflammatory response?

Why?

A

Mast Cells

Upon activation, begin two separate processes.

  1. Degranulation
    - release of histamine (vasodilation)
    - release chemical factors that attract more WBCs (neutrophils and eosinophils)
  2. Synthesis of substances for chemical defense
    - Platelet Activating Factor
    - activates prostaglandins
    - activates leukotrienes (vascular effects)
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9
Q

What to prostaglandins do?

A

Vascular effects

Produce pain response

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10
Q

What do histamines do? Who produces them?

A

Increases permeability of capillaries

(Allows WBCs and some proteins in to fight invaders)

Produced by mast cells (and basophils)

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11
Q

What would happen to the number of receptors with chronic hyperinsulinemia

A

Downregulation of insulin receptors

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12
Q

How do you get hyperinsulinemia?

A

Healthy pancreas but defective receptors.

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13
Q

What would be the result if the insulin protein receptors in the phospholipid bilayer were dysfunctional?

A

You would end up with hyperglycemia (Type 2 diabetes)

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14
Q

What would be the result if there was an absolute deficiency of insulin (pancreatic beta cells not working)

A

Hyperglycemia (Type 1 Diabetes)

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15
Q

What is one of the biggest factors in insulin resistance?

A

A BMI of more than 30

This is because adipocytes release Resistin, which competes with insulin (binds faster to insulin protein receptors than insulin does).

Resistance is at the cellular level.

This leads to hyperglycemia.

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16
Q

What is a ligand?

A

Any kind of molecule that attaches to a protein receptor on a cell membrane.

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17
Q

Where is insulin made?

A

The beta cells of the pancreas.

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18
Q

What will the cell do if it doesn’t have enough glucose? (If there are low ligand levels)

A

It will send a chemical signal that travels through the bloodstream, stimulating the pancreas to send out more insulin.

It might also up-regulate the number of protein receptors so that it can take in more.

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19
Q

What types of cells are insulin-independent?

A
  • Peripheral nerve cells
  • Retinal cells
  • Endothelial cells (lining arteries, veins, etc).
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20
Q

When is sorbitol produced?

A

When the cell has too much glucose.

Sorbitol is sticky and causes dysfunction in cells as well as H20 accumulation (behaves like sodium). Leads to problems in insulin-independent cells.

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21
Q

What is down-regulation? What precipitates it?

A

High ligand levels will cause a cell to protect itself from too much glucose. It does this by retracting its insulin protein receptors, thus stopping the inflow of glucose.

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22
Q

Who can protect themselves from too much glucose? Insulin-dependent cells or insulin independent cells?

A

Insulin-dependent cells can protect themselves with down-regulation.

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23
Q

What is diabetic neuropathy? What causes it? What does it feel like?

A

Too much glucose in insulin-independent cells of the peripheral nerves (fingers and toes) will lead to an accumulation of sorbitol (thru polyol pathway).

Sorbitol brings water with it. It will cause hydropic swelling and lysis.

It will start with burning/tingling and eventually lead to loss of sensation.

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24
Q

What is retinal neuropathy?

A

Buildup of sorbitol in cells (converted from excess glucose via polyol pathway) will lead to hydropic swelling and cell lysis in insulin-independent retinal cells.

First you will notice black spots, then changes in vision.

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25
Q

What is noncompliance? What causes it?

A

In vascular cells (insulin-independent), AGES (advanced glycated end products) bind glucose permanently with proteins.

Causes damage to endothelial cells.

Production of Nitric Oxide depleted. Arteries become stiff - arteriosclerosis.

Result: High BP, HTN

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26
Q

Does glucose follow insulin into the cell?

A

No. Insulin never enters the cell. It just activates the protein receptor that opens up a GLUT channel for glucose.

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27
Q

Which leads to hyperglycemia - Type 1 Diabetes or Type 2 Diabetes?

A

Both lead to hyperglycemia - it’s the reasons that differ.

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28
Q

Where is the dysfunction in Type 1 Diabetes?

A

In the pancreas/beta cells.

Due to genetic inheritance or, later in life, autoimmune problems.

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29
Q

Where is the causal dysfunction in Type 2 Diabetes?

A

Starts at the cell - the insulin receptors are dysfunctional.

Greatest risk factor is a BMI greater than 30.

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30
Q

What is Nephropathy? What causes it?

A

AGES (advanced glycated end products) permanently bind glucose to proteins.

Causes damage to the vascular tissue in the renal corpuscle.

Endothelial cell production of Nitric Oxide is depleted. Renal corpuscle tissue becomes stiff/non compliant - arteriosclerosis.

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31
Q

What are the 3 processes that might malfunction, causing glucose to be unable to enter a cell?

A

Reception (inability of insulin to attach to protein receptor)

Transduction (after insulin attaches, transmission malfunction inside the cell)

Response (failure of the glut channels to actually open)

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32
Q

Why does diabetes cause frequent urination and excessive thirst?

A

Hyperglycemia makes the kidneys try to excrete excess glucose that’s in the bloodstream.

Normally, the kidneys reabsorb all the glucose, but too much glucose in the blood will surpass the renal threshold and it will be detectable in the urine.

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33
Q

What is the primary job of the phospholipid bilayer?

A

To regulate the flow of substances into and out of the cell.

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34
Q

What do the pancreatic beta cells produce?

What about the alpha cells?

A

Beta: insulin

Alpha: Glucagon

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35
Q

What does glucagon do?

A

It travels to the liver, telling special cells there to release glycogen.

(Glycogen tells the cells to release ATP).

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36
Q

What is cardiac output?

How do you calculate it?

A

The volume of blood your heart pumps per minute.

HR x Stroke Volume = cardiac output.

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37
Q

What is an average Stroke Volume?

A

60-80 ml/Stroke

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38
Q

What physiological response will occur with a decreased stroke volume?

A

Decrease in Blood Pressure
(Decrease in cardiac output)
Heart will pump faster - Increase in heart rate.

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39
Q

What hormone do the adrenals release in a stressful event? What is its effect?

A

Epinephrine

It will attach to beta receptors in the SA node of the heart and increase heart rate.

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40
Q

What is a normal Serum K+ range?

A

3.5-5.0

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41
Q

What is hydropic swelling? What are some causes of it?

A

Cell swells due to increased water in the cell. (Can lead to cell lysis).

Can occur from:
Sodium entering the cell
-failure of sodium-potassium pump due to hypoxia
-hyperkalemia with serum potassium levels of 7+
-hypoparathyroidism with hypocalcemia
Sorbitol entering the cell
maybe Calcium entering the cell (contributing factor with hypoxia)

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42
Q

What would you expect to happen with a patient who has serum potassium levels of 5.9?

A

Cell membrane polarity in excitable cells will move closer to threshold.

-APs will be quick to generate and repolarize - cardiac dysrhythmias
-huge T-waves in EKG
(Possibly twitching, tetany, irritability)

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43
Q

What is the p-wave?

A

Little bump in EKG before the QRS complex.

Signifies atrial depolarization

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44
Q

What is the QRS complex?

A

Up/down squiggle after the p-wave and before the T-wave.

Signifies ventricular depolarization.

45
Q

What is the T-wave?

A

Bump that happens after the QRS complex and before the p-wave.

Signifies ventricular Repolarization.
If it’s big/spiking, it indicates high levels of potassium in system/hyperkalemia (electrolyte imbalance).
Dangerous.

46
Q

What might you suspect with a combative or confused patient and why?

A

Acidosis - (blood pH of less than 7.30) leads to a change in mental status.

Lysed cells due to hypoxia have lactic acid from anaerobic respiration as well as from lysosomes releasing their acids/enzymes.

47
Q

What is a normal body pH?

A

7.35

48
Q

How might you treat acidosis?

What might you want to consider if the patient has blood loss?

A 
Give O2 (oxygen is an acid buffer)
IV fluids - sodium bicarb

BUT, if the pt is going to need a transfusion, you can only give IV saline (0.9% isotonic solution).

49
Q

What benefits might IV saline have for a patient who has decreased blood volume?

A

It can help to restore blood volume which should improve blood pressure.

50
Q

How does Calcium relate to protein channels?

A

Calcium lines the pores on the outside of integral proteins

It regulates the flow of substances (particularly cations) into the cell.

Its double-positive charge repels sodium.
(During action potentials, the sudden change in the cell membrane’s polarity displaces calcium and allows sodium to enter).

51
Q

What are some of the risks of hyperparathyroidism?

A

Parathyroid glands produce PTH, which regulates calcium levels in the bloodstream (serum calcium).

Hyperparathyroidism can create hypercalcemia, which will block sodium from entering the cells.

If sodium can’t enter as easily, the charge of the cell membrane is farther away from threshold.

This will slow down APs, resulting in muscle weakness:

  • cardiac dysrhythmias
  • slowing down of smooth muscle movements (peristalsis)
  • weakness/lethargy (skeletal muscle)
  • inadequate stroke volume and cardiac output
52
Q

What are some of the risks of hypoparathyroidism?

A

Decreased parathyroid function leads to decreased production of PTH, which regulates serum calcium levels.

Too little calcium means that sodium isn’t prevented from entering the cells.

This brings the cell membrane closer to threshold, leading to hyperexcitability and spontaneous AP generation.

Can result in muscle spasticity:

  • twitching
  • irritability
  • tetany
  • cardiac dysrhythmias
53
Q

Why might fat-soluble medications be dangerous?

A

Fat soluble medications aren’t prevented from entering the cell - they diffuse readily and don’t require any special transport proteins.

As a result, they can accumulate and cause problems. (For example, Demerol can slow breathing and kill you, whereas Fentanyl won’t be allowed to enter cell when its limit has been reached).

54
Q

What is myoglobin? How does it relate to traumatic injury?

A

Myoglobin is an integral protein in the cell membranes of skeletal and cardiac myocytes. Its job is to bring extra O2 into the cells.

Damaged skeletal muscle will release myoglobin proteins into the bloodstream where they will clog up the filtration mechanism in Bowman’s corpuscle.

Some breakdown of myoglobin in the renal system will allow it to enter the urine, which will make it look brown. This condition is called rhabdomyolysis.

55
Q

What is rhabdomyolysis?

A

The release of myoglobin into the bloodstream due to cell lysis that obstructs renal perfusion and leads to “coca-cola urine”

56
Q

What is the difference between ischemia and hypoxemia? Why do we care?

A

Ischemia is decreased blood flow, usually local in nature, due to the constriction or blockage of blood vessels. Leads to local hypoxia.

Hypoxemia is a decrease in the oxygen-carrying capacity of the blood or a decrease in available oxygen. Leads to systemic hypoxia.

We care because it determines how we treat the problem.

57
Q

What is the most common cause of cellular injury?

A

Hypoxia: insufficient oxygen to cells.

58
Q

What is the first and primary problem that hypoxia will create in a cell?

A

There won’t be sufficient oxygen for the mitochondria to produce ATP. (If blood flow is inhibited, there won’t be enough glucose, either).

59
Q

Why does it matter whether the mitochondria can carry out aerobic respiration?

A

If they can’t carry out aerobic respiration, they can’t create sufficient ATP to power the sodium-potassium pump.

In addition, the lactic acid created as a byproduct of glycolysis will decrease pH to unsafe levels.

60
Q

Why is it important that the sodium-potassium pump keeps working?

A

It maintains the polarity of the cell membrane, as well as the concentration of potassium inside and the concentration of sodium outside the cell.

When the pump fails, it will allow sodium to enter the cell, bringing water with it. This will lead to hydropic swelling, permeability changes in the internal and external membranes, and eventually lysis (if O2 isn’t restored).

61
Q

In what situation might we find chromatin clumping? What will it do?

A

When we have intercellular pH increase due to lactic acid buildup inside the cell. Can be accumulate as the byproduct of anaerobic respiration (hypoxia) or the rupture of lysosomes.

Calcium influx can also cause chromatin clumping because the extra charge can create free radicals inside the cell, which can damage DNA.

Chromatin clumping will prevent the DNA from replicating - can’t carry out its essential functions - which will lead to cell injury and death.

62
Q

Lysis vs Apoptosis?

A

Lysis = violent. Leads to inflammation and sometimes necrosis.

Apoptosis = clean and tidy, programmed cell death. Safe packaging and elimination of all organelles.

63
Q

What is necrosis? Is it reversible or irreversible?

A

Necrosis is cell death that creates dysfunction in the surrounding tissue - this can lead to dysfunction in the organ.

Characterized by:

  • existence of eschar (black)
  • loss of cell membrane integrity
  • collateral damage to surrounding cells
  • inflammatory response

Necrosis is reversible - new cells can regrow.

64
Q

What is liquefactive necrosis? Is it reversible or irreversible?

A

Liquefactive necrosis occurs in ischemic brain injury when brain tissue is deprived of O2 for 6-7mins.

(It will happen faster in a warm environment and slower in a cold environment)

Cells will lyse due to lack of oxygen. In the brain, this is irreversible.

65
Q

How could closed-head injuries lead to liquefactive necrosis?

A

Swelling in the brain can cause pressure that will exceed your body’s stroke volume. This will prevent new blood from coming into your brain, creating an ischemic event.

66
Q

Why might the cold make you live longer when your brain is deprived of oxygen?

A
  • Keeps Hb tightly bound to O2
  • cholesterol will get firmer in the phospholipid bilayer, preventing some cell processes and keeping the body in a “hibernative” state.
67
Q

What is substance P?

A

A neurotransmitter that makes sure that the pain impulse is transmitted.

68
Q

What are the three kinds of intracellular communication?

A

Contact signaling, Remote signaling and Gap Junctions

69
Q

What is Contact signaling? What type of substances does it typically work with?

A

When a hormone or neurotransmitter uses a receptor on the cell to communicate.

Typically it works with water-soluble molecules. Insulin and substance P are examples.

70
Q

What is Remote signaling?

A

Typically fat-soluble molecules will gain entry into the cell without a receptor protein, and reach a receptor protein in the cell nucleus with its message.

Aldosterone uses remote signaling - sent from the adrenals, tells the cells to pull in sodium.

71
Q

What are Gap Junctions?

A

Cardiac cells (primarily) that share calcium ions (in order to have enough to reach AP).

A type of contact signaling where sharing ions/molecules is key.

72
Q

What ways can cell signaling fail?

A

Reception, transduction or response can fail.

73
Q

What phase of communication is being inhibited by Resistin in Type 2 Diabetes?

A

The reception phase.

74
Q

Define Atrophy

A

Cells shrink and revert to lower level of functioning.

Usually after 3+ days of disuse.

Disuse syndrome would entail multiple tissues.

75
Q

Define hypertrophy

A

Excess use causes cell size to enlarge.

Pathological example: Left Ventricle.

Hypertension causes resistance, which makes LV muscles hypertrophy. Instead of making the heart more effective, it decreases the blood volume and elasticity of the muscle (so it doesn’t snap back as effectively).

Frank Starling law (bigger the heart muscle, the less effective it is).

76
Q

Define afterload

A

Vascular resistance - the pressure the heart has to work against to eject blood.

77
Q

Define metaplasia

A

Cells lose contact inhibition and start piling on top of each other, but still function well.

Benign tumors/moles.

78
Q

Define dysplasia

A

Dysfunctional pileup of cells - irregular borders, chaotic, all different sizes.

Signifies DNA mutations. The more dysregulated mutations your body has, the higher your cancer risk.

79
Q

What are interferons and what do they do?

A

Interferons are cytokines (proteins) that are released by host cells that have been infected by a virus.

They will interfere with the virus’s ability to replicate in other cells.

Also:
activate Killer T cells and macrophages
Up-regulate MHC which increases the cell’s antigen presentation.

(Will cause flu-like symptoms)

80
Q

How do neutrophils and eosinophils know to go to the inflammation site? How do they get there?

A

Mast cells release chemotactic factors into the injury site during degranulation.

Neutrophils and eosinophils follow the chemotactic gradient.

81
Q

How do Mast Cells help increase vascular permeability?

A
  • Histamine granules (degranulation process) target protein receptors on endothelial cells
  • Platelet Activating Factor (synthesis process) causes the liver to release Bradykinin (promotes vasodilation)
  • Release of leukotrienes (promote vasodilation)
  • Release of Prostaglandins (promote vasodilation in addition to pain response)
82
Q

What are some of the effects of vasodilation on the inflammation site?

A
  • WBCs and platelets gain access to site.
  • Blood Serum leaks out, forming exudate
  • Serum albumin leaks out, drawing water along with it.
  • RBCs leak out

These things will lead to swelling and redness, maybe some heat. (The swelling will lead to limited movement).

83
Q

What are eosinophils’ special ability?

A

They create an enzyme in their lysosomes that allow them to dissolve the surface membranes of parasites.

84
Q

What are the two things that Basophils contain/release? What do they do?

A

Histamine - targets receptors on endothelial cells which results in vasodilation

Heparin - anticoagulant, to prevent formation of dangerous blood clots

85
Q

Why does serum albumin increase swelling?

A

When capillaries become more permeable, serum albumin leaks into the interstitial space, bringing water with it.

(Serum albumin creates on oncotic pressure)

86
Q

What is Platelet Activating Factor? What does it do? Who produces it?

A

A ligand produced by the mast cells, Platelet-activating factor works on the liver, causing it to release 3 things:

  • Clotting factors (build a fibrin mesh)
  • Opsonins (tag cells for phagocytosis)
  • Bradykinin (promotes vasodilation)
87
Q

What two molecules do the mast cells produce by way of arachidonic acid? What do they do?

A

Leukotrienes: promote vasodilation

Prostaglandins: produce pain and promote vasodilation.

88
Q

How does an NSAID take away pain?

A

It blocks the conversion of arachidonic acid to prostaglandins, preventing/inhibiting the pain response.

89
Q

What does a high percentage of Bands signify? Is it a good thing or a bad thing? What is this called?

A

A high percentage of bands (immature neutrophils) signifies that the segmented neutrophils (mature) have been used up.

It signifies a bad infection, as the bands have been pulled out of the bone marrow before they’ve reached their effectiveness potential.

A high number of bands in lab values is called a “left shift”

90
Q

What four things do Macrophages do?

A

Phagocytosis
Present Antigens to helper T cells
Create new blood vessels (angiogenesis)
Release cytokines and growth factors to promote wound healing.

91
Q

What can happen when neutrophils and macrophages die?

A

Local tissue damage

Increased pH of surrounding tissues (and sometimes blood, measurable in labs)

92
Q

How do antihistamines work?

A

They compete for the same protein receptor site on endothelial cells as histamine uses.

As a result, they inhibit vasodilation. (With proper dosing, they don’t block it entirely)

93
Q

What do platelets do? What happens if you have too many? Too few?

A

Platelets help with clotting by walling off the site.

Too many can increase the risk of clot formation.
Too few can result in a) hemorrhage, and b) spread of the antigen

94
Q

What’s another name for CD4 cells? What do they do?

A

CD4 cells are T-helper cells. They are lymphocytes - a type of WBC.

CD4 is actually the name of the protein that T-helper cells present for attaching to antigen-presenting macrophages. Allows them to learn the shape of the antigen so that they can pass the information along to B- and Killer T cells.

95
Q

How does HIV harm the immune system?

A

HIV neutralizes the CD4 protein on T-helper cells, preventing them from docking with the antigen-preventing macrophage.

96
Q

Once the T-helper cell has interacted with an antigen-presenting macrophage, what will it do?

A

Release cytokines to attract Naive B cells (to teach it the shape of the antigen)
Call more macrophages to the site
Activate the Killer T cells

97
Q

What does the Naive B cell do after it interacts with the T-helper cell?

A

It will differentiate into:

Plasma cells: antibody-creating factories

Memory cells: will live for decades with a memory of the antigen’s shape

98
Q

What do antibodies do?

A

They bind with the antigen, marking it for phagocytosis.

99
Q

What is a “plasma protein system”? Where does synthesis of the proteins in the systems begin? What three did we learn about?

A

Plasma protein systems are cascades that are initiated by the inflammatory response.

The synthesis begins in the Liver

  • Clotting System
  • Complement System
  • Kinin System
100
Q

What is the clotting system?

A

The clotting system is initiated by Platelet Activating Factor (created by the mast cells) which notifies the liver to start the cascade.

Its job is to prevent the spread of infection by physically walling off the area.
Uses a fibrin mesh, which has three jobs:
-framework for healing
-retains phagocytes
-traps pathogens in pus

101
Q

How would you test to see if the clotting system is activated?

A

Lab values for:

Fibrinogen (would increase)
ESR (would increase)

102
Q

What is the complement system? How is it initiated?

A

The complement system is initiated by Platelet Activating Factor (mast cells). It tells the liver to release opsonins, which tag antigens for phagocytosis.

103
Q

How would you test to see if the complement system has been activated?

A

Lab values:

CRP (c-reactive protein) increase

104
Q

What is the Kinin system? What is its job?

A

Initiated by Platelet Activating Factor, which tells the liver to produce Bradykinin.

Causes vasodilation, increasing vascular permeability.

105
Q

How would you test to see if the Kinin system has been activated?

A

Lab tests:

Bradykinin levels would increase

106
Q

What does Procalcitonin measure?

A

Increased lab values of procalcitonin signifies that the infection is bacterial.

107
Q

What does serum lactate indicate?

A

An increased serum lactate level indicates acidosis.

It will be increased if there is cellular hypoxia (anaerobic metabolism)
It increases with all types of vascular shock

108
Q

What vital signs can be affected by the inflammatory response? (Why)?

A

Decreased Level of Consciousness (Severe vasodilation from systemic inflammation, Acidosis from inflammation)

Decreased BP/MAP (can be exacerbated by inflammatory response due to depleted vascular volume)

Fever (Acidosis due to phagocyte activity)

Resp. Rate increase (trying to blow off CO2 to raise blood pH)

Decreased capillary refill (decreased blood volume due to systemic inflammation)

1st Semester Nursing (5 decks)

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