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Pathophysiology > Module 1 > Flashcards

Module 1 Flashcards

1
Q

Define atrophy and how it applies to pathophysiological processes

A

Atrophy: Decrease in the size of a tissue, organ, or the entire body. In atrophy of an organ or body part, there may be a reduction in the number or in the size of the component cells, or in both. Certain cells and organs normally undergo atrophy at certain ages or under certain physiologic circumstances. Atrophy in general is related to changes in nutrition and metabolic activity of cells and tissues.

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2
Q

A widespread or generalized atrophy of body tissues occurs when?

A

Under conditions of starvation, whether because food is unavailable or because it cannot be taken and absorbed due to the presence of disease. The unavailability of certain essential protein components and vitamins disturbs the metabolic processes and leads to atrophy of cells and tissues. Associated with the widespread atrophy due to lack of protein is the atrophy of certain tissues that is due to deficiencies of specific vitamins.

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3
Q

Define hypertrophy

A

Increase in size of cells (organs). Increase in cell size, the heart and kidneys are particularly prone to enlargement. It is associated with an increase accumulation of protein in the cellular components & not with an increase in cellar fluid. It is caused by hormone stimulation or increased functional demand.

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4
Q

What is hyperplasia?

A

An adaptive increase in the number of cells that can cause enlargement of tissues or organs

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5
Q

6 ways cells can change?

A

Atrophy, Hypertrophy, Hyperplasia, Metaplasia, Dysplasia, Anaplasia

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6
Q

Hypertrophy vs. hyperplasia

A

Hypotrophy-individual cells enlarge

Hyperplasia- adaptive increase in the number of cells that causes tissue enlargement

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7
Q

Which of the 6 ways in which cells change is considered precancerous?

A

Dysplasia

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8
Q

Metaplasia

A

An adaptive change of one cell type for another to suit the environment. Reversible replacement of one mature cell type by another (Epithelium changes in smokers)

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9
Q

What is an example of Metaplasia?

A

Squamous metaplasia of the bronchial epithelium due to smoking
or
Gastric or glandular metaplasia of the GE junction in Barrett’s Esophagus

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10
Q

Is metaplasia reversible?

A

yes, but it can also progress to a more detrimental growth (ie dysplasia)

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11
Q

Dysplasia

A

Disordered growth of tissues resulting from chronic irritation or infection. Abnormal changes in size, shape and organization of mature cells (can lead to cervical cancer)

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12
Q

How can cells get injured?

A
  • Hypoxia
  • Mechanical forces
  • Extremes of temperature
  • Electrical injuries
  • Chemical agents and drugs
  • Biological agents
  • Ionizing radiation
  • Nutritional imbalances
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13
Q

What is hypoxia?

A

A type of cell death. This is caused by a lack of oxygen to the cells. It causes ATP powered pumps to malfunction. ATP is depleted because little to no oxygen is given to the cell.

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14
Q

What happens during a hypoxic injury

A

Blood flow falls below a certain critical level that is required to maintain cell viability. The interrupted supply of oxygenated blood to cells results in anaerobic metabolism and loss of adenosine triphosphate (ATP), and cellular membrane disruption

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15
Q

Problems hypoxic injury creates

A

Disrupts the ability of mitochondria to produce ATP, which in turn prevents normal functioning of the Na/K pumps, which leads to leads to swelling & lysis. It is reversible if oxygen is restored quickly.

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16
Q

Mechanisms of cell injury:

1) Depletion of ATP: No energy
2) Impaired calcium homeostasis
3) Free radical injury

A

1) Depletion of ATP: No energy
2) Impaired calcium homeostasis: Activates pathways that lead to cell death
3) Free radical injury
- Generation of ROS
- Low chemical specificity, highly reactive
- Disrupts pathways
- Damages mitchocondrial DNA > apoptosis

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17
Q

What is ionizing radiation?

A

Ionizing radiation is radiation with enough energy so that during an interaction with an atom, it can remove tightly bound electrons from the orbit of an atom, causing the atom to become charged or ionized

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18
Q

how does ionizing radiation cause cell injury?

A

It affects cells by causing ionization of molecules and atoms in the cell, by directly hitting the target molecules in the cell, or by producing free radicals that interact with critical cell components. it can immediately kill cells, interrupt cell replication, or cause a variety of genetic mutations, which may or may not be lethal. Most radiation injury is caused by localized irradiation that is used in the treatment of cancer.

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19
Q

how does non-ionizing radiation cause cell injury?

A

unlike ionizing radiation which can directly break chemical bonds, nonionizing radiation exerts its effects by causing vibration and rotation of atoms and molecules. all of this vibrational and rotational energy is eventually converted to thermal energy.

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20
Q

Decreased oxygen concentration in the tissues

A

hypoxia

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21
Q

Decreased oxygen in the blood

A

hypoxemia

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22
Q

how does hypoxia cause cell damage?

A

It deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP. Damage occurs due to hypoxia, even if it starts out as hypoxemia.
-diminishes ATP production

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23
Q

hypoxia causes ATP depletion or power failure in the cell, what widespread effects on the cell’s structural and functional components will this have?

A

As oxygen tension in the cell falls, oxidative metabolism ceases, and the cell reverts to anaerobic metabolism, using its limited glycogen stores in an attempt to maintain vital cell functions. cellular pH falls as lactic acid accumulates in the cell. this reduction in pH can have adverse effects on intracellular structures and biochemical reactions.

  • Na/K+ ATPase cannot run fast enough so the cell swells up with water
  • anaerobic metabolism used = lactic acid produced and the acid damages cell membranes, intracellular structures, and DNA
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24
Q

free radicals

A

free radicals are molecules with an unpaired electron in the outer electron shell

  • extremely unstable and reactive
  • can react with normal cell components
  • damaging them
  • turning them into more free radicals
  • normally removed from body by antioxidants
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25
Q

injured cells accumulate what?

A

calcium

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26
Q

calcium

A

Cell usually maintains low intracellular calcium
when calcium is released into the cell, it :
-acts as a second messenger inside the cell
-turns on intracellular enzymes, some of which can damage the cell
-can open more calcium “gates” in the cell membrane
letting in more calcium
calcium cascade

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27
Q

the increased calcium level may inappropriately activate a number of enzymes with potentially damaging effects. These enzymes include:

A

the phospholipases that are responsible for damaging the cell membrane, proteases that damage the cytoskeleton and membrane proteins, ATPases that break down ATP and hasten its depletion, and endonucleases that fragment chromatin.

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28
Q

apoptosis

A

programmed cell death “cell suicide”

  • removes cells that are being replaced or have been worn out
  • removes unwanted tissue
  • normal process in the body
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29
Q

necrotic cell death

A

necrosis refers to cell death in an organ or tissue that is still part of a living person
unregulated death caused by injuries to cells
cells swell and rupture
inflammation results

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30
Q

how does necrosis differ from apoptosis?

A

differs in that it involves unregulated enzymatic digestion of cell components, loss of cell membrane integrity with uncontrolled release of the products of cell death into the intracellular space, and initiation of the inflammatory response.
In contrast to apoptosis, which functions in removing cells so new cells can replace them, necrosis often interferes with cell replacement and tissue regeneration.

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31
Q

apoptosis or programmed cell death how do damaged or worn out cells commit suicide

A

Turn on their own enzymes inside the cell
digest their own cell proteins and DNA
are then destroyed by white blood cells

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32
Q

apoptosis can be caused by?

A

signaling factor attached to death domains of cell surface receptors
mitochondrial damage inside the cell
protein p53 activated by DNA damage

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33
Q

metaplasia

A

Change in cell
represents a reversible change in which one adult cell type is replaced by another adult cell type
metaplasia usually occurs in response to chronic irritation and inflammation and allows for substitution of cells that are better able to survive under circumstances in which a more fragile cell type might succumb

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34
Q

Cardiovascular system pain

A

1) Costochondritis
2) Angina
3) Myocardial Infarction

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35
Q

Abdominal Pain

A

1) Pancreatitis
2) Cholecystitis
3) Cholelithiasis
4) Appendicitis
5) Peritonitis
6) Nephrolithiasis

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36
Q

Pelvic Pain

A

1) Ovarian Cysts

2) Testicular Torsion

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37
Q

Musculoskeletal Pain

A

1) Gout
2) Osteoarthritis
3) Rheumatoid arthritis
4) Sciatica
5) Osteomyelitis
6) Cellulitis

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38
Q

A MEDICAL SYMPTOM is?

A

A departure from normal function or feeling which is noticed by a patient, indicating the presence of disease or abnormality. A symptom is subjective, observed by the patient, and cannot be measured directly

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39
Q

AMEDICAL SIGNis?

A

Anobjective indication of some medical fact or characteristic that may be detected by aphysicianduring aphysical examination. Signs may have no meaning to the patient, and may even go unnoticed, but may be meaningful and significant to the healthcare provider in assisting thediagnosisof medical condition(s) responsible for the patient’ssymptoms.

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40
Q

A DIFFERENTIAL DIAGNOSIS (sometimes abbreviated DDx, ddx, DD, D/Dx) is?

A

A systematic diagnostic method used to identify the presence of a disease state where multiple alternatives are possible. This method is essentially a process of elimination or at least of obtaining information that shrinks the “probabilities” of candidate diseases

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41
Q

Patient presents with chest pain

What can your differential diagnosis (DDx) be?

A

1) Costochondritis
2) Angina
3) Myocardial Infarction

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42
Q

Patient presents with abdominal pain

What can your differential Dx be?

A

1) Pancreatitis
2) Cholecystitis
3) Cholelithiasis
4) Appendicitis
5) Peritonitis
6) Nephrolithiasis
7) Menstrual cramps
8) Gas

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43
Q

What are nociceptors?

A

Nociceptors are how we feel pain. Nociceptors are nerves that send pain signals to the brain and spinal cord. They have specialized receptors, or nerve endings that are triggered to fire by chemical changes in the body. Nociceptors detect temperature, pressure and stretching in and around their surrounding tissues.

  • The two main kinds of pain detected by nociceptors are somatic pain and visceral pain. Somatic pain comes from the skin and deep tissues, while visceral pain originates in the internal organs.
  • Nociceptors fire when damage is detected, sending pain signals to the spinal cord and the brain. Once the damage has been healed, nociceptors should stop firing.
  • They are free nerve endings that respond to stimuli which can be: chemical, mechanical, and thermal
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44
Q

Where are nociceptors located?

A
  • Under epidermis
  • Within joint & bone surfaces
  • Deep tissues
  • Muscles
  • Tendons
  • Subcutaneous tissue
    They are located throughout the body in the skin, internal organs, joints, muscles and tendons.
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45
Q

Nociceptors may be sensitive to:

A
  • extremes of temperature
  • mechanical damage
  • dissolved chemicals, such as chemicals released by injured cells
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46
Q

Sometimes even after the initial damage has healed, nociceptors may continue to fire, which can lead to? Give an example

A

chronic pain

I.e. In phantom limb pain, nociceptors continue to fire long after an amputated limb has been removed.

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47
Q

Specificity Theory of Pain

A

The intensity of pain is directly related to the amount of associated tissue injury.
More relevant with specific injury and acute pain
Less reliable for chronic pain or cognitive contributions to pain

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48
Q

What is a neuromodulator? How can it be triggered?

A

a substance, other than a neurotransmitter, released by a neuron and transmitting information to other neurons, altering their activities.

  • Substances that influence pain
  • Can be triggered by:
  • Tissue injury
  • Chronic inflammatory lesions
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49
Q

What are the different types of neuromodulators?

A

1) Excitatory Neuromodulators
- Substance P
2) Inhibitory Neuromodulators
- GABA
- Norepinephrine
- Endorphins

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50
Q

A chemical substance that regulates the activity of neurotransmitters at the synpase (it controls the strength of pain occuring) e.g. If your brak your leg, there will be heaps of neuromodulators trying to get to the CNS to tell you OUCH!

A

neuromodulator

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51
Q

Endorphins

A
  • Inhibitory Neuromodulator
  • Attach to opiate receptors
  • In afferent neurons
  • Inhibits release of excitatory neurotransmitters
  • Raises pain threshold
  • Opiate drugs
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52
Q

What are two effects that can occur between neural impulses?

A

It can be inhibitory (blocks the postsynpatic button neuron from firing) OR it can be excitiory (stimulates the neural impulse in another neuron)

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53
Q

What are the FIVE MAJOR neurotransmitters?

A

Acetylcholine, Norepinephnne, Dopamine, Serotonin, Endorphins

54
Q

What does Endorphins do?

A

Natural system for pain relief produced in the CNS like panadol. Its INHIBITORY so it blocks the pain where the pain is being registered

55
Q

natural, opiatelike neurotransmitters linked to pain control and to pleasure

A

endorphins

56
Q

Types of acute pain

A

Somatic, visceral, referred

57
Q

Somatic pain

A

Superficial - Musculoskeletal
Sharp(er) & well localized
Sensory nerves

58
Q

Visceral pain

A

Internal organs or blood vessels
Dull(er) & more poorly localized
Sympathetic nerve fibers

59
Q

Referred pain

A

Pain distant from point of origin

60
Q 
Costochondritis
S/S:
How do you differentiate from a heart attack?
Causes:
Tx:
A

Inflammation of the cartilage connecting a rib to the sternum
S/S: Sharp pain at the connection, Can mimic heart attack
How do you differentiate from a heart attack?
Causes: Usually unknown,Trauma?
Tx: Anti-inflammatory drugs i.e. Ibuprofen

61
Q

Angina Pectoris

A 
Chest pain caused by reversible myocardial ischemia
S/S: 
- Sudden severe chest pain lasts 3-5 minutes
- Pressure/squeezing
- Fatigue, Nausea, Shortness of Breath
Causes:
- Cardiovascular disease
- Anemias
Tx:
- Rest
- Nitrates – dilate arteries and veins
62
Q

Types of Angina Pectoris

A

Stable Angina > Effort typical -(atherosclerosis) > exercise, emotion, heavy metal > Pain
Variant Angina > Prinzmetal > a-receptor mediated V.C. with or without atherosclerosis > pain even at rest
Unstable Angina > Accelerated > severe type - decrease change in pattern - increase in frequency and/or duration of pain

63
Q

Types of Angina short version

A
  • chronic stable angina
  • variant or Prinzmetal’s angina
  • unstable angina
64
Q

Angina pectoris is usually a manifestation of?

A

atherosclerotic coronary artery disease

65
Q

stable angina

A

aka: typical, chronic, classic, extertional
- usually related to CAD
- usually induced by physical activity or stress and symptoms are worse in cold weather or after a large meal
- discomfort in left area of chest lasting for 1-15 min*responds to nitroglycerin within 10-15 min
* considered stable if there has been no change in frequency, etiology, or duration of symptoms in last 60 days
- can receive dental care: keep appointments short and unstressful
- must bring own nitro

66
Q

unstable angina (UA)

A
  • aka: preinfarctory angina, coronary insufficiency, crescendo angina, intermediate coronary syndrome, premature or impending MI
  • between stable angina and MI; an imbalance between myocardial O2 supply and demand
  • patients with UA should receive only minimal or emergency dental care after consulting MD
  • nitroglycerin may or may not relieve anginal pain
  • patient at high risk for MI, up to 50% of UA patients will have an MI once at hospital
  • vasoconstrictor contraindicated
67
Q

variant angina

A
  • aka: Prinzmetal’s, atypical, vasoplastic angina
  • occurs spontaneously, usually while person at rest and odd hours of day or night
  • more common in woman under 50
  • low risk for CAD
  • etiology translent spasm of coronary artery causing brief occlusion of vessel
  • may or may not have atherosclerosis
  • nitroglycerin usually provides prompt relief; use caution with vasoconstrictors
68
Q

S/S stable angina

A
  • generalized chest discomfort
  • pressure, burning, heaviness, squeezing, or choking
  • radiates to left shoulder, arm, neck, lower jaw, or tongue
  • diaphoresis (cold sweats)
  • pallor
  • nausea
  • vary in intensity
  • levine sign
  • last 1-15min
  • increased pulse and BP
69
Q

S/S unstable angina

A
  • same as stable but occur for no apparent reason
  • intensity may be more acute
  • may last up to 30 min
70
Q

S/S variant angina

A
  • some of same as stable: may also include palpitations, syncope, and dyspnea
  • more likely to occur at rest
  • often associated with dysrhythmias
71
Q

treatment of angina

A
  • terminate treatment
  • semisupine or upright position
  • assess CAB’s
  • administer O2, 2-6 liters/min via nasal cannula
  • monitor vital signs
  • conscious patient: administer sublingual or transmucosal nitroglycerin-dilates coronary blood vessels resulting in decreased cardiac workload
  • use patient’s own med if current, will feel tingling on tongue if fresh
  • administer one tablet every 5 min up to 3 doses-usually alleviates symptoms in 2-4 min
  • nitro contraindicated in hypertensive patients or has recently taken erectile dysfunction drugs
  • following administration, patient may experience tachycardia, flushing, pounding in head, and hypotension
  • may resume treatment if patient feels well enough
  • chest pains not relieved in anginal patient after second dose, contact EMS (*after 10 min call EMS if not better)
72
Q

Mechanisms that decrease blood flow

A

Vasospasm: artery becomes smaller
Fixed stenosis: narrowing of the arteries lumen
Thrombosis: blood clots reduce the blood flow

73
Q

Mechanisms that increase O2 consumption

A

Heart rate increase
Heart contractions stronger
Blood pressure increase

74
Q

Nitroglycerin was first used by William Murrell to treat anginal attacks in 1878, with the discovery published that same year

1) Dilation of coronary vessels __________ oxygen supply to the myocardium

2) At low doses, nitroglycerin will dilate veins more than arteries, thereby _________ preload
Dilating the veins ___________ cardiac preload and lowers the oxygen requirement of the heart

3) At higher doses, it also dilates arteries, thereby ___________ afterload
The lowering of pressure in the arteries ___________ the pressure against which the heart must pump, thereby decreasing afterload and again, lowers the oxygen requirement of the heart

A

1) Increases
2) reducing, decreases
3) reducing, reduces

75
Q

Overall effects of nitroglycerin

A 
Decreases chest pain, 
Decrease of blood pressure
Increases heart rate
Orthostatic hypotension
Tolerance
76
Q

Angina pectoris tests

A

1) EKG – may be normal
2) Stress Tests
3) Coronary Angiography and Cardiac Catheterization
- Dye w/X-rays to show coronary lumen
4) CBC
- Increase cholesterol
- Increased C-reactive protein (CRP)?
- Indicates inflammation somewhere in the body
- Increased risk for heart attack
- Anemia

77
Q

What is C-Reactive protein?

A

A substance produced by the liver in response to inflammation. Other names for CRP are high-sensitivity C-reactive protein (HS-CRP), or ultra-sensitive C-reactive protein (US-CRP).
- A high level of CRP in the blood is a sign that there may be an inflammatory process occurring in the body. Inflammation itself isn’t typically a problem, but it can indicate a host of other health concerns, including infection, arthritis, kidney failure, and pancreatitis. High CRP levels may put patients at increased risk for coronary artery disease, which can cause a heart attack.

78
Q

Erythrocyte sedimentation rate (ESR) is?

A

another test that determines inflammation somewhere in the body

79
Q

Myocardial infarction

A

AKA “Heart Attack”
Progressive ischemia with damage to myocardium (myocyte necrosis)
2 types
- Subendocardial MI
Thrombus dislodges and only myocardium directly beneath endocardium involved
- Transmural MI
Thrombus remains and myocardium involved transcends to epicardium

80
Q

Transmural MI

A

A transmural myocardial infarction refers to a myocardial infarction that involves the full thickness of the myocardium.

81
Q

Myocardial infarction S/S & Causes

A 
Dyspnea
Sudden severe chest pain with radiation
Nausea/Vomiting
Anxiety/dizzy/cough
Diaphoresis – profuse sweating
- Causes
Causes:
Cardiovascular disease – what are the risk factors?
82
Q

MI Tx (treatment)

A

Thrombolytic therapy – w/in 3 hours
Cardioprotection after MI:
Beta-blockers – blocks sympathetic innervation
ACE inhibitors – How does this work?

83
Q

Heart attack symptoms for men and women

A 
Men and women may experience some common symptoms, but there are differences.
Women:
- Nausea/vomiting
- Jaw pain
- Back pain
Men:
- Chest discomfort
- Arm pain
- Shortness of breath
84
Q

Myocardial infarction tests

A 
Tests:
- EKG
  STEMI – indicates transmural MI
  non-STEMI – indicates subendocardial MI
- BP – Initially decreases
SNS reflexively activates
Temporarily increases HR and BP
Abnormal extra heart sounds – LV dysfunction
Pulmonary congestion
Dull percussion
Inspiratory crackles at lung bases
85
Q

What does the ECG look like for a STEMI heart attack?

A

The baseline is elevated which is a sign that someone is suffering from a “STEMI” heart attack.

86
Q

What does the ECG look like for a “NSTEMI” heart attack?

A

Notice the baseline is depressed. This is seen on the ECG of someone with a “NSTEMI” heart attack.

87
Q

When confronted with environmental stresses that disrupt normal structure and function, the cell under-goes adaptive changes that permit survival and maintain function. The adaptation is a reversible, structural, or functional response to normal or adverse conditions; it enables the cell to maintain a steady state called homeostasis . These changes may lead to?

A

atrophy, hypertrophy, hyperplasia, dysplasia, or metaplasia.

88
Q

Cellular atrophy decreases the 1) ____ _______ and results in 2) ____ ________. Causes of atrophy may be 3)_______, 4) _________, or 5) _________. All three causes may result in 6) _______ _______ ______, 7) _______ ______ _______, or both. A 8) _______-_______ ______ degrades proteins to ubiquitin, a smaller protein, and then 9) ________ in the cytoplasm complete the proteolysis.

A

1) Cell substance
2) Cell shrinkage
3) Physiological (associated with normal development)
4) Pathologic (accompanying disease)
5) Disuse (because of lack of stimulation)
6) Decreased protein synthesis
7) Increased protein catabolism
8) Ubiquitin-proteosome pathway
9) proteosomes

89
Q

main points of hypertrophy

A
  • increases cell size
  • commonly seen in cardiac and skeletal muscle tissue
  • increase in cell components is related to an increased rate of protein synthesis
  • Mechanical signals, such as stretch, and trophic signals, such as growth factors, hormones, and vasoactive agents, are triggers for hypertrophy
  • Physiologic hypertrophy is observed in uterine tissue and mammary glands during pregnancy.
90
Q

What causes atrophy?

A
  • decreased use
  • decreased blood supply (if tissue is starving it will eat itself, it will eat the actin and myosin to stay alive)
  • decreased nutrition
  • change hormones (if you don’t have hormones that nurture those cells then the cells won’t)
  • lose innervate (muscle cells are innervated so if you cut that neuron supply off, then that muscle can’t contract anymore and if it’s not being used it will shrink down, an ie. is a cast)
91
Q

What is a result of atrophy?

A

1) cells form accumulations

- lipofucion

92
Q

What causes hypertrophy?

A
  • due to increased protein synthesis w/in the cell, or decreased protein breakdown
  • NOT due to increased cell volume or fluid
93
Q

Hypertrophy is pathologic in?

A

heart, kidney (if one kidney has a problem the other kidney will increase its size not number of nephrons but the size of the kidney to try and accomodate , and others

94
Q

prostate is an example of?

A

Hyperplasia

95
Q

Why is hyperplasia not typical in cardiac and skeletal muscle or nerves?

A

Because these three types of cells don’t replicate once they have been differentiated.

96
Q

Example of metaplasia?

A

Respiratory tract ciliated columnar epithelium replaced by stratified squamous epithelium

97
Q

Components of Blood

A

Plasma 55% Cellular elements 45%

98
Q

What does plasma contain?

A

1) Water
2) Ions (blood electrolytes): Sodium, Potassium, Calcium, Magnesium, Chloride, Bicarbonate
3) Plasma proteins: Albumin, Fibrinogen, Immunoglobulins (antibodies)
4) Substances transported by blood: Nutrients (such as glucose, fatty acids, vitamins), waste products of metabolism, respiratory gases (O2 and CO2), Hormones

99
Q

What is the major function of water in plasma?

A

Solvent for carrying other substances

100
Q

What is the major function for ions (blood electrolytes) in plasma?
Sodium, Potassium, Calcium, Magnesium, Chloride, Bicarbonate

A

Osmotic balance, pH buffering, and regulation of membrane permeability.

101
Q

What is the major function of plasma proteins: Albumin, Fibrinogen, Immunoglobulins (antibodies)

A

Albumin: Osmotic balance, pH buffering
Fibrinogen: Clotting
Immunoglobulins (antibodies): Defense

102
Q

What are the cellular elements in blood?

A 
1) Erythrocytes (red blood cells)
Number: 5-6 million
Function: Transport oxygen and help transport carbon dioxide
2) Leukocytes (white blood cells)
Number 5,000-10,000
Function: Defense and immunity
Types: Basophil, Eosinophil, Neutrophil, Lymphocyte, Monocyte
3) Platelets
Number 250,000-400,000
Function: Blood clotting
103
Q

Total body of water=

A

ICF (intracellular) + ECF (extracellular)

104
Q

Why is the capillary wall one cell thick?

A

This layer is so thin that molecules such as oxygen, water and lipids can pass through them by diffusion and enter the tissues. Waste products such as carbon dioxide and urea can diffuse back into the blood to be carried away for removal from the body. Capillaries are so small the red blood cells need to partially fold into bullet-like shapes in order to pass through them in single file.

105
Q

What happens at the capillary level of the cell tissues?

A

Oxygen is distributed, carbon dioxide is collected

Wastes are collected

106
Q

Diffusion:

A

Mixing of two or more substances from an area of high concentration to an area of low concentration
Example: Perfume in a room

107
Q

Osmosis:

A

Diffusion of WATER through a membrane from a solution of low solute concentration (high water potential) to a solution with high solute concentration (low water potential)

108
Q

What are the causes of hypoxia?

A

Can result from a reduced amount of O2 in the air, loss of hemoglobin or decreased efficacy of hemoglobin, decreased production of RBC’s, diseases of the respiratory & cardiovascular systems, and poisoning of the oxidative enzymes (cytochromes) w/in the cells

109
Q

What cellular response happens during a hypoxic injury?

A

W/in 1 minute after blood supply to the myocardium is interupted, the heart becomes pale & has difficulty contracting normally.

  • w/in 3-5 min. the ischemic portion of the heart ceases to contract because of a rapid decrease in mitochondrial phosphorylation, causing insufficient ATP production
  • lack of ATP leads to increased anaerobic metabolism, which generates ATP from glycogen when there is insufficient O2
  • Once glycogen stores are depleted even anaerobic metabolism ceases
  • a reduction in ATP causes the plasma membrane’s Na/K pump & Na/Ca exchange mechanism to fail, which leads to an intracellular accumulation of Na and Ca and diffusion of K out of the cell
  • Na and water can then enter the cell freely, and cellular swelling as well as early dilation of the endoplasmic reticulum results
  • Dilation causes ribosomes to detach from rough ER reducing protein synthesis
  • w/continued hypoxia, entire cell becomes swollen w/increased concentrations of Na, H20, and Cl and decreased concentrations of K
  • disruptions reversible if O2 restored
  • If not restored vaculoation occurs w/in cytoplasm & swelling of lysosomes and marked mitochondrial swelling result from damage to outer membrane
  • Continued hypoxic injury w/accumulation of Ca subsequently activates multiple enzyme systems resulting in membrane damage, cytoskeleton disruption, DNA & chromatin degradation, ATP depletion, and eventual cell death
  • W/plasma membrane damage, extracellular Ca readily moves into cell and intracellular Ca stores are released
  • Increased intracellular Ca levels activate cell enzymes that promote cell death by apoptosis
  • If ischemia persists, irreversible injury is associated structurally w/ severe swelling of mitochondria, severe damage to plasma membranes, and swelling of lysosomes
  • restoration of O2 can cause additional injury called reperfusion injury
110
Q

Hypoxia (main points)

A
  • Decrease in oxygen to cells
  • Interrupts oxidative metabolism
    • Anaerobic respiration takes over
    • More or less ATP produced? less
  • Increase in lactic acid> pH decreases –more acidic or basic? acidic
  • Sodium-Potassium pump fails with decrease in ATP production> Intracellular Na and Ca levels rise, K levels fall > swelling/edema occurs
  • Cell becomes ‘leaky’ and internal enzymes get into circulation
  • Internal enzymes can be measured in lab tests to estimate cellular damage
  • Possible reperfusion injury > free radical formation (more on this soon)
111
Q

ATP depletion

A

Loss of mitochondrial ATP and decreased ATP synthesis; results include cellular swelling, decreased protein synthesis, decreased membrane transport, and lipogenesis, all changes that contribute to loss of integrity of plasma membrane

112
Q

Reactive O2 species (Increase ROS)

A

Lack of O2 is key in progression of cell injury in ischemia; activated O2 species (ROS, O2-, H2O2) cause destruction of cell membranes and cell structure

113
Q

Ca++ entry

A

Normally intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals cause an increase in cytosolic Ca++ concentrations; sustained levels of Ca++ continue to increase w/damage to plasma membrane; Ca++ causes intracellular damage by activating a number of enzymes

114
Q

Cell injury: Injury induced by free radicals, especially reactive oxygen species (ROS); this form of injury is called oxidative stress. When does it occur?

A

When excess ROS overwhelm endogenous antioxidant systems. A free radical (electrically uncharged atom or group of atoms that has an unpaired electron)

  • unpaired electrons makes a molecule unstable; it becomes stabilized by donating/accepting an electron from another. When attacked molecule loses an electron > free radical
  • free radicals capable of injurious chemical bond formation w/proteins, lipids, & carbohydrates-key molecules in membranes & nucleic acids
  • free radicals=difficult to control & initiate chain reactions & highly reactive due to low chemical specificity
115
Q

Free radicals may be initiated within cells by?

A

1) absorption of extreme energy sources (ultraviolet light, radiation)
2) Activation of endogenous reactions by systems involved in electron & O2 transport (e.g. reduction of O2 to H20)
3) enzymatic metabolism of exogenous chemicals or drugs

116
Q

Free radicals cause several damaging effects by?

A

1) lipid peroxidation - destruction of polyunsaturated lipids, leading to membrane damage & increased permeability
2) protein alteration, causing fragmentation of polypeptide chains
3) DNA fragmenation, causing decreased protein synthesis
4) mitochondrial damage causing the liberation of calcium into the cytosol

117
Q

Extreme temps that cause cell injury

A

1) Heat
- Increase in metabolism
- Inactivating enzymes
- Cell membrane disruption
- Coagulation of blood vessels and tissue proteins
2) Cold
- Vasoconstriction

118
Q

Physical agents of cellular injury: Electrical

A
  • Disruption of nervous and cardiac impulses
    • Creates heat and damages tissues
    • Big problem?
  • Lethality > dependent on:
  • Current - The higher the current, the more likely it is lethal. Since current is proportional to voltage when resistance is fixed (ohm’s law), high voltage is an indirect risk for producing higher currents.
  • Duration - The longer the duration, the more likely it is lethal—safety switches may limit time of current flow
  • Pathway - If current flows through the heart muscle, it is more likely to be lethal.
  • High voltage (over about 600 volts). In addition to greater current flow, high voltage may cause dielectric breakdown at the skin, thus lowering skin resistance and allowing further increased current flow
119
Q

Skin Resistivity of electrical cell injury
Least
Intermediate
Most

A 
- Least		Nerves
			Blood
			Mucous membranes
			Muscle
- Intermediate	Dry skin
			Tendon
			Fat
- Most		Bone
120
Q

Chemical agents and drugs

A
  • Multiple ways to damage cell structures
    • Injure cell membrane
    • Block enzymatic pathways
    • Disrupt osmotic balance
  • Alcohol, OTC drugs, Prescription drugs, Recreation drugs
    • Ethyl alcohol damages gastric mucosa, liver, developing fetus
    • Acetaminophen when detoxified by the liver is converted into a highly toxic metabolite. This metabolite can be taken care of in the liver by glutathione. However, when large amounts of Acetaminophen are converted, the liver can’t keep up and massive liver necrosis can occur.
    • What drugs contain Acetaminophen?
  • Ethylene glycol
121
Q

Cellular injury biological agents

A
  • Viruses
    • Hijack the cells by being incorporated into the cells’ DNA
    • Genetic mutation
  • Bacteria
    • Release endotoxins that increase capillary permeability
      Increase swelling
122
Q

Nutritional imbalances of cellular injury

A
  • Nutritional
    1) Excess
    2) Deficiency
  • Obesity and diets high in saturated fats are thought to predispose persons to atherosclerosis
  • Deficiency examples:
    Iron-deficiency anemia, scurvy, beriberi, pellagra
123
Q

Cell death

A 
1) Apoptosis
Programmed cell death
2) Necrosis (autolysis):
- Coagulative
- Liquefactive
- Caseous (cheese like)
- Fat
- Gangrenous
124
Q

Typesof necrosis

A

1) Coagulative:
- Typically affects kidney
- Denaturation of proteins from gel to firm state
2) Liquefactive:
- Typically affects neurons/glial cells in brain
- Cells digested by their own hydrolases-tissue becomes soft
- walled off from healthy tissue, forming cysts
3) Caseous (cheese like)
- TB: Combo of coagulative and liquefactive
- Cells disintegrate/denature but debris is walled off
4) Fat:
- Caused by lipases-breast, pancreas, abdominal structures
- Saponification
5) Gangrenous
- Usually occur in extremities and it is due to physical injury and trauma. There are two types of gangrene which are dry gangrene and wet gangrene. Dry gangrene have no bacterial infection and the tissue appear dry. Whereas wet gangrene has bacterial super-infection & the tissue looks wet

125
Q

Cellular aging

A
  • Decreased
    • Oxidative phosphorylation decreased
      • Less ATP
    • Synthesis of
      • Nucleic acids
      • Cell receptors
      • Transcription factors
  • Decline in
  • Muscular strength
  • Cardiac reserve
  • Nerve conduction time
  • Vital capacity
  • Glomerular filtration rate (GFR)
  • Vascular elasticity
126
Q

Necrosis (autolysis): Coagulative

A
  • Typically affects kidney

- Denaturation of proteins from gel to firm state

127
Q

Necrosis (autolysis): Liquefactive

A
  • Typically affects neurons/glial cells in brain
  • Cells “digested” by their own hydrolases-tissue becomes soft
  • walled off from healthy tissues, forming cysts
128
Q

Necrosis (autolysis): Caseous (cheese like)

A
  • TB: combo of coagulative and liquefactive

- cells disintegrate/denature but debris is walled off

129
Q

Necrosis (autolysis): Fat

A
  • Caused by lipases-breast, pancreas, abd structures

- Saponification

130
Q

Necrosis (autolysis): Gangrenous

A

Usually occur in extremities and it is due to physical injury and trauma. There are two types of gangrene which are dry gangrene and wet gangrene. Dry gangrene have no bacterial infection and the tissues appear dry. Whereas wet gangrene has bacterial super-infection & the tissue looks wet

Pathophysiology (22 decks)

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