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185 Cards in this Set
- Front
- Back
What is Disease?
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Patter of response to some form of injury
-the physiological effect of an injury, not the injury itself |
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What 3 factors are true of all diseases?
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They have a
1. cause 2. set of manifestations 3. time of course |
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Is disease static?
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No it is dynamic
|
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Pathology occurs in the body because the injury does what?
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The injury overwhelms the body's ability to compensate
|
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Can a body's response to an injury bring about a disease? If so give an example.
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Yes.
-Renal artery stenosis which causes a drop in blood flow and the kidneys respond by causing hypertension |
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Describe the concept of "normal"
|
No absolute value exists for any biological parameter; there are only averages and a range around that average
|
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List the Sources of Variation for Disease.
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1. Genetic Variation
2. Age differences 3. Gender Differences 4. Situational Differences 5. TIme Variations 6. Laboratory Conditions |
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Define the Etiology of disease.
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The specific cause of the disease
|
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Give an example of a situational variation of disease.
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RBC count at sea level vs RBC count at high alititude
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Who is the best indicator for the value of normal for a particular disease?
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The patient him or herself through their past medical reports.
-What is their baseline |
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According to the pathophysiological model, what are the three aspects of a given disease process?
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1. Etiology
2. Mechanism of development: pathogenesis 3. Functional consequences: Clinical manifestations |
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What is pathogenesis?
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The mechanism of development of a disease
|
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What are clinical manifestations?
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The observable result of the injury or disease
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Where do all different types of etiologies converge?
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At the cell level
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What are the 3 categories of etiologies in nature?
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1. Extrinsic in nature
2. Intrinsic in nature 3. idiopathic (unknown) |
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What is the etiology of the most common type of hypertension?
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Idiopathic
|
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If the etiology of a disease is extrinsic in nature, what are the examples of possible sources?
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1. Inanimate source
a. Temperature b. Radiation c. Iatrogenic 2. Animate source a. virus, fungal bacteria or parasite |
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LIst the examples of etiologies that are intrinsic in nature.
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1. Inherited
2. Metabolic 3. Nutritional 4. Psychogenic 5. Autoimmune |
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What is an Iatrogenic condition?
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Disease that was caused by medical care (hospital acquired injury)
|
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Define pathogenesis.
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Process of going from an injury up to the clinical manifestation.
-Development of the disease state |
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What are the factors that effect pathogenesis?
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1. Time (how long are we exposed?)
2. Quantity (how much of the pathogen were they exposed to?) 3. Location (where was the exposure?) (What is the location of the infection?) 4. Morphological changes (What changes in the organ or tissues did the exposure cause?) |
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Define a sign. Give an example
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Objectively observable clinical manifestation
Ex. bruising |
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What is a symptom? Give an example
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Subjective manifestation of a disease
Ex. Nausea -can only be reported by the individual |
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What is the only clinical manifestation that is both a sign and a symptom?
How is it measured? |
Pain.
-Expressed by the patient and subjectively documented using the grimace scale |
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What are the four periods/phases of disease?
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1. Latent period
2. Prodromal period 3. Acute phase 4. Sub-clinical phase |
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What is the latent period of a disease?
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Describes the period of time between the onset of the injury and the very first manifestation of any signs or symptoms
|
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What occurs in the prodromal period?
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It is the first onset of symptoms. The patient begins to feel "sick" in a non-specific way
|
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What is the acute phase?
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Time from first symptoms of unwell to the most acute symptoms.
-Peak of sickness |
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Describe the sub-clinical stage.
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Point at which the disease state is firmly established and there are already functional consequences that are being compensated by the body
-Ex. Cancer cells present in the body but no tumor is seen. |
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Besides the main stages of disease, name 4 other ways to classify a disease or its stage.
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Disease can either be in a phase of exacerbation or remission
-Disease can be acute or chronic |
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How do you determine what a patient is suffering from?
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Base diagnosis on the information available from clinical methods and lab methods
|
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Give examples of clinical methods used to diagnose.
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They are the symptoms presented from the patient and the physical signs objectively observed by the provider
|
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What are the laboratory methods used to diagnose?
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-Urinalysis
-Blood analysis -Blood counts: cells -Blood chemistry: sugar, electrolytes, enzymes -Blood cultures: bacteriological exam -Serology: examination of blood for indicators of infection -Tissue Diagnosis: biopsies, aspirations -Electrocardiograms -Radiography |
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What is differential diagnosis?
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List all the possible diseases associated with the clinical and laboratory results and remove them one by one as symptoms don't meet the criteria
|
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What is the cellular basis of disease?
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All forms of injury will effect some set of cells in the body or can effect all of them.
-Starts off by effecting cell function |
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How do we maintain cellular function?
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By controlling the internal and external cell environment ECF
|
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What are the important factors in maintaing cellular homeostasis?
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1. Maintain cell volume
2. Electrolyte balance 3. Maintain adequate pH 4. Cell metabolism 5. Cell transport |
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How does a cell control its volume?
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By maintaining water and osmolyte balance
|
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Besides the main stages of disease, name 4 other ways to classify a disease or its stage.
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Disease can either be in a phase of exacerbation or remission
-Disease can be acute or chronic |
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What ion maintains the osmotic value of the ECF?
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Sodium
|
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Potassium maintains the osmotic value of what environment>?
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The ICF
|
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What system in the body is used to systemically maintain cell volume?
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The Renin-Angiotensin system
-ADH/Thirst system |
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Where does Bulk flow take place?
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At the capillary level
|
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What happens if plasma osmolarity goes up?
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ADH goes up and thirst goes up
|
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What is responsible for Na/K balance?
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Aldosterone
|
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What is the equation for total body water?
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ICF + ECF
|
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What 4 compartments does fluid move through?
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-Between ECF and ICF
-Between Plasm and interstitum |
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What is considered the 3rd space?
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The transcellular compartment; the fluid that lies between serous membranes
|
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Give some examples of transcellular compartments in the body
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Synovial fluid
-intrapleural fluid, intramyocardial fluid etc |
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Why is it difficult to remove fluid from the 3rd space?
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Because the turn over rate is not rapid and can accumulate quickly
|
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Other than Na/K balance, what other electrolyte are we concerned to balance in the cell and why?
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Calcium
-Ca can trigger a whole range of reactions in the body so if they change innappropriately and can kill the cell -Bicarbonate levels can change the pH of the cell and cause protein denaturation |
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What clinical manifestation occurs when fluid movement is disrupted?
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Edema
|
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What is edema?
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fluid built up between intersistial and intervascular space
|
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What are the major causes of edema?
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-Decreased plasma oncotic pressure
-increased interstitial oncotic pressure -increased capillary blood pressure -lymphatic obstruction |
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What causes a decreased plasma oncotic pressure?
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Losses or diminshed production of Albumin
|
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What is the term when the capillaries become more permeable to protein causing a change in pressure?
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Increased interstitial oncotic pressure
|
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When is it normal to have capillaries very premeable to protein?
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when there is an injury and acute inflammation is used as a healing method
|
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What is a vascular component contributing to hypertension?
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Increased capillary blood pressure
-venous obstruction |
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What is lymph edema?
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when the lymph vessels to an area are obstructed and cannot drain properly
|
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What are isotonic alterations?
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Have a change in TBW accompanied by proportional changes in electrolyte and water
|
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Give an example of an isotonic volume depletion.
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Hemmorhage: all volume in equal amounts is lost
|
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What are hypertonic alterations?
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Osmolarity of the ECF is elevated
|
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What are some examples of hypertonic alterations?
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-hypernatremia
-water deficit -hyperchloremia - |
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What is hypernatremia and how is it caused?
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Altered Na osmolarity in the cell.
-Inadequate fluid intake or an inappropriate administration of hypetonic saline |
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What happens in water deficit? Give an example of someone who will experience it.
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EIther inadequate water intake or impaired renal conservation of water
-Can happen to marathon runners who are sweating and not getting any water -May lead to hypotonic conditions (toxic effect of not profuse sweating) |
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What is hyperchloremia?
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This is an increase in serum chloride levels
-accompanies any excess of Na or deficit of bicarbonate -Can also be from excess ammonium chloride diuretic |
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What are some examples of HYPOTONIC Alterations?
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-Hyponatremia
-Excess Water -Hypochloremia |
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What are some causes of hyponatremia?
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-diuretics
-vomiting -diarrhea -burns |
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What can cause hypochloremia?
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Accompanies any deficit of Na or excess of bicarbonate or any vomiting (loss of HCl)
|
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What is Hypertonic Hypotonicity?
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Na concentration is reduced, but blood is hypertonic
-Occurs because you have an accumulation of some non-Na osmolite |
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What are the most common causes of hypertonic hypotoncity?
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usually excess glucose or cholesterol.
-they increase the osmlarity of the blood which increases the blood volume (water in) and then dilutes the electrolyte levels |
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Where are the earliest life threatening manifestations seen from alterations in Na levels?
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In the brain
-can cause seizures |
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What happens to the excitability of the cell when EC potassium levels go up?
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They also go up
|
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Why do increase EC potassium levels increase excitability inside the cell?
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The direction of flow for K is out. But excess + charge in the EC space stops K+ from flowing out and thus making the IC more + which deplorizes the cell
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HYPOkalemic EC fluid causes what kind of electrical change in the cell?
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a decrease in excitability in the cell
|
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What is a major life threatening effect of changes in K levels?
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Problems with cardiac function!
-Arrhythmias and possible cardiac arrest |
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Why can both hypo and hyperkalemia cause muscle weakness?
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hyper: too much excitement can cause tetany and muscle fatigue
hypo: decreases muscle excitability |
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How is K maintained systemically and at the cellular level?
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Systemically by the Aldosterone-mediated-renal regulation
Cellularly by the Na/K ATPase pumps |
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What type of movement will K exhibit during acidosis?
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K+ will move OUT of the cell
|
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What type of pH change in the body would warrant K moving into the cell? Why?
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Alkalosis
-decrease in ICF [H+] will make the inside of cell more negative and pull K+ into the cell |
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What ion does the cell get rid of or bring in to maintain neutral?
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Potassium
|
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What type of kalemia reading will a patient who is in alkalosis read?
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They will appear HYPOkalmeic because the alkalosis will pull the K into the cell taking it out the the ECF
|
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What effect does insulin have on K?
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It promotes the entry of K into the LIVER and MUSCLE which effects the circulating K levels
|
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What is the emergency treatment for High K levels and what must you also consider?
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Use and injection of INSULIN
-For non-diabetic pts this would cause a massive drop in blood glucose so glucose must be given at the same time |
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What are the catecholamines?
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NE and Epi
|
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What happens to K+ when NE or Epi attach to B2?
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K+ will enter the cell causing increased excitability
|
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Which receptor of NE and Epi cause K+ to leave the cell?
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Alpha 2: causes decreased excitability in the cell
|
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What two factors are the largest predictors of K serum levels?
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Insulin and pH
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What is diabetic acidosis?
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Have an extremely high level of K+ because of the lack of insulin to pull K+ into the cell and a build up of ketone bodies
|
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What should a nurse do for a pt with diabetic acidosis?
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Get them on an EKG in case of arrhythmias
|
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What is the normal pH range of arterial blood?
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7.38-7.42
|
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What organs are the primary regulators of acid-base balance?
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the Lungs and the Kidneys
|
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How does the body maintain pH?
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Through the use of buffer systems
|
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Give some examples of buffer systems in the body.
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HCO3-/H2CO3
-hemoglobin -proteins -phosphate |
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What is the most important buffer system in the body>
|
Bicarbonate system
|
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Where is CO2 converted into the bicarbonate buffer and what does it need?
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Converted in the cell
-Need carbonic anhydrase enzyme |
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How is the production of carbonic acid regulated in the body?
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Through respiration
-Increase respiration --> decrease CO2 |
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What organ controls the rate of bicarbonate reabsorption and H+ secretion?
|
The kidneys!
|
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What occurs more rapidly; changing CO2 levels or the kidneys reabsorption of bicarbonate and H+?
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The changing CO2 levels
|
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What are the two major causes of acid-base disturbances?
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1. Respiratory
2. Metabolic |
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What is respiratory acidosis?
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Cause by hypoventilation and the PCO2 levels go up
-Problem with gas exchange -Respiration will not be part of the compensation |
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What causes respiratory alkalosis?
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Hyperventilation
|
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How are respiratory based acid-base changes compensated?
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Through metabolic system
|
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If the acid base change is not caused by respiration, what is it from? How is it compensated?
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Called Metabolic and compensated by the respiratory system
|
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What are some common causes of metabolic acidosis
|
1. Renal Disease*
2. ketoacidosis 3. Uremia: build up of uric acid 4. Ingestion 5. diarrhea 5. Renal failure or Proximal Tubule acidosis (impaired ability to secrete H+) |
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Give some examples of causes of metabolic alkalosis
|
1. Renal Disease
2. Excess loss of non-carbonic acids, 3. prolonged vomiting 4. GI suction 5. Hyperaldosteronism 6. Diuretic Therapy 7. Excess bicarbonate intake |
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What are the steps in determining if the acid/base disturbance originates from the respiratory or metabolic system?
|
Step 1: is the pH acidic or basic?
Step 2: look at PCO2, is the change promoting acidosis or promoting alkalosis or promoting nothing? Step 3: Look at Bicarbonate: is the change promoting acidosis, alkalosis or nothing? --If the answer is bicarbonate then it is metabolic --If the answer is PCO2 then it is respiratory based |
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When looking at the compensation phase of acid/base readings, how can you tell the cause of the pH problem?
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It is the disturbance that matches the change in the pH (PCO2 or bicarb)
-The value in the other direction is the compensation |
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If you have a pH of 7.35
PCO2: high Bicarb: high What acid base problem is it? |
Partially compensated Respiratory Acidosis
|
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What is cell metabolism?
|
ability of the cell to produce enough energy to due work
|
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What forms of energy substrates are used for energy?
|
Ingested nutrients
1. AA's from protein 2. Glucose from polysaccharides 3. fats in the form of fatty acids and glycerol |
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What is the general pathway of a glucose molecule to make ATP?
|
Glycolysis --> pyruvate --> citric acide cycle --> oxidative phosphorylation
|
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Where does glycolysis take place?
|
in the cytosol
|
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How many ATP is produced during glycolysis of 1 glucose?
|
2 ATP for every 1 glucose
|
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How many ATP's are produced in the citric acid cycle?
|
2 ATP for every 1 glucose
|
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Where does citric acid cycle take place?
|
in the mitochondria
|
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Which Passages in cellular metabolism are anaerobic?
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Glycolysis and the citric acid cylce
|
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What is the only system in cellular metabolism that is aerobic?
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oxidative phosphorylation
|
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Which system takes place in the inner mitochondrial membrane of mitochondria?
|
oxidative phosphorylation
|
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How many ATP are yielded from oxidative phosphorylation?
|
32
|
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Why do we need O2?
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O2 is used to produce the highest yield of ATP which gives energy to all functions in the body.
|
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What are the categories of passive cell transport?
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-Simple
-Osmosis -Facilitated diffusion |
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What is involved in the development of a disease?
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The introduction of altered function or an injury
|
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What is the basis of all disease states?
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The malfunction of the cell
|
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What are examples of stressors that cause cell injury?
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-Increased functional demand
-deprivation of O2 -deprivation of nutrient delivery |
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Define coagulated necrosis
|
A cell is exposed to a stressor so severe that the cell is irreversibly injured and dies
|
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What does a cell do if it is exposed to a mild, yet chronic stressor?
|
It will adapt to maintain stability but it will inevitably change how it functions
|
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What is true of all cell adaptations once the stressor is removed?
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They are reversible.
-The cell will go back to normal function |
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What is dysplasia?
|
a manifestation of cell injury
|
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What is a hypoxic injury?
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Anything that limits or interrupts O2 delivery to the tissue
|
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Define ischemia.
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Diminished blood flow to an area
|
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What injury can result from ischemia?
|
Hypoxic injury
|
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Give some examples of conditions that lead to hypoxia.
|
-Ischemia
-Low ventilation -gas exchange problems -anemia |
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What condition has been the model of understanding hypoxic injury?
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Ischemia
|
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What is a complete and total interruption of O2 delivery?
|
Anoxia
|
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What does anoxia often precede?
|
Tissue infarction
|
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What is tissue infarction?
|
the death of the tissue as a result of cessation of blood flow to the area
|
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What is a free radical?
|
Element with a single unpaired electron its outermost shell
|
|
How do free radicals create damage/injury?
|
They desire to pair their unpaired electron and steal the electron from other structures includes bonds between compounds.
-In the process of getting their electron they create damage |
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Where do many free radicals come from
|
1. Product of normal metabolism
2. age |
|
What method is used by the anti-aging movement and what is the reason behind it?
|
-Limit calorie intake drastically
-this reduces cellular metabolism and thus prevents the production of free radicals that are a by product of metabolism |
|
Why are free radicals produced from metabolism usually not a problem?
|
we have endogenous anti-oxidants that neutralize them, but we can still have an accumulation as a part of aging
|
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What 3 mechanisms do reactive O2 species cause cell injury?
|
1. Lipid peroxidation
2. Interact with function of polypeptide chains 3.Cuase damage to DNA |
|
What is lipid peroxidation?
|
Reactive O2 species react with lipids of the membrane and cause damage.
-destruction of unsaturated fatty acids - attack the double bonds |
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What is reprofusion? Is it helpful?
|
The re-introduction of O2 to a area suffereing from hypoxic injury.
-Not always helpful, it is layering injury upon injury |
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Describe the negative aspect of reprofusion.
|
Layering injury on to of injury
1. First injury is hypoxic injury 2. Inflammatory response of the body to heal the injury is the second injury 3. The 3rd layer comes from the reintroduction of blood flow and introduction to even more reactive species |
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What is a crisis of energy?
|
Ischemia causing less O2 to be delivered to the mitochondria where it is needed for ATP production
|
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What is involved in the development of a disease?
|
The introduction of altered function or an injury
|
|
What is the basis of all disease states?
|
The malfunction of the cell
|
|
What are examples of stressors that cause cell injury?
|
-Increased functional demand
-deprivation of O2 -deprivation of nutrient delivery |
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How will the cell start to compensate when a hypoxic injury or crisis of energy occurs?
|
It will increase its rate of glycolysis
|
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Along with an increase in glycolysis, what other cellular mechanism is effected during a hypoxic injury?
|
Na/K ATPase pumps decrease causing accumulation of Na in the cell --> water flows in --> bloating --> necrosis
|
|
In what ways does lipid peroxidation damage the cell?
|
1. Can increase membrane rigidity
2. decrease activity of the membrane enzymes 3. alter avicity of membrane receptors 4. Alter permeability (Influx of water) |
|
What are the sources of production of reactive species?
|
1. Metabolism
2. Inflammation 3. Exposure to UV light or industrial pollutants |
|
What are the manifestations of cell injury?
|
1. Atrophy
2. Hypertrophy 3. Hyperplasia 4. Metaplasia and dyslplasia |
|
What is physiological atrophy?
|
Results from normal physiological function and often occurs in development
-energy will only go to the most important structure |
|
Describe pathological atrophy.
|
Is a decrease in functional demand
-AKA disuse atrophy -Is reversible! -Can result from hypoxia, disuse, nutritional or endocrine decrease |
|
What are the 2 possible causes of physiological hypertrophy?
|
1. Increased functional demand that is not pathological ie weightlifting
2. the developmental progression ie hypertrophy to create sex organs and then hypertrophy to finish growth |
|
What are the pathological reasons behind hypertrophy?
|
1. Pathological increase beyond what is normal: ex left ventricular hypertrophy
2. Persistent tissue injury: chronic inflammation 3. overstimulation by hormones |
|
All of the conditions that cause hypertrophy can also cause what other manifestation?
|
Hyperplasia
|
|
What cells will only experience hypertrophy and not hyperplasia?
|
non-dividing cells such as cardiac cells
|
|
Define hyperplasia. what is an example?
|
Increase in the number of cells in an organ or tissue without the cells increasing in size.
Psoriasis of the skin |
|
What are hematopoitic stem cells?
|
They are in bone marrow and can only produce cells found in the blood stream and WBCs
|
|
What is the name of the cell after its final differentiation?
|
Terminally differentiated cell
|
|
What are two properties of a terminally differentiated cell?
|
1. Functionally mature
2. Loses its ability to divide ---will be replaced eventually by newly differentiated cells |
|
What is metaplasia?
|
Terminally differentiated cell gets replaced by a less differentiated precursor cell type
-can be adaptive |
|
Give an adaptive example of metaplasia.
|
Common in LUNGS of smokers
-ciliated cells are replaced with simple columnar cells -The adaptation is that the less differentiated cells maintain the ability to divide |
|
What is the adaptive and pathological aspects of metaplasia?
|
Adaptive: the precursor cells that take over for damaged terminally differentiated cells can always divide and replace themselves if they are damaged
-Pathological aspect is that they are not fully functional themselves |
|
What is dysplasia?
|
Have complete derrangement of the tissue bed
-Density, size and rate of cell division are completely abnormal -Cancerous cells that have yet to form a tumor -No uniformity |
|
What are the examples of abnormal accumulations resulting from cell injury?l
|
1. Lipid Accumulations in the cell
2. Water accumulations 3. glycogen accumulations 4. foreign accumulations: tar from cigarette smoke on lungs |
|
What are the 3 causes of accumulations in the cell after injury?
|
Have an overall alteration in inracellular digestion because the pathway is
1. Overwhelmed 2. Impaired 3. It is exposed to a foreign substance and there is no way to repair |
|
Give an example of a disease that is caused by an over accumulation of vacuoles due to cell injury.
|
1. Tay-Sacks
-deficiency of an enzyme needed to digest a particular class of lipid 2. Fatty Liver disease -hepatocytes in the liver with significant accumulations of fat |
|
What does the liver appear like in fatty liver disease?
|
Has a palor appearance or even greasy
|
|
Describe how alcoholism causes fatty liver disease.
|
-when you consume alcohol, the ETOH is metabolized by the liver and the byproduct is acetyl aldehyde: hepatotoxic
-Causes the liver to accumulate fat -Can lead to chronic injury: serosis of the liver: not reversible! |
|
At what point of cell swelling is there no turning back or repair?
|
When the mitochondria or ER of the cell have become bloated. Permanent damage and eventual necrosis
|
|
What is necrosis? Why is it also called coagulative necrosis?
|
-Permanent cell death that is traumatic in nature and unintended
-When the cell starts to dies you see proteins denaturing and coagulating. |
|
What is programmed cell death?
|
Apoptosis
|
|
What are the stereotypical changes in the nucleus during coagulative necrosis?
|
1. Nucleus appears to be shrinking (pyknosis)
2. After shrinking nucleus looks like it has fallen apart 3. cells that are dead look like they have no nucleus because it has been broken down |
|
What is liquifactive necrosis and when does it occur?
|
-Necrosis of cells where the tissue liquefies ending with empty space being replaced with fluid
-happens in organs that have very little or no connective tissue and the cells cannot regenerate |
|
What is fat necrosis?
|
Necrosis of lipid tissue.
-fatty acids entering EC space that end up reacting with EC calcium and when when they react you get the formation of SOAP deposits! |
|
What type of necrosis occurs in tissue with minimal connective tissue and appears like cottage cheese? What is an example?
|
Caseous Necrosis
-lymph nodes in the lungs that are attacked by TB |
|
What are endogenous endonucleases and when are they used?
|
-Proteins that go in and start cleaving portions of the chromatin
-transcribed when the cell begins initiation of apoptosis |
|
How does the cell appear first during apoptosis?
|
Appears to be shrinking
-THe cell implodes on itself!!! |
|
How do you know that a cell died from apoptosis and not necrosis?
|
In apoptosis the cell implodes in on itself and its content do no leak out
-necrosis, the content can leak into the EC space |
|
List some incidences that will trigger apoptosis of a cell?
|
1. when many mistakes in DNA have occured
2. When a virus injects its DNA into the cell 3. certain types of stress 4. Can be triggered by the immune system |