Pathophys L1

Front 1

Define disease.

Back 1

a pattern of response to some form of injury

Front 2

Describe the relationship between disease and injury.

Back 2

Diseases are the physiological effect of the injury, NOT the injury

ex: HIV is the injury, AIDS is the disease

Front 3

What are 3 features that every disease has?

Back 3

Every disease has a range of:
1. causes
2. manifestations
3. time course (how long it takes to develop)

Front 4

Do many diseases have 1 cause, manifestation, and time course?

Back 4

no, very few

Front 5

What does it mean when we say that diseases are dynamic?

Back 5

diseases come about as an interplay between the nature of the injury and the response to the injury

Front 6

Our bodies have ways to compensate for injuries. What are 2 potentially adverse outcomes from the body's compensation attempts?

Back 6

Sometimes,
1. the injury overwhelms the response
2. the response brings about the disease

Front 7

What is renal artery stenosis?

Back 7

caused by the narrowing of the renal artery, either unilateral or bilateral

Front 8

How does renal artery stenosis effect the kidney's ability to interpret blood volume and blood pressure?

Back 8

the stenosis causes a decrease in renal perfusion, which causes the kidney's to interpret the BV and BP as low

this misinterpretation causes the kidney to elevate the BP and BV, resulting in congestion and hypertension

Front 9

What kind of compensatory example is renal artery stenosis?

Back 9

an example in which the RESPONSE of the body is the actual cause of the disease

Front 10

What is the treatment goal for a disease that is caused by the body's compensatory response?

Back 10

aim the treatment of the disease at reducing the body's response

Front 11

How do you know when someone is in a disease state?

Back 11

when their manifestations are deviations from normal

Front 12

What are some examples of biological parameters that have normal averages and ranges?

Back 12

1. genetic: different polymorphisms affect people's ability to metabolize and respond to drugs
2. age: body system functions change with age
3. gender: hematocrit, metabolic rate differ among men and women
4. situational differences: sea level vs. elevation
5. time differences: time of day, month
6. lab conditions: specific conditions might affect the parameter reading

Front 13

How can we best measure whether or not a patient has deviated from normal?

Back 13

have the patient serve as their own standard (ie know the individual norm of the patient)

Front 14

Define etiology.

Back 14

the disease's cause

Front 15

Define pathogenesis.

Back 15

the mechanism of disease development (specifically HOW the disease developed)

Front 16

What are clinical manifestations?

Back 16

the observable results of a disease (ie the functional consequences of disease development)

Front 17

Do you observe disease development to understand pathogenesis?

Back 17

no, you observe the clinical manifestations (ie lab results)

Front 18

At which level do all etiologies converge?

Back 18

the cell level: all etiologies effect cell function, which then go on to effect tissue and organ function

Front 19

What are 3 possible etiologic origins?

Back 19

1. extrinsic
2. intrinsic
3. idiopathic (unknown)

Front 20

Which common disease is idiopathic?

Back 20

primary hypertension (aka essential hypertension)

Front 21

Describe the different forms of disease states.

Back 21

Many disease states have forms of BOTH known causes and idiopathic causes

Front 22

What are 3 possible conditions that that may serve as extrinsic conditions for disease etiology?

Back 22

1. infectious (viral, parasitic, fungal, bacterial)
2. inanimate (extreme environmental conditions: temperature, radiation, chemical burns)
3. Iatrogenic conditions

Front 23

What are iatrogenic conditions?

Back 23

When someone has some condition that is caused by medical care (fairly common)

Front 24

What occurs when there is an injury that effects cell function and when the cell adapts in a maladaptive manner?

Back 24

altered or dysfunction of an organ results from pathogenesis

Front 25

What are 4 factors of pathogenesis that determine the direction of disease development?

Back 25

1. time
(how long were you exposed to the radiation?)
2. quantity
(how much radiation were you exposed to?)
3. location
(where was the exposure)
4. what morphological changes occurred?

Front 26

What do the factors of pathogenesis determine?

Back 26

the severity of manifestations and the prognosis of treatment

Front 27

What are 3 major forms of clinical manifestations?

Back 27

1. signs
2. symptoms
3. pain

Front 28

What is a sign?

Back 28

-an objectively observable clinical manifestation
-can be determined from a good physical exam
-may or may not be noticed by patient

Front 29

What is a symptom?

Back 29

a subjectively experienced feeling

-can only be reported by the patient

Front 30

What is one of the only clinical manifestations that can be both a sign and a symptom? Give examples.

Back 30

pain

sign: grimacing, tensing, elevated heart rate, diaphoresis
symptom: can only be measured subjectively

Front 31

Clinical manifestations change with time. List the 5 possible periods of disease duration.

Back 31

1. latent period
2. prodromal period
3. acute period
4. chronic period
4. subclinical period

Front 32

Define latent period.

Back 32

the period of time between the ONSET of the injury and the very FIRST manifestation of any sign or symptom

Front 33

Define prodromal period.

Back 33

usually the first manifestation of signs or symptoms (nonspecific: fever, malaise, etc.)

Front 34

Define acute period.

Back 34

the time when you have SPECIFIC signs and symptoms and the time in which the SEVERITY of signs and symptoms are greatest

Front 35

What are the 2 possible options for a disease after the acute phase?

Back 35

diseases will either:
1. resolve themselves and you recover
2. disease will go into a chronic phase

Front 36

Define the chronic phase of a disease.

Back 36

often the severity of the signs and symptoms are REDUCED (and sometimes they completely resolve), but the disease process is still ongoing

Front 37

What is a characteristic quality of chronic diseases?

Back 37

periods of exacerbation and remission (ie latent/ silent periods)

Front 38

Define subclinical stage.

Back 38

the point at which the disease state is firmly established, and there are already functional consequences that are either well compensated for by the body or not yet detected by clinical measures

Front 39

Give an example in which the body is compensating at the subclinical stage.

Back 39

if a renal disease patient has nephron loss, you might not see a decrease in GFR if the other nephrons are compensating

Front 40

Give an example in which clinical measures of a disease are still subclinical.

Back 40

there may be abnormal cancer cells present, but they have not produced a mass yet

Front 41

In making a diagnosis, your data is based on what?

Back 41

1. Clinical methods (signs & symptoms)
2. Laboratory methods
-Urinalysis
-Blood analysis
-Tissue diagnosis
-EKG
-Radiography

Front 42

Describe the process of using a differential diagnosis.

Back 42

based on all the individual pieces of information, you make a list of possible diagnoses.

the diagnoses on your list is exhaustive and may pertain to only 1+ pieces of data.

Then you can eliminate the options that don’t correspond to the vast majority of your clinical data to reach your diagnosis

Front 43

What is the source of all disease?

Back 43

cell injury

Front 44

How do we maintain cell health?

Back 44

control the immediate environment that our cells are exposed to

Front 45

We can't control intracellular conditions, what can we control to compensate for this?

Back 45

our homeostatic mechanisms can control extracellular fluid

Front 46

Which 5 factors are important in maintaining cellular homeostasis?

Back 46

1. cell volume
2. electrolyte balance
3. pH maintenance
4. cell metabolism
5. cell transport

Front 47

How can cell volume be controlled?

Back 47

control:
1. water balance
2. osmolyte balance

Front 48

What does electrolyte balance control?

Back 48

cell's excitability and MP (aim for appropriate reactions)

Front 49

Why is pH maintenance so important?

Back 49

changes in pH are not tolerated because they have narrow ranges and proteins are affected most

Front 50

Why can't many osmolytes cross the plasma membrane?

Back 50

they have the potential to exert osmotic pressure

Front 51

Name the 2 primary osmolytes

Back 51

1. Na
2. K

Front 52

Which conditions do we strive to maintain at all times?

Back 52

isotonic conditions

Front 53

Which system regulates water balance?

Back 53

ADH/Thirst system:

ADH increases water reabsorption (retaining water ONLY). this controls your level of thirst and .:. the amount of water you drink

Front 54

What happens to ADH when plasma osmolarity increases?

Back 54

ADH increases

Front 55

What are 2 ways in which Na and K are controlled?

Back 55

1. systemically (renin-angiotensin system)
2. intracellularly (Na/K ATPase pumps)

Front 56

What factors control the renin-angiotensin system?

Back 56

1. volume status
2. BP

Front 57

Describe the mechanism behind the renin-angiotensin system.

Back 57

renal baroreceptors sense BP change (and therefore a BV change)--->
release renin-->
angiotensin I-->
AT II-->
Aldosterone

1. a drop in BP causes a rise in everything
2. a rise in BP causes a drop in everything

Front 58

What is the function of aldosterone when it is released?

Back 58

it causes the kidneys to:
1. conserve Na
2. waste K

.:.controls Na-K balance

Front 59

What is the Na-K ATPase pump function?

Back 59

continuous pumping of Na OUT and K IN (cell)

Front 60

What happens if the cell can't operate the Na-K ATPase pumps?

Back 60

Na accumulates inside the cell, causing an INCREASE in cell volume

Front 61

What is the first sign of cell death?

Back 61

cell volume increase

Front 62

What are 3 components of ECF?

Back 62

1. intravascular space
2. interstitial fluid
3. transcellular fluid (aka third space)

Front 63

What is transcellular fluid?

Back 63

the fluid that lies between serous membranes

normally, it comprises a VERY tiny portion of the ECF

Front 64

When transcellular fluid accumulates, why is it difficult to get rid of it?

Back 64

the turnover of the fluid is not very rapid

Front 65

What is the formula for TBW (total body water)?

Back 65

TBW=ECF + ICF

Front 66

60% of our body is water. What percentages is the water in terms of ECF and ICF?

Back 66

40% ICF
20% ECF

*can change depending on %body fat

Front 67

What effect does a higher percentage of fat cells have on your water balance?

Back 67

Since fat cells contain less water than all other cells, the higher your % body fat, the less of your BW is represented by TBW

people with more body fat (obese, elderly) are more vulnerable to dehydration

Front 68

Free [Na] is greater __

Free [K] is greater __

Free [Ca] is greater __

Back 68

Na: ECF

K: ICF

Ca: ECF

Front 69

What happens when Ca levels rise?

Back 69

they can kill the cell quickly

Front 70

How do bicarbonate levels effect catalysis?

Back 70

they first effect the pH of the solution, which in turn effects protein function and .:. catalysis

Front 71

2 functions of edema?

Back 71

1. expected and useful
2. pathological

Front 72

What are 4 causes of edema?

Back 72

1. decreased plasma oncotic pressure
2. increased interstitial oncotic presure
3. increased capillary BP (CBP)
4. lymphatic obstruction

Front 73

What is the typical cause of decreased plasma oncotic pressure?

Back 73

losses/reductions in albumin (the factor that maintains BV)

Front 74

What are 2 conditions in which albumin levels decrease?

Back 74

1. liver disease
2. starvation states (not enough AA to make albumin)

Front 75

Describe the type of edema that is from a drop in plasma oncotic pressure.

Back 75

starvation belly/ liver cirrhosis belly fluid accumulation

Front 76

What is the normal value for interstitial oncotic pressure?

Back 76

0

Front 77

How does interstitial oncotic pressure increase?

Back 77

vascular injury or leaking of vasculature lets albumin into the tissue space, causing a pull of fluid into that space

Front 78

What is a potentially useful reason as to why the interstitial oncotic pressure would increase?

Back 78

acute inflammation: causes all of the tiny capillaries to become leaky, which allows albumin to leak into the interstitial space

this is an adaptive process that draws water in to help flush out a wound

Front 79

What are 2 possible causes for an increase in CBP?

Back 79

1. hypertension
(elevated pressure in all of arterial system)
2. venous obstruction
(causes pressure to back up into capillaries, causing edema)
3. volume overload
(causes more fluid throughout the whole system)

Front 80

How might a lymphatic blockage occur?

Back 80

1. tumor in lymph node
2. removed lymph node (so no longer have fluid drainage)

Front 81

What is the only way to prevent true lymphedema?

Back 81

to prevent it from happening in the first place

Front 82

Why do all capillary beds have lymphatic drainage?

Back 82

to help regulate interstitial fluid (the lymphatic vessels are supposed to clear excess fluid)

Front 83

Where do fluid/electrolyte imbalances often come from?

Back 83

alterations in:
1. Na levels
2. Cl levels
3. water levels (total fluid or water balance)

Front 84

What are 3 ways in which fluid/electrolyte imbalances present themselves?

Back 84

1. electrolyte values change
2. volume status changes (overload vs deficit)
3. isotonic, hypotonic, or hypertonic alterations

Front 85

Do isotonic, hypotonic, and hypertonic alterations tell us anything about volume status?

Back 85

NO! they tell us about the relative CONC. of water: solutes

Front 86

What are the qualities of ISOTONIC ALTERATIONS?

Back 86

1. we have NO change in plasma osmolarity
2. we DO have a change in TBW (and therefore total plasma volume), but the change (whether loss or gain) is proportional to the loss (loss or gain) in BOTH water and solutes

Front 87

What are 2 types of isotonic alterations?

Back 87

1. isotonic volume depletion
2. isvolumetric excesses

Front 88

Give 2 examples of isovolumetric depletion.

Back 88

1. hemmorrhage (we lost whole blood and all of its components in proportional amounts)
2. severe wound drainage

Front 89

Give 2 examples of isovolumetric excesses.

Back 89

1. excess IV fluid administration (etiologically iatrogenic)
2. hypersecretion of aldosterone (overall volume stays the same because Na and H20 are conserved in equal amounts)

Front 90

How do we know when we have hypertonic alterations?

Back 90

when the ECF osmolarity increases

Front 91

What is either a cause or consequence of hypertonic alterations?

Back 91

hypernatremia

Front 92

Hypertonic alterations:

What are 5 causes of hypernatremia?

Back 92

1. inadequate fluid intake
2. inappropriate administration of hypertonic saline
3. water deficit
4. inadequate renal concentration of H2O
5. hyperchloremia

Front 93

What is the cause of inadequate fluid intake and how is this related to Na increase?

Back 93

not consuming enough water

your total body Na is the same, but since your H2O volume is lower, your [Na] appears to be hypernatremic

Front 94

What are 3 presentations of water deficit (not consuming enough water)?

Back 94

1. apparent hypernatremia (same concept as inadequate fluid intake)
2. Na levels staying the same
3. Na levels going down

(ex: when people exercise, don't drink enough water, AND sweat profusely: person loses water and salt---their Na profile depends on how much water and salt they've lost)

Front 95

What is the most toxic effect in a water deficit situation? When does it occur?

Back 95

hyponatremia: occurs when someone is sweating profusely and ONLY drinking water (so not replacing the lost Na)

Front 96

What 2 situations cause inadequate renal concentration of water?

Back 96

1. kidneys not responding to ADH
2. body not producing ADH

Front 97

What is the effect of inadequate renal concentration of water?

Back 97

you're not conserving water, so your plasma osmolarity gets very high

Front 98

What is the directional relationship between Na and Cl?

Back 98

Cl follows Na

Front 99

What are 2 situations that can result in hyperchloremia?

Back 99

1. excess Na
2. deficit bicarbonte

Front 100

What is a common cause of hyperchloremia?

Back 100

if a person takes a diuretic that contains too much aluminum chloride

Front 101

What are 3 causes of hypotonic alterations?

Back 101

1. hyponatremia
2. excess intake of water (water excess)
3. hypochloremia

Front 102

What are 5 causes of hyponatremia?

Back 102

1. diuretics
2. vomiting
3. diarrhea
4. burns
5. dilutional hyponatremia

Front 103

How do diuretics cause hyponatremia?

Back 103

they universally operate by blocking Na reabsorption (with the exception of mannitol) .:. you lose Na

Front 104

How do burns cause hyponatremia?

Back 104

burns cause loss of interstitial fluid and .:. you lose Na

Front 105

What is dilutional hyponatremia?

Back 105

expansion of water content in the blood, diluting the Na that's present (gives a hyponatremic reading)

Front 106

What is SIADH and how does it cause hypotonicity?

Back 106

Where ADH levels are abnormally high, causing inappropriate conservation of water

Front 107

What is hypertonic hyponatremia?

Back 107

a condition in which:
1. blood osmolarity is elevated
2. Na concentration in the blood is reduced

(an unusual situation)

Front 108

What causes hypertonic hyponatremia?

Back 108

the accumulation of a non-Na osmolyte (ie blood glucose, cholesterol)

Front 109

What are the physiological effects of non-Na osmolyte accumulation?

Back 109

1. they increase the osmolarity of blood .:. increasing blood volume
2. increase the pulling pressure of the plasma, causing water to get pulled into the blood vessels and diluting the electrolytes (not a proportional rise in Na to this water volume change)