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Patho > Unit 1: Cellular Adaptation, Injury, and Death > Flashcards

Unit 1: Cellular Adaptation, Injury, and Death Flashcards

1
Q

Atrophy

A

decrease in cell size

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2
Q

Cellular adaptation can be physiologic (______ and ______ _____) or pathologic (due to a ________)

A

Cellular adaptation can be physiologic (normal and expected) or pathologic (due to a disease process)

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3
Q

Physiologic example of atrophy

A

ovaries atrophy with age, which coincides with menopause and the inability to reproduce

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4
Q

Pathological example of atrophy:
________________________________________________________

This is why you must always ____ _____ _____ to ________ ____ ___

A

long term use of exogenous steroids causes atrophy of the adrenal cortex

Why you must always slowly taper corticosteroids to re-stimulate adrenal cortex

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5
Q

Hypertrophy

A

Increase in cell size

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6
Q

Hypertrophy can be triggered by ______ (______) or tropic (______ _____ or ______ _____ signals

A

Can be triggered by mechanical (stretch) or tropic (growth factor or vasoactive agents) signals

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7
Q

Example of hypertrophy:

A

HF causes backup of blood in heart chambers 🡪 cardiac tissue is stretched 🡪 LV must pump harder to eject blood and maintain CO 🡪 increased functional demand 🡪 increase in cell size

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8
Q

Physiological example of hypertrophy, plus 2 points

A

exercising will increase functional demand 🡪 increases muscle mass

-Can become pathologic if excessive as muscle will break down (rhabdomyolysis – protein accumulation in kidneys)

-Reversible 🡪 when functional demand decreases (you stop working out so much), cell size returns to normal

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9
Q

Physiological example of hypertrophy, plus one point

A

uterus stimulated by pregnancy hormones to increase in size to support fetus

Reversible 🡪 when baby is delivered, uterus will return to normal size

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10
Q

Pathologic example of hypertrophy

A

Left Ventricular Hypertrophy (LVH)

-Anything that impairs the forward flow of blood and causes a decrease in cardiac output (hypertension, aortic stenosis, polycythemia, ect) causes the left ventricle to work harder to adequately pump blood to the body

Harder worker LV = increased functional demand of LV 🡪 LVH

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11
Q

Hyperplasia

A

Increase in number of normal cells

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12
Q

Physiologic example of hyperplasia

A

mammary glands increase in number in response to estrogen during pregnancy

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13
Q

Physiologic example of hyperplasia (2)

A

Liver regeneration

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14
Q

Pathologic example of hyperplasia

A

Endometrial cells increase in number

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15
Q

Pathologic example of hyperplasia (2)

A

long term irritation of one area can cause bone spurs

-Bone cells increase in number

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16
Q

Metaplasia is

A

Different cell maturation pathway signaled by cytokines & growth factors

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17
Q

Metaplasia is basically the _____ of ___ cells with ____ ____ cells

A

Replacement of normal cells with lower level cells

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18
Q

Metaplasia includes _________ of stem cells (epitheilia) or undifferentiated mesenchymal cells (connective tissue)

A

Reprogramming of stem cells (epitheilia) or undifferentiated mesenchymal cells (connective tissue)

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19
Q

Pathologic example of metaplasia

A

long term smoking causes constant irritation/inflammation and will change bronchial tissue

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20
Q

Metaplasia: what happens with long term smoking?

________ cells stop dividing into ______ ______ cells and begin dividing into _______ ________ cells (lower level and LESS FUNCTIONAL cells)

_______,______🡪 _______ _____

No ____ so _____ can’t escape = problems _____, ___________, etc

A

Bronchial cells stop dividing into columnar ciliated cells and begin dividing into squamous non-ciliated cells (lower level and LESS FUNCTIONAL cells)

Ciliated, columnar 🡪 stratified squamous

No cilia so mucus can’t escape = problems breathing, increased risk for infection, etc.

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21
Q

Second pathologic example of metaplasia

A

kidney stones cause constant irritation/inflammation and will change bladder tissue

transitional 🡪 stratified squamous

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22
Q

Dysplasia:

_______ cells that are ____ from the original cells from which they derived

______, _____, ______, and ______ are ______

Increased risk for progressing to ______( _____ cells)

A

Disorganized cells that are distant from the original cells from which they derived

Size, shape, organization, and function are different

Increased risk for progressing to neoplasia (cancer cells)

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23
Q

Pathologic example of dysplasia: most notably occurs in _____ ___

2 points

A

most notably occurs in cervical tissue

Cervical cells can become disorganized and increase the risk for development of cervical cancer

Why women get frequent pap smears

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24
Q

Hypertrophy + Hyperplasia 🡪 an increase in cell size and number can occur together

What’s a physiologic example of this?

_____ cells increase in size and number when ______ in response to _____to support the _____ _____

A

Uterine cells increase in size and number when pregnant in response to hormones to support the growing fetus

Once the baby is delivered, the uterus reverts back to its original size (reversible adaptation)

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25
Q

Hypertrophy + Hyperplasia 🡪 an increase in cell size and number can occur together

What’s a pathologic example of this?

_______ _____

-_______ cells are stimulated by ______ to grow in both size and number 🡪 forms _____ ____in the ______

  • Causes ______, ______, and decreases _______
A

Uterine fibroids

Uterine cells are stimulated by hormones to grow in both size and number 🡪 forms fibrous masses in the uterine lining

Causes discomfort, bleeding, and decreases fertility

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26
Q

4 common biochemical ways cells die or become injured –

A

Lack of ATP
Reactive Oxygen Species (ROS)
Ca+ in cell (AKA point of no return)
Membrane Permeability Defects

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27
Q

NaK ATPase pump transports…

A

Na+ out and K+ in

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28
Q

Common biochemical ways cells die or become injured –
Lack of ATP 🡪 no ______ metabolism and _____ ____ ___ fails 🡪 ___ can’t get out and ____ can’t get in 🡪 ______ follows Na+ into cell 🡪 cell _____ 🡪 organelles cannot function 🡪 ribosomal _______from ER 🡪 protein synthesis _____ 🡪 _______ in ____ ______ as there are no carrier proteins to transport _____ out of the cell

A

Common biochemical ways cells die or become injured –
Lack of ATP 🡪 no aerobic metabolism and NaK ATPase pump fails 🡪 Na can’t get out and K+ can’t get in 🡪 water follows Na+ into cell 🡪 cell swell 🡪 organelles cannot function 🡪 ribosomal detachment from ER 🡪 protein synthesis ceases 🡪 increase in lipid deposition as there are no carrier proteins to transport lipids out of the cell

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29
Q

NOTE:

the NaK ATPase pump maintains intracellular and extracellular ____ ______ and is crucial to keeping a cell functional and healthy

A

NOTE:

the NaK ATPase pump maintains intracellular and extracellular ionic concentrations and is crucial to keeping a cell functional and healthy

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30
Q

NaK ATPase pump transports Na+ out and K+ in

When it does not work, Na+ is ___ ______ _____🡪 cell ____ and loss of function of organelles; K+ is not pumped ___🡪 accumulation of __ _______ of the cell + _____ ____build up from anaerobic metabolism (because there is no ATP) 🡪 _________ _______ and __________

A

NaK ATPase pump transports Na+ out and K+ in

When it does not work, Na+ is not pumped out 🡪 cell swell and loss of function of organelles; K+ is not pumped in 🡪 accumulation of K+ outside of the cell + lactic acid build up from anaerobic metabolism (because there is no ATP) 🡪 metabolic acidosis and hyperkalemia

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31
Q

Reactive Oxygen Species (ROS) 🡪 in ______ (_______ stress), ROS will ______ the _____ _______ by ____ _______ (ROS steal electrons from lipids and disrupt CM structure) 🡪 organelles can come out of cell and substances can go into cell (like Ca+ or water) 🡪 _______ and _______ of cell

A

Common biochemical ways cells die or become injured –
Reactive Oxygen Species (ROS) 🡪 in excess(oxidative stress), ROS will destroy the cell membrane by lipid peroxidation (ROS steal electrons from lipids and disrupt CM structure) 🡪 organelles can come out of cell and substances can go into cell (like Ca+ or water) 🡪 apoptosis and necrosis of cell

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32
Q

ROS = atoms with _______ electron that are a normal byproduct cellular metabolism or can come from _______ sources (poor diet, stress)

A

ROS = atoms with unpaired electron that are a normal byproduct cellular metabolism or can come from exogenous sources (poor diet, stress)

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33
Q

Common biochemical ways cells die or become injured –
ROS will attempt to steal e- from other cells/structures in the body 🡪 chain reaction of molecules needing another e-
In excess, they overwhelm and outnumber their natural opponent, antioxidants (Vit A, E, C) 🡪 ______ ______

A

oxidative stress

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34
Q

Common biochemical ways cells die or become injured –
Ca+ in cell (AKA point of no return) 🡪 excess Ca+ will _____ ________ (no ATP) and other ______ function 🡪 activate enzymes that breakdown many substances 🡪 intracellular damage from enzymes and promote of apoptosis

A

Ca+ in cell (AKA point of no return) 🡪 excess Ca+ will decrease mitochondrial (no ATP) and other organelle function 🡪 activate enzymes that breakdown many substances 🡪 intracellular damage from enzymes and promote of apoptosis

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35
Q

Normally, there is a Ca+ pump that only allows for a small amount Ca+ inside of the cell

When disrupted, Ca+ floods the cell and there is ________ damage

Ca+ acts as an activator for many enzymes such as protease (breaks down proteins of CM and cytoskeleton), endonuclease (breaks down DNA), and ATPase

A

irreversible

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36
Q

Common biochemical ways cells die or become injured –
Membrane Permeability Defects 🡪 damage to the CM increases permeability and ____ for substances to come in and out of the cell _____ 🡪 decrease in proteins, co-enzymes, RNA, and ATP substrates
Can be caused by ROS from lipid peroxidation 🡪 Ca+ into cell and organelle dysfunction

A

Membrane Permeability Defects 🡪 damage to the CM increases permeability and allows for substances to come in and out of the cell freely 🡪 decrease in proteins, co-enzymes, RNA, and ATP substrates
Can be caused by ROS from lipid peroxidation 🡪 Ca+ into cell and organelle dysfunction

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37
Q

Free Radicals 🡪 _______ molecules with an _______ electron
Disrupt chemical bonds of CM 🡪 destroy CM and structure 🡪 cell death

A

Free Radicals 🡪 unstable molecules with an unpaired electron
Disrupt chemical bonds of CM 🡪 destroy CM and structure 🡪 cell death

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38
Q

Free radicals can damage the cell with 3 mechanisms:

A

Lipid peroxidation 🡪 destroys CM and allows for substances to go in/out

Protein modification 🡪 protein dysfunction (need proteins for so many cell functions)

DNA damage 🡪 genetic mutations 🡪 increases risk for cancer development

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39
Q

Free radicals inactivated by _________ and some enzymes, but if there is an imbalance of ROS and free radical inactivators 🡪 oxidative stress

A

Free radicals inactivated by antioxidants and some enzymes, but if there is an imbalance of ROS and free radical inactivators 🡪 oxidative stress

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40
Q

Ischemia

A

reduction/cessation of blood flow

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41
Q

Hypoxia

A

inadequate amount of oxygen in tissues

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42
Q

sign of irreversible cell damage when there is a lack of O2 🡪 mitochondrial dysfunction and loss of mitochondrial membrane integrity

A

Mitochondrial vacuolization

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43
Q

3 things to remember about a reduction in ATP

A
  • cellular swelling
  • decrease in protein synthesis
  • decrease in membrane transport
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44
Q

Which common biochemical derangements destroy the cell membranes and structure?

A

Reactive Oxygen Species (ROS)

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45
Q

An increase in Ca in the cell leads to

A

intracellular damage from enzyme activation

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46
Q

Membrane permeability defects lead to release of ________ _____, which leads to _______ _____

A

Membrane permeability defects lead to release of lysosomal enzymes, which leads to cellular digestion

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47
Q

When calcium enters the mitochondria,

A

the cell dies

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48
Q

A decrease in ATP does not effect

A

the movement of water pressure (passive)

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49
Q

Reactive Oxygen Species are a part of our physiology, they’re a byproduct of

A

cellular metabolism (but it does so in a manageable manner)

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50
Q

If ROS rises, but ______ do not rise, there’s an _____. This is not good (antioxidants don’t change- we get it exogenously)

This is imbalance is called _____ _____, which can lead to ____ _____

A

If ROS rises, but antioxidants do not rise, there’s an imbalance. This is not good (antioxidants don’t change- we get it exogenously)

This is imbalance is called oxidative stress which can lead to cell injury

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51
Q

Hypoxemia

A

Too little oxygen in the blood

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52
Q

Can ischemia lead to hypoxia

A

yes !

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53
Q

______ will produce ____, but you can have ______ without ______

A

Ischemia will produce hypoxia, but you can have hypoxia without ischemia

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54
Q

What is vacuolization?

A

A way to compensate for flooding of the cell (acute cellular swelling). It’s only temporary- it buys a little time before the cell dies

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55
Q

Cellular Injury Mechanisms: Hypoxia (1st part):
Obstruction or cessation of blood flow –> _______ –> _______ in mitochondrial oxygenation. This can lead to either ____ ________ of ______ (end) or _____ in ATP.

A

Cellular Injury Mechanisms: Hypoxia (1st pathway):
Obstruction or cessation of blood flow –>ischemia –> decrease in mitochondrial oxygenation. This can lead to either severe vacuolization of mitochondria (end) or decrease in ATP.

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56
Q

Cellular Injury Mechanisms: Hypoxia (1st pathway):
Obstruction or cessation of blood flow –>ischemia –> decrease in mitochondrial oxygenation. This can lead to either severe vacuolization of mitochondria (end) or decrease in ATP.

(1) From this decrease in ATP, this can lead to a decrease in ___ _____ –> _______ Na ______, ________ K ______, _______ Ca _______ –> _____ increases –> ____ ____ ______ increases

A

(1) From this decrease in ATP, this can lead to a decrease in Na pump –> Intracellular Na increases , Extracellular K increases, Intracellular Ca increases –> H2O increases –> acute cellular swelling increases

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57
Q

Cellular Injury Mechanisms: Hypoxia (1st pathway):
Obstruction or cessation of blood flow –>ischemia –> decrease in mitochondrial oxygenation. This can lead to either severe vacuolization of mitochondria (end) or decrease in ATP.

(1) From this decrease in ATP, this can lead to a decrease in Na pump –> Intracellular Na increases , Extracellular K increases, Intracellular Ca increases –> H2O increases –> acute cellular swelling increases

This causes 4 things: A _____ of the ____ ____, a _____ of ribosomes, a _____ in ____ ______, and ___ ____

A

A dilation of endoplasmic reticulum, a detachment of ribosomes, a decrease in protein synthesis, and lipid deposition

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58
Q

Cellular Injury Mechanisms: Hypoxia (2nd pathway):
Obstruction or cessation of blood flow –>ischemia –> decrease in mitochondrial oxygenation. This can lead to either severe vacuolization of mitochondria (end) or decrease in ATP.

(2) From this decrease in ATP, this can lead to an ____ in _____ ______, a ____ in ____, an _____ of ______, and a _____ in ____. Lastly, this pathway ends with ____ ___ ______

A

From this decrease in ATP, this can lead to an increase in anaerobic glycolysis, a decrease in glycogen, an increase of lactate, and a decrease in pH. Lastly, this pathway ends with nuclear chromatin clumping

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59
Q

Cellular Injury Mechanisms: Hypoxia (1st pathway):

Why do you think the decrease in ATP -> decrease in Na pump eventually leads to lipid deposition?

A

We need proteins to transport fat out of the cell. So when we have a reduction of protein synthesis, there’s no protein carrier that can transport the fat out of the cell.

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60
Q

What is chromatin

A

It’s part of the packaging of DNA, to form it into a chromosome. It binds DNA so that it’s not so prone to breaking

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61
Q

At a high altitude, oxygen is ____ due to _____

A

At a high altitude, oxygen is reduced due to pressure

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62
Q

Cellular Injury Mechanisms: Hypoxia

Increase in altitude -> decrease in effective FiO2 -> hypoxia -> reduction in ____ -> anaerobic metabolism -> increase in ____ ___ ->______ _____ -> increase in ___

A

Increase in altitude -> decrease in effective FiO2 -> hypoxia -> reduction in ATP -> anaerobic metabolism -> increase in lactic acid -> metabolic acidosis -> increase in K

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63
Q

Too much circulating potassium is called..

A

hyperkalemia

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64
Q

Hyperkalemia can lead to

A

abnormal heart rhythms or cessation heart beat (cardiac arrest)

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65
Q

Cellular Injury Mechanisms: Hypoxia

Increase in altitude -> decrease in effective FiO2 -> hypoxia -> reduction in ATP -> anaerobic metabolism -> increase in lactic acid -> metabolic acidosis -> increase in K

NaK ATPase pump failure -> increase in ___ and ___ -> decrease of ____ in the cell -> cell swell -> decrease in level of ______ (LOC) -> increase of circulating _____ (dysrhythmia, cardiac arrest)

A

NaK ATPase pump failure -> increase in Na and Ca -> decrease of K in the cell -> cell swell -> decrease in level of consciousness (LOC) -> increase of circulating *potassium** (dysrhythmia, cardiac arrest)

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66
Q

Cellular Injury Mechanisms: Hypoxia

Increase in altitude -> decrease in effective FiO2 -> hypoxia -> reduction in ATP -> anaerobic metabolism -> increase in lactic acid -> metabolic acidosis -> increase in K

NaK ATPase pump failure -> increase in Na and Ca -> decrease of K in the cell -> cell swell -> decrease in level of consciousness (LOC) -> increase of circulating *potassium** (dysrhythmia, cardiac arrest)

This change effects the whole body, but this is what happened in the lungs in particular:

______________ membrane damage –> ______ in ______ _______–> interstitial fluid –> ______ ______ –> _____ –>_____ -> dysrhythmia –> cardiac arrest

A

Capillary-alveolar membrane damage –> increase in capillary permeability –> interstitial fluid –> pulmonary edema –> hypoxia –> hypoxemia dysrhythmia –> cardiac arrest

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67
Q

Lipid peroxidation

A

destruction of unsaturated fatty acids (constitutes our cell membrane)

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68
Q

Radiation/toxins –> production of ROS –> Superoxide, Hydrogen peroxide, Hydroxyl radical

This can lead to three pathological effects:

A

Lipid peroxidation -> membrane damage

Protein modifications -> breakdown misfolding

DNA damage -> mutations

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69
Q

IRI

A

Ischemia-Reperfusion Injury

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70
Q

Ischemia-Reperfusion Injury (IRI) is a complication of

A

ischemia

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71
Q

Original problem= ischemia is commonly related to a stroke as there is a blood clot occluding a vessel and ceasing blood flow (ischemia).

During this ischemic episode, there is an increase in O2 consumption as the body attempts to metabolize the clot _______ are produced in the process. When the clot is freed (_______), blood flow and ___ is restored and the enzyme xanthine oxidase uses the catabolites and O2, which produces ____

A

During this ischemic episode, there is an increase in O2 consumption as the body attempts to metabolize the clot-catabolites are produced in the process. When the clot is freed (reperfusion), blood flow and O2 is restored and the enzyme xanthine oxidase uses the catabolites and O2, which produces ROS

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72
Q

Original injury of ischemia leads to cell ___ which is _______ (as long as there’s no accumulation of calcium. But when we get reinjured with the reperfusion injury, it leads to cell ___ (_____)

A

Original injury of ischemia leads to cell swell which is reversible (as long as there’s no accumulation of calcium. But when we get reinjured with the reperfusion injury, it leads to cell death (necrosis)

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73
Q

Between reperfusion and ischemic injuries, which is usually worse?

A

Reperfusion

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74
Q

IRI:
Enzyme conversion (______ _____) with o2 exposure

Increase of _____ consumption during ischemia –> ______ -> increase of _____ with ______ -> results in cell membrane _____, ATP ___, ______, and _____

A

Enzyme conversion (xanthine oxidase) with O2 exposure

Increase of ATP consumption during ischemia –> catabolites-> increase of ROS with reperfusion -> results in cell membrane damage, ATP loss, apoptosis, and necrosis

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75
Q

IRI:

______ ______ due to excess ROS from reperfusion and the cell’s inability to produce antioxidants during the ischemic episode 🡪 CM damaged 🡪 ____ influx into cells (overload in _______)🡪 mitochondrial dysfunction 🡪 ATP loss 🡪 apoptosis and necrosis

A

Oxidative stress due to excess ROS from reperfusion and the cell’s inability to produce antioxidants during the ischemic episode 🡪 CM damaged 🡪 Ca+ influx into cells (overload in mitochondria)🡪 mitochondrial dysfunction 🡪 ATP loss 🡪 apoptosis and necrosis

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76
Q

IRI:

ROS excess is perceived as a threat by the immune system and stimulate an _____ ____ 🡪 neutrophils respond and adhere to the vessel epithelium to reach injury site 🡪 neutrophils accelerate injury by increasing capillary permeability (brings more blood and O2 = more ROS!!!)

A

ROS excess is perceived as a threat by the immune system and stimulate an inflammatory response 🡪 neutrophils respond and adhere to the vessel epithelium to reach injury site 🡪 neutrophils accelerate injury by increasing capillary permeability (brings more blood and O2 = more ROS!!!)

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77
Q

IRI:
_________ _____🡪 cell lysis from MAC 🡪 more tissue injury

A

Complement activated

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78
Q

Treatment for IRI

A

antioxidants (reverse neutrophil adhesion) and anti-inflammatories

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79
Q

What is considered a major burn injury

A

Covers 20% or more of body area

80
Q

Cellular injury mechanism: burns

(major burn)
Nerves are _____, so the patient does not feel pain from the burn 🡪 patient feels pain from _____
Skin loses _____ & vapor functions

A

Nerves are destroyed, so the patient does not feel pain from the burn 🡪 patient feels pain from EDEMA
Skin loses barrier & vapor function

81
Q

Cellular injury mechanism: burns

_______ _____ ________ from the direct tissue damage from the burn and the MASSIVE inflammatory response from the extensive tissue damage for the first ___ hours prior to capillary seal (AKA burn shock)

A

Increased capillary permeability from the direct tissue damage from the burn and the MASSIVE inflammatory response from the extensive tissue damage for the first 24 hours prior to capillary seal (AKA burn shock)

82
Q

Hypoalbuminemia

A

Too little of the protein albumin level in the blood

83
Q

Hypovolemia

A

Too little circulating blood volume

84
Q

Burns:

↑ capillary permeability allows for fluid to escape the blood vessels and enter tissues/interstitial space (3rd spacing effect) 🡪 ____ and _________as albumin that normally resides in blood plasma is now able to pass through the damaged vessel and get into the ISS 🡪 ______ _____ ____ pressure (lower PULLING pressure) 🡪 no force to pull fluid back into blood vessel 🡪 MORE EDEMA 🡪 ______ and ________ 🡪 tissue ________ as there is less blood in the vasculature that is able to reach tissues

A

↑ capillary permeability allows for fluid to escape the blood vessels and enter tissues/interstitial space (3rd spacing effect) 🡪 edema and hypoalbuminemia as albumin that normally resides in blood plasma is now able to pass through the damaged vessel and get into the ISS 🡪 decreased capillary oncotic pressure (lower PULLING pressure) 🡪 no force to pull fluid back into blood vessel 🡪 MORE EDEMA 🡪 hypovolemia and hypotension 🡪 tissue ISCHEMIA as there is less blood in the vasculature that is able to reach tissues

85
Q

INFLAMMATORY RESPONSE further increases capillary permeability as ______ ______through vessel walls and create ______ that albumin and fluid can pass through 🡪 MORE EDEMA AND HYPOTENSION + formation of exudates from wound (dead neutrophils that have phagocytized debris)

A

INFLAMMATORY RESPONSE further increases capillary permeability as neutrophils diapedeses through vessel walls and create holes/rents that albumin and fluid can pass through 🡪 MORE EDEMA AND HYPOTENSION + formation of exudates from wound (dead neutrophils that have phagocytized debris)

86
Q

Ischemia with burns is no different that the ischemia you learned previously - lack of O2 reaching tissues 🡪 decreased ATP production 🡪 NaK ATPase pump fails 🡪 cell swell and hyperkalemia 🡪 _______ ________

A

Ischemia with burns is no different that the ischemia you learned previously - lack of O2 reaching tissues 🡪 decreased ATP production 🡪 NaK ATPase pump fails 🡪 cell swell and hyperkalemia 🡪 METABOLIC ACIDOSIS

87
Q

3rd spacing means

A

fluid moves to a third space- it’s usually in the vasculature or the cells- not the interstitial space

(same as edema)

88
Q

Burns:

Because the patient is severely hypotensive, there is a lack of blood reaching all organs 🡪 ____ of _____reaching organs 🡪 tissue ischemia🡪 MOF (______ ______ ____)and MODS, ROS from tissue damage, _______ ____ ______ (low blood volume and ischemia to heart) causing ischemia, and ____ with compensatory mechanisms when blood flow/O2 supply is temporarily restored

A

Because the patient is severely hypotensive, there is a lack of blood reaching all organs 🡪 lack of O2 reaching organs 🡪 tissue ischemia🡪 MOF (Multiple organ failure) and MODS, ROS from tissue damage, decreased cardiac output (low blood volume and ischemia to heart) causing ischemia, and IRI with compensatory mechanisms when blood flow/O2 supply is temporarily restored

89
Q

Burn-

Remember: increased capillary permeability happens in the first 24 hours after suffering a burn prior to capillary seal.

So, what are the markers of the first 24 hours of a burn?

A

the severe edema, hypotension, and MODS are markers of the first 24 hours of a burn

90
Q

Burns-
_______ response as the body is attempting to catch up with the metabolism created by the burn (mass tissue destruction = mass tissue repair/immune response/ect that require mass amounts of energy/nutrients!!!)

A

Hypermetabolic response as the body is attempting to catch up with the metabolism created by the burn (mass tissue destruction = mass tissue repair/immune response/ect that require mass amounts of energy/nutrients!!!)

91
Q

Hypermetabolic response is characterized by…

A

↑ HR, hyperpnea (fast breathing), ↑ core body temperature, ↑ blood glucose, cachexia (muscle wasting)

92
Q

Cachexia

A

break down/destruction of muscle and tissue

93
Q

The hypermetabolic response lasts ____ ____ ____injury - wound closure/repair (can last week’s/months/years

A

The hypermetabolic response lasts 24 hours after injury - wound closure/repair (can last week’s/months/years

94
Q

Immunosuppression following burn shock from massive stress response 🡪 patient is very susceptible to infection 🡪 ______ and _____ ______ are the main concerns

A

Immunosuppression following burn shock from massive stress response 🡪 patient is very susceptible to infection 🡪 wound and systemic sepsis are the main concerns

95
Q

Treatment –
First 24 hours (burn shock/↑ capillary permeability) 🡪

A

fluid/electrolyte replacement with colloidal IV fluids

Remember at this point, the patient is suffering from severe edema and hypotension, so we are trying to prevent tissue ischemia

96
Q

Treatment- following burn shock ->

A

nutrition, wound management, excisions/grafting, scar reduction, comfort measures, infection control, thermoregulation

97
Q

5 clinical manifestations of cellular injury

A
  • Fever
  • Increase HR (increase metabolism)
  • Increase in WBC - infection
  • Pain (release in bradykinins, pressure)
    _ Increase in serum enzymes (LDH, ALT, AST, CK)
98
Q

Another clinical manifestation of cellular injury is _____, malaise, and _____- but these are referred to as sickness behaviors- doesn’t matter what’s wrong with you

A

fatigue, malaise, anorexia

99
Q

Sequence of Cell Death:
1. ↓ ATP production

  1. NaK ATPase pump failure (active transport – needs ATP)
  2. Cellular swelling (NaCl influx into cells – water follows)
  3. Ribosome _______ from endoplasmic reticulum
  4. ↓ protein synthesis
  5. Intracellular ____ → _________ _____
  6. Cytoplasmic ________ (ER breaks off and tries to wall off/enclose the water)
  7. _______ leakage of ______ ________
  8. ________ of intracellular structures (nucleus, nucleolus, halting DNA/RNA synthesis)
  9. ________ ____ ______
A
  1. ↓ ATP production
  2. NaK ATPase pump failure (active transport – needs ATP)
  3. Cellular swelling (NaCl influx into cells – water follows)
  4. Ribosome detachment from endoplasmic reticulum
  5. ↓ protein synthesis
  6. Intracellular Ca++ → mitochondrial swelling
  7. Cytoplasmic vacuolation (ER breaks off and tries to wall off/enclose the water)
  8. Lysosome leakage of digestive enzymes
  9. Autodigestion of intracellular structures (nucleus, nucleolus, halting DNA/RNA synthesis)
  10. Plasma membrane lysis
100
Q

Apoptosis = programmed and orderly cell death (physiologic or pathologic)
The cell shrinks, nucleus fragments, chromatin condenses
Apoptotic bodies form and are phagocytized
Plasma membrane stays INTACT
There is NO inflammatory response

A

Apoptosis = _________ and orderly cell death (physiologic or pathologic)
The cell shrinks, nucleus fragments, chromatin condenses
Apoptotic bodies form and are phagocytized
Plasma membrane stays INTACT
There is ___ _______ ______

101
Q

Apoptosis EX

A

RBC has a programmed lifespan of 120 days

102
Q

Necrosis = cell death due to ________ irreversible cell injury or programmed cell death 🡪 messy and may harm other cells

Sum of pathologic cellular changes after local cell death & cellular autodigestion (autolysis)

Characterized by cell swelling, membrane blebs, breakdown of plasma membrane, rupture of organelles, and stimulation of an
_________response

Necrotic cells seen as an intruder

A

Necrosis = cell death due to unplanned irreversible cell injury or programmed cell death 🡪 messy and may harm other cells

Sum of pathologic cellular changes after local cell death & cellular autodigestion (autolysis)
Characterized by cell swelling, membrane blebs, breakdown of plasma membrane, rupture of organelles, and stimulation of an inflammatory response

Necrotic cells seen as an intruder

103
Q

4 types of necrosis

A

Coagulative
Liquefactive
Caseous
Fat

104
Q

Necrosis:
Coagulative

________ ________ due to ________

A

Protein denaturation due to hypoxia

105
Q

Necrosis:
Liquefactive

A

Hydrolysis causes cells to become soft/liquid
Cysts form to wall off liquid

necrosis with autophagy and cysts

106
Q

Necrosis: Caseous (and example)

A

Mass apoptosis of cells

Granulomas walls off dead cells

Ex: TB tubercles

necrosis enclosed by granuloma

107
Q

Necrosis: Fat
Lipase breaks down free fatty acids 🡪 ___________

A

Fat
Lipase breaks down free fatty acids 🡪 saponification

108
Q

Gangrenous necrosis is not a type of necrosis, it’s when you have a _____ ____ of tissue. It must include _____ and _______ invasion in order to develop gangrene.

A

Gangrenous necrosis is not a type of necrosis, it’s when you have a large area of coagulative necrosis. It must include hypoxia
and bacterial invasion in order to develop gangrene.

109
Q

Dry gangrene

A

Arterial insufficiency + bacteria

Usually occurs in distal extremities (feet/toes)

Skin becomes dry and turns black

110
Q

Wet gangrene

A

Impaired venous return + bacteria

Large area of liquefactive necrosis

Usually occurs in internal organs(sigmoid colon)

Neutrophils invade an infected area and softened it 🡪 cyst forms

Tissue area is cold, black, swollen, and very stinky

111
Q

Gas Gangrene =

A

Clostridium

Pockets of gas in tissue

112
Q

Which gangrene is coagulative?

A

Dry

113
Q

Which gangrene is liquefactuve?

A

Wet

114
Q

Necrosis with large area of tissue

A

Gangrenous

115
Q

Necrosis with protein denaturation

A

Coagulative

116
Q

Necrosis with autophagy and cysts

A

Liquefactive

117
Q

Necrosis enclosed by granuloma

A

Caseous

118
Q

Condition of internal organs with cold, swollen, black, and foul smelling tissue

A

Wet gangrene

119
Q

Osmosis

A

passive movement of water (no ATP) from a lower water concentration to a higher concentration

120
Q

Osmolality

A

Ratio of solute (ions) to solvent (water)

121
Q

Tonicity

A

Term used within the body to describe relative osmolality

122
Q

A high osmolality means

A

the solute is greater than the solvent

123
Q

A low osmolality means the

A

solute is less than the solvent

124
Q

Osmolality refers to specific _____/____ while tonicity describes relativity (inside of cell is more concentrated than outside of cell)

A

values/numbers

125
Q

A normal osmotic equilibrium is when

A

the solute (ions) is equal to the solvent (water)

126
Q

Hypertonic/Hyperosmotic solution:

________ solute to solvent ratio outside of the cell in the ECF (extracellular fluid)
The fluid ______ of the cell is ____ _______than the fluid _____ of the cell (fluid inside of the cell is less conc.)

A

HIGHER solute to solvent ratio outside of the cell in the ECF (extracellular fluid)

The fluid outside of the cell is MORE CONCENTRATED than the fluid inside of the cell (fluid inside of the cell is less conc.)

127
Q

Hypertonic/Hyperosmotic solution:

The fluid will move from _____ of the cell to _____ of the cell to attempt to dilute the ECF 🡪 ____ _____

A

move from inside of the cell to outside of the cell to attempt to dilute the ECF 🡪 CELL SHRINK

128
Q

Shrinkage of the cell is also known as

A

crenation

129
Q

What does a Hypertonic/Hyperosmotic solution do to the osmolality

A

Increases osmolality inside of the cell and decreases osmolality outside of the cell

130
Q

Hypotonic/Hyposmotic solution =

A

LOWER solute to solvent ratio outside of the cell in the ECF

131
Q

Hypotonic/Hyposmotic solution =

Fluid ______ of the cell is ____ _____ than the fluid _____ of the cell (fluid inside of the cell is more conc.)

A

Fluid outside of the cell is LESS CONCETRATED than the fluid inside of the cell (fluid inside of the cell is more conc.)

132
Q

Hypotonic/Hyposmotic solution

Fluid will move from the ECF into the cell to attempt to ______ the ______ of the cell 🡪 ____ ______

A

Fluid will move from the ECF into the cell to attempt to dilute the inside of the cell 🡪 CELL SWELL

133
Q

In an isotonic solution,

A

the solute to solvent ratio outside of the cell in the ECF is equal to the ratio inside of the cell

134
Q

Is there movement of water in an isotonic solution?

A

No

What the cell is trying to maintain with its environment (equal concentration)

135
Q

Capillary Hydrostatic Pressure = ____ ______ pressure from aorta to _____ capillaries

A

Capillary Hydrostatic Pressure = driving filtration pressure from aorta to arterial capillaries

136
Q

Capillary Hydrostatic Pressure is

A

PUSHING pressure

It PUSHES fluid from the vessel into the interstitial fluid (ISF)

137
Q

Capillary Oncotic Pressure = force _______ end that ______ filtration

A

Capillary Oncotic Pressure = force venous end that opposes filtration

138
Q

Capillary Oncotic Pressure =

  • _________ _________
  • ______fluid from the ISF into the vessel 🡪 brings fluid back _____ the vessel
  • Mainly due to the plasma protein ____
A
  • PULLING PRESSURE
  • PULLSfluid from the ISF into the vessel 🡪 brings fluid back into the vessel
  • Mainly due to the plasma protein albumin
139
Q

When the pushing forces push water into the interstitial pace, or the interstitial oncotic pressure is pulling water into the interstitial space, it leads to..

A

edema

140
Q

Capillary membrane damage = movement of _____ into the interstitial space, which changes the ______ and causes ______

A

Capillary membrane damage = movement of proteins into the interstitial space, which changes the pressures and causes edema

141
Q

Capillary membrane damage:

_______ in the capillary membrane (ex: due to neutrophil diapedesis with inflammation) allows for albumin to leave the vessel and enter the ISS (interstitial space)

Albumin in the ISS = _____ ______ _____ PRESSURE

The force pulling fluid back into the vessel is gone 🡪 fluid stays in the ISS 🡪 edema

Fluid is now unavailable for circulation causing ________ and ______

Fluid is now unavailable for metabolism causing cell ________

A

Capillary membrane damage:

Holes in the capillary membrane (ex: due to neutrophil diapedesis with inflammation) allows for albumin to leave the vessel and enter the ISS (interstitial space)

Albumin in the ISS = DECREASED CAPILLARY ONCOTIC PRESSURE

The force pulling fluid back into the vessel is gone 🡪 fluid stays in the ISS 🡪 edema

Fluid is now unavailable for circulation causing hypotension and ischemia

Fluid is now unavailable for metabolism causing cell dysfunction

142
Q

Edema = accumulation of fluid in the interstitial space (locally or systemically)

A

Edema = ________ of fluid in the _____ ______ (locally or systemically)

143
Q

Types of edema:

lymphedema (backup of lymph fluid), pitting edema (leaves an indentation), cerebral edema, pulmonary edema, ascites(fluid in the peritoneal cavity; associated with liver failure)

S/S = weight gain, swelling, puffiness, impaired wound healing (poor circ 🡪 decreased nutrient delivery)

A

________ (backup of lymph fluid), _______ edema (leaves an indentation), ________ edema, _________ edema, _______ (fluid in the peritoneal cavity; associated with liver failure)

S/S = weight gain, swelling, puffiness, impaired wound healing (poor circ 🡪 decreased nutrient delivery)

144
Q

Edema mechanisms:

_____ _______ _____ _____ due to venous obstruction, Na+/H2O retention, HF
Backup of fluid/more fluid from retention increases pushing pressure on arterial end

___ ______ _____ due to liver disease (can’t synthesize proteins) and protein malnutrition
Lower pulling pressure 🡪 fluid stays in ISS

__ _____ _____ due to inflammation (neutrophil diapedesis), burns, immune cell injury

_______ ________
due to infection, tumor, surgical removal 🡪 lymphedema

A

↑ capillary hydrostatic pressure due to venous obstruction, Na+/H2O retention, HF
Backup of fluid/more fluid from retention increases pushing pressure on arterial end

↓ plasma albumin due to liver disease (can’t synthesize proteins) and protein malnutrition
Lower pulling pressure 🡪 fluid stays in ISS

↑ capillary permeability due to inflammation (neutrophil diapedesis), burns, immune cell injury

Lymph obstruction
due to infection, tumor, surgical removal 🡪 lymphedema

145
Q

Renin-angiotensin-aldosterone system (RAAS) 🡪 maintains Na+ levels and BP (↑Na+/BP)

RAAS system is activated when ___ BP/BV, ___ serum ____, ___ _____ ____, ___

A

↓BP/BV, ↓serum Na+, ↑urine Na+, ↑K+

146
Q

JGA (Juxtaglomerular apparatus) of ______ release ______ into blood stream 🡪 Renin converts ______________ that is constantly circulating, into ___________ _🡪 _________ __ passes by pulmonary vessels 🡪 _________ _________ release _________ ________ _________ ______ 🡪 ______ converts ___________ ___ to ______ ____ 🡪 ______ ____ __________ _______ ______ 🡪 ↑peripheral resistance/.afterload to_____ 🡪 ______ ___ signals the _____ _____ to release __________ 🡪 aldosterone stimulates kidneys to _______ ___ and _____ and excrete ____ (as Na moves into blood, water follows) 🡪 Na+ and H2O retention results in _____🡪 ____ 🡪 ↑renal perfusion, causes RAAS system to end by ceasing renin release

A

JGA (Juxtaglomerular apparatus) of kidneys release renin into blood stream 🡪 Renin converts angiotensinogen that is constantly circulating into angiotensin 1 🡪 angiotensin 1 passes by pulmonary vessels 🡪 pulmonary vessels release angiotensin converting enzyme (ACE) 🡪 ACE converts angiotensin 1 to angiotensin 2 🡪 angiotensin 2 vasoconstricts blood vessels 🡪 ↑peripheral resistance/.afterload to ↑BP 🡪 angiotensin 2 signals the adrenal cortex to release aldosterone 🡪 aldosterone stimulates kidneys to reabsorb Na+ and H2O + excrete K+ (as Na moves into blood, water follows) 🡪 Na+ and H2O retention results in ↑BV 🡪 ↑BP 🡪 ↑renal perfusion causes RAAS system to end by ceasing renin release

147
Q

Water Balance Regulation:
Thirst perception 🡪
Osmolality receptors sense ________ (solute > solvent) 🡪 _________ stimulates _____ to get you to drink
Osmolality receptors can be triggered due to low ________ ______ or ____________ (high concentration of solute, like Na+)

A

Water Balance Regulation:
Thirst perception 🡪
Osmolality receptors sense hyperosmolality(solute > solvent) 🡪 hypothalamus stimulates thirst to get you to drink
Osmolality receptors can be triggered due to low plasma volume or hyperosmolality (high concentration of solute, like Na+)

148
Q

Water Balance Regulation:
ADH secretion from the ______ ______
ADH = ___ ____ hormone 🡪 stimulates _________of H2O from renal tubules

A

ADH secretion from the posterior pituitary
ADH = NO PEE hormone 🡪 stimulates reabsorption of H2O from renal tubules

149
Q

ADH controls

A

plasma osmolality

150
Q

ADH chart (1) Increase in ______ _____ will cause a detection by brain _________. OR a detection by __ _______ will cause a detection by _____ _____.—–> _________ —> increases _____ and fluid intake —-> decreases _____ _______

A

Increase in plasma osmolality will cause a detection by brain osmoreceptors OR a detection by volume receptor —-> hypothalamus —> increases thirst and fluid intake —> causes decrease in plasma osmolality

151
Q

ADH chart (2)
Increase in plasma osmolality will cause a detection by brain osmoreceptors OR a detection by volume receptor —-> hypothalamus —> pars nervosa of _____ ______ -> ____ -> renal _____ ______> end result: __________________________________

A

Increase in plasma osmolality will cause a detection by brain osmoreceptors OR a detection by volume receptor —-> hypothalamus —> pars nervosa of posterior pituitary -> ADH -> renal water retention-> end result: decrease in plasma osmolality and increase in plasma volume

152
Q

Baroreceptors and volume receptors increase ADH secretion when

(osmolality, BV, BP)

A

High osmolality, low BV, low BP

153
Q

What does ADH cause

A

ADH causes increased renal absorption of H2O 🡪 BP/BV increases, and osmolality decreases 🡪 posterior pituitary stops secreting ADH (negative feedback mechanism)

154
Q

Hypotonic fluid alteration = too little solute to solvent outside of the cell (inside of the cell is MORE conc and outside of the cell is more diluted)

A

Hypotonic fluid alteration = too _____ _____ to solvent outside of the cell (inside of the cell is ____ ____ and outside of the cell is more ______)

155
Q

What happens to the osmolality of the ECF in hypotonic fluid alteration

A

It decreases (outside of cell has a lower concentration)

156
Q

Hypotonic fluid alteration
Fluid moves _____ cell to decrease the osmolality of the intracellular fluid 🡪_____ _____

A

Fluid moves INTO cell to decrease the osmolality of the intracellular fluid 🡪 CELL SWELL

157
Q

Hyponatremia 🡪

A

too little Na+ in blood

158
Q

Hypotonic fluid alteration causes

A

renal failure = kidneys can’t reabsorb Na+

SIADH = excess ADH causing excessive H2O retention 🡪 large amount of fluid dilutes plasma 🡪 hyponatremia

159
Q

Hypotonic fluid alteration signs and symptoms

A

confusion, irritability, cerebral edema (remember cell swell even with neurons!!!), HA, lethargy, nausea, seizures, coma, hyper/hypovolemia

160
Q

ALWAYS think ____ when there is a Na+ imbalance!

A

neuro

161
Q

Hypertonic fluid alteration = too ____ solute to solvent ______ of the cell (inside of the cell is relatively ____ conc)

A

Hypertonic fluid alteration = too much solute to solvent outside of the cell (inside of the cell is relatively LESS conc)

162
Q

Hypertonic: Fluid moves from inside of cell to outside of the cell to decrease the osmolality of the ECF/plasma (depending on what cells this is occurring in) 🡪 _____ ______

A

cell shrinks

163
Q

Hypovolemia is associated with hypotonic alteration. It means there’s ____ _____ ____ ____ Whereas hypervolemia has _____ _____ ____ _____and is associated with hypertonic alteration

A

Hypovolemia is associated with hypotonic alteration. It means there’s too little blood volume. Whereas hypervolemia has too much blood volume and is associated with hypertonic alteration

164
Q

Membrane excitability: abnormal levels of potassium- there’s a problem with the

A

resting membrane potential

165
Q

With low potassium, (hypokalemia) it takes a ____ distance to reach the threshold potential which means it needs a ____ stimulus.

So, what type of manifestations can you expect to see in a patient with hypokalemia?

A

With low potassium, (hypokalemia) it takes a longer distance to reach the threshold potential which means it needs a stronger stimulus.

May see lethargy, muscle weakness, decreased muscle tone, decreased tendon reflexes

166
Q

With hyperkalemia, the resting membrane potential is ______. The distance is more ________ to reach the threshold potential, so it takes_____of a stimulus to initiate something (cells are easily excitable)

A

With hyperkalemia, the resting membrane potential is increased. The distance is more compressed, so it takes less of a stimulus to initiate something (cells are easily excitable)

167
Q

What manifestations can you expect to see from a patient who has hyperkalemia?

A

cardiac dysrhythmia, especially v-fib, muscle spasms, twitching/tremors

168
Q

The biggest sign of hyperkalemia is

A

ST segment depression

169
Q

Another sign of hyperkalemia is a

A

peaked T wave

170
Q

When there is a K imbalance, think

A

heart- K+ is essential for transmission/conduction of nerve impulses, normal cardiac rhythms, and skeletal/smooth muscle contraction

171
Q

Abnormal levels of calcium- the problem is with the

A

threshold potential

172
Q

Low __ and High __ will decrease excitability. High __ and Low __ will increase excitability

A

Low K and High Ca will decrease excitability. High K and Low Ca will increase excitability

173
Q

Hypercalcemia- increased _____ ____ and decreased ______. What manifestations can you see from this?

A

Increased threshold potential, decreased excitability

lethargy, muscle weakness, decreased muscle tone, decreased tendon reflexes

174
Q

Hypocalcemia- lower than normal threshold potential, decreased distance, more excitability.

What manifestations?

A

cardiac dysrhythmia, especially v-fib, muscle spasms, twitching/tremors

175
Q

ST depression and shallow T wave

A

hypokalemia

176
Q

ST depression and tall peaked T wave

A

hyperkalemia

177
Q

K and H relation:

_____: hydrogen is pushed into the cell and kicks out potassium and Mg

_____: Mg and K is pushed into the cell and kick out hydrogen to the blood

A
  1. Acidosis
  2. Alkalosis
178
Q

What always comes with hyperkalemia?

A

acidosis

179
Q

normal blood pH

A

7.35-7.45, 7.4 is ideal

180
Q

systemic increase in hydrogen (ion) concentration

A

acidosis

181
Q

systemic decrease in hydrogen (ion) concentration

A

alkalosis

182
Q

higher pH than 7.4 is

lower pH than 7.4 is

A

higher pH than 7.4 is alkalotic

lower pH than 7.4 is acidic

183
Q

________________ = partial pressure of CO2 (how much CO2 is in the arterial blood)
CO2 is acidic 🡪 high amounts of CO2 = acidosis (lower pH)

A

Respiratory component 🡪 PaCO2

184
Q

Metabolic component 🡪

A

HCO3-/bicarbonate

185
Q

More HCO3 means

A

it’s more basic/alkaline

186
Q

Metabolic component 🡪 HCO3-/bicarbonate

Bicarb levels are mediated by the _______ via reabsorption

Bicarb neutralizes H+ and increases pH

Think bicarb = BASIC

A

kidneys

187
Q

Normal levels of PaCO2

above ___ is ____
below ___ is ____

A

Normal: 35-45 40 is ideal

above 45 is acidic
below 35 is alkalotic

188
Q

Normal levels of HCO3

above ___ is ____
below ___ is ____

A

Normal: 22-26 24 is ideal

above 26 is alkalotic
below 22 is acidic

189
Q

Respiratory acidosis -

A

↑ PaCO2 (> 45) (ventilatory depression)

190
Q

Respiratory alkalosis

A

↓ PaCO2 (< 35) (alveolar hyperventilation)

191
Q

Metabolic acidosis

A

↓ HCO3 (< 22) (↑ acid or ↓ base)

192
Q

Metabolic alkalosis

A

↑ HCO3 (> 26) (↓ acid or ↑ base)

193
Q

body’s attempt to correct the acid base imbalance

A

compensation

194
Q

Natriuretic peptides 🡪 maintain BP and Na+ levels by inhibiting RAAS to ↓BP/Na+

RAAS antagonist 🡪 NPs _____________________________________

A

↓BP and ↑excretion of Na+/H2O (salt LOSS)

195
Q

Natriuretic peptides:
↑serum ____ (hypertonic) 🡪 hypothalamus signals ______ and causes you to drink to _ _______🡪 fluid shifts out of _______________________ ↓osmolality 🡪 __ ____/___ 🡪 ____ ______sensed by stretch receptors 🡪 ____/___ ______ 🡪 signals glomerulus to ____(make more urine to ↓BV) 🡪inhibits ____ and _____ _____ ___ from _____ Na+🡪 ↑excretion of Na+/H2O 🡪 ↑urination 🡪 ↓BV 🡪 ↓BP

A

Natriuretic peptides:
↑serum Na+ (hypertonic) 🡪 hypothalamus signals thirst and causes you to drink to ↓osmolality 🡪 fluid shifts out of cells and into plasma to ↓osmolality 🡪 ↑BV/BP 🡪 atrial stretching sensed by stretch receptors 🡪 ANP/BNP released 🡪 signals glomerulus to ↑GFR(make more urine to ↓BV) 🡪inhibits RAAS and proximal convoluted tubule from reabsorbing Na+ 🡪 ↑excretion of Na+/H2O 🡪 ↑urination 🡪 ↓BV 🡪 ↓BP

196
Q

Natriuretic peptides:
↑serum Na+ (hypertonic) 🡪 hypothalamus signals thirst and causes you to drink to ↓osmolality 🡪 fluid shifts out of cells and into plasma to ↓osmolality 🡪 ↑BV/BP 🡪 atrial stretching sensed by stretch receptors 🡪 ANP/BNP released 🡪 signals glomerulus to ↑GFR(make more urine to ↓BV) 🡪inhibits RAAS and proximal convoluted tubule from reabsorbing Na+ 🡪
result: ________________________________________________________________

A

↑excretion of Na+/H2O 🡪 ↑urination 🡪 ↓BV 🡪 ↓BP

197
Q
A

Patho (4 decks)

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