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Pathology 205 > fluids > Flashcards

fluids Flashcards

1
Q

water and ions

A

60 % of body weight is water- 40% of that is intracellualar

transcelluar- body in body cavity- 1%- stomach, brain

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2
Q

TRANSCELLULAR

A

TRANSCELLULAR- THIRD SPACE: Pericardial, Peritoneal, Pleural, Joint etc. spaces

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3
Q

hemostasis

A

what we put in is exixted everyday- if not then it will cause problem

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4
Q

NORMAL FLUID EXCHANGE

A

Hydrostatic pressure toward the arteriolar end of the capillaries pushes water out into tissues (FILTRATION).
Opposed by minor hydrostatic pressure of interstitial fluid
Oncotic pressure toward the venular end of the capillaries pulls water in the vessels (REABSORPTION)
Opposed by minor oncotic pressure in the interstitial fluid.
Small amount of water that remains in the interstitium is removed by lymphatics and returned to circulation.

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5
Q

increasec interstitial fluid

A

edema

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6
Q

transudate

A

protein poor vs exudates- protein rich

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7
Q

puffy eyes

A

kidney failure- in adults- water gets distributed while you sleep around the eyes- durign the day they get it at the ankles

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8
Q

hydrostatic pressure increases

A

when pregnant ex.

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9
Q

what are the four reasons for edema!!!!!!!!!!!!!!!!!

A
  1. decreese plasma proteins (decrease oncotic pressure):
    a) decrease protein intake:/synthesis Malnutrition
    b) increase protein loss Nephrotic syndrome
  2. Lymphatic blockage: obstruction by:
    a) Microorganisms (e.g. elephantiasis),
    b) Cancer cells (e.g. breast cancer – giving rise to orange peel skin)
  3.  fluid volume:
    a) Kidney failure (retention of sodium)
  4.  (hydrostatic) pressure with in the veins:
    a) Legs (prolonged standing);
    b) Generalized (heart failure)
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10
Q

Edema: Location and Extent

A 
Organs
Skin
Blister
Pulmonary edema
Heavy lungs, coughing up frothy fluid
Cerebral edema
Brain swelling and herniation of its contents into upper cervical spinal canal
Angioedema- throat- very bad
Preexisting cavities
Ascites
In peritoneal cavity
Hydrothorax
In pleural cavities
Hydropericardium
In pericardial cavity
Hydrocephalus
cerbrospinal fluid
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11
Q

brian edema

A

pushes against skull, or down the spinal cavity- respiration and circulation get compressed and die

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12
Q

ANASARCA

A

Protein malnutrition
Hydrops fetalis
Bad generalized edema!!!!- swells the whole body is also called ANASARCA.
-

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13
Q

Too much blood!Reddish swollen organs

A

may not be on exam

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14
Q

hemorrhage Types of vessels damaged:

A

Types of vessels damaged:
Cardiac!!!! ( VERY BAD AND BRAIN, EYE, PITUITARY GLAND)
Gunshot, Stab wound, infarction (often fatal)
Aortic
Trauma (motor vehicle accident), aortic aneurysm
Arterial
Penetrating wounds (knife, bullet), fractures
Venous
Trauma
Capillary
Trauma, venous pressure, weak capillary walls (scurvy)

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15
Q

hemorrhage- site

A

SITE:
Body cavities
Hemopericardium (pericardial space)

Bad sites to have bleeding
Brain
Into pericardial sac
Vitreous fluid of eye
Pituitary gland
Looks bad, but not so bad, per se
Black eye (periorbital hematoma)
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16
Q

ORIFICE- hemorrhaGE

A

Menorrhagia – menstrual

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17
Q

SIZE

A

Bleeding into the skin
Petechiae: Bleeding into skin less than 3 mm
Purpura: Bleeding into skin 3-10 mm
Ecchymoses: Bleeding into skin more than 10mm; also called Bruise

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18
Q

HOW MUCH BLOOD IS lost

A 
. How much blood lost?
Very small amounts: 
OK 
10%: 
1 U of blood
20%: 
feel sick
40%: 
hypovolemic shock
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19
Q

thrombosis

A

Transformation of fluid blood into solid aggregate of cells and fibrin within the vascular lumen.
Clot: Blood that has solidified anywhere else during life or within the vascular lumen after death.

only happens during life- liquid to solid in the blood vessels!!!!!!!!!!!!!!

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20
Q

embolism

A

Emboli are free particles / masses floating in blood stream that are not normally present in that state in normal blood.
Thrombi are said to embolize when they break free.
Emboli can come from Heart, Arteries, Veins, Capillaries

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21
Q

Thrombi: why do these form? Virchow’s triad

patients will need to know which of these caused the thrombosis to treat it

A

Blood vessel wall damage
Endothelial injury ( e.g. from vasculitis, atherosclerosis)
Blood flow abnormalities
Turbulence
Slowing of blood flow
Blood component alterations (hypercoagulable blood)
Pregnancy, Cancer, Severe burns
Disseminated intravascular coagulation (DIC)

22
Q

how can the bood flow to an organ be reduces

A

embolism,

23
Q

What would be the effect(s) of reduced or obstructed blood flow in the affected organ?

A

death, organ death, decrease in function,

24
Q

Thrombi: what are these composed of ? What do they look like?

A

Irregular swirling layers of red cells, fibrin, platelets and a few white cells (lines of Zahn).
Red (many red cells)
When flow is turbulent more red cells are included
White (layered, more fibrin)
When flow is laminar fewer red cells are included
Naked eye - have different colours
try and pull the clot away- thrombis will be attached to blood vessell wall vs post mortum clot will come out easily
the thrombis will be crumpis vs post-modern- like a worm

Under the microscope- will see the lines of Zahn

25
Q

know the difference btw post and premodern clots

A 
Non-adhesive
Soft
Chicken fat and currant jellyappearance
Attached
(hard and crumbly) Friable
Lines of Zahn
26
Q

Disseminated intravascular coagulation (DIC)

A

The clotting cascades are activated throughout the body. This is bad, since it tends to shut down organs due to microthrombi, and also causes bleeding due to consumption of clotting factors and activation of plasmin.
1 cause is systemic infection number 2 reason is cancer

27
Q

what do they look like DIC

A

angled blood cells

28
Q

Clinical effects of thrombi:

A

Occlude lumen of vessel
Death of the end organ or part of it (e.g. myocardial infarction (syn. Heart attack)
Narrow lumen = decreased blood flow = hypoxia & decreased function
May become source of Emboli

29
Q

What is the fate of thrombi:

- all these things can happen

A

Lysis : no sequelae
Organization (ingrowth of vessels and inflammatory cells)
Recanalization
Embolization (break free)

30
Q

recanalization

A

restoring flow

31
Q

embolization

A

break off and go a blood multiple small blodd vessels

32
Q

EMBOLISM

A

anything in the blood that should not be there
Any solid, liquid, or gaseous thing other than liquid blood that travels along the bloodstream. It will impact and lodge somewhere.
Thromboembolus: broken off thrombus
Liquid: Amniotic fluid, Fat
Solid:Cholesterol, Tumor
Gaseous: Air- bends

33
Q

what does embolism do (clinical effect)

A

Emboli travel from the site of origin till they get trapped at the next narrow point in the circulation
From leg veins - trapped in lungs
From heart - trapped in small vessels in other organs
Once trapped, obstruct the vessels and cause ischemic damage to the organs
(death - infarction), hypoxic injury.

34
Q

fat embolism

A

bone breaks and fat droplets travel in blood vessels

35
Q

what can travel in the blood

A

liquid (amniotic fluid, solid( tumor)

gases

36
Q

Clinical example of embolism; Pulmonary embolism

A

From Veins of Lower leg, abdomen
Effects:
May occlude main branches of Pulmonary Artery (e.g. Saddle embolus)
Small emboli cause small pulmonary infarcts
Air Embolism
“Bends”
can also happen for ppl sitting too long and when they get up the thrombi breaks off - travells to lungs and die

37
Q

thrombi and emboli vs

A

know

38
Q

infartion

A

necrosis by blockage of blood vessels
Death of Tissue from loss of Blood supply (ischemia)
Usually caused by thrombi

39
Q

what happens to the person in infarction

A 
What happens to infarcts?
PERSON:
May die (Stroke, heart attack)
ORGANS:
Heart – replacement of damaged cells by fibrous tissue (Repair)
Brain – liquefies and is absorbed
Liver – may regenerate
The organ may simply die and fall off (with or without secondary infection)- Gangrene
40
Q

What do infarcts look like?

A

Pale (white) infarcts result from arterial occlusion

no blood can get to it

41
Q

how to red infacts happen

A

Red infarcts result from venous occlusion, or hemorrhage (because of reperfusion or lots of collaterals) into a white infarct.
or restauration of a a infarct -adding mmore blood to it

42
Q

SHOCK

A

(low blood flow) Hypoperfusion of tissues leading to organ dysfunction
Shock is likely to deteriorate into a vicious cycle of organ failure and subsequent exacerbation of shock.
Reduced organ perfusion leads to:
Organ dysfunction
Secondary mediators of shock (e.g. TNF and IL-1) are produced by hypoperfused organs
Exacerbate effects of shock
Metabolic acidosis

43
Q

3 features of shock

A 
organ dysfunction
secondary
mediators of shock (e.g. TNF and IL-1)  are produced by hypoperfused organs
Exacerbate effects of shock
Metabolic acidosis
44
Q

3 causes of shock

A 
Pump failure (Heart)
Myocardial infarction
Arrythmia
Loss of fluid from circulation
Hemorrhage
Burns, Vomiting, Diarrhea
Loss of peripheral vascular tone
Pooling of blood in peripheral vessels
Anaphylactic Shock
Bacterial Sepsis (Septic Shock)
45
Q

3 stages of shocl

A 
Compensated shock
Blood shunted away from skin, gut, kidneys etc, to brain and heart and peripheral vasoconstriction to help maintain BP.
Blood pressure is maintained
Cold clammy skin, dry mouth
 Urine output
2. Progressive (decompensated) shock
Can not maintain heart and brain function
Low blood pressure
Altered consciousness

End-organ damage
Lungs (Shock lung: adult respiratory distress syndrome)
Kidneys etc.

Lactic acidosis and release of cytokines
Peripheral vasodilatation (warm skin)
Vascular permeability -> loss of fluids form circulation
  1. Irreversible Shock
    Circulatory Collapse
    Marked Hypoperfusion
    Loss of Vital Functions
46
Q

compensated shock

A 
Compensated shock
Blood shunted away from skin, gut, kidneys etc, to brain and heart and peripheral vasoconstriction to help maintain BP.
Blood pressure is maintained
Cold clammy skin, dry mouth
 Urine output
47
Q
  1. Progressive (decompensated) shock
A
  1. Progressive (decompensated) shock
    Can not maintain heart and brain function
    Low blood pressure
    Altered consciousness

End-organ damage
Lungs (Shock lung: adult respiratory distress syndrome)
Kidneys etc.

Lactic acidosis and release of cytokines
Peripheral vasodilatation (warm skin)
Vascular permeability -> loss of fluids form circulation
48
Q
  1. irreversible shock
A
  1. Irreversible Shock
    Circulatory Collapse
    Marked Hypoperfusion
    Loss of Vital Functions
49
Q

hemorhage

A

where are key cites where they are bad

50
Q

how much blood can we loose confortably

A

kno

51
Q

3 componenets of the triad

A

know

52
Q

3 causes of shack

A

and the 3 stages

Pathology 205 (23 decks)

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