fluids Flashcards
water and ions
60 % of body weight is water- 40% of that is intracellualar
transcelluar- body in body cavity- 1%- stomach, brain
TRANSCELLULAR
TRANSCELLULAR- THIRD SPACE: Pericardial, Peritoneal, Pleural, Joint etc. spaces
hemostasis
what we put in is exixted everyday- if not then it will cause problem
NORMAL FLUID EXCHANGE
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.
increasec interstitial fluid
edema
transudate
protein poor vs exudates- protein rich
puffy eyes
kidney failure- in adults- water gets distributed while you sleep around the eyes- durign the day they get it at the ankles
hydrostatic pressure increases
when pregnant ex.
what are the four reasons for edema!!!!!!!!!!!!!!!!!
- decreese plasma proteins (decrease oncotic pressure):
a) decrease protein intake:/synthesis Malnutrition
b) increase protein loss Nephrotic syndrome - Lymphatic blockage: obstruction by:
a) Microorganisms (e.g. elephantiasis),
b) Cancer cells (e.g. breast cancer – giving rise to orange peel skin) - fluid volume:
a) Kidney failure (retention of sodium) - (hydrostatic) pressure with in the veins:
a) Legs (prolonged standing);
b) Generalized (heart failure)
Edema: Location and Extent
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
brian edema
pushes against skull, or down the spinal cavity- respiration and circulation get compressed and die
ANASARCA
Protein malnutrition
Hydrops fetalis
Bad generalized edema!!!!- swells the whole body is also called ANASARCA.
-
Too much blood!Reddish swollen organs
may not be on exam
hemorrhage Types of vessels damaged:
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)
hemorrhage- site
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)
ORIFICE- hemorrhaGE
Menorrhagia – menstrual
SIZE
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
HOW MUCH BLOOD IS lost
. How much blood lost? Very small amounts: OK 10%: 1 U of blood 20%: feel sick 40%: hypovolemic shock
thrombosis
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!!!!!!!!!!!!!!
embolism
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
Thrombi: why do these form? Virchow’s triad
patients will need to know which of these caused the thrombosis to treat it
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)
how can the bood flow to an organ be reduces
embolism,
What would be the effect(s) of reduced or obstructed blood flow in the affected organ?
death, organ death, decrease in function,
Thrombi: what are these composed of ? What do they look like?
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
know the difference btw post and premodern clots
Non-adhesive Soft Chicken fat and currant jellyappearance Attached (hard and crumbly) Friable Lines of Zahn
Disseminated intravascular coagulation (DIC)
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
what do they look like DIC
angled blood cells
Clinical effects of thrombi:
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
What is the fate of thrombi:
- all these things can happen
Lysis : no sequelae
Organization (ingrowth of vessels and inflammatory cells)
Recanalization
Embolization (break free)
recanalization
restoring flow
embolization
break off and go a blood multiple small blodd vessels
EMBOLISM
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
what does embolism do (clinical effect)
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.
fat embolism
bone breaks and fat droplets travel in blood vessels
what can travel in the blood
liquid (amniotic fluid, solid( tumor)
gases
Clinical example of embolism; Pulmonary embolism
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
thrombi and emboli vs
know
infartion
necrosis by blockage of blood vessels
Death of Tissue from loss of Blood supply (ischemia)
Usually caused by thrombi
what happens to the person in infarction
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
What do infarcts look like?
Pale (white) infarcts result from arterial occlusion
no blood can get to it
how to red infacts happen
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
SHOCK
(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
3 features of shock
organ dysfunction secondary mediators of shock (e.g. TNF and IL-1) are produced by hypoperfused organs Exacerbate effects of shock Metabolic acidosis
3 causes of shock
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)
3 stages of shocl
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
- Irreversible Shock
Circulatory Collapse
Marked Hypoperfusion
Loss of Vital Functions
compensated shock
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
- Progressive (decompensated) shock
- 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
- irreversible shock
- Irreversible Shock
Circulatory Collapse
Marked Hypoperfusion
Loss of Vital Functions
hemorhage
where are key cites where they are bad
how much blood can we loose confortably
kno
3 componenets of the triad
know
3 causes of shack
and the 3 stages
