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PATHO FINAL EXAM "OLD" CH 7..8.9..10..11 > CHAPTER 7--HEMODYNAMIC DYSFUNCTION = 2 Q'S > Flashcards

CHAPTER 7--HEMODYNAMIC DYSFUNCTION = 2 Q'S Flashcards

1
Q

CELLS & TISSUES are dependant on

  1. Normal Fluid Environment = increase edema and decrease dehydration
  2. Adequate Blood supply
    - Thrombosis
    - Embolism
    - Infarction
    - Hemorrhage
A

know

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2
Q

______–Accumulation of excess fluid (transudate, exudate, lymph) in the intercellular (interstitial) tissue spaces and body cavities:

Body cavities are:

  1. pleural cavity (hydrothorax)
  2. peritoneal cavity (ascites )
  3. pericardial cavity (hydropericardium)

**Edema can be local or generalized

A

EDEMA

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3
Q

Pitting edema of the leg

reflects the “________” of the fluid- filled tissue

A

in-elasticity

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4
Q

Pathogenesis of Edema

  1. INCREASE capillary hydrostatic pressure (hemodynamic edema): protein-poor transudate
  2. INCREASE capillary permeability (inflammatory edema):protein-rich exudate
  3. DECREASE collodial osmotic pressure of plasma proteins: liver (dec. protein synthesis), kidney (nephrotic syndrome)
  4. INCREASE tissue osmotic pressure (sodium retention)
  5. obstruction of lymphatics (lymphedema): in malignancy, surgery, radiation therapy, or filariasis
A

KNOW

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5
Q

Causes of generalized edema
1. Cardiac = Left ventricular failure + Right ventricular failure
2. Renal–Acute glomerulonephritis & Nephrotic syndrome
3. Hepatic:–decreased protein synthesis & portal hypertension
4. 4. Nutritional: protein malnutrition
(kwashiorker or starvation)

A

KNOW

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6
Q

Causes of localized edema
1. Inflammatory edema
-INCREASE vascular permeability
-__________ hydrostatic pressure to arteriolar dilation
(= exudate)
2. Edema due to localized ________ obstruction
-thrombosis, varicose veins, compression
-hydrostatic pressure (= transudate)
3. Edema due to____________ obstruction
-surgery, cancer, parasites
-in early stage, edema is pitting ( = lymph)
-later, edematous tissue becomes fibrosed, thickened & non-pitting (elephantiasis)

A

INCREASE

venous

lymphatic

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7
Q

_________: INCREASE of blood due to active arterial dilation:

a. Physiologic : muscles during exercise
b. Pathologic: inflammation

__________: passive INCREASE of blood due to impaired venous drainage:

  • –localized as due to venous obstruction, or
  • -generalized as with right heart failure
A

Hyperemia

Congestion

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8
Q

Pulmonary congestion—Etiology: _____ ventricular failure (hypertension, myocardial infarction, rheumatic heart)
Alveolar capillaries: engorged, dilated, tortuous:
-edema of interstitial tissue
-transudate in alveoli
-hemorrhage

A

Left

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9
Q

Chronic passive congestion of the lungs
.
Increased venous pressure leads to extra vasation of
red blood cells into the alveoli and alveolar edema.
The hemosiderin formed from hemoglobin released from hemolyzed red blood cells is taken up by intraalveolar macrophages. These macrophages are
sometimes called “_____ _____ ______” because of
their association with pulmonary congestion with
congestive heart failure

.

A

“heart failure cells”

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10
Q

Liver congestion
Etiology—_______ side heart failure, pulmonary fibrosis, tricuspid stenosis, & thrombosis of hepatic vein or inferior vena cava

A

Right

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11
Q

Chronic passive congestion (nutmeg liver), gross. a “nutmeg” liver seen with chronic______ ________ of
the liver
.

A

passive congestion

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12
Q

__________— (blood clot):
A solid mass formed from blood constituents within heart and blood vessels during life. It is composed of layers of aggregated platelets and fibrin

A

Thrombus

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13
Q

Thrombosis is a normal hemostatic mechanism that stops _____-_____

A

bleeding:

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14
Q

Thrombosis is a normal hemostatic mechanism that stops bleeding.

  1. Formation of platelet plug:

-injury of __________ exposes subendothelial collagen
-adhesion of platelets to exposed collagen
-platelet release reaction: secretion of ADP platelet
aggregation (they aggregate on top of each other)

A

endothelium

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15
Q

Thrombosis is a normal hemostatic mechanism that stops bleeding.

  1. Coagulation of blood:

-activation of ________________ activates intrinsic pathway
-tissue thromboplastin released by injury activates
extrinsic pathway

3._________:—-prevents excess thrombus formation

A

Hageman factor (XII)

Fibrinolysis

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16
Q

Three important factors are involved in hemostasis

  1. Endothelial cells
  2. Blood platelet
  3. Coagulation factors
A

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17
Q

ENDOTHELI AL CELLS-Releasing antithrombotic or
thrombotic factors
A—-intact endothelial cells prevent thrombosis through;
1. Anti-platelet properties
2. Anti -coagulant properties
3. Fibrinolytic properties

B-Injured endothelial cells = initiate thrombosis
—Synthesize von WILLIBRANDS FACTOR–binds platelets to exposed subendothelial collagen (platelet adhesion)
-Release tissue factor (thromboplastin) = activates
__________ clotting pathway
:

A

extrinsic

18
Q

PLATELETS—-Derived from cytoplasmic fragmentation of megakaryocytes

  1. platelet ________ to subendothelial collagen mediated by von W factor
A

adhesion

19
Q

COAGULATION SYSTEM x 2

Intrinsic Pathway = Activation of XII
Extrinsic Pathway = Release of tissue thromboplastin

  • **Coagulation is confined to site of injury through:
  • natural anti-thrombin
  • removal of activated factors (liver & phagocytic cells)
  • dilution
A

know

20
Q 
THROMBOGENESIS
Predisposing factors (VIRCHOW'S TRIAD)
  1. Endothelial injury
  2. Alteration of normal blood flow
  3. Hyper-coagulability of blood
A

know

21
Q

Morphology of Thrombi
1. Arterial thrombi:
“ _______ ___ _____ “ which are the alternating pale pink bands of platelets with fibrin and red bands
of RBC’s forming true thrombus

  1. Venous thrombi—commonly (90% ) in veins of
    lower limbs—almost always occlusive
A

lines of Zahn

22
Q

________ veins of the legs = Severe varicosities of
the superficial leg veins have led to stasis dermatitis
and secondary ulcerations

A

Varicose

23
Q

Fate of Thrombi x 5

  1. _______: accumulate more platelets & fibrin to obstruct a critical vessel
  2. Fibrinolysis: re-establishment of lumen (fibrinolytic
    Activity)
  3. Thromboembolism: partial or complete detachment
  4. ___________: inward growth of granulation
    tissue
  5. Recanalization: capillaries of granulation tissues form
    anastomosing channels
A

Propagation

Organization (fibrosis)

24
Q

EMBOLISM

______:–an insoluble mass (solid, liquid, gaseous)
circulating in the blood
.
________:–occlusion or obstruction of a blood vessel by an embolus.

A

Embolus

Embolism

25
Q
  1. THROMBOEMBOLISM
    - Fragmented or _________ thrombi (98%)
    - Site of embolism depends of origin:
    i. pulmonary embolism
    ii. systemic embolism
A

detached

26
Q
  1. THROMBOEMBOLISM

Pulmonary embolism:
—Emboli are derived from thrombi of systemic veins,
mainly deep veins of legs (95%), superficial leg veins, pelvic,uterine, and periprostatic
–Multiple emboli over time may cause pulmonary
hypertension with ____ side heart failure

A

right

27
Q
  1. THROMBOEMBOLISM

Systemic embolism:
-Emboli are derived from mural thrombi:
a. mural thrombi due to _______ ___________
b. mitral stenosis & atrial fibrillation
c. aortic aneurysm or atheromatous plaque
—–Impacted in cerebral, renal, intestinal & splenic
branches, more frequently (70-75%) in ________ limbs.

A

myocardial infarction

lower

28
Q
  1. FAT EMBOLISM
    -2nd most frequent type of emboli
    -Fat globules enter blood after fracture of long bones
    or extensive trauma to fatty tissue (burns or surgery)
    -Effect: depends on their size:

More than 20 = Arrested in lung = Dyspnea
Less than 20 = Pass to systemic circulation

  1. AIR OR GAS EMBOLISM

a. _______
- Surgery or trauma to internal jugular vein
- During delivery or abortion: air enters ruptured uterine sinus
- Iatrogenic pneumothorax

b. ________:
(Caisson disease, Decompression sickness)
-occurs in caisson workers & sea divers
-breathing pressurized air = more air goes into solution in blood & tissues
-rapid decompression to sea level = dissolved gases come out of solution.
-because of low solubility of N2 = forms bubbles = act as emboli.

A

AIR:

GAS

29
Q

________–Area of localized ischemic necrosis
produced either by occlusion of arterial supply or
venous drain

A

INFARCTION

30
Q

Morphology of infarct

  1. ___________ coagulative necrosis (all infarcts) replaced by scar tissue
  2. Liquefactive Necrosis: in _____ or when infected.
A

Ischemic

CNS

31
Q

Types of infarct x 2

  1. __________________infarct—arterial obstruction in
    SOLID ORGANS with poor collateral circulation (end artery) e.g. spleen, heart, kidney, brain
  2. ____________________infarct
    -obstruction of venous outflow & congestion
    -LOOSE ORGANS e.g. lung
    -organs with double blood supply (liver, lung) or
    collateral vessels (small intestine)
    -twisted pedicle of ovary or test
A

Pale,white,anemic

Red,hemorrhagic

32
Q

Septic infarct

  • infected embolus
  • organs normally containing ________ (e.g.intestine)
  • bacteria from blood (secondary infection)
A

bacteria

33
Q

SHOCK—DECREASE tissue perfusion associated with DECREASE in effective cardiac output.

3 Types of SHOCK

  1. Cardiogenic (decreased cardiac output)
  2. Hypovolemic
  3. Shock due to peripheral sequestration of blood volume
A

know

34
Q 
1.\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ shock
Decreased cardiac output due to heart failure
-myocardial infarction
-massive pulmonary embolism
-cardiac tamponade
-arrhythmias
  1. ____________- shock
    Decreased cardiac output due DECREASED blood volume
    -hemorrhage
    -fluid loss e.g. burn, diarrhea, vomiting
  2. Shock due to _________ sequestration of blood
    volume
    -endotoxin of gram negative bacteria (septic shock)
    -chemical mediators of allergy (anaphylacticsh shock)
    -anesthesia, spinal cord injury (neurogenic shock)
A

Cardiogenic

Hypovolemic

peripheral

35
Q

3 Stages of shock:

  1. compensation
  2. impaired tissue perfusion (decompensation)
  3. irreversible stage
A

know

36
Q

3 Stages of shock:

  1. Stage of _____________
    Decreased cardiac output = mild hypotension = reflex sympathetic stimulation.
    -tachycardia
    -peripheral vasoconstriction:
    i. skin:cold & clammy
    ii. renal arterioles: decreased glomerular filtration
    = decreased urine output
A

compensation

37
Q

3 Stages of shock:

  1. Stage of impaired tissue perfusion (stage of ______)
    a. Prolonged stagnation & edema Vasoconstriction
    b. Promotes anaerobic glycolysis = lactic acidosis, dilation of arterioles = Blood stagnation & edema
    c. Tissue necrosis
A

decompensation

38
Q

3 Stages of shock:

  1. ________ stage

a. Failure of peripheral vasoconstriction (capillary hypoxia & acidosis = vasodilation
b. fall in blood pressure
c. impairment of perfusion of brain (neuronal degeneration) & heart (further decrease in cardiac
output, death)
d. Full recovery is possible with the early detection and correction of the CAUSE of shock

A

Irreversible

39
Q

High mortality rate x 2

  1. Cardiogenic shock— due to existing_______ diseases
  2. Septic shock—— due to the difficulty in ______ control
A

cardiac

infection

40
Q

Factors that favor RECOVERY from shock X 3

  1. Availability of early treatment of
    - Initiating cause
    - Hypovolemia
  2. Younger age
  3. Good general health
A

know

41
Q

Factors that favor SHOCK FAILURE X 5

  1. Delay in treatment
    - Failure in removing the initiating cause
  2. Old age
  3. Poor health
  4. Pre-existing CVD & lung diseases
  5. Complications as infection & necrosis
A

know

PATHO FINAL EXAM "OLD" CH 7..8.9..10..11 (5 decks)

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