Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

Accumulation of fluid in tissues or body cavities

A

EDEMA - tissues
EFFUSIONS - body cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Increased blood volume w/n tissues

A

hyperemia
congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pathologic counterpart of hemostasis

A

Thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

A detached intravascular solid, liquid or gaseous mass that is carried by the blood from its point of origin to a distant site where it often causes tissue dysfunction or infarction

A

Embolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Area of ischemic necrosis caused by occlusion of either arterial supply or venous drainage

A

Infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

State in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion — cellular hypoxia

A

Shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

4 main mechanisms of edema formation

A
  1. INCREASED hydrostatic pressure
  2. DECREASED oncotic pressure
  3. INCREASED vascular permeability
  4. Lymphatic OBSTRUCTION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

General morphologic appearance of edema

A
  1. Clearing and separation of ECM
  2. Subtle cell swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

58/M w/ hx of MI presented w/ paroxysmal noctunal dyspnea (PND)
CXR - bilateral pleural effusion

diagnosis, mechanism of edema, kind of effusion

A

Congestive Heart Failure
Increased Hydrostatic Pressure
Transudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

32/M, hx of remittent fever and productive cough, developed dyspnea
CXR -R pleural effusion w/ L parenchymal infiltrates

diagnosis, mechanism of edema, kind of effusion

A

Parapneumonic effusion; CAP MR
Increased vascular permeability
Exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

57/M chronic alcoholic, increase in abdominal girth. Chem showed low serum albumin and elevated ALT and AST. Abdominal UTZ showed moderate ascites

diagnosis, mechanism of edema, kind of effusion

A

Decreased oncotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

34/F, known case of breast cancer stage 2 (T2N0M0), s/p MRM, developed left arm swelling

mechanism of edema

A

Lymphatic obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Transudate

A

abnormalities in Starling forces
normal vascular permeability
absent plasma protein leak
low protein content of fluid
<1.012
absent fibrin
absent inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Exudative

A

increased vascular permeability
presence of plasma protein leak
high protein content in fluid
>1.012
present fibrin
present inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

It is an ACTIVE process d.t. augmented blood flow from ARTERIOLAR DILATION of increased O2 demand; affected tissue is REDDER than normal because of engorgement w/ OXYGENATED blood

A

Hyperemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

It is a PASSIVE process d.t. IMPAIRED VENOUS RETURN out of a tissue, has BLUE-RED color d.t. accumulation of DEOXYGENATED blood in the affected tissue

A

Congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

24/F w/ large left atrial myxoma that obstructed flow of blood into the left atrium. Autopsy of the lung showed engorged alveolar capillaries, alveolar septal edema and focal intraalveolar hemorrhage.

Diagnosis

A

Acute pulmonary congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

34/F died from acute R sided HF sec to saddle embolus. Autopsy of the liver showed distended central vein and sinusoids, centrilobular ischemic necrosis and periportal fatty change

Diagnosis

A

Acute Hepatic Congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

55/M died of complications from congestive heart failue. Autopsy of the lung showed thickened and fibrotic alveolar septa and hemosiderin laden macrophases.

Diagnosis

A

Chronic Passive Congestion, Lung

20
Q

60/M died of complications from HF. On autopsy, liver is heavier than normal and has nutmeg like appearance. Sections show centrilobular hemorrhage, hemosiderin laden macrophages and hepatocyte loss of variable degrees.

Diagnosis

A

Chronic Passive Congestion, liver

21
Q

Components of Virchow Triad

A

Endothelial Injury
Stasis
Hypercoagulability

22
Q

Major contributor to the development of ARTERIAL thrombi

A

Turbulence or Endothelial injury

23
Q

Major contributor to the development of VENOUS thrombi

A

Stasis

24
Q

Any alteration of the COAGULATION pathway that predisposes to thrombosis
Can be primary (Factor V Leiden, Protein C and S deficiency), or secondary (cancer, atrial fibrillation and prolonged immobilization)

A

Hypercoagulability

25
Q

Lamination composed of PALE PLATELETand FIBRIN deposits alternating w/ DARKER RED cell rich layers signify formation of thrombus in flowing blood
Present in ANTEMORTEM THROMBOSIS

A

Lines of Zahn

26
Q

MC siteof ARTERIAL THROMBOSIS

A

Coronary > Cerebral > Femoral

27
Q

MC site of VENOUS thrombosis

A

Superficial or deep veins of the leg

thrombi - superficial leg veins - RARELY embolize
thrombi - deep leg veins - MC source of venous emboli

28
Q

Fates of Thrombus

A

PROPAGATION - thrombi accumulate additional platelets and fibrin
EMBOLIZATION - thromb dislodge and travel to other sites in the vasculature
DISSOLUTION - rapid shrinkage and total disappearance of recent thrombi
ORGANIZATION AND RECANALIZATION -thrombi becomes incorporated in the vessel wall w/ formation of new capillary channels that restore blood flow

29
Q

MC and most dreaded sequelae of DVT

A

Pulmonary Embolism

30
Q

Embolus occluding the bifurcation of the pulmonary trunk
Associated w/ sudden death d.t. acute R sided HF

A

Saddle embolus

31
Q

65/F, known case of DVT came from a 17 hr flight, developed respiratory dstress w/ R ventricular wall dysfunction on 2D echo.
Diagnosis

A

Pulmonary Embolism

32
Q

45/F, known case of thyrotoxic heart disease and chronic atrial fibrillation developed sudden L sided weakness and loss of sensation.

Type of Embolism

A

Systemic thromboembolism (from mural thrombus)

33
Q

38/M, known case of Non Hodgkin Lymphoma, developed sudden R sided weakness. Has had a recent admission for a month and has a history of cardiac pathology.

Phenomenon observed in the patient

A

Paradoxical Embolism (Cardiac pathology is PFO)

34
Q

32/M involved in a motorcycle accident and sustained mid-shaft right femoral fracture w/o any blunt or penetrating head and chest trauma.
Developed progressive respiratory distress and died. Autopsy shows fat globules in pulmonary vasculature.

Diagnosis

A

Fat Embolism

35
Q

25 G1P1 (1001) developed respiratory distress, seizures and refractory bleeding post partum and died. Autopsy showed fetal skin and lanugo in pulmonary vasculature.
Diagnosis

A

Amniotic Fluid Embolism

36
Q

30/M diver, developed respiratory distress and joint pain after rapid ascent. Work up showed gas bubbles in pulmonary vasculature and joints.
Diagnosis

A

Air Embolism (Decompression sickness)

37
Q

Infarcts that tend to occur in LOOSE tissues and in those w/ DUAL CIRCULATIONS previously congested tissues or when FLOW IS REETABLISHED AFTER AN INFARCTION (i.e. angioplasty of obtructed artery

A

Red(Hemorrhagic) Infarct

*pulmonary and bowel infarcts

38
Q

Infarct that tend to occur in SOLID ORGANS w/ END ARTERIAL circulations

A

White (Anemic) Infarct

*Myocardial and Splenic Infarcts

39
Q

55/M known case of MASSIVE MI, developed VENTRICULAR FIBRILLATION and died.

Kind of Shock

A

Cardiogenic Shock

40
Q

65/M with RUPTURED ABDOMINAL AORTIC ANEURYSM, died.

Kind of Shock

A

Hypovolemic Shock

41
Q

23/M, college student and doremr, developed COUGH and COLDS for 2 days followed by REMITTENT HIGH GRADE FEVER w/ DUSKY ECCHYMOSES on the lower extremities. At ER, px was STUPUROUS w/ BP = 50 palpatory.

Diagnosis andKind of Shock

A

Meningococcemia
Septic Shock

42
Q

25/F, suffered from a BEE STING, developed GENERALIZED WHEALS, PERIORBITAL EDEMA and RESPIRATORY DISTRESS. BP = 70/50 .

Kind of Shock

A

Anaphylactic Shock

43
Q

28/F, suffered from a BLUNT TRAUMA of the BACK after a vehicular accident, was HYPOTENSIVE for several days and was started on VASOPRESSORS for management.

Kind of Shock

A

Neurogenic Shock

44
Q

Antiphospholipid Antibody Syndrome (APAS)

A

one or more antiphospholipid (aPL) autoantibodies
*anti-cardiolipin
*lupus anticoagulant
*anti-B2 glycoprotein

AND

recurrent thrombosis or pregnancy complications
thrombocytopenia

44
Q

Antiphospholipid Antibody Syndrome (APAS)

A

one or more antiphospholipid (aPL) autoantibodies
*anti-cardiolipin
*lupus anticoagulant
*anti-B2 glycoprotein

AND

recurrent thrombosis or pregnancy complications
thrombocytopenia

45
Q

Paradox of APAS

A

thrombosis
thrombocytopenia
prolonged aPTT

Pathology (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions