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PATHOLOGY > THROMBOTIC DISEASES AND EMBOLISM > Flashcards

THROMBOTIC DISEASES AND EMBOLISM Flashcards

1
Q

DEFINE THROMBOSIS

A

THROMBOSIS:
THE FORMATION, DEVELOPMENT OR PRESENCE OF A THROMBI OR THROMBI

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2
Q

STATE 3 COMPONENTS OF VIRCHOW TRIAD.

A
  1. ENDOTHELIAL INJURY
  2. ABNORMAL BLOOD FLOW (STASIS OR TURBULENCE)
  3. HYPERCOAGULABILITY (PRIMARY OR SECONDARY)
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3
Q

WHAT IS THROMBUS?

A

THROMBUS:
A STATIONARY BLOOD CLOT ALONG THE WALL OF A BLOOD VESSEL, FREQUENTLY CAUSING VASCULAR OBSTRUCTION.

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4
Q

THROMBUS INVOLVED IN THE PATHOGENESIS OF: (CLUE: 5 DISEASE)

A
  1. MYOCARDIAL INFARCTION
  2. CEREBROVASCULAR DISEASE
  3. PERIPHERAL ARTERIAL DISEASE
  4. DEEP VEIN THROMBUS
  5. PULMONARY EMBOLISM
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5
Q

THE MOST COMMON SITES OF THROMBUS FORMATION WITHIN THE ARTERIAL SYSTEM ARE:

A
  1. LEFT ATRIUM
  2. LEFT VENTRICLE
  3. CAROTID ARTERIES
  4. ABDOMINAL AORTA
  5. LOWER LIMB VASCULATURE
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6
Q

WHEN DOES ARTERIAL THROMBOEMBOLISM OCCUR?

A

ARTERIAL THROMBOEMBOLISM OCCUR WHEN A PIECE OF THROMBUS TRAVELS FROM ITS SITE OF FORMATION TO A MORE DISTAL PART OF THE ARTERIAL CIRCULATION.

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7
Q

WHAT HAPPEN WHEN ARTERIAL THROMBOEMBOLISM OCCUR?

A

IT WILL CUTS OFF THE OXYGEN SUPPLY TO THE SUBTENDED TISSUE RESULTING IN ISCHEMIA AND IF THIS IS PROLONGED, TISSUE INFARCTION OCCUR.

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8
Q

EMBOLI FROM
1. THE HEART WILL TRAVEL TO THE ___
2. THE ARTERY WILL TRAVEL TO THE ___

A
  1. THE HEART WILL TRAVEL TO ANY ART OF THE ARTERIAL CIRCULATION
  2. THE ARTERY WILL TRAVEL TO THE DISTAL TO ITS SITE OF ORIGIN.
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9
Q

THE MOST COMMONLY AFFECTED ORGANS OR TISSUES IN ARTERIAL THROMBOEMBOLISM ARE:

A

1 BRAIN
2. UPPER OR LL
3. INTESTINE

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10
Q

WHERE DOES SUPERFICIAL VENOUS THROMBI OCCUR?

A

IN THE SAPHENOUS VEINS

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11
Q

WHERE DOES THE DEEP VEIN THROMBUS ALWAYS OCCUR?

A

IN THE DEEP LEG VEIN (EX: ILIAC VEIN, FEMORAL VEIN, POPLITEAL VEIN)

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12
Q

WHAT IS THE CM OF SUPERFICIAL VENOUS THROMBI?

A
  1. LOCAL CONGESTION
  2. SWELLING
  3. PAIN
  4. TENDERNESS
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13
Q

SUPERFICIAL VENOUS THROMBI CAN LEAD TO THE DEVELOPMENT OF

A

INFECTION
VARICOSE ULCERS

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14
Q

DEEP VEIN THROMBI IS (PRONE/RARELY) EMBOLIZE.

A

PRONE

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15
Q

MANY DVTS ARE (SYMPTOMATIC/ ASYMPTOMATIC)

A

SYMPTOMATIC

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16
Q

STATE 5 RF OF VENOUS THROMBOSIS

A

INHERITED RF
1. DEFICIENCY OF PROTEIN S
2. DEFICIENCY OF PROTEIN C
3. FACTOR V LAIDEN MUTATIONS
4. ANTITHROMBIN DEFICIENCY
MODIFIED RF
1. TRAUMA
2. SURGERIES ESP ORTHOPEDIC SURGERIES
3. BEDRIDDEN
4. OCP
5. PREGNANCY

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17
Q

STATE THE CM OF DVT

A
  1. DISTAL OEDEMA
  2. PAIN
  3. TENDERNESS
  4. REDNESS
  5. HEAT
  6. CYANOSIS
  7. SUPERFICIAL VEIN DILATATION
  8. SWELLING
18
Q

DESC THE DEVELOPMENT OF THROMBUS

A
  1. THE FUNCTION OF THE VENOUS VALVE IS TO PREVENT THE BACKFLOW OF BLOOD AND CREATE A SLOW CIRCULATION IN THAT SPECIFIC AREA.
  2. FIBRIN, A FIBROUS CLOTTING PROTEIN, WILL ACCUMULATE IN THE SLOW MOVING VENOUS BLOOD TRAPPING THE BLOOD CELLS.
  3. FIBRIN TRAPPED BLOOD CELL COMBINE WITH PLATELET FORMING A PLATELET AGGREGATION.
  4. BY TIME, THE PLATELET AGGREGATION WILL INCREASES AND THIS WILL OCCLUDE THE BLOOD VESSEL CREATING A SLOWER CIRCULATION AS WELL AS LEADING TO SWELLING AND PAIN IN THE REGION.
19
Q

WHAT IS POST THROMBOTIC SYNDROME?

A

POST THROMBOTIC SYNDROME OCCURS IN 1/3 OF PATIENT,
IT OCCUR AFTER MONTHS OR YEARS OF A LOWER LIMB DVT
VENOUS THROMBI THAT PERSIST CAN DESTROY VENOUS VALVES AND VENOUS RETURN IS IMPAIRED WHICH CAN LEAD TO VENOUS HPT

20
Q

STATE THE SIGNS AND SYMPTOMS OF POST THROMBOTIC SYNDROME.

A

SYMPTOMS:
1. PAIN
2. CRAMPS
3. HEAVINESS
4. ITCHING
5. PARAESTHESIA
6. WORSE AT END OF THE DAY AND AFTER STANDING FOR LONG PERIODS

SIGNS
1. REDNESS
2. INDURATION
3. PATCHY HYPERPIGMENTATION
4. VENOUS ECTASIA
5. VENOUS ULCERATION

21
Q

HOW TO PREVENT DVT?

A
  1. EARLY AMBULATION POST OPERATIVELY
  2. GRADUATED COMPRESSION STOCKING
  3. INTERMITTENT PNEUMATIC COMPRESSION DEVICES
  4. FOOT PUMPS
  5. ANTICOAGULANT THERAPY
  6. IVC FILTERS
22
Q

DEFINE EMBOLUS.

A

EMBOLUS;
A DETACHED INTRAVASCULAR SOLID, LIQUID OR GASEOUS MASS THAT IS CARRIED BY THE BLOOD CIRCULATION TO THE DISTAL PART OF THE ORIGIN WHERE IT OFTEN LEAD TO TISSUE DYSFUNCTION OR INFARCTION.

23
Q

STATE 3 DIFFERENT TYPES EMBOLISM.

A
  1. PULMONARY EMBOLISM
  2. FAT EMBOLISM
  3. AMNIOTIC FLUID EMBOLISM
24
Q

PULMONARY EMBOLISM IS THE (MOST/LEAST) COMMON FORM OF THROMBOTIC EMBOLISM

A

MOST

25
Q

PE ORIGINATE FROM

A

DEEP VEIN THROMBOSIS

26
Q

STATE 3 RF OF PE.

A
  1. BED RIDDEN
  2. SURGERY ESP ORTHOPEDIC SURGERY
  3. TRAUMA
27
Q

STATE THE MORPHOLOGY OF PE.

A
  1. A LARGE EMBOLUS APPEAR LIKE A SADDLE EMBED IN THE MAIN PULMONARY ARTERY IR ITS MAJOR BRANCHES.
  2. SMALL EMBOLI ALWAYS APPEAR IN THE MEDIUM SIZED OR SMALL SIZED PULMONARY ARTERIES.
  3. RED INFARCT
  4. A WEDGE SHAPED CAN BE SEEN AT THE BASE AT THE PLEURAL SURFACE OR AT THE APEX POINTING TOWARD THE HILUS OF THE LUNG.
  5. IN HISTOLOGY, COAGULATIVE NECROSIS CAN BE SEEN
28
Q

STATE THE CLINICAL CONSEQUENCES OF PE.

A
  1. MAJORITY OF PE IS ASYMPTOMATIC AND IT CAN BE HEALED VIA RESOLUTION.
  2. RISK OF RECURRENCE IS HIGH
  3. SUDDEN DEATH D/T MASSIVE PE CAN OCCUR IF THE EMBOLUS IS LARGE OR THERE IS MULTIPLE SMALL EMBOLI.
29
Q

SYSTEMIC THROMBOEMBOLISM CAN BE SEEN IN PATIENT WITH

A
  1. INTRACARDIAC MURAL THROMBI
  2. ATHEROMATOUS PLAQUE WITH THROMBUS
  3. VALVE VEGETATION
  4. ATRIAL THROMBUS
  5. OLD MYOCARDIAL INFARCT
  6. RECENT MYOCARDIAL INFARCT
30
Q

A 17-year-old man underwent operation after sustaining fracture of his right femur
following a motor vehicle accident. On the second postoperative day, he suddenly
became dyspnoeic and confused. Physical examination revealed petechial rash on his
neck and anterior thorax.
The MOST likely condition that has developed in this patient is
a. Air embolism
b. Fat embolism
c. Marrow embolism
d. Septic embolism

A

b. FAT EMBOLISM

31
Q

DEFINE FAT EMBOLISM.

A

SOFT TISSUE CRUSH INJURY OR RUPTURE OF MARROW VASCULAR SINUSOID SUCH AS LONG BONE FRACTURE WILL RELEASE MICROSCOPIC FAT GLOBULES INTO THE CIRCULATION.

32
Q

STATE THE FAT EMBOLISM SYNDROME.

A
  1. SYMTOMATIC IN MINORITY OF PATIENTS
  2. CHARACTERISED BY:
    - PULMONARY INSUFFICIENCY
    - NEUROLOGIC SYNDROME
    - ANEMIA
    - THROMBOCYTOPENIA
    - DIFFUSE PETECHIAL RASH
  3. CLINICAL SIGNS AND SYMPTOMS APPEAR 1 TO 3 DAYS AFTER INJURY
  4. THE PATHOGENESIS INVOLVE BOTH MECHANICAL OBSTRUCTION AND BIOCHEMICAL INJURY.
33
Q

WHAT IS AMNIOTIC FLUID EMBOLISM?

A
  1. AMNIOTIC FLUID EMBOLISM OCCUR AS A COMPLICATION OF LABOUR AND CAN HAPPEN IMMEDIATELY DURING POSTPARTUM PERIOD.
34
Q

WHAT IS THE SIGN AND SYMPTOMS OF AMNIOTIC FLUID EMBOLISM?

A
  1. DYSPNEA
  2. CYANOSIS
  3. SHOCK
  4. NEUROLOGIC IMPAIRMENT
  5. HEADACHE
  6. SEIZURE
  7. COMA
    “DI CS NANTI SAKIT KEPALA SAMPAI COMA”
35
Q

STATE THE UNDERLYING CAUSE OF AMNIOTIC FLUID EMBOLISM.

A

THE UNDERLYING CAUSE OF AMNIOTIC FLUID EMBOLISM IS THE ENTRY OF AMNIOTIC FLUID AND ITS CONTENT INTO THE MATERNAL CIRCULATION VIA TEARS IN THE PLACENTAL MEMBRANES AND/OR UTERINE VEIN RUPTURE.

36
Q

DEFINE AIR EMBOLISM.

A

GAS BUBBLES WITHIN THE CIRCULATION CAN COALESCE TO FORM FROTHY MASSES THAT OBSTRUCT VASCULAR FLOW AND CAUSE DISTAL ISCHEMIC SHOCK.

37
Q

STATE THE CAUSED OF DECOMPRESSION SICKNESS.

A

IT IS CAUSED BY SUDDEN CHANGE IN THE ATMOSPHERIC PRESSURE.

38
Q

STATE THE INDIVUALS AT RISK OF DECOMPRESSION SICKNESS.

A
  1. SCUBA AND DEEP SEA DIVERS
  2. UNDERWATER CONSTRUCTION WORKERS
  3. PERSONS IN UNPRESSURIZED AIRCRAFT IN RAPID ASCENT.
39
Q

HOW DOES DECOMPRESSION SICKNESS OCCUR IN A DEEP SEA DIVER?

A

DURING A DEEP SEA DIVE:
1. WHEN AIR IS BREATHED AT HIGH PRESSURE, HIGH AMOUNT OF GAS PARTICULARLY NITROGEN ARE DISSOLVED IN THE BLOOD AND TISSUES.
2. IF THE DIVER ASCENDS TOO RAPIDLY, THE NITROGEN EXPANDS IN THE TISSUE AND BUBBLES OUT OF SOLUTION IN THE BLOOD TO FORM GAS EMBOLI CAUSING TISSUE ISCHEMIC.

40
Q

WHAT IS THE TREATMENT FOR DECOMPRESSION SICKNESS.

A

PLACING THE AFFECTED PERSONS IN A HIGH PRESSURE CHAMBER TO FORCE THE GAS BACK INTO SOLUTION

41
Q

STATE THE COMMON SITE OF CAISSON DISEASE.

A
  1. FEMORAL HEADS
  2. TIBIA
  3. HUMERI
42
Q

WHAT IS MEANT BY FOREIGN BODY EMBOLISM.

A

FOREIGN BODY EMBOLISM
1. USUALLY A/W IV DRUG ABUSE
2. PRESENCE OF MG TRISILICATE (TALC) IN THE INTRAVENOUS MIXTURE
3. IT WILL ELICIT A GRANULOMATOUS RESPONSE IN THE ORGANS IN WHICH THEY LODGE.

PATHOLOGY (13 decks)

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