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Pathology MBBS > Hemodynamic Disorder > Flashcards

Hemodynamic Disorder Flashcards

1
Q

Various causes of oedema

A
  1. Increased hydrostatic pressure
  2. Reduced plasma osmotic pressure
  3. Sodium and water retention
  4. Lymphatic obstruction (non pitting)
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2
Q

Periorbital oedema is a characteristic of

A

Renal dysfunction

Oedema in the parts of the body containing loose connective tissue

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3
Q

The examples of impaired venous return causing increased hydrostatic pressure and edema

A

Congestive heart failure
Constrictive pericarditis
Ascites (liver cirrhosis)
Venus obstruction or compression: thrombosis, external pressure
Lower extremity inactivity with prolonged dependency

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4
Q

Examples of arteriolar dilation leading to increased hydrostatic pressure

A

Heat

Neurohumoural dysregulation

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5
Q

Reduced plasma osmotic pressure leading to oedema is caused by

A

Protein losing glomerulopathy (nephrotic syndrome)
Liver cirrhosis
Malnutrition
Protein losing gastroenteropathy

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6
Q

Causes of lymphatic obstruction leading to oedema

A

Inflammatory
Neoplastic
Post-surgical
Post-irradiation

This does not cause pitting edema

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7
Q

Causes of sodium retention leading to oedema

A

Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium:
Renal hypoperfusion
Increased RAAS secretion

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8
Q

Microscopic features of oedema

A

Clearing and separation of the extra cellular matrix

Subtle cell swelling

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9
Q

Features of pulmonary oedema

A

The lungs are often 2 to 3 times their normal weight
On sectioning , a frothy blood tinged fluid is seen
It is a mixture of air, edema and extravasated RBCs

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10
Q

Features of brain oedema

A

Maybe localised or generalised
Swollen brain exhibits narrow sulci distended gyri
Impressions are seen on the skull
Herniation of the brain may occur through the Foramen Magnum or the brainstem vascular supply maybe compressed leading to death

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11
Q

Common causes of pulmonary oedema

A

Left ventricular failure
Renal failure
Acute respiratory distress syndrome
Pulmonary inflammation or infection

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12
Q

The effects of pulmonary oedema

A

It impedes gas exchange hypoxaemia
A favourable environment for bacterial infection
It is often worsened by plural effusions which may further compromise gas exchange by compressing the underlying pulmonary parenchyma

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13
Q

Virchow’s triad

A
  1. Endothelial injury
  2. Alterations in normal blood flow
  3. Hypercoagulabilty of blood
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14
Q

Primary causes of thrombophilia

A
  1. Factor V Leiden mutation
  2. Prothrombin gene mutation
  3. Protein C deficiency
  4. Protein S deficiency
  5. Antithrombin III deficiency
  6. Hyperhomocysteinemia
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15
Q

Acquired causes of thrombophilia

A
  1. Hyperhomocysteinemia
  2. Pregnancy
  3. OCPs
  4. Prolonged bed rest
  5. Immobilisation
  6. Microangiopathic haemolytic anaemias
  7. APLA -Anti phospholipid syndrome
  8. Nephrotic syndrome
  9. Prosthetic cardiac valves
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16
Q

Examples of microangiopathic haemolytic anaemia

A
  1. HUS
  2. TTP
  3. DIC
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17
Q

Haemorrhaging infarct or red infarct

A
  1. Seen in organs with dual blood supply
    Lung, liver
  2. Loose connective tissue containing organs like ovary
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18
Q

White or pale infarct

A

Single vessel supply (end artery)

Heart , spleen, kidney

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19
Q

Pulmonary embolism

A

Commonly caused by deep vein thrombosis
Saddle embolism:
Present at the bifurcation of vasculature leading to sudden cardiac death

20
Q

Air embolism

A

Caissons disease or decompression sickness or chokes (when affects lungs)

21
Q

Fat embolism

A 
Fracture of long bones
2-3 days after fracture:
1. Thrombocytopenia➡️ rash 
2. Delirium
3. Irritability
4. Dyspnea
22
Q

Amniotic fluid embolism

A

Pregnancy complication like abruptio placentae

Cyanosis is seen

23
Q

In chronic venous congestion of liver, liver is seen as

A

Nutmeg liver

24
Q

Heart failure cells

A

They are haemosiderin laden macrophages
Seen in the lungs of patients with CHF (congestive heart failure)
Prussian blue is the special stain used for heart failure cells

25
Q

Petechiae

A

Petechiae are minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces
Causes:
1. low platelet counts (thrombocytopenia)
2. defective platelet function
3. loss of vascular wall support

26
Q

Purpura

A

Purpura are slightly larger (3 to 5 mm) hemorrhages. Purpura can result from the same disorders that cause petechiae, as well as trauma, vascular inflammation (vasculitis), and increased vascular fragility.

27
Q

Ecchymoses

A

Ecchymoses are larger (1 to 2 cm) subcutaneous hematomas (bruises). Extravasated red cells are phagocytosed and degraded by macrophages
The characteristic color changes of a bruise result from the enzymatic conversion of hemoglobin (red-blue color) ➡️ bilirubin (blue-green color) ➡️ hemosiderin (golden-brown).

28
Q 
Internal bleeding (e.g., a hematoma) does not lead to iron deficiency
Why
A

Iron is efficiently recycled from phagocytosed red cells

29
Q

The general sequence of events leading to hemostasis at a site of vascular injury is

A
  1. Arteriolar vasoconstriction
  2. Primary hemostasis: the formation of the platelet plug
  3. Secondary hemostasis: deposition of fibrin
  4. Clot stabilization and resorption
30
Q

α granules of platelets

A

α-granules have the adhesion molecule P-selectin on their membranes and contain:
1. proteins involved in coagulation:-
fibrinogen, coagulation factor V, vWF
2. protein factors that may be involved in wound healing:-
fibronectin
platelet factor 4 (a heparin-binding chemokine)
platelet-derived growth factor (PDGF)
transforming growth factor-β

31
Q

Dense or δ granules of platelets

A

Dense (or δ) granules contain:

  1. ADP and ATP
  2. Ca2+
  3. serotonin
  4. epinephrine.
32
Q

On contact with proteins like collagen and vWF of subendothelial connective tissue, platelets undergo a sequence of reactions that culminate in the formation of a platelet plug

A
  1. Platelet adhesion (via vWF)
  2. Platelets rapidly change shape following adhesion
  3. Secretion (release reaction) of granule contents occurs along with changes in shape; these two events are often referred to together as platelet activation.
  4. Platelet aggregation ➡️ platelet contraction and secondary hemostatic plug formation
33
Q

Recruitment of platelets

A

ADP is a component of dense-body granules; thus, platelet activation and ADP release begets additional rounds of platelet activation, a phenomenon referred to as recruitment.

34
Q

Platelet activation is triggered by

A

Platelet activation is triggered by a number of factors, including the coagulation factor thrombin and ADP.

Thrombin activates platelets through a special type of G-protein coupled receptor referred to as a protease activated receptor (PAR), which is switched on by a proteolytic cleavage carried out by thrombin

35
Q

Glanzmann thrombasthenia

A

inherited deficiency of GpIIb-IIIa results in a bleeding disorder

The conformational change in glycoprotein IIb/IIIa that occurs with platelet activation allows binding of fibrinogen, a large bivalent plasma polypeptide that forms bridges between adjacent platelets, leading to their aggregation.

36
Q

prothrombin time (PT) assay assesses

A

the function of the proteins in the extrinsic pathway (factors VII, X, V, II (prothrombin), and fibrinogen).

In brief, tissue factor, phospholipids, and calcium are added to plasma and the time for a fibrin clot to form is recorded.

37
Q

partial thromboplastin time (PTT) assay screens the

A

function of the proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen).

In this assay, clotting of plasma is initiated by the addition of negative- charged particles (e.g., ground glass) that activate factor XII (Hageman factor) together with phospholipids and calcium, and the time to fibrin clot formation is recorded.

38
Q

Factor XII deficiency

A

Individuals with factor XII deficiency do not bleed and in fact may be susceptible to thrombosis.

The paradoxical effect of factor XII deficiency may be explained by involvement of factor XII in the fibrinolysis pathway

39
Q

the most important activator of factor IX, in vivo

A

factor VIIa/tissue factor complex

40
Q

the most important activator of factor X

A

factor IXa/factor VIIIa complex

41
Q

The mild bleeding tendency seen in patients with factor XI deficiency is likely explained by

A

the ability of thrombin to activate factor XI (as well as factors V and VIII), a feedback mechanism that amplifies the coagulation cascade.

42
Q

Among the coagulation factors, thrombin is the most important, because

A
  • Conversion of fibrinogen into crosslinked fibrin.
  • Platelet activation.
  • Proinflammatory effects.
  • Anti-coagulant effects
43
Q

Coagulation normally is restricted to sites of vascular injury by:

A
  1. Limiting enzymatic activation to phospholipid surfaces (by activated platelets or endothelium)
  2. Circulating inhibitors of coagulation factors, like antithrombin III (facilitated by heparin-like molecules on endothelial cells)
  3. Thrombomodulin on normal endothelial cells (which bind thrombin and convert it into an anticoagulant)
  4. Fibrinolytic pathways (e.g., by association of t-PA with fibrin).
44
Q

Platelet inhibiting effects of endothelium

A
  1. Shields platelets from subendothelial vWF and collagen
  2. Releases a number of factors that inhibit platelet activation and aggregation like prostacyclin, NO and adenosine diphosphatase
  3. Binds and alters the activity of thrombin
45
Q

Major prothrombotic alterations in endothelium following injury

A
  1. Downregulation of thrombomodulin by cytokines
  2. Downregulation of protein C and tissue factor protein inhibitor
  3. Secretion of Plasminogen activator inhibitors (PAI), decreasing fibrinolysis and downregulating t-PA

thrombin activation stimulates platelets and facilitates inflammation through PARs expressed on platelets and inflammatory cells.

46
Q

Effects of abnormal blood flow on thrombosis

A
  1. Promote endothelial cell activation and enhanced procoagulant activity (through flow-induced changes in endothelial gene expression)
  2. Stasis allows platelets and leukocytes to come into contact with the endothelium
  3. Stasis also slows the washout of activated clotting factors and impedes the inflow of clotting factor inhibitors.

Pathology MBBS (17 decks)

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