Haemodynamic disorder and shock Flashcards
Regarding non-inflammatory oedema, which of the following statements is correct?
A Has a protein content > 2g/dl
B Has a cholesterol content of < 45mg/dl
C Is caused by raised plasma colloid pressure
D Has a specific gravity > 1.012
B
Explanation
A non-inflammatory oedema or transudate has a low protein content, a specific gravity of < 1.012, a serum cholesterol of < 45mg/dl and a protein content of <2g/dl. It is caused by increased hydrostatic pressure and a decreased plasma colloid pressure
Non-thrombocytopaenic purpura is associated with which of the following?
A Meningococcaemia
B Aplastic anaemia
C Systemic lupus erythematosus (SLE)
D Human immunodeficiency virus (HIV)
A
Explanation
Non-thrombocytopaenic purpura is a type of purpura (red or purple skin discoloration) not associated with thrombocytopaenia. Causes include menigococcaemia, Henoch-Schonlein purpura (HSP), hereditary telangiectasia and congenital cytomegalovirus. The bleeding disorder is due to vessel wall abnormality. The platelet count and coagulation tests (PT,PTT) are usually normal, pointing by exclusion to the underlying problem
Thrombocytopaenia is caused by a decreased production of platelets (HIV, aplastic anaemia), decreased platelet survival (SLE, HIV), sequestration of platelets (hypersplenism) and dilutional, for instance by massive transfusion.
Reduction in platelet number, a count <100000 platelets/uL is generally considered to constitute thrombocytopaenia. Levels <20000uL may be associated with spontaneous bleeding. 20000-50000 is associated with post traumatic bleeding. PT and PTT are normal
Regarding increased vascular permeability due to endothelial contraction, which of the following statements is false?
A It is due to formation of endothelial gaps
B It occurs quickly and is short lived
C It is the most common mechanism of increased vascular permeability
D It is most common in capillaries
D
Explanation
The endothelium is responsible for normal fluid exchange and microvascular permeability. During inflammation the endothelium becomes leaky. Formation of endothelial gaps in venules is the most common mechanism. It is short-lived (15-30min) and usually reversible. Other mechanisms include cytoskeletal reorganization (endothelial retraction), increased transcytosis, direct endothelial injury, delayed or prolonged leakage, leukocyte mediated endothelial injury, and leakage from new blood vessels
Which of the following is not a cause of oedema?
A Increased lymph flow
B Increased interstitial colloid pressure
C Decrease oncotic pressure
D Increased venous pressure
A
Explanation
Pathophysiologic categories of oedema;
- Increased hydrostatic pressure
- Reduced plasma oncotic pressure
- Lymphatic obstruction
- Sodium retention
- Inflammation
Regarding amniotic fluid embolism, which of the following statements is correct?
A There is an increased risk in primagravida patients
B Increased risk in prolonged labour
C Mortality of 30%-50%
D Occurs in 1:40 000 births
D
Explanation
Amniotic fluid embolisms occur more often in multigravids at a rate of 1:40000. Increased risk factors include;
Precipitous or tumultuous labour (listed as risk factors in UpToDate, traumatic labour, caesarean section, operative vaginal delivery, abruption, placenta previa, cervical or uterine laceration, medical induction of labour, eclampsia, foetal distress, grand multiparity and advanced maternal age
The underlying cause is the infusion of amniotic fluid or foetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins
Mortality is in the range of 80% (5th highest cause of maternal mortality)
Note: The older editions of Robbins state an incidence rate of 1:50000. The eighth edition reports a rate of 1:40000
Regarding thrombotic and antithrombotic properties which of the following statements is correct?
A Tissue thromboplastins activate the intrinsic cascade
B Increased plasminogen activator extends thrombus
C Thrombomodulin can bind and activate thrombin into an anticoagulant
D Clot retraction is independent of platelets
C
Explanation
Tissue thromboplastins do not activate the intrinsic pathway but rather the extrinsic pathway. Clot retraction is dependant on release of multiple coagulation factors from platelets trapped in a fibrin mesh. Increased plasminogen decreases thrombus. Thrombomodulin binds and converts it from a procoagulant into an anticoagulant via its ability to activate protein C, which inhibits clotting by inactivating factors Va and VIIIa
Passive hyperaemia is caused by, which of the following mechanisms?
A Exercising muscle
B Arteriolar dilatation
C Portal hypertension
D Inflammatory mediator release
C
Explanation
Passive hyperaemia (congestion) is caused by portal hypertension, congestive cardiac failure, isolated venous obstruction and hepatic obstruction. Exercise, inflammatory mediator release, arteriolar dilatation are all active causes of hyperaemia
Passive hyperaemia is CONGESTION or STASIS
Extra:
Web search: Passive hyperaemia is when blood can’t properly exit an organ, so it builds up in the blood vessels. This type of hyperaemia is also known as congestion.
TB: hyperaemia is an active process resulting from arteriolar dilation and increased blood flow., as occurs at sites of inflammation or in exercising skeletal muscle. Hyperaemic tissues are redder than normal because of the engorgement with oxygenated blood.
Congestion (passive hyperaemia) is a passive process resulting form impaired outflow if venous blood form a tissue. It can occur systemically, as in cardiac failure, of locally as a consequence of an isolated venous obstruction.
Not sure why the term of passive hyperaemia was used in a question because it does not appear to be mentioned in the TB
Which of the following options best defines the pathophysiology underlying shock?
A Lactic acid production
B Decrease blood volume
C Cellular hypoxia resulting from impaired tissue perfusion
D Low cardiac output
C
Explanation
Shock is defined as cellular hypoxia resulting from impaired tissue perfusion. It is caused by a reduction in cardiac output and/or effective blood volume
Which of the following is the central pathophysiological feature of shock?
A Hypotension
B Cellular hypoxia at a tissue level
C Cardiac failure
D Decreased blood volume
B
Explanation
Shock is defined as cellular hypoxia resulting from impaired tissue perfusion. It is caused by a reduction in cardiac output and/or effective blood volume
Septic shock may cause all of the following, except?
A Vasoconstriction
B Acute renal failure (ARF)
C Adult respiratory distress syndrome (ARDS)
D Disseminated intravascular coagulopathy (DIC)
A
Explanation
Features of septic shock include systemic vasodilitation (giving rise to hypotension), diminished myocardial contractibility, widespread endothelial injury (causing disseminated intravascular coagulopathy, DIC) and activation causing systemic leukocyte adhesion along with pulmonary alveolar capillary damage (e.g. adult respiratory distress syndrome, ARDS)
The process of blood coagulation involves which of the following?
A Alpha 2 macroglobulin
B The action of plasmin on fibrin
C The removal of peptides from each fibrinogen molecule
D The action of antithrombin 3
C
Explanation
Alpha 2 macroglobulin (A2MG), antithrombin III and the action of plasmin are all anticoagulants
Extra: Alpha 2 macroglobulin acts as an antiprotease and is able to inactivate an enormous variety of proteinases. It functions as an inhibitor of fibrinolysis by inhibiting plasmin and kallikrein. It functions as an inhibitor of coagulation by inhibiting thrombin. Alpha 2-macroglobulin may act as a carrier protein because it also binds to numerous growth factors and cytokines, such as platelet-derived growth factor, basic fibroblast growth factor, TGF-β, insulin, and IL-1β.
Note: the inhibiton of thrombin will prevent coagulation. Althouugh A2MG has a plasmin inhibition, I dont think it will be procoagulant
Regarding the complement system which of the following statements is correct?
A The alternative pathway is stimulated by Ag-Ab interaction
B C5a initiates arachadonic acid metabolite release from neutrophils and monocytes
C C6-9 forms the membrane attack complex (MAC)
D C3 inhibits the final common pathway
B
Explanation
MAC is the cytolytic endproduct of the complement cascade; it forms a transmembrane channel, which causes osmotic lysis of the target cell.The classic pathway is stimulated by the Ag-Ab interaction. C3 complement activates the final complement pathway. C5-C9 forms the membrane-attack complex (MAC). MAC is the cytolytic endproduct of the complement cascade; it forms a transmembrane channel, which causes osmotic lysis of the target cell. The critical step in complement activation is the proteolysis of complement C3. Which ever pathway is activated they all lead to the formation of C3 convertase which splits C3 into C3a and C3b. C3a involved in the recruitment and activation of leukocytes. C3b then goes onto activate and form the MAC (through C5-C5a, C5b. C5b binding to C5-C9). C5a activates the lipoxygenase pathway of AA metabolism in neutrophils and macrophages, causing release of more inflammatory mediators. Leukocyte activation, adhesion, and chemotaxis. C5a activates leukocytes, increasing their adhesion to endothelium, and is a potent chemotactic agent for neutrophils, monocytes, eosinophils, and basophils. C3a and C5a have anaphylatoxin activity, directly triggering degranulation of mast cells as well as increasing vascular permeability and smooth muscle contraction.
With regard to emboli, which of the following statements is correct?
A Arterial emboli most often lodge in the viscera
B Amniotic fluid emboli are associated with the highest mortality
C All emboli consist of either gas or solid intravascular mass
D Pulmonary emboli are rarely multiple
B
Explanation
The major sites of arteriolar embolisation are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lessor degree. Pulmonary emboli are frequently multiple and cause 200 000 deaths per year in the USA. A patient who has had one pulmonary embolus is at a high risk of having more. Emboli consist of a solid (fat, tumor, bone fragment), liquid, gas or foreign body material e.g. shrapnel or a bullet. The incidence is only 1:40000 deliveries but the mortality is >80%. Amniotic fluid embolism is the fifth most common cause of maternal death world wide. It accounts for 10% of maternal deaths in the USA a year and results in>85% of permanent neurological deficits in survivors
Regarding the veins of the lower limb, which of the following statements is correct?
A Thrombosis in the superficial veins is a common source of emboli
B Dermatitis is a common consequence of Buerger’s disease
C Varicosity development has no genetic component
D Phlegmasia alba dolens is associated with iliofemoral vein thrombosis, occurring in pregnant females
D
Explanation
Superficial vein thrombosis is not a common source of emboli. Pain, ulcers and gangrene (thromboangitis obliterans) are a common consequence of Buerger’s disease. Varicosity development is genetically based. Deep veins account for >90% of cases of thrombophleblitis and phlebothrombosis. 10% of venous thrombosis occurs in the superficial veins
Fat embolism syndrome is associated with which of the following options?
A A mortality of greater than 20%
B The core clinical feature is the presence of neurological abnormalities
C Although 90% of skeletal injuries cause fat emboli, less than 10% of patients develop symptoms
D Symptoms typically develop after 4 days
C
Explanation
Fat embolism occurs in 90% of individuals with skeletal injuries, but less than 10% of such patients show any clinical findings. However, a minority of patients develop fat embolism syndrome.
Fat embolism syndrome is the term used when patients become symptomatic. It is characterised by pulmonary insufficiency, neurological symptoms, anaemia and thrombocytopaenia.10% of cases are fatal. The fat causes physical (obstructive) and biochemical (free fatty acid, FFA, inflammation) injury
Typically these symptoms develop 1-3 days after injury and occur suddenly
Thrombocytopaenia is attributed to platelet adhesion to fat globules and subsequent aggregation or splenic sequestration; anaemia results from a similar red cell aggregation or haemolysis.
A diffuse petechial rash (20-50% of cases) is related to rapid onset of thrombocytopaenia and can be a used diagnostic feature.
Non-inflammatory oedema is characterised by which of the following?
A A high protein content > 2g/dl
B Caused by a decrease in intravascular hydrostatic pressure
C An elevated level of atrial natriuretic peptide (ANP)
D A specific gravity > 1.012
C
Explanation
A non inflammatory oedema or transudate has a low protein content, a specific gravity of < 1.012, a serum cholesterol of < 45mg/dl and a protein contant of <2g/dl. It is caused by increased hydrostatic pressure and a decreased plasma colloid pressure. Atrial natriuretic peptide’s (ANP) main function is to increase sodium excretion from the kidney due a raised right atrial pressure. Other actions include an increase in capillary permeability, leading to extravasation of fluid and oedema.
Which of the following factors is part of the intrinsic pathway of coagulation?
A VIIa
B II
C X
D XI
D
Explanation
Calcium is found in the common pathway of the coagulation cascade, together with factors I, II, V, X.
The tissue factor pathway (also know as the extrinsic pathway) contains factor VII and is activated by coagulation factor III (tissue factor, thromboplastin). The intrinsic pathway contains factors VIII, IX, XI, XII and is activated by exposing factor XII to thrombogenic surfaces
Which of the following are features of a post mortem clot?
A Presence of Lines of Zahn
B Supernatant resembling chicken fat
C Presence of fibrin deposits in the thrombus
D Adherence to vascular walls
B
Explanation
Lines of Zahn imply the development of a thrombosis at the site of blood flow. These lines represent pale platelet and fibrin deposits alternating with darker red cell rich layers. Such lines signify that a thrombus has formed in flowing blood. Postmortem clots are gelatinous (due to the lack of fibrin) with a dark red dependent portion where red cells have settled by gravity and a yellow “chicken fat” upper portion. They are usually not attached to the underlying wall.
Which of the following is a feature of non-inflammatory oedema?
A Decreased intravascular hydrostatic pressure
B A protein content > 2g/dl
C Specific gravity >1.012
D Right atrial pressure is high
D
Explanation
A non inflammatory oedema or transudate has a low protein content, a specific gravity of < 1.012, a serum cholesterol of < 45mg/dl and a protein contant of <2g/dl. It is caused by increased hydrostatic pressure and a decreased plasma colloid pressure. Atrial natriuretic peptide’s (ANP) main function is to increase sodium excretion from the kidney due a raised right atrial pressure. Other actions include an increase in capillary permeability, leading to extravasation of fluid and oedema.
Which of the following amounts of air is liable to produce significant pulmonary air embolism?
A 10ml
B 100ml
C 1ml
D 20ml
B
Explanation
Generally, small amounts of air in the arterial system are broken up in the capillary bed and absorbed from the circulation without producing symptoms, however the injection of 2 or 3mL of air into the cerebral circulation can be fatal. Furthermore, as little as 0.5mL of air in the left anterior descending coronary artery has been shown to cause ventricular fibrillation
Traditionally, it has been estimated that more than 5mL/kg of air displaced into the intravenous space is required for significant injury (shock or cardiac arrest) to occur. However, complications have been reported with as little as 20mL of air (the length of an unprimed IV infusion tubing) injected intravenously (rare). Basically, the closer the vein of access is to the right heart, the smaller the lethal volume is.
Extra:
Volume of Air in a Lethal Venous Air Embolism: a case report, https://anesthesiology.pubs.asahq.org/
Discussion: In summary, estimates of 200–300 ml air have been reported to be lethal. This is the first report in an adult human to document an exact lethal volume of air, 200 ml (albeit in a patient with congestive heart failure), rather than to estimate retrospectively the lethal volume after the incident of fatal venous air embolism. It is still unclear whether this amount, 200 ml, represents the minimum volume of air considered to be lethal to healthy adult humans.
The most common haemodynamic mechanism in the production of pulmonary oedema is?
A Lymphatic obstruction
B Increase oncotic pressure
C Increase hydrostatic pressure, as occurs in left ventricular failure (LVF)
D Decrease oncotic pressure
C
Explanation
Pulmonary oedema occurs because of left sided heart failure. Decreased cardiac output causes a reduction in renal perfusion, which leads to the activation of the renin-angiotensin-aldosterone system. This in turn induces the retention of salt and water and the expansion of the interstitial and intravascular volumes, resulting in a greater hydrostatic pressure and pulmonary oedema
Regarding factor VIII, which of the following statements is correct?
A Factor VIII combines with factor X to activate thrombin
B A deficiency of 50% of the normal levels of factor VIII gives rise to mild disease
C Factor VIII deficiency causes a prolonged prothrombin time (PT)
D Factor VIII is useful in the treatment of haemophilia B
B
Explanation
Factor VIII joins with factor IX to activate factor X. It is used to treat haemophilia A as only the intrinsic pathway is affected. Those with less than 1% of normal levels have a severe form of the disease, 2-5% moderate and 6-50% mild. In haemophilia A, laboratory tests reveal a prolonged partial thromboplastin time (PTT), normal bleeding time, normal prothrombin time (PT) and normal platelet count.
Haemohilia B is a factor IX deficiency.
Haemophilia A is the most common hereditary (X-linked recessive trait) disease associated with life threatening bleeding
Note: PT measures factors (1,2,5,10), 7 AND aPTT measures factors (1,2,5,10), 8, 9, 11, 12
Deficiency of which of the following factors DOES NOT cause an increased Prothrombin time?
A V
B X
C VIII
D VII
C
Explanation
Prothrombin time (PT) assess the extrinsic and common coagulation pathways. The clotting of plasma after addition of an exogenous source of tissue thromboplastin (e.g. brain extract) and Ca+ ions is measured in seconds. A prolonged PT cab result from a deficiency or dysfunction of factor V, VII, X, prothrombin and fibrinogen.
Factor VIII is part of the intrinsic pathway and will affect the partial thromboplastin time (PTT)
What is the pathological name for a 4mm tissue haemorrhage lesion under the skin?
A Purpura
B Ecchymoses
C Diatheses
D Petechaie
A
Explanation
1-2mm haemorrhages into the skin, mucous membranes, or serosal surfaces are called PETECHIAE. Typically associated with increased intravascular pressure, low plt count, defective plt function and clotting deficits.
> 3mm haemorrhages are called PURPURA and may associated with similar traumas to petechaie as well as trauma, vasculitis and increased vascular fragility (amyloidosis)
> 1-2cm subcutaneous haematomas are called ECCHYMOSES and are typical after traumas but may be exacerbated by any of the aforementioned conditions.
Massive collections of blood in one or tother body cavities are called haemothorax, haemopericardium, haemoarthrosis and haemoperitoneum.
Apart from fibrinogen, which clotting factors does Prothrombin time test for?
A II, V, VII, X
B VIII, V, II, X
C VIIa and tissue factor
D XII, XI, IX, VIII
A
Explanation
Prothrombin time is an in vitro measurement, measured after addition of tissue factor, phospholipids and calcium. It evaluates function of extrinsic pathway proteins (VII, X, II, V and fibrinogen).
Partial thromboplastin time (PTT) is an in vitro measurement, measured after the addition of negatively charged particles (e.g. ground glass). It screens for function of intrinsic pathway proteins (XII, XI, IX, VIII, X, V, II and fibrinogen).
Robbins pocket companion textbook
A 5-year-old boy develops recurrent haematomas and bruising. He is testing for clotting disorders. Haemophilia B is a clotting disorder characterized by a deficiency in which coagulation factor?
A IX
B X
C Prothrombin
D VIII
A
Explanation
Haemophilia B is an X-linked recessive disease caused by factor IX deficiency. It is clinically indistinguishable from Haemophilia A.
