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Haemodynamic Disorders Flashcards

(45 cards)

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1
Q

What is a thrombus?

A

Intravascular mass formed in life consisting of red blood cells, platelets and fibrins

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2
Q

Virchow’s triad

A

Endothelial injury, stasis, hypercoagulabiliy

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3
Q

Common clinical states leading to thrombus

A

Venous stasis
Contact activation
Paraneoplastic syndrome
Estrogen (pro-coagulator)
Endothelial injury

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4
Q

Causes of venous stasis

A

Prolonged bed rest, immobilisation, atrial fibrilation

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5
Q

Causes of contact activation

A

Prosthetic heart valve (anti-coagulants are needed for life)

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6
Q

Causes of paraneoplastic syndrome

A

Cancer cells secreting clotting factors (lung/pancreas)

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7
Q

Causes of high estrogen levels

A

Oral contraceptives, late pregnancy

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8
Q

Causes of endothelial injury

A

Post-surgery, post-birth

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9
Q

Fates of thrombi

A

Dissolution by fibrinolysis - for new thrombi, old thrombi are more cross-linked
Propagation - accumulation of more platelets
Organisation and recanalisation - ingrowth of new capillaries to restore flow
Embolisation - detachment and lodging in a distant site, may become infected (septic emboli)

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10
Q

Causes of edema

A

Increased capillary hydrostatic pressure
Decreased capillary oncotic pressure
Sodium and water retention
Increased vascular permeability and active hyperaemia - AKA local inflammation giving exudate
Obstruction of lymphatic drainage

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11
Q

Causes of increased capillary hydrostatic pressure

A

Local - impaired venous drainage (e.g. DVT)
General - congestive heart failure, portal hypertension

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12
Q

Causes of decreased capillary oncotic pressure

A

Nephrotic syndrome (loss of proteins in urine)
Hypoalbuminemia (liver damage causing decreased albumin synthesis)
Malnutrition

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13
Q

Causes of sodium & water retention

A

Low renal perfusion leading to activation of RAAS system

Low renal perfusion could be due to two reasons:
Low blood volume (as a result of high capillary hydrostatic pressure and low capillary oncotic pressure, increased transudate and hence decreased blood volume)
Low blood pressure (left heart failure)

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14
Q

Causes of obstruction of lymphatic drainage

A

Filariasis (elephantiasis)
Neoplasm - Lymphoma
Post-surgical/radiation damage

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15
Q

Cardiac causes of edema

A

RHF leading to backpressure effects on systemic circulation, increased venous pressure and increased capillary hydrostatic pressure > transudate and edema

Decreased cardiac output causing low renal perfusion and hence RAAS activation and ADH secretion > increased sodium and water retention, increased plasma volume and increased capillary hydrostatic pressure > transudate and edema

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16
Q

What is an embolus?

A

Detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant its point of origin

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17
Q

Types of embolism

A

Pulmonary embolism
Systemic thromboembolism
Air embolism
Fat embolism
Amniotic fluid embolism

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18
Q

Pulmonary embolism

A

Typically venous in origin (e.g. DVT)
May cause:
Sudden death - saddle embolism is lodged in the bifurcation of the pulmonary trunk
Pulmonary hypertension > strain right heart
Pulmonary infarction is uncommon because lungs have dual blood supply

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19
Q

Systemic thromboembolism

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A

Typically arterial in origin:
Intramural emboli due to LV infarction and LA fibrillation
Aortic aneurysm and atherosclerotic plaques

Results in vascular occlusion anywhere in the systemic circulation

20
Q

Fat embolism & effects

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A

Typically caused by fracture of long bones which contain fatty marrow
May cause:
Vascular occlusion and pulmonary insufficiency
Neurologic disturbances
Thrombocytopenia and anemia as RBCs and platelets adhere and aggregate to fat globules, leading to increased splenic sequestration
Petechiae can be a diagnostic feature

21
Q

Air embolism

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A

Iatrogenic injury (surgery or laparoscopic procedures)
Chest wall injury
Decompression sickness - gas dissolved in tissues, esp. N2, bubbles out quickly with rapid ascent after deep sea diving
Decompression sickness can present with:
Joint pain (bubbling out in joints)
Respiratory distress
Ischemic necrosis

Treated with hyperbaric chambers

22
Q

Amniotic embolism

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A

Rare obstetric complication where amniotic fluid and fetal tissue infuses into maternal circulation due to tear in placental membrane or uterine rupture
Can cause pulmonary circulation obstruction
Circulating fetal tissues can cause disseminated intravascular coagulation

23
Q

What is an infarct?

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A

Necrosis due to ischemia due to occlusion in either arterial supply or venous drainage

**Venous occlusion only leads to infarct when the tissue is drained by a single efferent vein (e.g. testis, ovaries) - if not, bypass channels can open up and the result is merely congestion

24
Q

Causes of infarction

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A

Thrombotic/embolic occlusion - most common cause
Extrinsic vessel compression - tumour, herniated sac, edema in a limited space (e.g. anterior compartment syndrome - anterior tibialis muscle swells too big for sheath)
Torsion of vessles - spermatic cord, bowel volvulus (red)

25
Morphology of infarcts (how to classify?)
Classification by colour: - Red infarct has a superimposed hemorrhage, in organs with loose tissue and dual blood supply (e.g. lung, liver) - White infarct in organs with firm tissue and end blood supply (e.g. heart, spleen, kidney) Classification by infection - Bland infarct - no infection - Septic infarct - infection, and potential to become abscess Changes in morphology over time
26
Ischaemia results in
1. Remains viable because of compensation - Ischemic atrophy and reduced function (e.g. renal artery stenosis causing kidney atrophy) - Establish collateral blood flow (e.g. heart w R & L circumflex arteries) 2. Healing by fibrosis, replace infarcted area with fibrous tissue (e.g. can happen in heart, but more susceptible to heart failure) 3. Infarct
27
Typical bleeding patterns of abnormal vasculature
Petechiae and purpura on skin and mucous membranes Significant haemorrhage into joints, GIT, urinary tract, etc Normal PT, PTT, bleeding time, platelet count
28
Causes of abnormal vasculature
Infections such as meningococcus and rickettsioses that cause disseminated intravascular coagulation & vasculitis Drug reactions - deposition of drug induced immune complexes on blood vessel walls causing vasculitis (type III hypersensitivity) Weakened vasculature: Scurvy - vitamin C deficiency causes low collagen synthesis; Cushing's syndrome - high cortisol, catabolism of protein Hereditary hemorrhagic telangiectasia - AD disorder causing formation of dilated, torturous, thin-walled blood vessels that bleed easily Perivascular amyloidosis - weakened vessel walls
29
Causes of hemorrhage
Traumatic Abnormal vasculature Platelet defects (qualitative/quantitative) Coagulation factor deficiency
30
Patterns of hemorrhage
Mucous/subcutaneous hemorrhage: petechiae, purpura, ecchymosis Hemorrhage into a bodily cavity: hemothorax, hemopericardium, hemoperitoneum, hemathrosis Hemorrhage contained within tissue: hematoma
31
Reactions to hemorrhage
Initial: SNS, increase blood volume Compensate for volume loss: RAAS activation, sodium and water retention, redistribution of blood flow Long-term: Replace RBC via bone marrow
32
Clinical consequences of hemorrhage
Hypovolemic shock: If more than 20% of blood volume lost rapidly Compression by hematoma - extradural hematoma increases intracranial pressure Iron deficient anemia: Chronic bleed externally (e.g. GIT) - will not be iron deficient if bleed is into bodily cavity because iron will be recycled
33
What is shock?
Inadequate perfusion of all cells and tissues leading to hypoxia and reversible cellular injury, and if severe, irreversible cellular injury and death
34
Types of shock
Hypovolemic shock Cardiogenic shock Distributive shock Obstructive shock
35
Hypovolemic shock
Low blood volume due to hemorrhage, severe burns, diarrhea, vomiting
36
Cardiogenic shock
Pump failure due to MI, cardiac tamponade, ventricular arrhythmias/fibrillation
37
Distributive shock
Widespread vasodilation. Neurogenic shock Anaphylactic shock Septic shock
38
Obstructive shock
Pulmonary embolism, pericardial embolism
39
Stages of shock
1. Initial non-progressive stage 2. Progressive stage 3. Late irreversible stage
40
Initial non-progressive stage of shock
Neurohumoral responses kick in to maintain BP - Baroreceptor reflex - increased sympathetic stimulation - Catecholamine (NE, E, dopa) release - RAAS, ADH activation and release Redistribution of cardiac output: - Peripheral vasoconstriction - Autoregulation of cerebral and cardiovascular blood flow to maintain perfusion
41
Progressive phase (stages of shock)
Persistent hypoxia - increased anaerobic glycolysis, widespread tissue injury and death Metabolic imbalances - lowered blood pH (lactic acidosis) which blunts vasomotor response Increased risk of disseminated intravascular coagulation due to the cell injury and death everywhere
42
Late irreversible phase
Widespread cell injury and death > release of lysosomal contents into circulation, aggravating shock Irreversible loss of vital functions - Acute tubular necrosis - shutdown of kidneys - Myocardial ischemia and infarction
43
Vicious cycles of shock
Heart (myocardial damage, infarction) + Gut (fluid loss, bacterial liberation) + Lung (alveolar damage, decreased perfusion) + Kidney (tubular damage, acidosis) + Liver (decreased lactate catabolism, acidosis) Metabolic acidosis: depresses cardiac function and decreases the response of vasopressors [basically, all contribute to metabolic acidosis, and metabolic acidosis aggravates the organ damage]
44
Clinical presentations of shock
Hypovolemic shock, cardiogenic shock: weak and rapid pulse, tachypnea, cold, clammy and cyanotic skin Anaphylactic shock, septic shock: weak and rapid pulse, tachypnea, warm, flushed skin
45
Pathophysiology of septic shock
Endotoxin (lipopolysaccharides) on gram negative bacteria cell wall bind to endotoxin receptors on macrophages, activating them and causing cytokine release: - Widespread vasodilation causes decreased tissue perfusion, causing hypoxic injury and decrease in plasma pH - Decreased cardiac contractility - Increased risk of disseminated intravascular coagulation: endothelial injury and endothelial activation by cytokines cause formation of microthrombi and organ damage > depletion of coagulation factors increases bleeding tendency - Hyperglycemia: stress hormones (cortisol, catecholamines) promote insulin resistance

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