Circulatory Disorders Flashcards
1
Q
Oedema Fluid Distribution
A
Fluid distribution:
- Approximately 60% of the body is composed of water (2/3rd intracellular fluid, 1/3 extracellular). 80% interstitium + 20% plasma
determined by opposing forces of:
- Plama colloid osmotic pressure- keeps fluid in vessels (venous end)
- Vascular hydrostatic pressure- pushes fluid out (arterial end)
Any diseases–> ↑ hydrostatic pressure +/or ↓colloid osmotic pressure → ↑ interstitial fluid
2
Q
Oedema
A
Oedema
- Oedema → abnormal accumulation of fluid within interstitial tissues (exceeds lymphatic drainage)
- Fluid collection named by location e.g. hydrothorax, hydropericardium & hydroperitoneum (ascites)
- Anasarca- severe generalised oedema- most noticeable in subcutaneous tissues
- Histo: Clear spaces are a big give away
- Two types of oedema fluid:
- Non inflammatory oedema (haemodynamic- usually assoc. with something in the cardiovascular system) → ↓ protein/cell transudate
- Inflammatory oedema → protein/cell rich exudate
3
Q
Oedema
(Characteristics and Consequences)
A
- Gross: yellow, gelatinous fluid occupies body cavities or expands tissues affected by it
- Micro: as expansion of the tissue with clear spaces
- Subcutaneous oedema is generally ↓ severe than oedema of brain etc but usually indicates more severe underlying condition such as cardiac disease/ renal failure
4
Q
Four Mechanisms of Oedema
(VERY IMPORTNANT)
A
- increased intravascular hydrostatic pressure
- Decreased osmotic pressure- Any conditions that can lead to lack or loss of albumin
- increase vascular permeability- usually inflammatory in origin
- decreased lymphatic drainage - blockage of lymphatic flow (inflammation/compression)
5
Q
Increased Intravascular Hydrostatic Pressure
(Oedema: out of vessel)
A
- Occurs due to ↑ blood volume in the microvasculature which may be due to active ↑ flow of blood (hyperaemia-excess of blood) or passive accumulation of blood (congestion)
- Regional ↑ in HP→ localised oedema (due to obstruction/ compression or vascular malformation).
This is from inefficient lymphatics or palatinate lymphatics. Skin is thickened and feels cooler (cooler fluctuant skin). ex: dog–> congenital lymphoedema
- Systemic ↑ in HP→ generalised oedema (most common cause= CVD). Vascular congestion
- Congestion & ↑ hydrostatic pressure can occur in:
- Portal venous system in right hand side (RHS) congestive heart failure → ascites (accumulation of protein-containing (ascitic) fluid within the abdomen). Clear and gelatinous material in the abdominal cavity
- Pulmonary venous system → in LHS congestive heart failure → pulmonary oedema. Get prominent interlobular septa and frothy oedema fluid in bronch. If you cut through them, fluid often comes out from cut surface
6
Q
Decrease in Plasma Osmotic Pressure
(Oedema- not enough into vessel)
A
- Occurs due to ↓ plasma proteins (albumin) → ↑ fluid filtration & ↓ absorption → generalised oedema (always lead to generalized oedema)
- Hypoalbuminaemia → ↓ synthesis by the liver or ↑ lost from the circulation
- ↓ hepatic production may be as a result of severe liver diseases such as cirrhosis (e.g. fluke/toxic injury-ragwort) or protein malnutrition or malabsorption
- Excessive loss from circulation may be due to: Protein losing enteropathy (e.g. IBD), Severe haemorrhage associated with parasitism (e.g. Haemonchus), Protein losing nephropathy (nephrotic syndrome) or Plasma exudation associated with severe burns
7
Q
Increased Vascular Permeability
(oedema- more fluid into interstitial)
A
- Occurs due to inflammatory or immunologic stimuli
- ↑ permeability–> proteins escape into interstitial fluid & ↑ the osmotic pressure –> Fluid drawn into interstitial fluid from the plasma –>oedema (purpose is to dilute an inflammatory agent)
- But If stimulus is ongoing–> leakage of plasma proteins & emigration of leukocytes –> a cell-rich exudate
- Examples: viral & bacterial infections, endotoxic shock & anaphylaxis
8
Q
Decreased Lymphatic Drainage
(Oedema- lack of removal of fluid from interstitial space)
A
- many causes:
- Lymph vessel compression (by granuloma/ tumour) or constriction (due to fibrosis)
- Internal blockage (thrombus/ embolus,
- Congenital malformation –> apalsia or hyperplasia (congenital lymphodema)
- Surgical removal of lymph nodes: ex: cancer near by taken out with draining lymphnodes
- Lymphangitis (inflammation) or Intestinal lymphangiectasia (can be acquired/ congenital)
-Usually results in a localised oedema → lymphoedema
9
Q
Haemorrhage
A
- Extravasation of erythrocytes–> tissue (whereas congestion is within an intact blood vessel)
- Due to abnormal function or integrity of endothelium, platelets or coagulation factors (inherited or acquired)
- Two types: Rhexis → big hole in vessel, Diapedesis → lots of little holes
- causes:
- Endothelial Injury
- Developmental collagen disorders
- Collagen defect sin guinea pigs & primates with Vit C deficiency - Have collagen in basement membrane, vessels may be more prone to hemorrhage
- decreased platelet numbers (thrombocytopaenia)
- Abnormal platelet function (thrombocytopathy)
- Decreased concentration or function of coagulation factors
10
Q
Haemorrhage by Rhexis
A
physical/ traumatic rupture of a blood vessel
- Causes: inherited or acquired abnormalities in blood vessels: Vascular erosion by microorganisms, inflammatory reactions, abscesses or invasive neoplasms
11
Q
Haemorrhage by Diapedesis
A
- Endothelial injury by endotoxins, infectious agents (e.g. CAV 1) and chemicals (e.g. uraemic toxins)
- Developmental collagen disorders
- Collagen defects in guinea pigs and primates with vitamin C deficiency
- ↓ platelet numbers (thrombocytopaenia)
- decreased production–> megakaryocyte damage (Neoplasm in BM)
- increased destruction–> immune mediated disease
- increased use–> DIC (increased consumption of platelets) -
Abnormal platelet function (thrombocytopathy)
- Inability to adhere or aggregate at the site of a vascular injury- Could be missing these receptors.. Primary platelet malfunction
- Inherited defects such as in Glanzmann’s thrombasthenia
- Secondary platelet dysfunction- deficiencies of factors necessary for normal platelet function
- Von Willebrand’s disease → most common inherited canine bleeding disorder -
↓ concentration or function of coagulation factors
- Inherited deficiencies of coagulation factors - severe liver disease
- ↓ production of coagulation factors- e.g due to severe liver disease, as most produced here
- ↓ production of vitamin K dependent coagulation factors (vitamin K deficiency or inhibitors of the Vit K activity- Some clotting factors are depending on vitamin K)
- ↑ use of coagulation factors → due to ↑ consumption associated with DIC
12
Q
Patterns of Tissue Haemorrhage
A
- Petechiae: minute 1-2mm haemorrhages (minor vascular damage)
- Purpura: >3mm haemorrhages (more extensive vascular damage)
- Suffusive haemorrhage: larger continuous areas of haemorrhage
- Haematoma: accumulation of haemorrhage within a focal confined space (ears/ spleen following tumour)
- Ecchymoses: 1-2cm subcutaneous haematomas (bruises)- RBCs phagocytised & degraded by macrophages (Haemoglobin → bilirubin →haemosiderin)
13
Q
Loss of Blood
A
- Epistaxis (nose bleed): May originate anywhere in the respiratory system
- Gastric haemorrhage: melena (black tar appearance of faeces) indicates upper GIT bleeding
- Haematochezia: passage of fresh blood in the faeces- indicates bleeding in lower GIT
- Dysentery: severe diarrhoea containing mucus & blood ± fever, abdominal pain, tenesmus
- Haematuria: blood in urine (to distinguish, centrifuge & rbcs should accumulate at bottom)
- Haemoglobinuria: RBC breakdown products in urine following intravascular haemolysis
14
Q
Significance and Consequences
(Haemmorhage)
A
- Clinical significance of haemorrhage depends on: the volume, rate & site of bleeding
- Usually blood loss localised & stopped by haemostatic processes
- Rapid loss <20% of the blood volume/ slow losses of larger amounts–> little impact on healthy adults
- >20%→ hypovolaemia, ↓ tissue perfusion & haemorrhagic (hypovolaemic) shock
- Extensive bleeding can cause jaundice from massive breakdown of RBCs
- Bleeding in brain –> ↑ intracranial pressure–> compromised blood supply & may cause herniation of BS
- Chronic or recurrent external blood loss–> causes a net loss in iron–> iron deficiency anaemia
15
Q
Hyperaemia & Congestion
A
Both cause local ↑ blood volumes → engorgement of the vascular bed (increase hydrostatic pressure and oedema)
Hyperaemia- active process in which arterial dilation –>↑ blood flow (tissues appear bright red)
- Physiologic hyperaemia occurs during ↑ O2 demand (muscle activity), dissipation of heat (from skin), digestion of food
- Pathologic hyperaemia occurs during early vascular response to an inflammatory stimulus
- ex: cat with gingivitis. bright red hyperaemic gingiva –> due to dilation of blood vessels with oxygenated erythrocytes
- Histo: Multiple dilated capillaries, filled with erythrocytes, there are dark blue dots all around (indicate lymphocytes)
Congestion- passive process → ↓ outflow of blood from a tissue- can be localised or generalised, acute or chronic
ex: displacement of organ, dog with intestinal torsion
* Congested tissues → dusky red-blue colour (due to cell stasis & accumulation of deoxygenated blood)
16
Q
Localised Congestion
A
obstruction/compression of venous outflow
- Neoplastic or inflammatory mass
- Displacement of an organ (intestinal torsion)
- Fibrosis resulting from healed injury
17
Q
Generalised Congestion
A
- ↓ passage of blood through the heart or lungs → due to heart failure or pulmonary fibrosis
- RHS heart failure → portal vein & hepatic congestion
- LHS heart failure → pulmonary congestion (mitral valve endicardiotis)
- External compression of the heart → cardiac tamponade (due to traumaticreticulopericarditis)
18
Q
Acute Passive Congestion
A
- sudden disruption of venous return to the heart
- can occur with acute cardiac failure- in lungs causes dark red colour& they become heavier than normal, in spleen- enlarged, red pulp becomes engorged with RBCs. In liver- causes enlargement & dark reddish brown colour
- engorged pulonary vessels in the lung
- arrythmias
- Barbituate euthanasia: causing relaxation of smooth muscle. tribeculae of the spleen, allows tissue to be congested with erythrocytes
19
Q
Chronic Passive Congestion
A
- In long standing chronic passive congestion, the lack of blood flow–> tissue hypoxia–> ischemia &fibrosis
- (hemosiderin containing macrophages can be seen- heart failure cells cells). due to RBCs lysing
- In liver- rounded edges can be seen grossly, histologically- multifocal haemorrhages, most common cause= chronic HF
- Nutmeg liver: Dark red areas are intra (or centri) lobular (necrosis from having lack of blood supply). Enlarged, bulging rounded liver lobes. Portal areas are where you have your hepatic arteries.
- Usually large, rounded, and bulging liver lobes with chronic
20
Q
Post Mortem Vascular Changes
A
- Vascular congestion, oedema & haemorrhages can occur agonally
- Need to distinguish from pathological changes
- After death before the blood clots, it undergoes gravitational pooling → hypostatic congestion
21
Q
Embolism
A
Particulate matter travelling within the vascular system which lodges in vessels too small to permit further passage (emobilisation) –> ischemic necrosis & infarction of hypoxic tissue
- Thromboemboli are emboli derived from fragments of a thrombus
- Clinical consequences depends on:
- Type of vessel occluded- occlusion of artery= more likely to cause infarction
- Rate of development & duration of occlusion- slower rate –> may develop alternate perfusion path
- Prior perfusion & viability of the tissue
- Degree of collateral circulation in affected tissue- dual blood supply–> ↓ risk of infarction
- Vulnerability to hypoxia (most vulnerable= neurones)
- Return of oxygenated blood flow to a prolonged ischaemic area
- Pulmonary thromboemboli- Venous thromboemboli typically lodge in the pulmonary circulation
- Systemic thromboembolism- Arterial thromboemboli often arise from intracardiac mural thrombi
- Other types- fibrocartilaginous emboli, bacterial emboli, neoplastic emboli
22
Q
Infarction
A
- An area of peracute ischemia that undergoes coagulative necrosis
- Ischemia: perfusion of tissue= inadequate to meet metabolic demands
- Occlusion of either the arterial supply/ venous drainage by:
- Thromboembolic arterial occlusions (most common)
- Vasospasm
- Extrinsic compression of a vessel
- Torsion or traumatic rupture of a vessel
- Gross: Wedge shaped area of discolouration (usually darker than surrounding tissue due to haemorrhage), may develop–> pale centre with dark red rim (due to necrosis & swelling). In organs with spongey consistency (lung/ spleen) dark red colour will remain. Eventually scar tissue replaces damage
23
Q
Haemostasis
A
• Normal physiological response for prevention & cessation of bleeding/haemorrhage after disruption of a vessel wall- Involves the interaction between endothelium, platelets & coagulation factors- cease blood loss after disruption of vessel wall
-Mediators released by damaged endothelial cells. get reflex vasoconstriction at site of injury
Tightly regulated process, to keep fluidity and clotting in balance
- Pathological haemostasis → haemorrhage (too little) or thrombosis (too much clotting)
- Activation of clotting → thrombin →circulating, soluble fibrinogen → insoluble fibrin
- Fibrinolysis: prevents/limits inappropriate clotting in the circulation
