pathology 7 - disorders of the circulation Flashcards

0
Q

what is hyperaemia? what may you see?

A

due to locally increased blood flow - arteriolar dilation increases blood flow - active process
‘erythema’ = red!

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1
Q

how to disorders of the circulation arise?

A

diseases of the heart and BV. also due to conditions which alter the volume and distribution of blood and body fluids.

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2
Q

what is congestion? each side? what may it cause?

A

reduced outflow of blood so therefore, builds up eg. right sided heart failure would make liver congested as it backs up.
left sided would cause congestion in the lungs again due to backup. passive process - can cause cyanosis (blue/pruple colouration to the skin ) , hypoxia.

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3
Q

what may you see in the abdomen omentum with hyperaemia? what is normal? if have peritonitis?

A

would see fat and narrow blood vessels normally. peritonitis - hyperaemia occurs so see very red omentum and high amounts of fibrin. large blood vessels.

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4
Q

if have liver congestion due to the right sided heart failure (passive) what would you see?

A

lobules on the surface and hypoxia occurs - centre of lobules may be degenerating - centrilobular congestion

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5
Q

what is haemorrhage?

A

escape of blood from vessels due to vascular damage. eg. surface wound (external) or internally . haematoma/haemothorax. /failure of clotting mechanisms.

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6
Q

what are the 4 types of haemorrhage, classified by size?

A
  1. petechiae - very small 1-2mm locally increased vascular pressure/decreased platelet function. will see many of them
  2. purpura - slightly larger but still in capillaries. due to trauma/increased fragility and vasculitis
  3. ecchymoses - larger again - bruising.
  4. rhectic/suffusive - major bleed eg. due to fracture no longer just in capillaries.
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7
Q

haematoma?

A

haemorrhage into a discrete area eg. under skin blood blister.

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8
Q

haemoparicardia?

A

haemorrhage into the pericardia

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9
Q

haemarthrosis?

A

into the joints

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10
Q

epistaxis?

A

nose bleed

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11
Q

haematochezia? haemomelena?

A

chezia - urinary system (fresh blood)

melena - digested blood in faeces.

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12
Q

what can the effects of haemorrhage be? local? generalised?

A

local - depends on location eg. intracerebral
generalised - systemic - loss of 10% leads to anaemia
30-40% leads to hypovolaemic shock
acute - regenerative anaemia
chronic - iron deficiency.

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13
Q

what is haemorrhage diathesis?

A

increased tendancy to haemorrhage. following unjury eg. defective clotting.

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14
Q

what is haemostasis?

A

the maintenance of vascular integrity and blood flow. - arrests any bleeding from ruptured/damaged BV.

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15
Q

explain the process of haemostasis and fibrinolysis? explain how platelets are adhered to damaged cells? explain the ‘sludging effect’? what is the main role of platelets? primary plug formed by?
what does tissue factor III do ? (also called?) acts with? what is formed?
explain secondary haemostasis? ploymerization does what?
what are FDP’s and how are they formed? EG?

A
  1. vascular injury - causes arterioles to constrict followed by platelet adherance (tissue factor and von williebrand factor)vascular shutns help to redistribute blood away from the injured area. increased blood viscosity and RBC packing occur due to plasma loss through leaky endothelium. ‘sludging effect’
  2. activated platelets changee from round discs to flat plates and release granules that recruit more platelets and form the haemostatic plug (primary)
  3. tissue factor III or thrombopastin is exposed to injury. acts with factor VII to initiate the coagulation cascade - THROMBIN formed. from prothrombin.
  4. thrombin converts fibrinogen to fibrin. (insoluble) it accumulates and forms a meshwork that recruits and activates more platelets. this is then polymerized to form a plug which stops haemorrhage (secondary haemostasis!!)
  5. along with the coagulation cascade, the fibrinolytic cascade is also activated. it prevents over-production or persistence of fibrin. plamsinogen converted to plasmin which breaks down fibrin into FDP’s. (d-dimer) DIC.
16
Q

PLATELETS ALSO CALLED? what can they do/

A

thrombocytes! they can contract

17
Q

explain the kinin system? eg?

A

associated with inflammation. eg. bradykinin - vasodilator. increases vascular permeability which allows increasd leukocyte migration. + contracts smooth muscle and pain.

18
Q

explain the complement system?

A

another cascade system. which contributes to inflamm, phagocyctosis of microbes and cell lysis.

19
Q

what is the role of TXA2?

A

from platelets and activates aggregation and vasoconstriction.

20
Q

PGI2? what does it do and where from?

A

prostaglandin from endothelial cells which inhibits platelets and vasodilator.

21
Q

heamorrhagic diseases. cause increased tendency to bleed. may not show up until trauma/surgery. eg. Increased vascular fragility?

A

damage by toxins, drug induced, diabetes mellitus, allergies

22
Q

haemorrhagic disease - inadequate haemostatic respone?

A

thrombocyte (platelet) deficient. clotting factor deficient. eg. thrombocytopaenia - low platelets (bone marrow disease)

23
Q

which cells produce platelets in bone marrow?what could affect this? cayse which disease?

A

inadequate haemostatic response. megakaryocytes produce platelets in the bone marrow. bacterial, protzoal, drugs, bracken fern poisoning.

24
Q

haemorrhagic diseases - platelet destruction?

A

usually idiopathic. eg. FELV/ DIC. Thrombopathias - abnormal platelet function in bassett hounds common.

25
Q

haemorrhagic diseases - VON WILLIEBRANDS DISEASE.

A

factor VIII related. poor platelet reaction. (intrinsic system) leads to prothromin to thrombin normally which then leads to fibrinogen to fibrin. may not notice until surgery.

26
Q

haemorrhagic disease - Vitamin K deficiency? what else do you need for the coagulation cascade?

A

liver failure. co-factor for enzymes involved in coagulation. maldigestion of fat. ( also need calcium for the coagulation cascade)