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Principles Of Pathology > Haemodynamic disorders, Thromboembolic Disease and shock > Flashcards

Haemodynamic disorders, Thromboembolic Disease and shock Flashcards

1
Q

What are the four factors responsible for oedema?

A

Increase hypostatic pressure

Decrease osmotic pressure- lose proteins

Increase vascular permeability

Blockage of lymphatic flow

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2
Q

How can oedema occur and be classified into?

A

Regional- Tumour, volvulus in the intestine.

Systemic- Heart pressure, congestion, haemorrhage etc. CHD

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3
Q

What happens during acute hepatic congestion?

A

Distension of central veins and sinusoids. Resulting in centrilobular necrosis. https://s3.amazonaws.com/brainscape-prod/system/cm/173/340/820/a_image_thumb.png?1450629341

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4
Q

What can aetiological factors that can occur causing acute hepatic congestion and what can be an indicator of this?

A

Chronic RHS heart failure. This is also known as nutmeg liver. Breakdown of red blood cells, haemosiderin laden macrophages.

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5
Q

What can aetological factors can affect pulmonary oedema etc?

A

LHS heart failure.

Acute- engorged alveolar and focal- intra alveolar. Haemorrage by diapedesis-leukocyte extravasation.

Chronic- Septa thickening over a chronic amount of time. Heart failure cells within the alveoli can be a good indicator.

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6
Q

What diseases can affect hepatic congestion by a decrease in osmotic pressure?

A

Dogs- Copper chronic disease

Horse- Ragwort

Sheep- Liver fluke

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7
Q

How does Ragwort poisoning of horses occur?

A

Alkaloids intoxication. Causes megalocytosis, fibrosis and bile duct proliferation.

Causes antimitotic affects on the hepatocytes

Megalocytosis- mitotic inhibition with continued nucleoprotein synthesis, increase in the size of the nuclei.

Aflatoxins

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8
Q

What is the difference between haemorrhage and congestion?

A

Congestion- Intact blood vessels are distended with erythrocytes

Haemorrhage- Accumulation of extravasated erythryocytes

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9
Q

Why does haemorrhage occur and what are the two types?

A

Occurs because of abnormal function or integrity of one or more of the factors that influence haemostasis. The endothelium, platelets or coagulation factors.

The two types are:

Rhexis- traumatic or physical rupture of a vessel wall

Diapedesis-the escape of blood from vessels where it may be difficult to detect a disruption to the vessel wall.

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10
Q

What is the significance or consequence of haemorrhage?

A

Depends on the loss however can lead to hypovolaemia, reduced tissue perfusion, haemorrhagic hypovolaemic shock.

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11
Q

What are the causes of diapedesis?

A

Endothelial injury by endotoxins, infectious agents and chemicals.

Immune complexes (type III hypersens.)

Collagen disorder or defects

Decreased platelet numbers (thrombocytopaenia) or abnormal platelet function (thrombocytopathy)

Decreased concentration or function of coagulation factors

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12
Q

What would you call blood in the urine?

A

Two terms:
1. Haematuria- when centrifuged the colour of the urine will become clear as the RBC sediments seperate.

  1. Haemoglobinuria- The other will not
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13
Q

What is haemostasis?

A

Cessation of blood loss after disruption of a vessel wall. Involves the interaction of endothelial, platelets and coagulation factors. Activation of clotting factors culminates in thrombin generation and conversion of circulating fibrin into insoluble fibrin. Can lead to a THROMBIS

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14
Q

Can you illustrate a primary haemostasis?

A

https: //s3.amazonaws.com/brainscape-prod/system/cm/173/406/980/a_image_thumb.png?1450716218
https: //s3.amazonaws.com/brainscape-prod/system/cm/173/406/980/a_image_thumb.png?1450716276

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15
Q

Can you illustrate a secondary haemostasis?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/407/045/a_image_thumb.png?1450716339

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16
Q

Can you illustrate the thrombo-anti thrombotic events in secondary haemostasis?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/407/074/a_image_thumb.png?1450716398

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17
Q

What is the coagulation cascade?

A

Amplifying series of enzymatic reactions where inactive proenzymes are converted to active forms (clotting factors).

The extrinsic pathway is most important pathways activated by TF when vascular damage has occured.

Culminating in thrombin formation adn generation of insoluble fibrin from fibrinogen.

Coagulation factors- plasma proteins produced mainly by the liver, some require vitamin K for function.

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18
Q

Name some anti coagulation factors?

A

Antithrombin III produced by the liver and endothelium, inhibits the activity of thrombin

Proteins C and S are vitamin K depedent proteins that inactive factors VA and VIIIa

Tissue factor pathway inhibitor produced by endothelium prevents activation of extrinsic coagulation cascade.

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19
Q

How does damaged endothelium become prothrombotic?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/407/811/a_image_thumb.png?1450716995

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20
Q

What is virchow’s triad?

A

Its states the three things together can lead to a thrombosis:

  1. Endothelial injury
  2. Hypercoagulability
  3. Abnormal blood flow
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21
Q

What are the causes of endothelial damage?

A
  1. Immune mediated vasculitis
  2. Toxins- Endotoxins
  3. Local extensions of infection = hepatic abscess
  4. DIC
  5. Infectious agents
  6. Vitamin E/ Selinium deficiency
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22
Q

What is FIP and what does it cause?

A

Feline infectious peritonitis

Mutated feline coronavirus

Can lead to a thrombosis

A strong CMI is imminent in protecting against FIP

There are two forms:
Dry form- weak CMI, virus can persist in MO release of inflammatory mediators and cause perivascular pyogranulomatous inflammation

Wet form (effusion not oedema- body cavity)- no CMI, continued viral replication production of non neutralizing antibodies and immune complex formation and deposition in vessel walls.

23
Q

What are the causes of stasis and turbulence?

A
  1. Cardiac disease (cardiomyopathy)
  2. Aneurysm (copper deficiency in pigs)
  3. Hypovolaemia (diarrhoea)
  4. Local stasis or reduced flow (intestinal torsion)
  5. Inactivity
  6. Ulcerated atherosclerotic plaques
24
Q

What is amyloidosis and how can we distinguish this?

A

We can distinguish this by using a congo red staining.

It is the progressive depostion of proteinaceous material causing pressure atrophy to adjacent cells.

Example of glomerular nephropathy

Leads to antithrombin III deficiency- thrombosis

25
Q

What is an embolus and what can this occur from?

A

Free floating foreign material within the blood

Breaking bones

26
Q

What is a thromboemboli?

A

Thromboemboli, are emboli derived from fragments of a thrombus.

27
Q

What is the consequence of embolisation?

A

Inevitably emboli lodge in vessels too small to permit further passage creates embolisation.

The consequence of embolisation is the vulnerability to ischaemia, size of the blood vessel occluded and presence of a collateral blood supply.

28
Q

What would endocarditis look like in histology?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/410/677/a_image_thumb.png?1450719014

29
Q

What is a saddle thrombis? clinical signs

A

Cold legs, painful, Slight paralysis.

Can lead from HCM- hypertrophic cardio myopathy

so a saddle thrombis is in the ratification of the iliac arteries

left atrial dilation

hypertrophic cardiac myocytes

Increase turbulence

30
Q

What is shock?

A

Characterized by systemic hypotension due to either low cardiac output

Consequences are cellular hypoxia meaning cellular death

There are three types= cardiogenic, hypovolaemic, and blood maldistribution

Blood maldistribution= analphylactic, septic, and neurogenic shock

31
Q

Whats the intial stage of shock?

A

An intial non progressive phase: Reflex compensatory mechanisms

  1. baroreceptors detect= adrenaline output
  2. Decrease plasma volume stimulates ADH release and angiotensin system
  3. Increase peripheral resistence ADH and angiotensin system
  4. Net affect is tachycardia
32
Q

What is the second stage of shock?

A

Progressive stage= widespread due to hypoxia

Intracellular aerobic respiration is replaced by anaerobic glycolysis.

Metabolic acidosis, arterioles dilate and the blood begins to pool in microcirculation

Decrease in cardiac output, endothelial cells at risk of developing anoxic injury

33
Q

What is the final stage of shock?

A

This is the irreversible stage:

  1. Membrane transport mechanisms are impaired, lysosomal enzymes are released, structural integrity is lost and necrosis occurs.
  2. Vital organs such as the heart and kidney are affected and begin to fail.
  3. As each organ fails there is a reduction in the metabolic support each system provides to the others.
34
Q

What is Haemorrhagic Viral disease and some viruses from them?

A

VHFs are caused by four main viruses:

Arenavirus

Bunyavirus

Flavivirus

Filovirus

35
Q

What are the characteristics of VHFs?

A
  1. They are all RNA viruses, and all covered, or enveloped, in a fatty lipid coating
  2. The viruses are geographically restricted to the areas where their host species live.
  3. Humans are not the natural reservoir for these viruses. Humans are infected when they come into contact with infected hosts. However, accidental transmission from the host, humans can transmit the virus to one and another.
  4. Their survival is dependent on an animal or insect host, called the natural reservoir.
36
Q

What carries viruses that cause viral haemorrhagic fevers?

A
  • Viruses associated with most VHF are zoonotics.
  • Viruses naturally reside in an animal reservoir host or athropod vector.
  • Rodents and athropods are the main reservoirs for viruses causing VHFs.
  • The hosts of some viruses remain unknown- Ebola and mauburg viruses are well known.
37
Q

How are VHF’s transmitted?

A

The viruses are carried in rodents reservoirs which are transmitted when humans have contact with faeces, saliva any bodily excretion.

The viruses associated with athropod vectors are spread most often when the vector mosquito or tick bites.

However some of these vectors may spread virus to animals, livestock for example.

38
Q

What are arenaviruses?

A

They are ss RNA divided into “old world” arenaviruses and new world RNA viruses.

39
Q

What are hantaviruses and how are they spread?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/489/441/a_image_thumb.png?1450795453

40
Q

What are bunyaviruses?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/489/450/a_image_thumb.png?1450796752

41
Q

What are flaviviruses?

A

They are positive strand RNA viruses that cause widespread human and animal infections. Many are arboviruses- athropod carries. Such as

  • dengue virus
  • yellow fever
  • bovine pestiviruses
42
Q

What are filoviruses?

A

They are negative stranded- enveloped RNA viruses.

Though generally flawed found in athropods and rodents.

Commonly known as Ebola and Marburg virus

43
Q

Again what are the characteristics of VHFs?

A
  • They are all RNA viruses that are covered or enveloped in a fatty lipid coating
  • The viruses are geographically restricted to the areas where their host species live.
  • Humans are not the natural reservoir for these viruses. Humans are infected when they come into contact with infected hosts.
  • Their survival is dependent on an animal or insect host, called the natural reservoir.
44
Q

What happens when these VHF’s infect?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/493/410/a_image_thumb.png?1450797942

45
Q

what is BVDV?

A

Bovine virus diarrhoea virus- Pestivirus

46
Q

How does BVDV infect?

A

Acute infection=

  • mild disease
  • virus clearence 10-14 days
  • antibody has a slow plateau
  • recognition of more genetic diversity
47
Q

What are the clinical signs of BVDV?

A
  • Severe haemorraghic syndrome
  • mucosal disease
  • reproductive failure
48
Q

What is different in BVDV in infected cattle?

A

BVDV is a reproductive disease and can infect foetus.

Can lead to abortions, stillbirths and calcified foetus.

Can lead to PI calves.

49
Q

What is a PI animal/calf

A

Infection of the pregnant dam.

PI stands for persistent infections.

Usually stunted growth and PI dams can make PI calves.

Depending on when the PI dam was infected can lead to consequences on the calf.

Early pregnancy= Early foetal lost, congenital lost, PI animals

Mid preg.= Congenital abnormalities

late preg.= active immunity

50
Q

What are the biotypes of BVDV?

A

There are two biotypes which can lead to different signs:

non-cytopathogenic= PI

cytopathogenic= mucosal disease

51
Q

Can you illustrate the cytopathogenic biotype in terms of how the calves will be born?

A

https://s3.amazonaws.com/brainscape-prod/system/cm/173/496/013/a_image_thumb.png?1450801206

52
Q
A
53
Q

Can you summarise the main points about BVDV?

A

BVDV is a bovine pestivirus, is a major endemic pathogen affecting the health and fertility in a cattle.

Causes infertility, congenital infections, abortions and death.

Infections in early pregnancy can create the persistently infected calf. And with it the dam can be immune.

Has a variable pathogenesis and it is highly mutuable.

54
Q

What are the importances of viral diseases?

A
  1. Viruses are ubiquitous
  2. They have evolved with their natural hosts
  3. Viruses are always evolving rapidly.

Principles Of Pathology (8 decks)

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