GENPATH Haemodynamic Disorder Flashcards

1
Q

Effects of blood loss

Acute - […]

Chronic - […]

A

Effects of blood loss

Acute - shock

Chronic -* iron deficiency anemia*

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2
Q

3 important factors that prevent thrombosis
[…]

A

3 important factors that prevent thrombosis
**1. smooth endothelial wall
2. PGI2 (prostacyclin)
3. Laminar blood flow

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3
Q

Air embolism pathology?

[…]

Treatment?
[…]

A

Air embolism pathology?

**Divers who surface too rapidly. bubbles form. go to any organ.
Lungs –> choking
muscles –> bends/pains
Brain –> seizures/staggers/drowsiness

Treatment?
putting patient’s in high pressure chamber to decompress and dissolve bubble

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4
Q

Amniotic fluid embolism pathology?

  • […]
  • […]
  • […]
  • […]
  • […]

Diagnosed by?
[…]

A

Amniotic fluid embolism pathology?

  • amniotic fluid get into amniotic vein
  • get to hearts/lungs/brains of mother
  • high mortality
  • can cause DIVC from the prostaglandins in amniotic fluid
  • rare obstetric complication

Diagnosed by?
- **presence of fetal squamous cells (foetal squames) in mother’s blood **

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5
Q

Briefly describe the spectrum of pulmonary or pulmonary vascular conditions that can develop as a result of the deep vein thrombus embolising to the pulmonary vasculature [6m] (vvvv IMPT!!!!!)

[…]

[…]

[…]

A

Briefly describe the spectrum of pulmonary or pulmonary vascular conditions that can develop as a result of the deep vein thrombus embolising to the pulmonary vasculature [6m] (vvvv IMPT!!!!!)

***Pulmonary thromboembolism: “saddle” embolism of bifurcation of pulmonary trunk, leading to occlusion of right ventricle outflow and lack of blood flow to left heart. Subsequent fall in CO results in a lack of blood in systemic circulation. Systemic hypoxia, hypotension and cardiac arrest ensures, leading to sudden death

*Pulmonary infarction: embolism into branch of artery, causing infarction (despite dual blood supply). This is also called “red” infartion, and can lead to haemorrhagic necrosis.

Pulmonary hypertension: showers of small thromboemboli occluding small branches of pulmonary arteries. Increases pulmonary vascular resistance and causes pulmonary hypertension. Overtime, the increased afterload and back pressure effects in the right heart leads to RV hypertrophy and RH failure
*

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6
Q

Clinical consequences of

venous thrombosis
[…]

arterial thrombosis
[…]

A

Clinical consequences of

venous thrombosis
**- edema (from local vascular occlusion)
- embolism

arterial thrombosis
**- cerebral necrosis (cerebral artery)
- myocardial necrosis (coronary artery)
- renal necrosis (renal artery)

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7
Q

Clinicopathological consequences of shocks in vital organs
- Damage to organs can worsen shock and consequently culminate in a vicious cycle leading to […].

A

Clinicopathological consequences of shocks in vital organs
- Damage to organs can worsen shock and consequently culminate in a vicious cycle leading to* multiple organ failure*.

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8
Q

Define embolus

An embolus is […]

A

Define embolus

An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

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9
Q

Define Hyperaemia

[…]

A

Define Hyperaemia

vessels of the microcirculation contain more blood than normal

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10
Q

Define Oedema

[…]

A

Define Oedema

An excessive extravascular accumulation of fluid

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11
Q

Define shock

[…]

A

Define shock

A state of inadequate perfusion of cells and tissues leading to reversible hypoxic injury and, if severe or prolonged enough, to irreversible cell and organ injury and death

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12
Q

Definition of infarction

[…]

A

Definition of infarction

Necrosis due to ischaemia

usually occlusion of artery. Sometimes occlusion of venous drainage

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13
Q

Describe the mechanisms in which nephrotic syndrome can cause generalised oedema. [8]

[…]

A

Describe the mechanisms in which nephrotic syndrome can cause generalised oedema. [8]

***Nephrotic syndrome → loss of albumin in urine → hypoalbuminemia → drop of plasma oncotic pressure → loss of fluid from vascular space to interstitial space → oedema (3m)

Decreased venous return to heart → reduced CO → reduced renal blood flow → activation of RAAS → sodium and water retention by kidney (4m)

***Secretion of ADH – water retention by kidney (1m)
*

Alright so the key idea is the compromised glomerular filtration in nephrotic syndrome leading to loss of albumin in urine. Then can start your performance from there alr.
Dont forget RAAS, dont forget ADH.*

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14
Q

Embolus a […]
- Embolism is the process!
- Causes vascular […] –> […], […] of target organs
- Can be septic if emboli carries pathogens (e.g infective endocarditis)

Pulmonary Embolism
- Venous emboli from lower limb secondary to DVT –> veins –> R heart –> pulmonary arteries
- Sudden occlusions can be fatal, usually clinically silent. Can cause pulmonary infarction and hypertension as well.
- Embolism at bifurcation of pulmonary arteries = […] Embolism
- Embolism that crosses ASD/VSD –> lodged in systemic circulation = […] Embolism

Systemic Embolism
- Most arise from […] mural thrombi or vegetations (on heart valves)
- White infarct occurs in most solid organs
- Red infarct occurs in spongy organs and organs of dual blood supply due to necrosis of surrounding vasculature (local haemorrhage)

A

Embolus a **detached intravascular solid, liquid (fat, amniotic fluid) or gaseous (air, nitrogen) mass that is carried by the blood to a site DISTANT from point of origin **
- Embolism is the process!
- Causes vascular occlusion –> ischema, necrosis of target organs
- Can be septic if emboli carries pathogens (e.g infective endocarditis)

Pulmonary Embolism
- Venous emboli from lower limb secondary to DVT –> veins –> R heart –> pulmonary arteries
- Sudden occlusions can be fatal, usually clinically silent. Can cause pulmonary infarction and hypertension as well.
- Embolism at bifurcation of pulmonary arteries = Saddle Embolism
- Embolism that crosses ASD/VSD –> lodged in systemic circulation = Paradoxical Embolism

Systemic Embolism
- Most arise from intracardiac mural thrombi or vegetations (on heart valves)
- White infarct occurs in most solid organs
- Red infarct occurs in spongy organs and organs of dual blood supply due to necrosis of surrounding vasculature (local haemorrhage)

Special types of Embolism:
Fat embolism
- Traumatic fracture releasing fat in bone marrow –> vascular occlusion, can lead to endothelial injury

Gas embolism
- Gas bubbles in circulation coalesce and obstruct blood flow
- Eg. when disconnecting heart lung machine during cardiac bypass surgery, injections, decompression sickness (nitrogen expands in the tissue and bubbles out)

Amniotic fluid embolism
- Amniotic fluid enters maternal circulation via tears in placenta
- Causes acute R heart failure, **Disseminated intravascular coagulation **(DIC)
- Most common cause of maternal death in developed world

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15
Q

Endothelial injury predisposes to thrombosis by
[…]

A

Endothelial injury predisposes to thrombosis by
**- loss of non-reactive surface
- exposure to subendothelial collagen
- local depletion of PGI2 and plasminogen activator
- release of tissue thromboplastin (tissue factor)

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16
Q

Example of active hyperaemia and their causes

Physiological:
- […]
- […]

Pathological
- […]

A

Example of active hyperaemia and their causes

Physiological:
- Blushing (nervous impulse)
- Exercising (functional demand)

Pathological
- **acute inflammation **

17
Q

Exudate vs Transudate (IMPT)

Exudates:
- […] protein content
- […] plasma fibrinogen
- […] specific gravity
- […] inflammatory cells

Exudate indicates […], Transudate indicates […]

A

Exudate vs Transudate (IMPT)

Exudates:
- higher protein content
- has plasma fibrinogen
- High specific gravity
- Many inflammatory cells

Exudate indicates inflammation, Transudate indicates haemodynamic disorders

18
Q

Factors that increase thrombotic tendancy (name 5)
[…]

A

Factors that increase thrombotic tendancy (name 5)
**- Atrial fibrillation
- Prosthetic cardiac valves
- Post-operative or post-partum state
- Prolonged bed rest or immobilisation
- Disseminated cancer
- Oral contraceptives (oestrogen)

  • trauma
  • surgery
  • autoimmune diseases
  • “economy class syndrome”
  • catheters
  • post pregnancy
  • increased platelets
  • Factor V or prothrombin mutations
  • defects in fibrinolysis or antithrombin III
19
Q

Haemorrhage
- bleeding. What else u want me to say HAHAHAH

Can be caused by:
- Trauma
- Abnormal vessels
- Platelets problems (thrombocytopenia, qualitative platelet defect)
- Coagulation factor deficiency

Location and extent (terminologies buffet!!)
Subcutaneous:
- 1-2mm, petite = […] –> platelet deficiency, abnormal vessels
- 1cm, small bruises = […] –> platelet deficiency, abnormal vessels
- 2-3cm, big bruises = […] –> coagulation factor deficiency

Into body cavities:
- in joints = […]
- Haemothorax –> trauma
- Haemopericardium –> ruptured MI
- Haemoperitoneum –> ruptured ectopic pregnancy

Within tissue
- severe = […]
- trivial = bruise

CONSEQUENCES
- Acute = […] if blood loss > 20%
- Compression of soft tissue by haematoma (e.g extradural haematoma)
- Chronic = […] anaemia in external blood loss (e.g menstration, GI bleed).

RESPONSES
- initial = sympathetic […] to maintain BP and Flow
- Compensatory = Fluid retention by […] & […], redistribution of blood flow via vasoconstriction
- Long Term = […] of lost RBCs

A

Haemorrhage
- bleeding. What else u want me to say HAHAHAH

Can be caused by:
- Trauma
- Abnormal vessels
- Platelets problems (thrombocytopenia, qualitative platelet defect)
- Coagulation factor deficiency

Location and extent (terminologies buffet!!)
Subcutaneous:
- 1-2mm, petite = Petechiae –> platelet deficiency, abnormal vessels
- 1cm, small bruises = Purpura –> platelet deficiency, abnormal vessels
- 2-3cm, big bruises = Ecchymoses –> coagulation factor deficiency

Into body cavities:
- in joints = Haemarthrosis
- Haemothorax –> trauma
- Haemopericardium –> ruptured MI
- Haemoperitoneum –> ruptured ectopic pregnancy

Within tissue
- severe = Haematoma
- trivial = bruise

CONSEQUENCES
- Acute = hypovolemic shock if blood loss > 20%
- Compression of soft tissue by haematoma (e.g extradural haematoma)
- Chronic = Iron deficiency anaemia in external blood loss (e.g menstration, GI bleed).

RESPONSES
- initial = sympathetic vasoconstriction to maintain BP and Flow
- Compensatory = Fluid retention by RAAS & ADH, redistribution of blood flow via vasoconstriction
- Long Term = replacement of lost RBCs

Note that Iron defiency anaemia DOES NOT occur in haematoma as phagocytes can recycle iron in Hb.

20
Q

Hyperaemia
- Vessels of the microcirculation contain […] blood than usual
- Active hyperaemia can be due to functional demand (exercising), nervous impulses (blushing) and acute inflammation
- Presents as […] (tissues appear red and engorged due to accumulation of oxygenated blood)

Congestion
- is passive hyperaemia due to impaired […]
- Localized congestion is due to […]
- Systemic congestion is due to […]
- Presents as […] (tissues appear blue due to accumulation of deoxygenated blood)
- Organs appear firm, heavy, enlarged & cyanotic!!

A

Hyperaemia
- Vessels of the microcirculation contain more blood than usual
- Active hyperaemia can be due to functional demand (exercising), nervous impulses (blushing) and acute inflammation
- Presents as Erythema (tissues appear red and engorged due to accumulation of oxygenated blood)

Congestion
- is passive hyperaemia due to impaired venous outflow
- Localized congestion is due to venous blockage
- Systemic congestion is due to cardiac failure
- Presents as Cyanosis (tissues appear blue due to accumulation of deoxygenated blood)
- Organs appear firm, heavy, enlarged & cyanotic!!

21
Q

Name two types of edema and examples of their causes

Localised
a. […]
b. […]
c. […]

Generalised
a. […]

b. […]

c. […]

A

Name two types of edema and examples of their causes

Localised
a. impaired venous drainage (eg. venous thrombosis)
b. increased vascular permeability (eg. inflammation)
c. obstruction/destruction of lymphatics (eg. filariasis, cancer)

Generalised
a. Cardiac edema (Congestive heart failure)
- increased venous pressure
- RAAS
- ADH

b. Renal edema (Nephrotic syndrome)
**- Hypoproteinaema (decreased oncotic pressure)
- sodium retention (RAAS) (increased hydrostatic pressure)
- ADH

**c. Hepatic edema
- hypoproteinaema (such as albumin) (decreased oncotic pressure)

22
Q

**Pots: Chronic Venous Congestion (Liver) **
- Congestion leads to […] of organ
- […] congestion leads to characteristic […] appearance (where got look alike sia…..)

Gross Description:
- Liver, diffused lesion
- Diffusely enlarged liver with variegated “[…]” dark and lighter appearance

Microscopic Features
- Centrilobular necrosis due to relative ischemia
- Small areas of change
- Viable hepatocytes around portal triad with congested sinusoids

A

Pots: Chronic Venous Congestion (Liver) **
- Congestion leads to *enlargement
of organ
- *Centrilobular
congestion leads to characteristic nutmeg appearance (where got look alike sia…..)

Gross Description:
- Liver, diffused lesion
- Diffusely enlarged liver with variegated “nutmeg” dark and lighter appearance

Microscopic Features
- Centrilobular necrosis due to relative ischemia
- Small areas of change
- Viable hepatocytes around portal triad with congested sinusoids

23
Q

Pots: Chronic Venous Congestion (Lung)

Gross Description:
- […] Lungs (3 lobes), parasaggital, diffuse lesion
- Diffusely […], […] appearance, heavy
- Edema, congestion, hemosiderin deposition
- […] fluid when lung is slightly squeezed

Microscopic Features:
- Venous congestion
- Fluid present in alveolar spaces (secondary to increased hydrostatic pressure)
- Abundant alveolar macrophages that have engulfed dead RBCs ([…] macrophages)

A

Pots: Chronic Venous Congestion (Lung)

Gross Description:
- Right Lungs (3 lobes), parasaggital, diffuse lesion
- Diffusely enlarged, brownish appearance, heavy
- Edema, congestion, hemosiderin deposition
- Frothy fluid when lung is slightly squeezed

Microscopic Features:
- Venous congestion
- Fluid present in alveolar spaces (secondary to increased hydrostatic pressure)
- Abundant alveolar macrophages that have engulfed dead RBCs (Haemosiderin laden macrophages)

FYI Haemosiderin laden macrophages are also called “heart failure cells”, which are indicative of LH failure.

24
Q

Shock (Mnemonic: NACHOS)
- Inadequate perfusion of cells and tissues –> leading to reversible hypoxic injury –> irreversible injury and death if severe/prolonged
- Mean arterial pressure <60mmHg or systolic BP <80mmHg

N[…] Shock
- Withdrawal of sympathetic tone in the body, caused by trauma to head/ anesthetic drugs –> loss of basal level of sympathetic discharge that maintains arteriole tone –> arterioles dilate –> decreased TPR –> decreased BP
- Examples include severe head trauma and abnormal anesthetic response

A[…] Shock
- IgE-mediated hypersensitivity causing increased inflammation throughout whole body –> histamine –> widespread vasodilation + capillary permeability increased –> fluid leaves vascular compartment (exudation) –> decreased BP
- Examples include bee stings, allergies

C[…] Shock
- Cardio-GENIC so its problem with the heart itself. Heart not pumping adequately –> decrease CO –> decrease BP
- Examples include STEMI, cardiac failure, bradycardia, arrhythmias

H[…] Shock
- loss of volume –> Starling’s Law –> decrease CO –> decrease BP
- Examples include Haemorrhage, Vomitting, Diarrhea, Severe Burns

O[…] Shock
- Blood clots from other parts of the body affecting return of blood to LV –> decrease CO –> decrease BP
- Examples include Deep Vein Thrombosis or any clots that dislodge from anywhere

S[…] Shock
- Disseminated infection
- Inflammation: Cytokine storm, vasodilation, increased vascular permeability
- Hypercoagulable state: […] activation –> increase prothrombotic factors –> disseminated intravascular coagulation (DIC) –> systemic thrombosis of small vessles –> hypoperfusion
- Examples include endotoxics from gram -ve bacteria lipopolysaccharides (LPS)

A

Shock (Mnemonic: NACHOS)
- Inadequate perfusion of cells and tissues –> leading to reversible hypoxic injury –> irreversible injury and death if severe/prolonged
- Mean arterial pressure <60mmHg or systolic BP <80mmHg

Neurogenic Shock
- Withdrawal of sympathetic tone in the body, caused by trauma to head/ anesthetic drugs –> loss of basal level of sympathetic discharge that maintains arteriole tone –> arterioles dilate –> decreased TPR –> decreased BP
- Examples include severe head trauma and abnormal anesthetic response

Anaphylatic Shock
- IgE-mediated hypersensitivity causing increased inflammation throughout whole body –> histamine –> widespread vasodilation + capillary permeability increased –> fluid leaves vascular compartment (exudation) –> decreased BP
- Examples include bee stings, allergies

Cardiogenic Shock
- Cardio-GENIC so its problem with the heart itself. Heart not pumping adequately –> decrease CO –> decrease BP
- Examples include STEMI, cardiac failure, bradycardia, arrhythmias

Hypovolemic Shock
- loss of volume –> Starling’s Law –> decrease CO –> decrease BP
- Examples include Haemorrhage, Vomitting, Diarrhea, Severe Burns

Obstructive Shock
- Blood clots from other parts of the body affecting return of blood to LV –> decrease CO –> decrease BP
- Examples include Deep Vein Thrombosis or any clots that dislodge from anywhere

Septic Shock
- Disseminated infection
- Inflammation: Cytokine storm, vasodilation, increased vascular permeability
- Hypercoagulable state: endothelial activation –> increase prothrombotic factors –> disseminated intravascular coagulation (DIC) –> systemic thrombosis of small vessles –> hypoperfusion
- Examples include endotoxics from gram -ve bacteria lipopolysaccharides (LPS)

Damage to organs can worsen shock and consequently culminate in a vicious cycle leading to multiple organ failure!!!

25
Q

Thrombus is an […]
- Thrombosis is the process in which a thrombus is formed
- It is predisposed by (Virchow’s triad):
(1) […],
(2) […] ,
(3) […]

Fates of a Thrombi
- […]
- […]
- […]
- […]

A

Thrombus is an intravascular mass formed during life from constituents of blood
- Thrombosis is the process in which a thrombus is formed
- It is predisposed by (Virchow’s triad):
(1) Endothelial injuries,
(2) Stasis or turbulence of blood flow ,
(3) Hypercoagulable states

Fates of a Thrombi
- resolution / lysis (yay!)
- Propagation
- organisation & recanalisation (this is still ok)
- **embolism (this is really bad) **

26
Q
A
27
Q

What are the definitions of

Thrombus
[…]

Thrombosis
[…]

A

What are the definitions of

Thrombus
an intravascular mass formed during life from constituents of blood

Thrombosis
process in which thrombus is formed