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MRSC - Part B > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the pathology of AL amyloid?

A

clonal proliferation of plasma cells producing amyloidal monoclonal antibodies (soluble precursor to AL amyloid)

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2
Q

What is the pathology of AA amyloid?

A

macorphages producing interleukins stimulate hepatocytes to secrete serum amyloid protein A (a soluble precursor to AL amyloid)

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3
Q

Give examples in which AA Amyloid can occur?

A

It is an acute phase protein seen in
Rheumatoid arthritis
IBD
TB
Bronchiectasis
RCC

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4
Q

Clinical features of AL amyloidosis

A

Kidneys - protinuria and nephrotic syndrome
Heart - Restrictive cardiomyopathy and arrhythmias
Nervous system - Peripheral neuropathy, carpal tunnel, autonomic neuropathy (hypotension)
GI tract - malabsorption, obstruction, perforation
Periorbital purpura

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5
Q

Clinical features of AA amyloidosis

A

Hepatomegaly
Splenomegaly
Kidneys - proteinuria, nephrotic syndrome -> CKD

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6
Q

Which thyroid cancer is associated with amyloidosis and why?

A

Medullary
Amyloid is composed of calcitonin

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7
Q

What are starling’s forces?

A

Hydrostatic pressure = “push” force of fluid within the capillary
Oncotic pressure = “pull” force of plasma proteins causes water to move into capillary due to osmosis

In arteries - hydrostatic > oncotic, fluid moves out of capillaries
In veins - oncotic > hydrostatic, fluid moves into veins

Hypoalbuminaemia -> decreased oncotic pressure
Portal hypertension/right sided heart failure -> Increased hydrostatic pressure
There less fluid moves back into capillaries and collects in 3rd spaces.

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8
Q

What is the pathophysiology of atherosclerosis?

A

Endothelial dysfunction -> Migration of macrophages -> Formation of foam cells with lipid core

Migration of vascular smooth muscle cells forms fibrous cap

Cap rupture leads to thrombosis

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9
Q

Name some chemical mediators of inflammation

A

Vasoactive mediators: histamine/serotonin
Arachidonic acid derivatives: Prostaglandins
Cytokines: Interleukins/tumour necrosis factor
Platelet activating factor
Complement factors

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10
Q

What is the complement cascade?

A

Formation of membrane attack complex from proteins that binds to cell membrane and causes cell death by osmotic lysis.
Activated:
C3 coming into contact with micro-organisms
Classic antigen-antibody complex
Lectin pathway via mannose binding

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11
Q

Stages of inflammation

A
  1. Vasoconstriction
  2. Vasodilation
  3. Increased vascular permeability
  4. Migration of neutrophils to site
  5. Phagocytosis by neutrophils
  6. Resolution vs chronic inflammation
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12
Q

Definition of abscess

A

collection of pus surrounded by granulation/fibrous tissue

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13
Q

Definition of sinus

A

blind ended tract, lined by granulation tissue, that connects 2 epithelial surfaces

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14
Q

What is chronic inflammation?

A

prolonged inflammation with active inflammation, tissue injury and healing all happening at the same time.
characterised by cell types present such as macrophages, lymphocytes and plasma cells

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15
Q

Define granuloma

A

focal collection of activated epilthelioid macrophages at the site of persistent stimulus

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16
Q

Define granulomatous inflammation

A

Chronic inflammation characterised by macrophages and giant cells

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17
Q

Examples of granulomatous conditions

A

Caseating eg TB
Non caseating eg Sarcoidosis/Crohn’s disease

18
Q

What is the shelf life of red blood cells?

A

35 days when stored in the fridge

19
Q

Stages of fracture healing

A
  1. Haematoma formation
  2. Granulation tissue formation
  3. Bony callus formation
  4. Bone remodelling
20
Q

Stages of haemostasis

A
  1. Vasospasm
  2. Platelet plug
  3. Coagulation cascade
  4. Fibrin plug
21
Q

What is the histology seen in Hashimoto’s and Grave’s disease?

A

Hashimoto’s - intense lymphocytic infiltrate with acinar destruction and fibrosis
Grave’s - Diffuse hyperplasia with hypertrophy of follicular cells.

22
Q

Define disseminated intravascular coagulation

A

widespread activation of coagulation and consumption of coagulation factors and platelets, leading to bleeding

23
Q

Stages of wound healing (+ timeframe +cells involved)

A
  1. Haemostasis (mins to hours)
  2. Inflammation (days, neutrophils and macrophages)
  3. Proliferation (1-6 weeks, fibroblasts)
  4. Remodelling (6+ weeks, myofibroblasts)
24
Q

Definition of ARDS

A

Rapid onset of respiratory failure characterised by widespread inflammation

25
Q

What is the berlin criteria

A

Used in ARDS

Acute onset (<7 days)
Bilateral lung infiltrates
PaO2/FiO2 ratio <200mmHg
CPAP >5cm H20
No cardiac failure (PAWP <18mmHg)

26
Q

What is the monroe kelly doctrine

A

the volume of the brain, CSF and blood within the cranium is constant. The cranium is a rigid space therefore if one component increases, another must decrease or the ICP will increase.

27
Q

Define compartment syndrome

A

Increased interstitial pressure in osteofascial compartments resulting in microvascular compromise

-> reduced perfusion and tissue necrosis (muscle and nerves)

28
Q

What is the difference between spinal and neurogenic shock?

A

Spinal - flaccid paralysis, areflexia, and parasthesia associated with spinal cord injury, often temporary

Neurogenic shock - disruption to sympathetic innervation resulting in unopposed parasympathetic innervation -> bradycardia and hypotension due to decreased peripheral vascular resistance.

29
Q

Physiological consequences of hypothermia

A

Coagulopathy
Platelet dysfunction
Enzymatic dysfunction
Cardiac Arrhythmias
Increased affinity of O2 binding to Hb -> Hypoxia of tissues
Coma

30
Q

What 3 elements contribute to surgical infections?

A

Causative infectious agent
Susceptible host
Poorly perfused, closed space

31
Q

What are the cytological features of malignancy?

A

Abnormal/increased mitosis
Increased size of nucleus
Pleomorophism
Hyperchromatism
Increased nucleoli

32
Q

What are the histological features of malignancy?

A

Basement membrane involvement
Necrosis
Vascular/lymphatic invasion
Angiogenesis
Disruption of tissue architcture

33
Q

Features of class II and III shock

A

Class II (blood loss 15-30%) - HR >100, normal BP, UO 20-30 ml/hr, anxious and confused, CRT 2-3

Class III (blood loss 30-40%) - HR > 120, High BP, UO 5-10 ml/hr, confused and lethargic, CRT 3-4

34
Q

What is the pathophysiology of ARDS

A

It is rapid onset respiratory failure with widespread pulmonary infiltrates characterised with non cardiogenic oedema and results in hypoxaemia and decreased lung compliance.

Inflammatory response characterised by vascular endothelium and alveolar epithelium damage, oedema, surfactant deficiency and reduced compliance -> severe impairment of gas exchange.

3 stages: exudative, proliferative and fibrosis.

35
Q

What does CEPOD stand for

A

confidential enquiry into patient outcomes and death

36
Q

Management of ARDS

A

Treat underlying cause!

37
Q

What is ERAS?

A

Enhanced recovery after surgery

Early mobilisation
Early oral nutrition
Early removal of catheters and drains
Multimodal non opioid analgesia
Prevention of PONV

38
Q

What is the physiological response to fluid bolus?

A

Increased circulating volume ->
Increased venous return ->
Increased cardiac output ->
Increased tissue perfusion

Due to carotid and aortic arch baroreceptor response - When blood pressure increases, baroreceptors fire more, which signals the brain to decrease heart rate and increase vascular tone.

39
Q

How do arterial lines measure blood pressure?

A

Arterial catheter is connected to pressure transducer which converts the pressure changes to an electrical signal

40
Q

What is frank starling’s law?

A

The law states that when the volume of blood in the ventricles increases, the heart’s stroke volume also increases. This is because the cardiac muscle contracts with greater force when it’s stretched before contraction.

41
Q
A

MRSC - Part B (4 decks)

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