Pathology

Question 1

What is the pathology of AL amyloid?

Answer 1

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

Question 2

What is the pathology of AA amyloid?

Answer 2

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

Question 3

Give examples in which AA Amyloid can occur?

Answer 3

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

Question 4

Clinical features of AL amyloidosis

Answer 4

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

Question 5

Clinical features of AA amyloidosis

Answer 5

Hepatomegaly
Splenomegaly
Kidneys - proteinuria, nephrotic syndrome -> CKD

Question 6

Which thyroid cancer is associated with amyloidosis and why?

Answer 6

Medullary
Amyloid is composed of calcitonin

Question 7

What are starling’s forces?

Answer 7

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.

Question 8

What is the pathophysiology of atherosclerosis?

Answer 8

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

Question 9

Name some chemical mediators of inflammation

Answer 9

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

Question 10

What is the complement cascade?

Answer 10

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

Question 11

Stages of inflammation

Answer 11

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

Question 12

Definition of abscess

Answer 12

collection of pus surrounded by granulation/fibrous tissue

Question 13

Definition of sinus

Answer 13

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

Question 14

What is chronic inflammation?

Answer 14

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

Question 15

Define granuloma

Answer 15

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

Question 16

Define granulomatous inflammation

Answer 16

Chronic inflammation characterised by macrophages and giant cells

Question 17

Examples of granulomatous conditions

Answer 17

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

Question 18

What is the shelf life of red blood cells?

Answer 18

35 days when stored in the fridge

Question 19

Stages of fracture healing

Answer 19

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

Question 20

Stages of haemostasis

Answer 20

1. Vasospasm
2. Platelet plug
3. Coagulation cascade
4. Fibrin plug

Question 21

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

Answer 21

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

Question 22

Define disseminated intravascular coagulation

Answer 22

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

Question 23

Stages of wound healing (+ timeframe +cells involved)

Answer 23

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

Question 24

Definition of ARDS

Answer 24

Rapid onset of respiratory failure characterised by widespread inflammation

Question 25

What is the berlin criteria

Answer 25

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

Question 26

What is the monroe kelly doctrine

Answer 26

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.

Question 27

Define compartment syndrome

Answer 27

Increased interstitial pressure in osteofascial compartments resulting in microvascular compromise -> reduced perfusion and tissue necrosis (muscle and nerves)

Question 28

What is the difference between spinal and neurogenic shock?

Answer 28

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.

Question 29

Physiological consequences of hypothermia

Answer 29

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

Question 30

What 3 elements contribute to surgical infections?

Answer 30

Causative infectious agent Susceptible host Poorly perfused, closed space

Question 31

What are the cytological features of malignancy?

Answer 31

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

Question 32

What are the histological features of malignancy?

Answer 32

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

Question 33

Features of class II and III shock

Answer 33

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

Question 34

What is the pathophysiology of ARDS

Answer 34

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.

Question 35

What does CEPOD stand for

Answer 35

confidential enquiry into patient outcomes and death

Question 36

Management of ARDS

Answer 36

Treat underlying cause!

Question 37

What is ERAS?

Answer 37

Enhanced recovery after surgery Early mobilisation Early oral nutrition Early removal of catheters and drains Multimodal non opioid analgesia Prevention of PONV

Question 38

What is the physiological response to fluid bolus?

Answer 38

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.

Question 39

How do arterial lines measure blood pressure?

Answer 39

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

Question 40

What is frank starling's law?

Answer 40

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.