Cell Pathology Flashcards

Question 1

Q

Principles of tumours

What is Neoplasia?

*LOB: Compare and contrast benign and malignant tumours, and understand that malignancy (cancer) is defined by invasive growth and metastatic potential.

Answer

A

State of autonomous cell division
An abnormal mass of tissue which shows uncoordinated growth and serves no useful purpose

They are clonal- originating from a single cell which has acquired genetics mutations

may be benign or malignant

Question 2

Q

Principles of tumours

What are the features of a benign neoplasm?

*LOB: Compare and contrast benign and malignant tumours, and understand that malignancy (cancer) is defined by invasive growth and metastatic potential.

Answer

A

Slower growing
well circumscribed
often encapsulated
not locally invasive growth
no metastatic potential

Question 3

Q

Principles of tumours

What are the features of a malignant neoplasm?

*LOB: Compare and contrast benign and malignant tumours, and understand that malignancy (cancer) is defined by invasive growth and metastatic potential.

Answer

A

faster growing
poorly circumscribed
non-encapsulated
locally invasive growth
metastatic potential

Question 4

Q

Principles of tumours

What are the microscopic features of a malignant neoplasm?

*LOB: Compare and contrast benign and malignant tumours, and understand that malignancy (cancer) is defined by invasive growth and metastatic potential.

Answer

A

may or may not closely resemble cell of origin - variable differentiation
many mitoses
high nuclear:cytoplasmic ratio
cells and uclei vary in shape and size (pleomorphism)

Question 5

Q

Principles of tumours

What are the microscopic features of a benign neoplasm?

*LOB: Compare and contrast benign and malignant tumours, and understand that malignancy (cancer) is defined by invasive growth and metastatic potential.

Answer

A

vary closely resembles cell of origin- very well differentiated
few mitoses
normal nuclear:cytoplasmic ratio
cells are uniform throughout the tumour

Question 6

Q

Principles of tumours

What is tumour grade?

*LOB: Define tumour grade and stage and explain how they differ from one another, giving examples of grading and staging systems used in clinical practice

Answer

A

Grade reflects how closely the cancer resembles the normal tissue

Well differentiated = cells resemble normal
Poorly differentiated = cells do not resemble normal

GRADE= aggressiveness

Question 7

Q

Principles of tumours

Examples of tumour grading

*LOB: Define tumour grade and stage and explain how they differ from one another, giving examples of grading and staging systems used in clinical practice

Answer

A

Grade 1= well differentiated, less aggressive
Grade 2= moderately differentiated.
Grade 3= poorly differentiated, more aggressive.

Question 8

Q

Principles of tumours

What is tumour staging?

*LOB: Define tumour grade and stage and explain how they differ from one another, giving examples of grading and staging systems used in clinical practice

Answer

A

Malignant tumours are staged
Used to determine how much cancer there is and where it is located- spread

most important prognostic factor and helps to plan most appropriate treatment

Question 9

Q

Principles of tumours

What is TMN?

*LOB: Define tumour grade and stage and explain how they differ from one another, giving examples of grading and staging systems used in clinical practice

Answer

A

T- Tumour spread
N- regional lymph node metastases
M- presence of distant metastases

When combined they give an overall ‘stage’ assigned
I,II,III,IV= 1 least to IV most advanced.

Question 10

Q

Principles of tumours

What is epithelial Dysplasia

*LOB: Define dysplasia and explain the concept of premalignancy (precancer), recognising that carcinoma in situ is a synonym for severe dysplasia

Answer

A

a pre-maligant condition
characterised microscopically by varying degrees of decreased differentiation, more mitoses, cellular/ nuclear pleomorphism

Dysplasia is classified according to the severity of changes seen of histology
normal, mild, moderate, severe or low/high grade

Question 11

Q

Principles of tumours

Dysplasia and carcinoma in situ

*LOB: Define dysplasia and explain the concept of premalignancy (precancer), recognising that carcinoma in situ is a synonym for severe dysplasia

Answer

A

Carcinoma in situ- is a severe dysplasia at certain anatomical sites

Think: Cancer that hasnt moved

they have not yet invaded the basement membrane

Question 12

Q

Principles of tumours

Why is basement membrane invasion important?

*LOB;Define dysplasia and explain the concept of premalignancy (precancer), recognising that carcinoma in situ is a synonym for severe dysplasia

Answer

A

Dysplasia and carcinoma in situ havent invaded- this is precancerous
It does not have access to potential routes to metastasis such as blood vessels and lymph

This is sometimes called “pre-cancer”

Question 13

Q

Principles of tumours

Other premalignancies

*LOB: Give examples of the different terminology used for premalignancy in different anatomical sites

Answer

A

Cervical Intraepithelial Neoplasia (CIN):
Ductal Carcinoma in Situ (DCIS):
**Lobular Carcinoma in Situ (LCIS): **
Actinic Keratosis: solar keratosis,often caused by sun exposure
Lentigo MalignaA type of melanoma in situ,
Barrett’s Esophagus: A condition where the normal squamous epithelium of the esophagus is replaced by columnar epithelium
Adenomatous Polyps: These are premalignant growths classified as tubular, villous, or tubulovillous.
Endometrial Hyperplasia: abnormal thickening of the endometrium
Prostatic Intraepithelial Neoplasia (PIN): The presence of abnormal cells in the lining of the prostate ducts
Leukoplakia: A white patch in the mouth that can become cancerous, often associated with tobacco use.
Erythroplakia: A red patch in the oral cavity with a higher malignant potential than leukoplakia.

Question 14

Q

Principles of tumours

Why is identifying pre-cancer important?

*LOB: Explain why it is preferable to treat a patient with precancer rather than cancer and outline how this forms part of the rationale for the breast, cervical and bowel cancer screening programmes

Question 15

Q

Principles of tumours

Carcinoma histological types

*LOB: Recall that the most common histological types of cancers in adults are carcinoma, melanoma and lymphoma/leukaemia. Recall that germ cell tumours, sarcomas and central nervous system tumours are less common types of cancer.

Answer

A

Origin: Epithelial cells (lining of organs and tissues).
Subtypes:
Adenocarcinoma (e.g., breast, prostate, colon).
Squamous cell carcinoma (e.g., skin, lung, esophagus).
Transitional cell carcinoma (e.g., bladder).

Question 16

Q

Principles of tumours

Melanoma histological types

*LOB: Recall that the most common histological types of cancers in adults are carcinoma, melanoma and lymphoma/leukaemia. Recall that germ cell tumours, sarcomas and central nervous system tumours are less common types of cancer.

Answer

A

Origin: Melanocytes (cells that produce pigment in the skin).
Locations: Skin, eyes, mucous membranes.

Question 17

Q

Principles of tumours

Lymphoma/Leukemia: histological types

*LOB: Recall that the most common histological types of cancers in adults are carcinoma, melanoma and lymphoma/leukaemia. Recall that germ cell tumours, sarcomas and central nervous system tumours are less common types of cancer.

Answer

A

Lymphoma: Cancer of the lymphatic system (e.g., Hodgkin’s lymphoma, non-Hodgkin’s lymphoma).

Leukemia: Cancer of blood-forming tissues (e.g., bone marrow), leading to the overproduction of abnormal white blood cells.
Subtypes: Acute and chronic forms of lymphocytic and myeloid leukemia.

Question 18

Q

Principles of tumours

Germ Cell histological types

*LOB: Recall that the most common histological types of cancers in adults are carcinoma, melanoma and lymphoma/leukaemia. Recall that germ cell tumours, sarcomas and central nervous system tumours are less common types of cancer.

Answer

A

Origin: Germ cells (cells that develop into sperm or eggs).
Common Locations: Testes, ovaries.
Examples: Seminoma, non-seminomatous germ cell tumors.

Question 19

Q

Principles of tumours

Sarcomas histological types

*LOB: Recall that the most common histological types of cancers in adults are carcinoma, melanoma and lymphoma/leukaemia. Recall that germ cell tumours, sarcomas and central nervous system tumours are less common types of cancer.

Answer

A

Origin: Mesenchymal tissue (connective tissues like bone, muscle, fat).
Examples: Osteosarcoma (bone), liposarcoma (fat), rhabdomyosarcoma (muscle).

Question 20

Q

Principles of tumours

Central Nervous System (CNS) Tumors: histological types

*LOB: Recall that the most common histological types of cancers in adults are carcinoma, melanoma and lymphoma/leukaemia. Recall that germ cell tumours, sarcomas and central nervous system tumours are less common types of cancer.

Answer

A

Origin: Brain and spinal cord tissue.
Examples: Gliomas (including glioblastoma), meningiomas, medulloblastoma.

Question 21

Q

Breast Pathology

Breast lumps undergo triple assessment… why?

*LOB: Describe the ‘triple assessment’ approach to investigation of a breast lump

Answer

A

Clinical
– Radiological (mammography, ultrasound)
– Pathological (Needle test – either FNA cytology or core biopsy (or both)

pre-operative diagnostic accuracy is approximately 99%

Question 22

Q

Breast Pathology

Common Breast Lump Diagnoses

*LOB: Describe the ‘triple assessment’ approach to investigation of a breast lump

Answer

A

Young
1. Fibroadenoma
2. Fibrocystic change
3. Carcinoma

Old
1. Carcinoma
2. Fibroadenoma
3. Fibrocystic Change

Question 23

Q

Breast Pathology

How are FNA and core biopsies reported?

*LOB: Describe the ‘triple assessment’ approach to investigation of a breast lump

Answer

A

C= FNA cytology / B= Biopsy

C1/B1 = inadequeate or not diagnositc
C2/B2 = Benign (confidently say not (pre) malignant)
C3/B3 = equivocal, favour benign
C4/B4 = equivocal, favour malignant
C5/B5= malignant

Question 24

Q

Breast Pathology

What is fibrocystic change?

*LOB: Describe the pathology of fibrocystic change and fibroadenoma

Answer

A

variety of benign non-neoplastic changes
Seen 25-45 years old
Changes affect the TDLU with fibrosis and cysts

clinical breast pain, tenderness, lumpy (esp during 2nd half cycle)

Tx reassure, analgesic, cyst aspiration, exicision

TDLU (terminal duct lobular unit) functional unit of breast w acini duct

Question 25

Q

Breast Pathology

What is fibroadenoma?

*LOB: Describe the pathology of fibrocystic change and fibroadenoma

Answer

A

commonest benign tumour of breast
women < 30 y.o
clinical firm mobile painless lump

Pathology well circumscribed tumour composed of well differentiated glands connective tissue stroma

Tx observe or excise

Question 26

Q

Breast Pathology

What is fibrocystic change?

*LOB: Describe the pathology of fibrocystic change and fibroadenoma

Answer

A

variety of benign non-neoplastic changes
Seen 25-45 years old
Changes affect the TDLU with fibrosis and cysts

clinical breast pain, tenderness, lumpy (esp during 2nd half cycle)

Tx reassure, analgesic, cyst aspiration, exicision

TDLU (terminal duct lobular unit) functional unit of breast w acini duct

Question 27

Q

Breast Pathology

How is a sentinel node identified?

*LOB: Explain the concept of the ‘sentinel’ node in breast cancer and indicate how the status of the axillary sentinel node affects the management of the axilla and the patient’s prognosis

Answer

A

Dye and isotope (Technetium-99m) technique
One or several nodes may have taken up the dye and radioactive tracer (the ‘sentinel nodes’)
The nodes are removed and submitted to the pathologist for examination

Tumour present
A level I, II and III axillary clearance

Question 28

Q

Breast Pathology

The Wide Local Excision Specimen

*LOB: Explain the concept of the ‘sentinel’ node in breast cancer and indicate how the status of the axillary sentinel node affects the management of the axilla and the patient’s prognosis

Answer

A

The wide local excision specimen contains a 17mm grade 3 invasive ductal carcinoma. The tumour is completely excised: the closest margin to the tumour is 2mm posteriorly. The sentinel node is negative for malignancy’

* Invasive ductal carcinoma
* What does grade 3 tell us and why is it important?
– it is a poorly differentiated tumour ie. highly aggressive behaviour
* Why is the 17mm tumour size important?
– the size of the primary tumour determines the ‘T’ stage (T1c) in TNM
* Why is the negative sentinel node important?
– Mrs Patel does not require an axillary clearance
– the node status is N0 in TNM

Question 29

Q

Breast Pathology

What are important risk factors for breast cancer?

*LOB: Describe important risk factors for developing breast cancer

Answer

A

lifetime oestrogen exposure (breast cancer is hormone-driven):
– female sex
– ↑age (rare before 40)
– early menarche, late menopause
– long term oral contraceptive pill
– HRT >10 years
– obesity – peripheral aromatisation of androgens to oestrogens
* family history. 5-10% of breast cancers are familial
– germline BRCA1 and BRCA2 (both tumour suppressor genes) mutations
– both inherited in an autosomal dominant fashion
– women with mutations in these genes have a lifetime risk of breast cancer up to 85%
– germ-line mutations in other high risk genes such as TP53 and PTEN are less common

Question 30

Q

Breast Pathology

Most common invasive breast cancer

*LOB: Identify the most common and second most common types of invasive breast cancer to be invasive ductal carcinoma and invasive lobular carcinoma respectively

Answer

A

Invasive Ductal Carcinoma (IDC): This is the most common type of invasive breast cancer, accounting for about 70-80% of all cases. IDC begins in the milk ducts and invades the surrounding breast tissue. It can spread (metastasize) to other parts of the body if not treated.

Invasive Lobular Carcinoma (ILC): This is the second most common type, making up about 10-15% of invasive breast cancers. ILC starts in the milk-producing lobules and can also invade surrounding breast tissue and spread to other areas of the body.

Question 31

Q

Breast Pathology

How does ER affect cancer Tx?

*LOB: Describe the important prognostic factors for invasive breast cancer (tumour grade, stage, ER status and HER2 status, completeness of excision)

Answer

A

Oestrogen receptor (ER) expression by breast carcinomas correlates with aggressiveness and predicts response to therapy:

– ER positive tumours
* tend to be lower grade and less aggressive
* likely to respond to hormonal therapy

– ER negative tumours
* tend to be higher grade and more aggressive
* unlikely to respond to hormonal therapy

Question 32

Q

Breast Pathology

How does HER2 affect cancer Tx?

*LOB: Describe the important prognostic factors for invasive breast cancer (tumour grade, stage, ER status and HER2 status, completeness of excision)

Answer

A

HER2 (c-erbB-2) is an oncogene
* HER2 over-expression by an invasive carcinoma is associated with:
– more aggressive behaviour ie. poorer prognosis
– good response to Herceptin (a monoclonal antibody against HER2 receptor)

Question 33

Q

Breast Pathology

What is DCIS?

*LOB: Explain how DCIS is a precursor (precancer) of invasive breast cancer and outline how its detection is a key aim of the breast screening programme

Answer

A

Ductal Carcinoma in Situ (DCIS)

abnormal cells are found in the lining of the breast milk ducts but have not spread beyond the ducts into the surrounding breast tissue

DCIS does not usually form a palpable mass so how is it detected? mammogram of microcalcifications

If left untreated, in about 20-30% of cases DCIS will
progress to cancer

DCIS is included in the ‘5’ reporting category but shouldnt be as no invasion.

Question 34

Q

Breast Pathology

What is Paget’s disease of the Nipple?

*LOB: Explain how DCIS is a precursor (precancer) of invasive breast cancer and outline how its detection is a key aim of the breast screening programme

Answer

A

a clinical appearance due to the presence of
DCIS cells in the epidermis ie. it is a manifestation of DCIS
* Although it is a manifestation of DCIS, in most cases there is also an
underlying invasive carcinoma

DCIS is included in the ‘5’ reporting category but shouldnt be as no invasion.

Question 35

Q

Cardiovascular

What is the difference between haemostasis and thrombosis?

*LOB: Compare and contrast haemostasis and thrombosis

Answer

A

Hameostasis
* formation of solid plug from blood
* coagulation cascade and fibirnolytic system

thrombosis
* inappropriate activation of haemostasis-
* overwhelms the fibrinolytic and coagulation inhibitors

Question 36

Q

Cardiovascular

Quick Recap of the Haemostasis mechanism

*LOB: Compare and contrast haemostasis and thrombosis

Answer

A

1) Vessel wall injury
2) Adhesion and aggregation of platelets
3) Primary plug
4) Exposure of tissue factors to initiate the coagulation cascade.
5) Broken down by the activation of the fibrinolytic system

Question 37

Q

Cardiovascular

What is a clot vs a thrombus?

*LOB: Compare and contrast haemostasis and thrombosis

Answer

A

Clot is without platelets and occurs in stationary blood such as after death or in a test tube.

Question 38

Q

Cardiovascular

What is Virchows triad?

*LOB: Explain the importance of Virchow triad and list its components

Answer

A

Endothelial Injury: atherosclerosis, vasculitis, trauma
Abnormal Flow: Turbulance and stasis
Hypercoagulability blood cell, alteration in coag factor

Arterial Thrombosis= Atherosclerosis,
Venous= stasis and hypercoag.

Question 39

Q

Cardiovascular

What is a clot vs a thrombus?

*LOB: Compare and contrast haemostasis and thrombosis

Answer

A

Clot is without platelets and occurs in stationary blood such as after death or in a test tube.

Question 40

Q

Cardiovascular

Define embolism

*LOB: Define embolism, list common types of emboli and describe how they may cause clinical effects

Answer

A

obstruction of an artery, typically by a clot of blood

Thromboembolism from the venous system will occlude pulmonary artery
Thromboembolism from the arterial system/ LH heart will occlude systemic artery

Question 41

Q

Cardiovascular

Types of emboli

*LOB: Define embolism, list common types of emboli and describe how they may cause clinical effects

Answer

A

Thromboembolism
Stroke = cerebral artery
PE = pulmonary artery
MI= Coronary artery
Other systemic including bowel etc

Fat Embolism
After long bone fractures etc, respiratory distress neuro and petechial rash
Air Embolism Trauma, surgery, decompression
Amniotic Rapid CV collapse, DIC
Septic Infection (infective endocarditis) causes abscesses and infarction

Question 42

Q

Cardiovascular

What is the difference ischamia and infarction?

*LOB: Define ischaemia and infarction

Answer

A

A decrease in blood flow to a tissue, resulting in hypoxia, or insufficient oxygen.

Ischaemia partial and reversible damage
Infarction complete blockage with necrosis

Question 43

Q

Cardiovascular

What is the mechanism of stable angina?

*LOB: Explain the mechanism by which atherosclerosis causes disease using the example of gradual stenosis of a stable plaque - stable angina

Answer

A

Gradual enlargement of a stable atherosclerotic plaque
luminal stenosis

THINK= flow =radius^4

Results in mismatch of O2 demand and supply
Myocardial Ischamia
Cardiac type pain

On exertion, relieved by rest.

Question 44

Q

Cardiovascular

What is the mechanism of Myocardial Infarction?

*LOB: Explain the mechanism by which atherosclerosis causes disease using the example of rupture of a vulnerable plaque with occlusion at the site of rupture - myocardial infarction

Answer

A

Elevated troponin- damage molecule released

Sudden plaque disruption and thrombosis in a vulnerable plaque
OCCLUSION at the site

Repair results in scar formation which reduces electrical conductivity

Plaque rupture in the left anterior descending (LAD) artery can cause a ST-elevation myocardial infarction (STEMI),

Question 45

Q

Cardiovascular

Why do MI commonly occur in the LAD?

*LOB: Explain the mechanism by which atherosclerosis causes disease using the example of rupture of a vulnerable plaque with occlusion at the site of rupture - myocardial infarction

Answer

A

Has the poorest prognosis
Narrows towards the ventricle so smaller lumen- more likely to occlude.
Supplies oxygen to the SAN
So arrythmia can occur- systemic heart damage.

Question 46

Q

Cardiovascular

Ventricular Fibrilation

*LOB: Outline the important complications of myocardial infarction

Answer

A

Presents as cardiac arrest
K+ release from nectrotic myocytes which induce arrythmia in the hyper excitable tissue around the infarct
Inferior MI are more likely to be associated with arrythmia than other MIs

No the only arrythmia

Question 47

Q

Cardiovascular

Cardiac Tamponade

*LOB: Outline the important complications of myocardial infarction

Answer

A

blood accumulates in the pericardial sac after myocardial rupture (usually of the free wall of the left ventricle)

increased pressure compresses heart

CLINCAL Hypotension, distended neck veins, muffled heart sounds

Question 48

Q

Cardiovascular

Interventricular septum

*LOB: Outline the important complications of myocardial infarction

Answer

A

a connection between the right and left ventricles, resulting in a ventricular septal defect (VSD).

CLINICAL sudden heart failure with loud systolic murmur.
Left to right shunt so pulmonary hypertension

Question 49

Q

Cardiovascular

Mitral Regurgitation

*LOB: Outline the important complications of myocardial infarction

Answer

A

papillary muscle dysfunction or rupture, which impairs the function of the mitral valve,

CLINICAL pulmonary oedema, heart failure, systolic murmur

Question 50

Q

Cardiovascular

Mural Thrombus

*LOB: Outline the important complications of myocardial infarction

Answer

A

thrombus on the inner ventricular wall

CLINICAL stroke, renal infarction, peripheral ischaemia.

Question 51

Q

Cardiovascular

Pericarditis

*LOB: Outline the important complications of myocardial infarction

Answer

A

y: Inflammation of the pericardium can occur as a direct result of the infarct (acute pericarditis) or later as part of an autoimmune reaction known as Dressler’s syndrome (weeks to months post-MI).

Question 52

Q

Cardiovascular

Ventricular Aneurysm

*LOB: Outline the important complications of myocardial infarction

Answer

A

No the only arrythmia

Question 53

Q

Cardiovascular

Short Term MI complications

*LOB: Outline the important complications of myocardial infarction

Answer

A

arrythmia
cardiogenic shock
acute heart failure
papillary muscle rupture

Question 54

Q

Cardiovascular

Pulmonary Embolism

*LOB: Describe the aetiology and effects of medium-sized pulmonary emboli and understand the importance of venous thromboembolism prevention

Answer

A

Pulmonary emboli DVT particularly from the legs or pelvis.

VTE is both DVT and PE

A medium-sized PE blocks a moderate branch of the pulmonary artery, reducing blood flow to parts of the lung.
This causes hypoxia, increased pulmonary artery pressure, and strain on the right ventricle.

CLINICALshortness of breath, chest pain, tachycardia, and sometimes hemoptysis.

PREVENT compression stockings, mobilisation post surgery, anticoagulant therapy.

Question 55

Q

Cardiovascular

Ischaemic Stroke

*LOB: Explain the mechanism by which atherosclerosis causes disease using the example of rupture of a vulnerable plaque with embolism - ischaemic stroke

Answer

A

Sudden rupture of cerebral artery due to atherosclerosis
Embolism from a distant site.

Question 56

Q

Cardiovascular

AAA

*LOB: Explain the mechanism by which atherosclerosis causes disease using the example of aneurysm formation - abdominal aortic aneurysm

Answer

A

AAAs are usually asymptomatic until a complication occurs

Chronic inflammation and degradation of the vessel’s structural components (e.g., collagen and elastin) cause progressive dilation of the aortic wall, leading to an aneurysm.

As the aneurysm enlarges, it becomes more prone to rupture, which can cause life-threatening internal bleeding.

Rupture (retroperitoneal ‘leak’ or free rupture)

Question 57

Q

Cardiovascular 2

What is the spectrum of Ischaemic Heart Disease?

*LOB: Explain the concept of systemic hypertension and recall important causes of secondary hypertension

Question 58

Q

Cardiovascular 2

What is Hypertension?

*LOB: Explain the concept of systemic hypertension and recall important causes of secondary hypertension

Answer

A

Incidence of complications is proportional to the BP

BP above which treatment does good = 140/90

Essential / primary 95%
Secondary 5%

Question 59

Q

Cardiovascular 2

Causes of Secondary HTN

*LOB: Explain the concept of systemic hypertension and recall important causes of secondary hypertension

Answer

A

Cushing’s Syndrome
Acromegaly
Renal Artery Stenosis (RAAS activation)
Polycycstic Kidney Disease
Coarctation of the Aorta (ductus arteriosum) (High BP in upper body, poor in lower)

Question 60

Q

Cardiovascular 2

Effects of hypertension on vessels

*LOB: Describe the effects of systemic hypertension on blood vessels, the heart, kidney and brain

Answer

A

accelerates atherosclerosis and arteriosclerosis

Question 61

Q

Cardiovascular 2

What is hyaline arteriosclerosis?

*LOB: Describe the effects of systemic hypertension on blood vessels, the heart, kidney and brain

Answer

A

Hyaline most common- leakage of plasma across endothelium and excess ECM production -> hyaline change in wall

Increases rigidity so the arterial tree has less compliance
Reduces flow in affected vessel

Shifts the autoreg curve to the right so more susceptible to hypotension- why low BP shock elderly

Question 62

Q

Cardiovascular 2

Effects of hypertension on heart

*LOB: Describe the effects of systemic hypertension on blood vessels, the heart, kidney and brain

Answer

A

Accelerates coronary artery atherosclerosis

LV compensatory hypertrophy
increase in myocardium cell size
when fails, progressive left ventricular failure

A Fib
Thrombi may form in the atria, and these may embolise
Cardiac output may fall

Question 63

Q

Cardiovascular 2

Effects of hypertension on kidneys

*LOB: Describe the effects of systemic hypertension on blood vessels, the heart, kidney and brain

Answer

A

Progressive hyaline arteriosclerosis in the renal arterioles causes chronic and progressive renal ischaemia

Tubular atrophy
Intersisitial Fibrosis
Progressive Glomerular Scleorsis
Progressive CKD

Question 64

Q

Cardiovascular 2

Effects of hypertension on brain

*LOB: Describe the effects of systemic hypertension on blood vessels, the heart, kidney and brain

Answer

A

Intracerebral haemorrhage, which presents clinically as a stroke

the haemorrhage is due to rupture of tiny (~1mm diam) Charcot-Bouchard aneurysms which form in arterioles weakened by long-standing hypertension

Subarachnoid Haemorrhage
or Berry Aneurysms due to atherosclerosis in people with a congenital weakness in the media of cerebral vessels

Ischaemic (infarct-type) stroke (80%) occlusion of a cerebral artery by a thromboembolus

Answer 63

A

Mr Hughes, a 55yo man, presents to A&E with sudden onset of central chest pain. He describes it as a tearing pain between his shoulder blades
O/E HR 105bpm, BP 180/130mmHg, heart sounds are normal
ECG shows features of left ventricular hypertrophy. There is no ST depression or elevation

Answer 64

A

Tear in the intimate causing a split in the media.

True lumen is narrowed, false lumen fills with blood

Answer 65

A

What are the major risk factors for developing aortic dissection?
hypertension
connective tissue disorders resulting in an abnormal media eg. Marfan, Ehler-Danlos
pregnancy

Answer 66

A

Tear in the intimate causing a split in the media.

True lumen is narrowed, false lumen fills with blood

Answer 67

A

Type A involves the ascending aorta
Type B does not involve the ascending aorta

Answer 68

A

Rupture into pericardium (tamponade)
Rupture resulting in reduced flow/ occlusion of carotid artery (stroke)
Stretching of aortic valve.
*

Answer 69

A

2 cusps attatched by chordae tendinae to papillary muscle of left ventricle

Answer 70

A

Three semilunar cusps

Answer 71

A

Stenosis failure of valve to open- chronic development

Regurgitation failure to close- acute or chronic

Mitral Regurgitation
Mitral Stenosis
Aortic Regurgitation
Aortic Stenosis
Tricuspid Regurgitation
Tricuspid Stenosis
Pulmonary Regurgitation
Pulmonary Stenosis

Answer 72

A

age-related calcification of a tricuspid valve - the commonest cause in the UK
cusp calcification of a congenitally bicuspid valve
post-rheumatic fever (this is uncommon in the UK)

Blood flow into the aorta during systole is impeded
so LV must generate high pressure

Answer 73

A

Angina
Syncope on exertion
Heart failure

. The two options for valve intervention are conventional aortic valve replacement and transcatheter aortic valve implantation

Aortic stenosis is also an important cause of unexpected sudden death (arrhythmias)

Ejection systolic Murmur

Answer 74

A

infection of part of the endocardium, usually the endocardial surface of a valve

Due to highly pathogenic/normal valve or normally pathogenic/abnormal valve

**usually bacterial: **
Streptococci, usually S. viridans (40-50%) – weakly pathogenic
Staphylococci, eg. S. aureus (20-30%) – highly pathogenic
S. aureus is the most common cause of infection in iv drug users

less commonly fungi eg. Candida, Aspergillus

Answer 75

A

a thrombus containing microorganisms on the surface of a valve

As the organisms of Infective Endocarditis replicate they become enmeshed within layers of platelets and fibrin on the valve surface, forming vegetations

Answer 76

A

Blood cultures
3 sets of blood cultures from different sites, taken a minimum of 1 hour apart and before starting antibiotics
confirms the diagnosis and guides appropriate antibiotic therapy

Echocardiography
transoesophageal echocardiography toidentify vegetations and any complications

Answer 77

A

Damage to the mitral valve with development of regurgitation

Part of the vegetation has broken away from the valve to form an embolus

Formation of antigen-antibody immune complexes
the antigen is probably derived from the micro-organism and the antibody is produced by the body in response to it

If deposited in renal glomerulus, reduces flow - kidney injury

Answer 78

A

2nd most common valve lesion (after aortic stenosis

Mitral valve prolapse
There is accumulation of glycosaminoglycans in cusp tissue (‘myxomatous degeneration’) → the cusps become enlarged and one of the cusps ‘prolapses’ back into the LA during systole

Answer 79

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Acute Infective Endocarditis, post MI rupture

Answer 80

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syndrome which occurs when the pumping action of the heart is inadequate for the needs of the body

common: prevalence of 2-3% of population; ∼ 20% in 70-80 year olds
serious: mortality is 30% in the first year and 10% each year after

Answer 81

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a sudden major insult to the left side of the heart
no time for compensation
CO falls
Complication of MI in left ventrivle

CLINICAL Severe breathlessness due to pulmonary oedema, cardiogenic shock

sudden severe congestion in the pulmonary venous system and rapid accumulation of fluid in the alveolar spaces and interstitium
cardiogenic schok if underperfusion of organs

Answer 82

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to chronic left ventricular failure
chronic ischaemic heart disease (due to coronary artery atherosclerosis)
hypertension
valvular (mitral/aortic) heart disease
*

Answer 83

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ISAL = I See All Leads.

Inferior (II, III, avf)

Septal (V1,V2)

Anterior (V3,V4)

Lateral (V5,V6, I, avl)

OR LII LI SSAALL (Lilly Sal)

Answer 84

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Response to cellular injury
Aim to remove injurous agents, clear damaged tissue/ components, trigger healing
intended to be protective response but may be harmful when inappropriately activated.

Answer 85

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Acute inflammation – usually a transient phenomenon

cell injury + neutrophils + vascular changes

Chronic inflammation – a more persistent form of inflammation

persistent cell injury
+
lymphocytes, macrophages, plasma cells
+
fibrosis

Answer 86

A

Endogenous
Infectious agents such as viruses
Physical trauma

Endogenous
Autoimmune
Neoplasm

Answer 87

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heat (calor)
redness (rubor)
swelling (‘tumor’)
pain
loss of function

Neutrophils are the primary inflammatory cell

Parameter     | Value         | Reference Range
-------------------------------------------------
Hb            | 130g/L        | 12-16g/dL
MCV           | 84fL          | 78-97fL
WCC           | 15.5x10^9/L   | 4-11x10^9/L
Neutrophils   | 18.5x10^9/L   | 1.5-8.0x10^9/L
Lymphocytes   | 3.2x10^9/L    | 1.1-4x10^9/L
CRP           | 245mg/L       | 0-5mg/L

Answer 88

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Vascular changes:
* increased capillary permeability
* Arteriole dilation
* Expansion of capillary bed
* Venule dilation

Answer 89

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Fluid, fibrin and neutrophils
Part of swelling.

Fibrin acts as a solid scaffold for Neutrophils to move around the area of inflammation

Edema expands the extracellular matrix
Deposits of fibrin and plasma proteins

Answer 90

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CRP is an acute phase protein secreted by the liver
Bacterial infections are potent stimulators of acute phase protein production

Induced by IL-6
Acts as opsonin and complement activator

Answer 91

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Regeneration/ Resolution
Repair with scarring
Progression to chronic inflammation

Answer 92

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There is complete restoration of normal structure and function
Conditions which favour resolution:
limited tissue destruction without significant damage to the connective tissue framework
damaged cells are able to regenerate eg. epithelia

Answer 93

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SKIN GRAFT

Answer 94

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Fibrous scar formation

Organisation – the process by which the inflammatory exudate is replaced by granulation tissue

Granulation tissue - a fragile complex of proliferating interconnecting capillaries, fibroblasts and some macrophages

Scar formation - granulation tissue is replaced by a scar. The scar is laid down by fibroblasts. A scar is composed mainly of fibrous tissue. Collagen fibres are the main component of fibrous tissue.

Answer 95

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substantial tissue destruction leading to significant damage to the connective tissue framework
damaged cells are unable to regenerate eg. nerve, cardiac/skeletal muscle

BUT scar lacks specialised function- think ECG changes in scarred heart.

Answer 96

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Chronic inflammation is said to occur when inflammation persists for weeks, months or longer
Chronic inflammation is usually due to persistent injury
lymphocytes, macrophages and plasma cells are the main types
In chronic inflammation there is usually an attempt to heal by fibrosis (scarring)

Answer 97

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Three processes occur simultaneously:
persistent tissue injury and destruction at the surface
an on-going inflammatory response to limit the damage
the main inflammatory cells are macrophages, lymphocytes & plasma cells
attempts to organise and heal by fibrosis (scarring) at the base of the ulcer

Answer 98

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Granulomatous inflammation is a specific type of chronic inflammation
A granuloma is an aggregate of activated (epithelioid) macrophages
[-oid = resembles  ‘epithelioid’ = resemble epithelial cells]
infections eg. mycobacteria
sarcoidosis
Crohn’s disease

Answer 99

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the tissue maintains a cheese-like appearance.
tissue structure is destroyed.
Caseous necrosis is enclosed within a granuloma.
Caseous necrosis is most notably associated with tuberculoma. The dead tissue appears as a soft and white proteinaceous dead cell mass.

Answer 100

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Chronic inflammation is said to occur when inflammation persists for weeks, months or longer
Chronic inflammation is usually due to persistent injury
lymphocytes, macrophages and plasma cells are the main types
In chronic inflammation there is usually an attempt to heal by fibrosis (scarring)

Answer 101

A

arterial
Intimate layer
Modifiable risk
Smoking
Hypertension
Diabetes mellitus
Dyslipidaemia (abnormal lipoprotein levels ie. high ratio of LDL:HDL)

Answer 102

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Atherosclerosis shows the following features:
persistent injury - to the endothelium
chronic inflammatory cells - macrophages and lymphocytes
healing by fibrosis - collagenous cap

SO IT IS CHRONIC INFLAMMATORY

Answer 103

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immune response to M. Tuberculosis is the formation of an organized granuloma.
It consists mainly in the recruitment at the infectious stage of macrophages, highly differentiated cells such as multinucleated giant cells, epithelioid cells and Foamy cells, all these cells being surrounded by a rim of lymphocytes.
Although in the first instance the granuloma acts to constrain the infection, some bacilli can actually survive inside these structures for a long time in a dormant state.
For some reasons, which are still unclear, the bacilli will reactivate in 10% of the latently infected individuals, escape the granuloma and spread throughout the body

Answer 104

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Cortisol (from adrenal cortex): Regulates metabolism, immune response, and stress adaptation.
Aldosterone (from adrenal cortex): Maintains blood pressure by regulating sodium and potassium balance.
Growth Hormone (GH): Stimulates growth, metabolism, and tissue repair.
Thyroid Hormones (T3, T4): Regulate metabolic rate, heart rate, and temperature.
Prolactin: Promotes milk production in females.

Answer 105

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Hypothalmus releases:
GHRH (Growth Hormone-Releasing Hormone) stimulates the release of GH (Growth Hormone).
TRH (Thyrotropin-Releasing Hormone) stimulates the release of TSH (Thyroid-Stimulating Hormone).
CRH (Corticotropin-Releasing Hormone) stimulates the release of ACTH (Adrenocorticotropic Hormone).
The posterior pituitary releases hormones produced by the hypothalamus, such as:
ADH (Antidiuretic Hormone) for water balance.
Oxytocin for childbirth and lactation.

Answer 106

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Regulates stress response through CRH → ACTH → Cortisol.

Answer 107

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Regulates metabolism through TRH → TSH → Thyroid hormones (T3, T4).

Answer 108

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Regulates reproductive function through GnRH → LH & FSH → Estrogen, Progesterone, Testosterone.

Answer 109

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Cushings Syndrome
weight gain, hypertension, and diabetes.

Answer 110

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Addisons Disease

Cortisol deficiency causes fatigue, low blood pressure, and hyperpigmentation.

Answer 111

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Acromegaly
Excess GH leads to enlarged hands, feet, and facial features.

Answer 112

A

Hypothyroidism/Hyperthyroidism:
Metabolism and energy levels

Think SWEATING

Answer 113

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Diabetes Insipidus: ADH deficiency causes excessive urination and dehydration.

Answer 114

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Therapeutic administration of exogenous glucocorticoids (ie. iatrogenic)

A pituitary adenoma secreting ACTH is the commonest cause of endogenous Cushing’s syndrome
An adrenal adenoma secreting cortisol
Ectopic ACTH production.

Answer 115

A

Bilateral idiopathic adrenal hyperplasia (60-70% of cases)

An adrenal cortical adenoma which secretes aldosterone

Answer 116

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Excess aldosterone results in:
- excess Na+ reabsorption into blood
→ hypernatraemia
- excess K+ loss into urine
→ hypokalaemia

The excess Na+ retention results in excess H20 reabsorption
→ ↑ circulatory volume → ↑ CO → ↑ BP

Answer 117

A

Phaeochromocytoma is a tumour arising in the adrenal medulla.
The tumour cells secrete excessive amounts of catecholamines (usually adrenaline) which is not under negative feedback control

Answer 118

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Both MEN 1 and MEN 2 are inherited in an autosomal dominant fashion
MEN 2 is due to a germline mutation in the RET proto-oncogene and is characterised by:
parathyroid adenoma or hyperplasia
phaeochromocytoma
medullary carcinoma of thyroid (almost inevitable  prophylactic thyroidectomy)

MEN 1 is due to a germline mutation in the MEN1 tumour suppressor gene and is characterised by:
parathyroid adenoma or hyperplasia (usually the first to present, as hypercalcaemia)
gastroenteropancreatic endocrine tumours
pituitary adenomas

Patients and their relatives with MEN 1 or MEN 2 should be managed in specialised endocrine clinics with the help of a geneticist

Answer 119

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Used for diagnosing adrenal insufficiency by checking the adrenal response to ACTH.

Answer 120

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Assesses thyroid function by measuring the pituitary response to TRH.

Answer 121

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Synacthen (ACTH analog) is used to stimulate adrenal glands and measure cortisol production, diagnosing adrenal insufficiency.

Answer 122

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IGF-1 (Insulin-like Growth Factor 1): Elevated levels are the key marker for acromegaly, as IGF-1 reflects average GH levels over time.

Oral Glucose Tolerance Test (OGTT) with GH measurement: Normally, glucose suppresses GH levels. Failure to suppress GH after glucose ingestion is diagnostic of acromegaly

Answer 123

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Serum Cortisol: Low cortisol levels, particularly in the morning, are suggestive of adrenal insufficiency.
ACTH (Adrenocorticotropic Hormone) Levels: Elevated ACTH levels, along with low cortisol, confirm primary adrenal insufficiency.
Synacthen (ACTH Stimulation) Test: Measures cortisol response to synthetic ACTH. Failure to produce adequate cortisol confirms adrenal insufficiency.
Electrolytes: Low sodium and high potassium levels may indicate Addison’s disease.

Answer 124

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24-hour Urinary Free Cortisol: Elevated cortisol levels in a 24-hour urine collection are indicative of Cushing’s syndrome.
Dexamethasone Suppression Test: In Cushing’s syndrome, cortisol fails to suppress after dexamethasone administration.
Midnight Salivary Cortisol: Cortisol is normally low at midnight, but remains elevated in Cushing’s syndrome.
ACTH Levels: Can help differentiate between ACTH-dependent (e.g., Cushing’s disease) and ACTH-independent causes (e.g., adrenal tumors).

Answer 125

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Hypothyroidism: Low levels of free T4 and T3.
Hyperthyroidism: Elevated levels of free T4 and T3.

Thyroid Antibodies:Anti-TPO (Thyroid Peroxidase Antibody) and Anti-Tg (Thyroglobulin Antibody): Elevated in autoimmune thyroiditis (Hashimoto’s thyroiditis, Graves’ disease)

Answer 126

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Antinuclear Antibody (ANA): Used in screening for systemic autoimmune conditions like lupus.
Anti-dsDNA: Specific for systemic lupus erythematosus (SLE).
Anti-Sm, Anti-Ro, Anti-La: Used for various autoimmune conditions (e.g., Sjogren’s syndrome).
Rheumatoid Factor (RF) and Anti-CCP: Used in diagnosing rheumatoid arthritis.

Answer 127

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Serum and Urine Osmolality: Diabetes insipidus is characterized by low urine osmolality (diluted urine) and high serum osmolality (concentrated blood).
Water Deprivation Test: Failure to concentrate urine during water deprivation indicates diabetes insipidus.
Desmopressin (ADH) Response Test: Helps differentiate between central (responds to ADH) and nephrogenic (no response to ADH) diabetes insipidus.

Answer 128

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Serum Prolactin Levels: Elevated levels indicate hyperprolactinemia, which can be due to various causes (e.g., prolactinomas, medications, hypothyroidism).
TSH and Free T4: Hypothyroidism can cause elevated prolactin, so thyroid function tests are often done.
MRI of the Pituitary: Used to check for prolactin-secreting pituitary adenomas (prolactinoma).

Answer 129

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. 24-hour Urinary Free Cortisol (UFC)
Purpose: Measures the amount of free cortisol excreted in urine over 24 hours.
Use: This test helps assess whether cortisol is being overproduced. Elevated levels are suggestive of Cushing’s syndrome.
Inpatient Application: Patients may have multiple collections to improve diagnostic accuracy. It is particularly useful in inpatient settings for confirming cortisol excess.
2. Low-Dose Dexamethasone Suppression Test (LDDST)
Purpose: Assesses the response of cortisol to synthetic glucocorticoid (dexamethasone).
Procedure: Dexamethasone is administered, and cortisol levels are measured the following morning.
Use: In normal individuals, dexamethasone suppresses cortisol production. Failure to suppress cortisol indicates Cushing’s syndrome.
Inpatient Application: This test can be performed with close monitoring to assess cortisol suppression over time.
3. Midnight Plasma Cortisol
Purpose: Measures cortisol levels during the night when cortisol is normally at its lowest.
Use: Elevated midnight cortisol levels are highly suggestive of Cushing’s syndrome.
Inpatient Application: Inpatient settings are ideal for this test, as patients can be closely monitored and blood drawn precisely at midnight.
4. Midnight Salivary Cortisol
Purpose: A non-invasive test that measures cortisol levels in saliva at midnight.
Use: Like plasma cortisol, elevated levels at midnight indicate a loss of normal circadian rhythm, which is typical in Cushing’s syndrome.
Inpatient Application: Useful in inpatient care where compliance with timing can be closely ensured.
5. High-Dose Dexamethasone Suppression Test (HDDST)
Purpose: Differentiates between pituitary-dependent Cushing’s disease and other causes (e.g., ectopic ACTH production or adrenal tumors).
Procedure: A higher dose of dexamethasone is given, and cortisol levels are measured.
Use: Cortisol suppression after high-dose dexamethasone suggests a pituitary cause (Cushing’s disease). Lack of suppression suggests ectopic ACTH production or adrenal tumors.
Inpatient Application: This test is often performed under close supervision in an inpatient setting for accurate monitoring.
6. Plasma ACTH Levels
Purpose: Measures the level of ACTH in the blood to help differentiate between ACTH-dependent and ACTH-independent Cushing’s syndrome.
Use:
Low ACTH levels suggest an adrenal cause (ACTH-independent Cushing’s).
Normal or elevated ACTH levels indicate ACTH-dependent causes, such as a pituitary adenoma (Cushing’s disease) or ectopic ACTH production.
Inpatient Application: Frequent blood draws and precise timing of sample collection are often necessary, making it suitable for an inpatient setting.
7. CRH Stimulation Test
Purpose: Helps distinguish between pituitary and ectopic causes of ACTH production.
Procedure: CRH (Corticotropin-Releasing Hormone) is administered, and ACTH and cortisol levels are measured before and after.
Use: In Cushing’s disease (pituitary adenoma), ACTH and cortisol levels rise after CRH administration. In ectopic ACTH production, there is no response.
Inpatient Application: Inpatients are closely monitored during this test to manage any reactions and ensure accurate timing of sample collection.

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