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MRCS Part B - Paul Edit > Pathology 3 Mo's Notes > Flashcards

Pathology 3 Mo's Notes Flashcards

1
Q

What are two causes of gallbladder adenocarcinoma?

A
  • Cholelithiasis; gall stones
  • Chronic cholecystitis
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2
Q

What are risk factors for gallbladder adenocarcinoma?

A

Modifiable
smoking
gall stones
obesity
Non-modifiable
age >70
female
family history
primary sclerosing cholangitis

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3
Q

Where does gall bladder adenocarcinoma spread to?

A

* Porta hepatis lymph nodes
* Liver (segment V)
* CBD
* Stomach
* Duodenum

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4
Q

What are three types of necrotising fasciitis?
What causes them?

A

*Type I (polymicrobial ie, more than one bacteria involved)
*Type II (haemolytic group A streptococcus, and/or staphylococci including methicillin-resistant strains/MRSA)
*Type III (gas gangrene eg, due to clostridium)

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5
Q

What are some common organisms associated with necrotising fasciitis?

A
  • Group A streptococcus (Strep. Pyogenes)
  • Staph. aureus
  • Clostridium perfringens
  • Bacteroides fragilis
  • MRSA
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6
Q

What are four differentials for hospital patient taking antibiotics with bloody diarrhoea?

A

* C difficile - pseudomembranous colitis
* Ischemic colitis
* Hospital acquired infective gastroenteritis, norovirus
* Inflammatory bowel disease

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7
Q

What is the pathogenesis of pseudomembranous colitis?

A

abx -> disruption of microbiota -> increase in C.diff -> release of toxins that disrupt epithelial function -> infiltration of neurophils from crypts -> produce mucopurulent pseuodmembranes

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8
Q

What is the appearence of the bowel in pseudomembranous colitis?

A

Yellow patches on the bowel

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9
Q

What is the classification for perforated diverticulitis? Describe it

A

0 = mild clinical - PO abx
1 = confined pericolic inflammation or phlegamon - abx +/- IR drainage
2 = Distant abscess - surgical drainage
3 = Purulent peritonitis - Hartman’s
4 = faecal peritonitis - Hartman’s

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10
Q

What is the pathogenesis of diverticulitis?

A

Congenital
Acquired

Low fibre diet
Elevated intraluminal pressure
Outpouchings of bowel at areas of weakness in the inner circular muscular layer (where NV penetrate)
This is weaker in the large bowel due to outer longitudinal layer forming the taeniae coli

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11
Q

What are five complications of diverticular disease?

A
  • Infections
  • Diverticulitis
  • Perforation, paracolic abscess, focal peritonitis
  • Fistula (colovesical, vaginocolic, ileocolic)
  • Bleeding
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12
Q

How to manage diverticulitis?

A

Conservative (for uncomplicated diverticulitis)
* Fluids
* NPO
* Antibiotics
* CT guided percutaneous drainage of collection should be considered
Surgery (perforations): staged procedure:
* Diverting colostomy
* Hartmann
* Resection anastomoses

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13
Q

Define an ulcer

A

An ulcer is a local defect of the mucous membrane or the skin due to gradual disintegration of the surface epithelial cells

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14
Q

What are three modifiable risk factors for peptic ulcer disease?

A
  • H-pylori infection
  • NSAIDs
  • Smoking
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15
Q

What is h.pylori?

A

Gram negative microaerophilic spiral bacteria found in the stomach

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16
Q

How does H. pylori survive in acidic stomach?

A

H. pylori survives in acidic conditions by producing urease, which catalyzes hydrolysis of urea to yield ammonia thus elevating the pH of its environment.

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17
Q

How does H. pylori cause gastritis?

A

H. pylori produce
proteases and
phospholipases
+
toxic ammonia produced from breakdown of urea
damage gastric mucosa and cause inflammation

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18
Q

What four mechanisms by which H-pylori can colonize the stomach?

A

1- Flagella, which allow the bacteria to be motile in viscous mucus
2- Urease, which generates ammonia from endogenous urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach
3- Adhesins, which enhance bacterial adherence to surface foveolar cells
4- Toxins, such as that encoded by cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development by poorly defined mechanisms

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19
Q

What 2 types of gastric cancer can be caused by h.pylori?

A
  • Adenocarcinoma
  • MALT (Mucosal associated lymphoid tissue tumor)
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20
Q

How to treat h.pylori?

A

7 days twice daily of
Full dose of PPI + metronidazole 400 mg + clarithromycin 250mg,

or

Full dose of PPI + amoxicillin 1g + clarithromycin 500mg

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21
Q

How do PPIs work?

A

PPI binds irreversibly to H+/K+ ATPase enzyme (proton pump) on gastric parietal cells and blocks secretion of H+, which combine with CI- in the stomach lumen to form HCL.

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22
Q

What is the function of HCL in the stomach?

A
  • Activate pepsinogen to pepsin which help in proteolysis
  • Antimicrobial
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23
Q

How can NSAIDs cause PUD?

A
  • Topical irritant effect on the epithelium
  • Impairment of the barrier properties of the mucosa
    * Suppression of gastric prostoglandin synthesis (inhibitors of cyclooxygenase)
  • Reduction of gastric mucosal blood flow
  • Interference with the repair of superficial injury
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24
Q

What are 3 causes of hypercalcemia?

A
  • Malignancy
  • Hyperparathyroidism (PTH adenoma)
  • Renal failure
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25
Q

What is frozen section?

A

It’s a pathological laboratory procedure to perform rapid microscopic analysis of a specimen.

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26
Q

Epithelium of gastric mucosa in antrum?

A

Simple columnar with mucosal and goblet cells

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27
Q

What are histological features of parathyroid adenoma?

A
  • Uniform, polygonal chief cells with small, centrally placed nuclei.
  • A few nests of larger oxyphil cells are present as well. Uncommonly, adenomas are composed entirely of this cell type (oxyphil adenomas).
  • A rim of compressed, non-neoplastic parathyroid tissue, generally separated by a fibrous capsule, is often visible at the edge of the adenoma
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28
Q

What is a common ectopic site for parathyroid glands? Why?

A

Superior mediastinum
thymus originates from the third branchial arch as does the inferior thyroid, drags it down

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29
Q

Briefly describe types of hyperparathyroidism

A

All have high PTH
1. Primary
Adenomas - high calcium, low phosphate
2. Secondary
Secondary to chronically low calcium - low or normal calcium, low vit d
3. Tertiary
Persistent hyperplasia of PTH - calcium high, phosphate low

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30
Q

What is the normal oesophageal lining?

A

Non keratinized stratified squamous epithelium

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31
Q

What is the stain used in immunohistochemistry?

A

Cytokeratin

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32
Q

What is the general outline for T in TMN?

A

Tis = high grade dysplasia
T1 = confined to submucosa or more superficial
T2 = into muscular layer
T3 = adventitia
T4 = into adjacent tissues/organs

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33
Q

What are some risk factors for gastric cancer?

A

modifiable
h.pylori
pernicious anaemia

non-modifiable
HNPCC
FAP

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34
Q

Describe the pathophysiology of gastric cancer

A

Normal mucosa → Chronic gastritis → Intestinal metaplasia → Dysplasia → Intramucosal carcinoma → Invasive gastric carcinoma

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35
Q

What is the WHO classification of gastric cancer? types

A
  1. tubular adenocarcinoma - most common
  2. papillary carcinoma
  3. mucinous adenocarcinoma
  4. Poorly cohesive carcinomas
  5. Mixed carcinoma
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36
Q

Borrmann classification system for gastric cancer?

A

Macroscopic appearance of the lesion:
* Polypoid growth
* Fungating growth
* Ulcerating growth
* Diffusely infiltrating growth (linitis plastica)

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37
Q

Which para-neoplastic conditions associated with gastric cancer?

A
  • Acanthosis nigricans
  • Dermatomyositis.
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38
Q

What are some complications from total gastrectomy? early/late

A

Early
* Anastomotic leak
* Pancreatitis
* Cholecystitis
* Hemorrhage
* Infection.

Late
* Dumping syndrome
* Vitamin B12 deficiency (lack of intrinsic factor)
* Metabolic bone disease
* Recurrence of malignancy

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39
Q

What is dumping syndrome? early/late

A

Loss of the reservoir function of the stomach (e.g. following gastrectomy) results in the rapid transit of highly osmotically active substances into the duodenum following meals

Early 30 minutes - increase in osmolaity = fluid shift = abdo pain, diarrhoea, tachycardia + hypotension

Late 2-3 hours - increase in cardonhydrate = high glucose = reactive hyperinsulinaemia = hypoglycaemia

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40
Q

What are haemorrhoids?

A

Swollen or inflamed perianal veins that make up the anal cushions

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41
Q

What is the pathogenesis of haemorrhoids?

A

prolonged/repeated downward stress due to straining during defecation causes loss of ligaments resulting in prolapse

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42
Q

Describe the pathogenesis of atherosclerosis

A
  1. endothelial injury - smoking, HTN, hyperlipidaemia
  2. endothelial dysfunction causing monocyte and macorphage recruitment and activation
  3. Fatty streak (atheroma) formation due to formation of foam cells (combination of macrophages and lipids)
  4. Fibroatheroma due to chonic inflammation - ECM desposition, collagen and smooth muscle proliferation
  5. Complicated lesion - surface defect with haematoma/thrombosis
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43
Q

What are some risk factors for atherosclerosis? modifiable/non-modifiable

A

Non-modifiable
* Genetic abnormalities
* Family History
* Increasing age
* Male gender

Modifiable
* Hyperlipidemia
* Hypertension
* Cigarette smoking
* Diabetes
* Inflammation

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44
Q

How is a thrombus formed?

A

Rupture of an atheromatous plaque
Exposure of collagen
Platelet activation - release ADP + thromboxane = further platelets and vasospasm
Collagen is activated leading to a growing thrombus

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45
Q

Mechanism of myocardial infarction?

A

Vascular obstruction
Anaeobic respiration = increase in lactic acid
Loss of contractility
Myocyte death by necrosis after 30 minutes

46
Q

What is malignant melanoma?

A

Malignant neoplasm of melanocytes (melanin producing cells), mainly arising in skin.

47
Q

What skin conditions associated with melanoma?

A
  • Albinism
  • Giant congenital pigmented naevus
  • Fitzpatrick skin type 1
  • Dysplastic naevus, multiple nevi
48
Q

Risk factors for malignant melanoma?

A
  • Immunocompromised patients
  • Past history of melanoma
  • Red hair, sun exposure
  • skin conditions
49
Q

What are some key features on a pathology report for malignant melanoma?

A
  • Size
  • Breslow thickness: measured in mm. From the top of stratum granulosum to the deepest point of tumour involvement
  • Depth of invasion (Clark’s levels)
  • Ulceration, mitoses, lymphovascular invasion
  • Immunohistochemistry staining
50
Q

What is the KI67 index?
What number indicates a poor prognosis?

A

cancer cells : normal cells
>10 is bad
10 - 2 is intermediate

51
Q

What are some poor prognostic factors for malignant melanoma?

A
  • Increased tumor thickness (Breslow thickness)
  • Increased depth of invasion
  • Type of melanoma: nodular, amelanotic melanoma
  • Presence of ulceration
  • Presence of lymphatic or perineural invasion
  • Presence of regional or distant metastasis
  • Male, old age
52
Q

How does Breslow thickness affect management?

A

<0.8 = no further Rx if no FHx and no Rfx
0.8 - 1 mm depth = 1cm margin
1- 2mm depth = 1 - 2 cm margin
>2mm depth = 2cm margin

+/- sentinel lymph node biopsy

53
Q

What are some types of malignant melanoma?
Which have the best and worst prognosis?

A

superficial spreading (best) 70%
nodular 20%
amelanotic (worst)
acral
mucosal
lentigo

54
Q

What tumour markers are used for malignant melanoma?

A

S100B
HMB45

55
Q

What genes are associated with malignant melanoma?

A

CDK2a
CDK4
BRCA2
BRAF
NF-1

56
Q

What is the five year prognosis for the stages of malignant melanoma?

A

1 90%
2 70%
3 50%
4 25%

57
Q

What is the surgical sieve?
VITAMINS

A

Vascular
Infection
Trauma
Autoimmune
Metabolic
Inflammatory
Neoplasia

58
Q

What is Virchow’s triad?

A
  • Hypercoagulable state
  • Venous stasis
  • Endothelial injury
59
Q

What is SIRS?

A

Systemic Inflammatory response syndrome

= 2 or more of
* Body temperature less than 36 °C (96.8 °F) or greater than 38 °C (100.4 °F)
* Heart rate greater than 90 bpm
* Tachypnea >20
* WCC <4 or >12
* Hyperglycemia
* Altered mental state

60
Q

Define ARDS

A

Diffuse alveolar damage and lung capillary endothelial injury
Acute, diffuse, inflammatory form of lung injury

61
Q

What are the differentials for BCC?

A
  • SCC
  • TB
  • Actinic keratosis
  • Seborrheic keratosis
  • Verruca vulgaris
62
Q

What is the natural history of BCC?

A
  • Indolent with slow progression
  • Locally destructive but limited potential to metastasize (never metastasize)
63
Q

What are the margins for BCC excision?

A

4mm for low risk
6mm for high risk (>2cm lesion, lymph nodes)

64
Q

What is the characteristic appearance of Reed-Sternberg cells?
What disease?

A

owl eye appearance - bilobed nucleus with prominent eosinophilic inclusion-like nucleoli
Hodgkin’s lymphoma

65
Q

Mechanism of lymphatic spread?

A

Malignant tumors release growth factors such as VEGF-C to induce lymphatic vessel expansion (lymph angiogenesis) in primary tumors and in draining sentinel LNs, thereby promoting LN metastasis

66
Q

What is sickle cell disease?

A

Autosomal recessive - ish
point mutation in beta haemoglobin
causes distortion of the shape of red cells results in stacking, reduced oxygen carrying capacity and increased coagulability

67
Q

What are four complications of sickle cell anaemia?

A
  • Vaso-occlusive crisis: triggered by infection, dehydration, acidosis, affecting the bones (painful bone crisis as in hand-foot syndrome), lungs (acute chest syndrome), brain (stroke and retinopathy), spleen (autosplenectomy)
  • Sequestration crisis: in children, massive entrapment of sickle cell in the spleen will lead to rapid splenic enlargement and hypovolemic shock
  • Aplastic crisis: due to infection of red cell progenitors by parvo-virus
  • Chronic tissue hypoxia: organ damage (spleen, heart, kidney, lungs)
  • Increased susceptibility of infection with encapsulated organisms
68
Q

How does anutosplenectomy occur in sickle cell disease?

A

sickled red cells are trapped in red pulp
results in chronic erythrostasis, splenic infarction, fibrosis and atrophy

69
Q

In what surgical conditions is sickle cell disease relevent?

A
  • Gall stones
  • Autosplenectomy
  • Avascular bone necrosis
  • Osteomyelitis
  • Pulmonary hypertension
  • Heart failure
70
Q

What are common organisms in infection post splenectomy?
Why?

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Neisseria meningitidis
    Encapsulated organisms
71
Q

What are the most common primary brain tumours in the elderly?
HG/LG

A

High-grade:
* Gliomas and glioblastoma multiforme.
* Medulloblastoma.

Low-grade:
* Meningiomas.
* Acoustic neuromas.
* Neurofibroma.
* Pituitary tumors.
* Pineal tumors.
* Craniopharyngiomas.

72
Q

How do brain tumours present?

A

Symptoms of SOL + raised ICP

  • Headache, which is typically worse in the mornings.
  • Nausea and vomiting.
  • Seizures.
  • Progressive focal neurological deficits, e.g. diplopia associated with a cranial nerve defect, visual field defects, neurological deficits affecting the upper and/or lower limb.
  • Cognitive or behavioral symptoms.
  • Symptoms relating to location of mass, for e.g. frontal lobe lesions associated with personality changes, disinhibition and parietal lobe lesions might be associated with dysarthria.
73
Q

What is the pathology? Describe it

A

Polycystic kidney disease
Enlargement of the kidney with multiple cyst formations

74
Q

What genes are associated with PKD? How are they inherited

A

PKD1 + 2
autosomal dominant

75
Q

describe the pathogenesis of cyst formation in ADPKD

A

hyperplasia of renal tubules
formation of saccular cysts that fill with fluid from glomerular filtrate
continued proliferation causes cysts to seperate
continue proliferation causes destruction of the cortex

76
Q

What organs in the abdomen are prone to cyst formation?

A
  • Liver
  • Ovaries
  • Pancreas
  • Spleen
77
Q

What are complications of PKD?

A
  • Renal failure
  • Infection
  • Hypertension
78
Q

What types of graft rejection are there?
Describe each; time. cause.

A

Hyperacute
minutes of clamp release
Due to pre formed antibodies* e.g. ABO mismatch, or IgG
Immediate loss of graft occurs

Acute
Days to weeks after surgery
Cell mediated = necrosis of parenchymal cells
Antibody mediated = necrosis of endothelial tissues (vasculitis like)
Rx = high dose IV steroids/IV Ig

Chronic
atherosclerosis + fibrosis results in atrophy

79
Q

What are risk factors for cryptorchidism?

A
  • Family history
  • Low birth weight, premature birth
  • High abdominal pressure (gastroschisis)
  • Down syndrome
80
Q

What are some complications of cryptorchidism?

A

Infertility, inguinal hernia, testicular torsion

81
Q

What types of testicuar tumours are there?

A

95% Germ cell
** Seminomatous tumors**
** Nonseminomatous tumors**

5% non germ cell
Embryonal carcinoma
Yolk sac (endodermal sinus) tumor
Choriocarcinoma
Teratoma
** Sex Cord-Stromal tumors**
o Leydig cell tumor
o Sertoli cell tumor

82
Q

What biological markers are used for testicular tumours?

A
  • bHCG
  • AFP
  • Lactate dehydrogenase
83
Q

When is bHCG raised in testicular tumours?

A

Seminomas 10% - these are 95% of all testicualar CA
NSGCT 60% - these are 5% of all testicular CA
Choriocarcinomas 100%

84
Q

How is LDH used in testicular tumours?

A

Monitor tumour volume, necrosis and response to oncology

85
Q

When is AFP raised in testicular tumours?

A

some NSGCTs but not in pure seminomas

86
Q

What is the most common testicular cancer in men aged 20 to 40?

A

Seminoma

87
Q

What is the most common testicular tumour in men aged over 60?

A

Non-Hodkin lymphoma

88
Q

What type of bony mets in prostate cancer?
Why?

A

Sclerotic
Due to increased ostoeblastic acitivity

89
Q

What is pus?

A

Pus is the product of acute inflammation composed of cellular and fluid, exudative phases.

90
Q

What type of stain for TB?

A

Ziehl–Neelsen stain

91
Q

What organisms cause osteomyelitis?
in sickle cell?

A

s.aureus
streptococcus
enterbacter
salmonella (sickle cell)

92
Q

What is the classification system for osteomyelitis?
Describe it

A

Cierny Classification
Anatomical Location
1. Medullary
2. Superficial
3. Localised
4. Diffuse
Host Type
A. Normal
B. Immunocomprimised
C. treatment is worse to patient than infection

93
Q

What are the 5 steps of pathogenesis of osteomyelitis?

A

1- Invasion and Inflammation
2- Suppuration
3- Necrosis (sequestration)
4- New bone formation
5- Resolution

Bacteria enter - express adhesins - further spread
Leads to devascularisation -necrosis + reabsorption - floating dead bone (squestrum) - reservoir for infection
An involucrum can also form, following the sequestrum formation, whereby the region becomes encased in a thick sheath of new periosteal bone.

94
Q

What is sequestrum?

A

Dead bone that has become separated during the process of necrosis from normal or sound bone. It is a reservoir of infection.

95
Q

What is involucrum?

A

Reactive woven or lamellar bone depositions forming a shell of living tissue around a sequestrum
Or Thick sheath of periosteal new bone surrounding a sequestrum.

96
Q

What is the management of osteomyelitis?

A

medical management of risk factors
cultures
IV abx - long term
surgical debridement

97
Q

What are some differential diagnosis for swollen knee?

A
  • OA and overuse syndrome
  • Septic arthritis, infections (gonorrhea, Lyme disease, TB, brucellosis)
  • Gout
  • Pseudogout (Ca+2 pyrophosphate deposition disease)
  • Hemarthrosis
  • Tumors
  • Trauma (ligamentous injury, fractures, patellar dislocation, meniscus injury, etc.)
  • Polyarthritis (RA, Reiter’s syndrome, Juvenile rheumatoid arthritis)
98
Q

Compare gout and pseudogout
crystal type, crystal shape, birefringence, site, radiography

A
99
Q

What are some complications of blood transfusion?

A
  • Acute hemolytic reactions
  • Febrile non- hemolytic transfusion reaction
  • Delayed hemolytic transfusion reactions
  • Transfusion related acute lung injury
100
Q

What is DIC?

A

It is a pathological consumptive coagulopathy due to activation of the coagulation and fibrinolytic systems, activation of the latter leads to formation of micro thrombi in many organs with the consumption of the clotting factors and platelets.

101
Q

What activates intrinsic and extrinsic pathways?
What measures them?

A
  • Intrinsic pathway is activated by vessel injury which will lead to activation of factor 12
  • Extrinsic pathway is activated by tissue thromboplastin released by the damaged cells
  • APTT tests for intrinsic pathway
  • PT tests for extrinsic pathway and the common pathway
102
Q

Briefly outline types of hypersensitivity reactions?
name, mediators, examples, time
ACID EGG T

A
103
Q

What are the stages of bone healing

A

1. Hematoma formation (mass of clotted blood) at fracture site.
Tissue in fracture site swells, very painful, obvious inflammation, and bone cells are dying.
2. Fibrocartilaginous callus develops over a 3 to 4-week period.
This process involves
* Capillary growth in the hematoma
* Phagocytic cells invading and cleaning-up debris in injury site
* Fibroblasts and osteoblasts migrating into site and beginning reconstruction of bone
Note that the fibrocartilaginous callus serves to splint the fracture.
3. Bony callus begins forming after 3 to 4 weeks after injury and is prominent 2 to 3 months following the injury. Continued migration and multiplying of osteoblasts and osteocytes result in the fibrocartilaginous callus turning into a bony callus.
4. Remodeling. Any excess material of the bony callus is removed and compact bone is laid down in order to reconstruct the shaft. Remodeling is the final stage.

104
Q

What is hepatitis c virus?

A

Is a single-stranded RNA virus from family flaviviruses

105
Q

What the presentation acute hepatitis?

A

Acute hepatitis presents as jaundice (mixed CB and UCB) with dark urine (due to CB), fever, malaise, nausea, and elevated liver enzymes (ALT > AST)

106
Q

What is hepatitis?

A

Is inflammation that disrupts hepatocytes and small bile ductules

107
Q

What is the pathological sequence in hepatitis c virus?

A
  1. Acute Hepatitis
  2. Chronic Hepatitis
  3. Liver cirrhosis & portal hypertension
  4. Liver cell failure
  5. HCC
108
Q

What are some causes of chronic liver failure?

A

chronic hepatitis B, chronic hepatitis C, nonalcoholic fatty liver disease, and alcoholic liver disease.

109
Q

What are some risk factors for hepatitis C?

A
  • Intravenous drug abuse
  • Multiple sex partners
  • Having had surgery within the last 6 months
  • Needle stick injury
  • Multiple contacts with an HCV-infected individual
  • Employment in the medical or dental field
110
Q

What is cirrhosis of the liver?

A

End-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes

111
Q

What are some clinical features and sequalae of liver cirrhosis?

A

Portal hypertension
o Ascites
o Congestive splenomegaly/hypersplenism
o Portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae)
o Hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)
Decreased detoxification
o Mental status changes, asterixis, and eventual coma (due to raised serum ammonia)
o Gynecomastia, spider angiomas and palmar erythema due to hyperestrinism
o Jaundice
Decreased protein synthesis
o Hypoalbuminemia and edema
o Coagulopathy due to decreased synthesis of clotting factors.
Hepatocellular carcinoma

MRCS Part B - Paul Edit (29 decks)

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