histo path Flashcards
1
Q
Neutrophils
A
Acute inflammation (sterile or non-sterile)
Raised due to corticosteroid use
2
Q
Macrophages
A
Late acute inflammation
Chronic inflammation (including granulomas e.g. Sarcoidosis)
3
Q
Lymphocytes
A
Chronic inflammation
Lymphoma (sheets of clonal cells ie. Identical)
4
Q
Plasma Cells
A
Chronic inflammation
Myeloma
5
Q
Eosinophils
A
Allergic reactions
Parasitic infections
Tumours e.g. Hodgkin’s disease
6
Q
Mast Cells
A
Allergic reactions
Parasitic infections
7
Q
Fontana stain :
A
+ve for melanin
identifying Capsule-Deficient Cryptococcus Neoformans and typical Cryptococcus Neoformans.
8
Q
Congo Red stain :
A
+ve for Amyloid (Apple green birefringence)
9
Q
Prussian Blue:
A
+ve for iron (haemochromatosis)
10
Q
Go-to stain for most histological samples is?
A
Hemotoxylin and Eosin (H&E).
11
Q
what happens to serum transferrin in iron def anaemia and why ?
A
Serum Transferrin increases in IDA, as the liver increases transferrin production to
bind to as much available iron it can to compensate for low iron levels
12
Q
Evolution of MI – Histological findings**:
A
Under 6 hours - normal by histology (CK-MB also normal)
6–24 hrs - loss of nuclei, homogenous cytoplasm, necrotic cell death
1-4 days - infiltration of polymorphs then macrophages (clear up debris)
5-10 days - removal of debris
1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
Weeks-months - strengthening, decellularising scar tissue.
13
Q
most common cause of RV failure
A
Most common cause is secondary to LVF but can be primarily caused by chronic severe pulmonary hypertension
most common cause of LVF is CAD
14
Q
what is dilated cardiomyopathy and is its mechanism of heart failure ?
A
dilated = too thin
systolic dysfunction
15
Q
restrictive cardiomyopathy what is it ?
A
too stiff
diastolic dysfunction
16
Q
Hypertrophic obstructive cardiomyopathy (HOCM) - what is it ?
A
– septal hypertrophy resulting in an outflow tract obstruction
17
Q
pathogensis of rheumatic fever ?
A
you get a strep throat infection usually 2-4 weeks before
cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens
18
Q
main pathogen of infection preceeding rheumatic fever ?
A
Lancefield group A strep is the main pathogen.
19
Q
what is criteria for rheumatic fever ?
A
Jones criteria
eviednce group A strep infection + 2 major criteria or 1 major + 2 minor criteria
Major criteria:
Carditis
Arthritis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules
Minor criteria:
Fever
Raised CRP/ESR
Migratory arthralgia
Prolonged PR
Prev. rheumatic fever
Malaise
Tachycardia
Evidence of GAS infection:
Positive throat culture
Elevate AsO
Recent scarlet fever
20
Q
rheumatic fever important histology to know
A
Histology: Beady fibrous vegetations (verrucae), Aschoff bodies (small giant-cell granulomas) and Anitschkov myocytes (regenerating myocytes).
21
Q
treatment for rheumatic fever ?
A
NSAIDs (e.g. ibuprofen) are helpful for treating joint pain
Aspirin and steroids are used to treat carditis
Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood.
Monitoring and management of complications
22
Q
in infective endocarditis, the Bacteraemia secondary to:
A
- Poor dental hygiene (Strep. Viridans)
- IVDU
- Soft tissue infection
- Dental treatments
- Cannulas/lines
- Cardiac and valvular surgery/pacemakers
- Previously damaged valve e.g. post-rheumatic fever
23
Q
difference between acute and subacute infective endocarditis ?
A
Acute:
- staph aureus / strep pyogenes
high virulence
vegetation is larger and more localised
spread is to the aorta
Subacute:
Strep. viridans, Staph. epidermis, HACEK* (culture -ve), Coxiella, Mycoplasma,candida
Low
Friable, soft thrombi. A few mm in size.
Chordae
24
Q
what valve in infective endocarditis ?
A
Usually mitral/aortic valve unless IVDU when right-sided valves involved.
25
what is the common cardiac murmur in infective endocarditis ?
New murmur (MR/AR usually)
26
what criteria for diagnosing infective endocarditis
Duke Criteria:
Major:
○ Positive blood culture growing typical IE organisms or 2 positive cultures >12hrs apart
○ Evidence of vegetation/abscess on echo or new regurgitant murmur
Minor:
○ Risk factor (e.g. prosthetic valve, IVDU, congenital valve abnormalities)
○ Fever >38
○ Thromboembolic phenomena
○ Immune phenomena
○ Positive blood cultures not meeting major criteria
Diagnosis:
● 2 major
● 1 major + 3 minor
● 5 minor
27
how to manage infective endocarditis ?
Treatment: Start with broad spectrum Abx once cultures taken. Then treat according to sensitivities.
Subacute: Benzylpenicillin + gentamicin; or vancomycin for 4 weeks.
Acute: Flucloxacillin for MSSA, rifampicin + vancomycin + gentamicin for MRSA. (S. aureus IE is very nasty so make sure there is cover for this).
28
give path, cause, and murmur for these valve diseases:
aortic stenosis
Narrowed aortic valve high velocity, high pressure flow
Calcification (old age), congenital bicuspid valve
Crescendo-decrescendo, radiates to carotids
29
give path, cause, and murmur for these valve diseases:
aortic regurg
Incompetent aortic valve blood flows back into LV after systole
Infective endocarditis, dissecting aortic aneurysm, LV dilation, connective tissue disease e.g. Marfans, Ank Spon
Early diastolic, with collapsing pulse
30
give path, cause, and murmur for these valve diseases:
mitral stenosis
Narrowed mitral valve high velocity, high pressure flow. Back pressure in left atrium dilatation
Rheumatic fever
Mid diastolic, opening click
31
give path, cause, and murmur for these valve diseases:
mitral regurg
Incompetent mitral valve blood flows back into left atrium during systole
Infective endocarditis, connective tissue disease, post-MI, rheumatic fever, left ventricular dilation (functional MR)
Pansystolic,Radiates to axilla
32
histology chronnic bronchitis
Dilatation of the airways, goblet cell hyperplasia and hypertrophy of mucous glands
33
histology of bronchiectasis
Permanent fibrotic dilatation of the bronchi
34
histology of asthma
SM cell hyperplasia, excess mucus (goblet cell hypertrophy), inflammation
Whorls of shed epithelium (Curschmann spirals), eosinophils, Charcot-Leyden crystals
35
histrology of emphysema
Loss of the alveolar parenchyma distal to the terminal bronchiole
36
what is Interstitial Lung Disease and how does it present ?
inflammation and fibrosis of pulmonary tissue - features of restrictive lung disease (FEV1/FVC > 70%)
chronic shortness of breath
fine end inspiratory crackles
ground glass / honeycomb appearance on CT CAP
causes can be: idiopathic pulmonary fibrosis, drug induced. sarcoid., eosinophillic, smoking related
37
outline stages of lobar pneumonia
Lobar pneumonia* – Fibrinosuppurative consolidation.
Stages:
1.Consolidation;
2. Red Hepatisation (neutrophilia);
3. Grey Hepatisation (Fibrosis);
4. Resolution
Typically high virulence organisms (Strep. Pneumoniae – rust coloured sputum)
38
which lung cancer has strongest correlation with smoking ?
squamous cell carcinoma
39
which lung cancer has associations with PTHrP secreion ?
squamous cell carcinoma
40
where in the lung is squamous cell carcinoma most commonly?
proximal bronchi (ie central)
41
what lung cancer is most common in women and non smokers?
adenocarcinoma
42
where in the lung do you find adenocarcinoma ?
peripherally
43
where do you find small cell carcinoma in the lung ?
proximal bronchi (central)
has a strong relationship to smoking
44
which lung cancer is associated with SIADH ?
small cell carcinoma
45
which lung cancer is associated with ectopic ACTH secretion ?
small cell carcinoma
46
flushing + diarrhoea + bronchoconstriction
carcinoid syndrome ( release of serotonin)
47
how to stage lung cancer ?
Staging – most important prognostic factor:
* Tumour (T1-4) – based on size and invasion of pleura, pericardium
* Lymph node metastasis (N0-2) - N0 – lymph node not involved by tumour, N1 or N2 - lymph nodes involved. 1 vs 2 depends on extent of involvement
* Distant metastasis (M0 or 1) - M1 – tumour has spread to distant sites
48
what is Mesothelioma:
Arise from either parietal or visceral pleura. It spreads widely within the pleural space and usually associated with extensive pleural effusion, chest pain and dyspnoea.
There is a long latent period of 25-45 years for development of asbestos-related mesothelioma.
49
"iron laden macrophages "
history for acute intra alevolar fluid
Pulomary oedema
50
CXR Findings in pulomary oedema
* CXR findings: Alveolar opacification (batwing appearance), Kerley B-lines, (cardiomegaly suggesting a cardiac cause), fluid in horizontal fissure.
51
Squamous cell
oesophageal carcinoma associated with....
alochol and smoking
52
signet ring cell carcinoma
gastric cancer
53
how does coeliac present ?
Symptoms (of malabsorption): Steatorrhoea, abdo pain, bloating, n&v, ↓wt, fatigue, IDA, failure to thrive, rash (dermatitis herpetiformis).
Also associated with hyposplenism so may need extra vaccines.
54
gold standard Ix for coeliac disease
Gold standard Ix: Upper GI endoscopy and duodenal biopsy (villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes) while eating gluten.
NB normal villous:crypt ratio is ~ 2:1.
55
gold standard Ix for hirschprung's disease
* Gold standard Ix: Full thickness biopsy – hypertrophied nerve fibres, no ganglia
56
what is Carcinoid Syndrome
* Diverse group of tumours of enterochromaffin cell origin, Produce 5-HT (serotonin)
* Commonly found in the bowel (but also lung, ovaries, testes)
* Usually slow growing
57
how are cancers of colon / rectum classified ? important histo risk factors ?
Classified based on architecture as tubular, tubulovillous or villous.
* Large size is most important risk factor for malignancy, in addition to degree of dysplasia and increased villous component.
58
what type of cancer is colorectal cancer ?
98% are adenocarcinoma, 45% in rectum
59
Familial adenomatous polyposis (FAP) - what is it?
1. 70% AD mutation in APC tumour suppressor gene (C5q1), 30% AR mutation in DNA mismatch repair genes.
2. Present 10-15yrs - >100 adenomatous polyps required for diagnosis, usually 100-1000s seen. ALL will → adenocarcinoma if left untreated by 30yrs therefore most have prophylactic colectomy.
3. Increased risk of neoplasia elsewhere, e.g.: ampulla of Vater and stomach
60
Cholecystokinin
responsible for stimulating digestion of fat and protein. Made by I-cells in the duodenum. Causes release of digestive enzymes
61
different endocrine function of the different cells of the pancreas
Alpha cells: glucagon increases blood glucose
Beta cells: insulin decreases blood glucose
Delta cells: somatostatin regulates the above cells
D1: a vasoactive peptide, stimulates the secretion of H20 into pancreatic system
PP: pancreatic polypeptide, self regulates secretion activities
62
scoring system for acute pancreatitis
Glasgow scale
63
causes of acute pancreatitis
‘I GET SMASHED’: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, Hyperlipidaemia, ERCP, Drugs e.g. thiazides
64
what bloods good to assess for pancreatitis
* NB: Amylase only transiently increased. Serum lipase is more sensitive.
65
marker for pancreatic cancer ?
CA19.9 >70IU/mL
66
what surgery for pancreatic cancer ?
Whipple’s procedure – surgical resection
67
Multiple Endocrine Neoplasia (MEN)**
go through the types
* MEN 1= ‘PPP’ - Parathyroid hyperplasia/adenoma, Pancreatic endocrine tumour (often phaeochromocytoma), Pituitary adenoma.
* MEN 2A- Parathyroid, Thyroid, Phaeochromocytoma
* MEN 2B- Medullary Thyroid, Phaeochromocytoma, Acoustic Neuroma. Marfanoid phenotype
68
outline the pathophysiology of liver injury
* A normal liver has hepatocytes with microvilli. Stellate cells which lie quiescent in the space of Disse (space between hepatocytes and sinusoid)
* Chronic inflammation causes the loss of microvilli and activation of stellate cells, which produce collagen.
* They become myofibroblasts that initiate fibrosis by deposition of collagen in the space of Disse.
* Myofibroblasts contract constricting sinusoids and increasing vascular resistance.
* Undamaged hepatocytes regenerate in nodules between fibrous septa
69
spotty necrosis
acute hepatitis
(small foci of inflammation and infiltrates)
70
causes of acute hepatitis
Acute Hepatitis
* Can either be caused by viruses (Hepatitis A to E) or by drugs
71
define liver cirrhosis
Diffuse abnormality of liver architecture that interferes with blood flow and liver function.
Histopathology of a cirrhotic liver:
Hepatocyte necrosis
Fibrosis
Nodules of regenerating hepatocytes
Disturbance of vascular architecture
72
The major causes of cirrhosis include:
1. Alcoholic liver disease
2. Non-alcoholic fatty liver disease
3. Chronic viral hepatitis (hep B+/-D and C)
4. Autoimmune hepatitis
5. Biliary causes: Primary biliary cirrhosis & Primary sclerosing cholangitis
6. Genetic causes:
a) Haemochromatosis- HFE gene Chr 6
b) Wilson’s disease- ATP7B gene Chr 13
c) Alpha 1 antitrypsin deficiency (A1AT)
d) Galactosaemia
e) Glycogen storage disease
7. Drugs e.g. methotrexate
73
size of regenerating nodules and are these 2 different types called and what can cause each ?
It can also be classified according to the size of the regenerating nodules into:
MICRONODULAR (nodules < 3mm) - uniform liver involvement
* Caused by: alcoholic hepatitis, biliary tract disease
MACRONODULAR (nodules > 3mm) - variable nodule size
* Caused by: viral hepatitis, Wilson’s disease, alpha1 antitrypsin deficiency
74
modified child's pugh score is for what?
predicts survival
75
microscopic characteristics of alcholic hepatitis
hepatocyte ballooning
mallory denk bodies
micronodular sclerosis
76
histology in primary billiary cholangitis
* Histology: bile duct loss with granulomas [HIGH YIELD]
77
which antibodies in primary biliary cholangitis ?
* Anti-mitochondrial antibodies in > 90% [HIGH YIELD]
78
which antibodies in primary sclerosing cholangitis
p-ANCA [HIGH YIELD]
79
onion skinning fibrosis
primary sclerosing cholangitis
80
USS and ERCP findings in primary sclerosing cholangitis
* US scan: bile duct dilatation
* ERCP: shows beading of bile ducts
81
inheritance of haemochromatosis ?
Autosomal recessive [HIGH YIELD]
82
inheritance of wilson's disease ?
Autosomal recessive [HIGH YIELD]
83
what stain in wilson's
Copper stains with Rhodanine stain
84
● Kayser Fleischer rings
wilson's disease
85
features pf haemochromatosis
● Skin bronzing (melanin deposition)
● Diabetes
● Hepatomegaly with micronodular cirrhosis
● Cardiomyopathy
● Hypogonadism
● Pseudogout
86
features of wilson's disease
● Liver disease: acute hepatitis, fulminant liver failure or cirrhosis
● Neuro disease: parkinsonism, psychosis, dementia (basal ganglia involvement)
● Kayser Fleischer rings: copper deposits in Descemet’s membrane in cornea
87
treatment for haemochromatosis
Venesection
Desferrioxamine
88
treatment for wilson's
Lifelong penicillamine.
Good prognosis with early treatment but any neuro damage is permanent and may require liver transplant.
89
what is Cholangiocarcinoma linked to ?
primary sclerosing cholangitis
90
whta is the MOST COMMON malignant liver lesion
secondary tumours
91
most common renal stone ?
o Calcium Oxalate
92
prostate cancer type most common in men over 50
* Adenocarcinoma is the commonest form in men over 50y.
92
grading for prostate cancer
Gleason score
* 1-5 based on differentiation (5 is worst – least differentiated and most aggressive)
* Take a biopsy and classify the most common pattern seen and the worst pattern seen
* Add these two numbers together to get a result out of 10
* Expressed as X+Y=Z
93
sx, histo, mx for benign prostatic hyperplasia
* Dihydrotestosterone-mediated hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large nodules
* Nodule formation compresses prostatic urethra leading to outflow tract obstruction
* Symptoms: difficulty urinating, retention, frequency, nocturia, overflow dribbling
* Histology: nodule formation, prostatic epithelial ducts with duct spaces
* Management: TURP, 5α reductase inhibitors, alpha blocker (tamsulosin, aware of BP effects)
93
staghorn calculi made from
o Magnesium Ammonium Phosphate
94
what is a blood marker used in prostate cancer
prostate specific antigen (PSA)
95
most common testicular tumours
Most testicular tumours are germ cell tumours – arising from germ cells in the testes. Commonly seen in men aged 20-45
intratubular germ cell neoplasia
96
different types of germ cell testicular tumours and which is most common
* Seminoma: most common type of germinal tumour. Peak age: 30s. Radiosensitive.
* Teratoma: occur at any age from infancy to adult life. Regarded as malignant when occurs in the post-pubertal male. Chemo sensitive. Biologic markers for germ cell tumours: AFP, HCG, and LDH
* Embryonal carcinoma – resembles embryonic tissue
* Yolk sac tumour
* Choriocarcinoma
97
type of non germ cell tumour testicular
Leydig cell tumour (derived from stroma), Sertoli cell tumour (derived from sex cord)
98
most common malignant renal cell carcinoma
clear cell
99
give both benign and malignant renal tumours
benign
1. papillary adenoma
2. oncocytoma
3. angiomyolipoma
malignant
1. renal cell carcinoma - clear cell / papillary / chromophobe
2. nephroblastoma / Wilm's tumour
3. transitional cell carcinoma
100
most common bladder cacner ?
transitional cell tumour
101
what type of bladder cancer more frequent in countries with endemic urinary schistosomiasis.
Squamous Cell Carcinoma:
102
list the nephrotic and nephritic syndromes
Nephrotic syndrome:
* Primary
o Minimal change disease
o Membranous glomerular disease
o Focal segmental glomerulosclerosis
* Secondary – e.g. Diabetes, amyloidosis, SLE
Nephritic syndrome:
* Acute post-infectious (aka Post-streptococcal)
* IgA nephropathy (aka Berger Disease)
* Rapidly progressive glomerulonephritis
* Alport’s syndrome (aka Hereditary nephritis)
* Thin basement membrane disease (aka Benign familial haematuria)
As a general rule, the glomerular vessels are very delicate and so deposition of immune complexes (which may release inflammatory substances and cause further damage) will reduce their function.
103
nephrotic syndrome triad
1. Proteinuria (>3g/24h / protein:creatinine ratio >300mg/mmol)
2. Hypoalbuminaemia (<30 g/L)
3. Oedema
104
periorbital swelling in children ?
minimal change disease
105
frothy urine is due to ?
proteinuria
106
why is it called minimal change disease ?
no changes under light microscope
but under electron microscope --> loss of podocyte foot processes
107
features of nephritic syndrome
Syndrome characterised by: PHAROH
* Proteinuria (less than nephrotic syndrome)
* Haematuria (coke-coloured urine)
* Azootemia – (high urea and creatinine)
* Red Cell Casts (in urine – these are red cells that have clumped together & have leaked out into the tubules)
* Oliguria
* Hypertension
108
muddy brown casts
acute tubular necrosis
109
time frame of post-strep glomerulonephritis and what organism? compare it to IgA nephropathy
Occurs 1-3 weeks after streptococcal throat infection or impetigo (usually Lancefield Group A beta-haemolytic strep = Strep. pyogenes).
* Presents 1-2 days (earlier than Acute postinfectious GN!) after an URTI with frank haematuria*
110
what is HEREDITARY NEPHRITIS (ALPORT’S SYNDROME)
* Hereditary glomerular disease caused by mutation in type IV collagen alpha 5 chain
* X linked
* Nephritic syndrome + sensorineural deafness + eye disorders (lens dislocation, cataracts)
* Presents at 5-20yrs with nephritic syndrome progressing to ESRF
111
differentials of asymptomatic haematuria in renal path
Asymptomatic Haematuria
If this appears in an SBA – the differentials include:
1. THIN BASEMENT MEMBRANE DISEASE (Benign familial haematuria)
2. IgA NEPHROPATHY (Berger disease)
3. ALPORT SYNDROME
IgA and Thin basement membrane are more common causes of asymptomatic haematuria than of nephritic syndrome. Differentiation between thin basement membrane and IgA is clinically difficult.
If there are no histological findings included in the questions clinical differences include IgA being more likely to cause frank haematuria, more likely to cause a change in renal function Cr raised) and slightly more common in the Asian population.
112
causes of acute tubular necrosis
Causes:
* Hypovolaemia → Pre-renal ARF → Ischaemia of nephrons (EMQ: cured hypovolaemia but persistent ARF).
* Nephrotoxins – drugs (aminoglycosides, NSAIDs), radiographic contrast agents, myoglobin (e.g. secondary to rhabdomyolysis), heavy metals
Damage to tubular epithelial cells → cells shed and block of tubules as casts → reduced flow and increased haemodynamic pressure in nephron → reduced pressure gradient across BM → acute renal failure → tubular glomerular feedback reduces blood supply to kidneys further.
Most common cause of acute renal failure
Histopathology: Necrosis of short segments of tubules
113
how does Thrombotic thrombocytopaenic purpura presetn ?
PENTAD:
* MAHA
* Thrombocytopenia
* Renal failure
* Fever
* Neurological Sx e.g. confusion, seizures
114
causes of acute renal failure
PRE-RENAL
* Most common cause of acute renal failure
* Caused by renal hypo-perfusion e.g. hypovolaemia, sepsis, burns, acute pancreatitis, and renal artery stenosis.
RENAL
* Acute Tubular Necrosis (ATN): commonest renal cause of ARF.
* Acute glomerulonephritis.
* Thrombotic microangiopathy.
POST-RENAL
* Obstruction to urine flow as a result of stones, tumours (primary & secondary), prostatic hypertrophy and retroperitoneal fibrosis
115
chronic kidney disease stages
1 Kidney damage with normal renal function (often proteinuria) >90
2 Mildly impaired 60-89
3 Moderately impaired 30-59
4 Severely impaired 15-29
5 Renal failure (generally requires replacement therapy) <15 (or if being treated with renal replacement therapy)
116
adult polycyctsic disease inheritance and which mutations
* Autosomal dominant inheritance. 85% due to mutations in PKD1 on chromosome 16 (encoding polycystin-1), 15% due to mutations in PKD2 on chromosome 4 (encoding polycystin-2)
117
‘wire loop capillaries’
lumpy-bumpy granular fashion
Lupus Nephritis
Depending on site and intensity of immune complex deposition clinical presentation may be: isolated urinary abnormalities, acute renal failure, nephrotic syndrome or progressive chronic renal failure.
Renal Histology: Immune complex deposition in capillaries ‘wire loop capillaries’, deposition of immune complexes & complement in the GBM in a lumpy-bumpy granular fashion.
Class 1: Minimal mesangial disease, looks near normal on light microscopy
Class 2: Mesangial proliferative disease
Class 3: Focal subendothelial deposits
Class 4: Diffuse subendothelial deposits
Class 5: Subepithelial immune deposits (membranous disease)
Class 6: Advanced sclerosis (>90%)*
118
define pelvic inflammatory disease
Pelvic Inflammatory Disease (PID / Salpingitis)
Infection ascending from vagina and cervix up to uterus and Fallopian tubes, leading to inflammation (endometritis, salpingitis) and the formation of adhesions.
119
causes of PID (give organisms as well)
* Ascending bacteria from lower genital tract - Neisseria gonorrhoea, Chlamydia trachomatis, enteric bacteria
* Secondary to abortion/termination of pregnancy – S. aureus, Streptococcus, C. perfringens, Coliforms
120
clinical features of PID
Clinically: bilateral lower abdo pain, deep dyspareunia, vaginal bleeding/discharge, fever, adnexal tenderness, and cervical excitation
121
violin-string” peri-hepatic adhesions
PID causing...
10% have Fitz Hugh Curtis syndrome – formation of scar tissue along liver capsule - RUQ pain from peri-hepatitis + “violin-string” peri-hepatic adhesions [BUZZWORD]
122
what is Fitz Hugh Curtis syndrome
* 10% have Fitz Hugh Curtis syndrome – formation of scar tissue along liver capsule - RUQ pain from peri-hepatitis + “violin-string” peri-hepatic adhesions [BUZZWORD]
123
complications of PID
Complications:
* 10% have Fitz Hugh Curtis syndrome – formation of scar tissue along liver capsule - RUQ pain from peri-hepatitis + “violin-string” peri-hepatic adhesions [BUZZWORD]
* Infertility
* ↑Risk of ectopic pregnancy
* Bacteraemia → SEPSIS
* Tubo-ovarian abscess
* Chronic PID
* Peritonitis
* Plical fusion – fimbrial ends of fallopian tubes adhere together
124
define endometriosis
Endometriosis
Presence of endometrial glands or stroma in abnormal locations outside the uterus e.g. ovaries, uterine ligaments, rectovaginal septum, Pouch of Douglas, pelvic peritoneum
125
clinical features of endometriosis
Clinically:
* Cyclical pelvic pain, dysmenorrhoea, deep dyspareunia, ↓fertility
* Cyclical PR bleeding, haematuria, bleeding from umbilicus (depending on site of endometrial deposits)
* Nodules/tenderness in vagina, posterior fornix or uterus; immobile and retroverted uterus in advanced disease
126
chocolate cysts
* Endometriomas = blood-filled “chocolate cysts” on ovaries [BUZZWORD]
127
powder burns
endometriosis
Macroscopically:
* Red-blue to brown vesicles - “powder burns” [BUZZWORD]
* Endometriomas = blood-filled “chocolate cysts” on ovaries [BUZZWORD]
`
128
bulky uterus
adenomyosis
Similar to endometriosis; presence of ectopic endometrial tissue deep within the myometrium
129
outline adenomyosis - presentation etc
Adenomyosis
Similar to endometriosis; presence of ectopic endometrial tissue deep within the myometrium
Clinically: heavy menstrual bleeding, dysmenorrhoea, and deep dyspareunia.
BUZZWORDS: “Bulky uterus”, “Subendothelial linear striations”, “Globular uterus”.
Complications:
* Malignant transformation
* Red degeneration during pregnancy
130
fibroids clinical presentation
Clinically:
* Heavy menstrual bleeding, dysmenorrhoea, pressure effects (urinary frequency, tenesmus)
* Subfertility
* In pregnancy: red degeneration of fibroids (haemorrhagic infarction → severe abdo pain), post-partum torsion
131
most common type of endometrial cancer
Postmenopausal bleeding is endometrial cancer until proven otherwise
Adenocarcinomas (85%), squamous cell carcinoma (15%)
132
Postmenopausal bleeding is ........ until proven otherwise
endometrial cancer
132
staging for endometrial cancer
Staged with FIGO system:
* Stage 1 – Cancer ONLY in uterus
* Stage 2 – spread to CERVIX
* Stage 3 – spread to PELVIC AREA
* Stage 4 – METASTASIS to rectum/bladder/distal organs
133
most common ovarian cyst ?
follicular cyst
* Due to non-rupture of the dominant follicle/failure of atresia in a non-dominant follicle
* Commonly regress after several menstrual cycles
134
most common type of ovarian carcinoma
– 90% are epithelial ovarian cancers
135
Histology: columnar epithelium, Psammoma bodies
in ovarian cancer
Serous cystadenoma (subtype of benign epithelial ovarian cancer)
136
Most common benign ovarian epithelial tumour
serous cystadenoma
137
Histology: mucin secreting cells [BUZZWORD]
in ovarian cancer
mucinous cystadenoma (subtype of benign epithelial ovarian cancer)
138
Histology: clear cells, clear cytoplasm, Hobnail appearance
in ovarian cancer
clear cell
139
Histology: tubular glands [BUZZWORD]
in ovarian cancer
endometrioid
140
Most common ovarian tumours in younger women (15-21 yo)
what are they and outline /.... .
Shows differentiation toward somatic structures
Mature teratomas (dermoid cyst) 95% of teratomas: Benign; usually cystic;
Differentiation of germ cells into mature tissues (e.g. skin, hair, teeth, bone, cartilage); usually bilateral and asymptomatic.
Immature teratomas:
Malignant, usually solid;
Contains immature, embryonal tissues
Secrete AFP
141
Histology: Call-Exner bodies [BUZZWORD]
in ovarian cancer
Granulosa-Theca cell tumour
(subset of sex cord/ stroma tumours )
Produce E2
Look for oestrogenic effects – irregular menstrual cycles, breast enlargement, endometrial/breast cancer
Histology: Call-Exner bodies [BUZZWORD]
142
Histology: Mucin producing signet ring cells [BUZZWORD]
in ovarian cancer
Krukenberg tumour
Malignancy of the ovary that has metastasised from usually gastric / colonic cancer
Histology: Mucin producing signet ring cells [BUZZWORD]
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how to stage ovarian cancer ?
FIGO staging
* Stage I: ONLY in ovaries
* Stage II: spread to PELVIS
* Stage III: spread to ABDOMEN (including regional LN metastases)
* Stage IV: METASTASIS outside abdominal cavity
The true abdominal cavity consists of the stomach, duodenum (first part), jejunum, ileum, liver, gallbladder, the tail of the pancreas, spleen, and the transverse colon
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Risk of malignancy index (RMI)
– scoring system used to estimate the likelihood of a malignant cyst – cut-off score 200:
RMI = U x M x Ca-125
U = Ultrasound
* 1 Point for each feature: multilocular, evidence of solid areas, evidence of metastases, ascited and bilateral lesions
* Overall ultrasound score summarised between 0 and 3 with 0=no ultrasound features, 1=1 ultrasound feature and 3=2-5 ultrasound features
M = Menopause
* 1 point for premenopausal
* 3 points for post-menopausal
Ca-125
* Measured in iu/ml
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outline normal histology of cervix and and how CIN can progress and where
Normal cervical histology:
Outer cervix (continuous with vagina) covered by squamous epithelium; endocervical canal lined by columnar glandular epithelium. The squamocolumnar junction (SCJ) separates them.
Transformation zone (TZ): the area where columnar epithelium transforms into squamous cells (=squamous metaplasia). This is a normal physiological process. This area is susceptible to malignant change due to high rates of cell turnover
CIN: Dysplasia at the TZ as a result of infection by HPV 16 & 18.
Graded mild, moderate or severe dyskaryosis on cytology, but graded CIN 1-3 on histology (from biopsy).
* CIN 1 = dysplasia confined to deepest 1/3 of epithelium
* CIN 2 = lower 2/3
* CIN 3 = full thickness, but basement membrane intact
60-90% of CIN 1 reverts to normal over 10-23 months
30% of CIN 3 progress to cervical cancer over 10 years if left untreated
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figo staging for cervical cacner
Staged using FIGO system
* Stage 0: CIN
* Stage I: ONLY
* Stage II: spread into UPPER 1/3 VAGINA
* Stage III: spread into PELVIC SIDE WALL and/or LOWER 1/3 VAGINA Stage IV: METASTASIS beyond pelvis to bladder/bowel
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CIN 1-3 on histology (from biopsy).
* CIN 1 = dysplasia confined to deepest 1/3 of epithelium
* CIN 2 = lower 2/3
* CIN 3 = full thickness, but basement membrane intact
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what separates endo cervix and ecto cervix ? Normal cervical
histology:
Outer cervix (continuous with vagina) covered by squamous epithelium; endocervical canal lined by columnar glandular epithelium. The squamocolumnar junction (SCJ) separates them.
Transformation zone (TZ): the area where columnar epithelium transforms into squamous cells (=squamous metaplasia). This is a normal physiological process. This area is susceptible to malignant change due to high rates of cell turnover
CIN: Dysplasia at the TZ as a result of infection by HPV 16 & 18.
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what is the triple assessment in breast
Triple assessment comprises:
1. Clinical Examination
2. Imaging – USS/mammography – decision based on density of breast tissue –dense=USS, less dense=mammography – general age cut-off 35
3. Cytology and histology –
* Cytopathology (obtained via fine needle aspiration (FNA)) – cells spread across a slide, stained and Coded from C1 (inadequate sample), C2 (benign), C3 (atypia), C4 (suspicious of malignancy) to C5 (malignant)
* Histopathology (obtained via core biopsy) – intact tissues removed showing architectural and cellular detail and coded B1 (normal), B2 (benign), B3 (uncertain), B4 (suspicious) to B5 (malignant). B5a = DCIS, B5b = invasive carcinoma
o NOTE: histopathology = gold-standard for diagnosis of breast cancer. Normal breast histology is a ductal-lobular system lined by inner glandular epithelium
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outline the non neoplastic breast conidtionns
Acute Mastitis**
* Presentation: painful, red breast, hot to touch and fever
* Either lactational (more common) or non-lactational
* Lactational is usually secondary to S. aureus infection (often polymicrobial) via cracks in the nipple & due to stasis of milk
* FNA cytology shows an abundance of neutrophils [BUZZWORD]
* Management: continued expression of milk + antibiotics +/- surgical drainage
* Non-lactational – keratinising squamous metaplasia block lactiferous ducts leading to peri-ductal inflammation and rupture.
Fat Necrosis
* Inflammatory reaction to damaged adipose tissue (typically obese, middle-aged women).
* Presents as painless breast mass/skin thickening/mammographic lesion (may mimic carcinoma displaying skin tethering/niplle retraction)
* Causes – trauma, radiotherapy, surgery, nodular panniculitis
* Cytology – empty fat spaces , histiocytes and giant cells [BUZZWORDS]
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breast mouse
fibroadenoma
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breast histo
empty fat spaces , histiocytes and giant cells
fat necrosis
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breast histo / cytology
shows an abundance of neutrophils
acute mastitis
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breast cytology
Nipple discharge – proteinaceous material and macrophages
duct ectasia
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breast histo
papillary mass within a dilated duct lined by epithelium
intraductal papiloma
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breast histo
central, fibrous, stellate area
radial scar
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branching”/”leaf-like fronds”/”artichoke appearance
phyllodes tumour
(breast)
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breast histo
dilated large ducts which may become calcified
fibrocystic disease
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different histo for invasive breast carcinoma
Invasive breast carcinoma (80%) – malignant epithelial tumours which infiltrate within breast, capacity to spread to distant sites.
* They can be histologically subcategorised into ductal, lobular, tubular and mucinous.
* Invasive ductal = carcinoma that cannot be subclassified into another group. Most common. Big, pleiomorphic cells [BUZZWORD] – invasive cells move intro stroma
* Invasive lobular = cells aligned in single file chains/strands.
* Tubular carcinomas = well-formed tubules [BUZZWORD] with low grade nuclei. Rarely palpable as <1cm.
* Mucinous carcinoma = cells produce abundant quantities of extracellular mucin [BUZZWORD] which dissects into surrounding stroma.
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common site of intraparenchymal haemorrhagic stroke
* Common site= basal ganglia
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* Commonest form of adult brain tumours
Secondary tumours are metastatic lesions from other parts of the body
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Most common, aggressive primary brain tumour in adults
Glioblastoma multiforme (G4) - BAD
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2 most common brain tumours in children
1. astrocytoma
2. medulloblastoma
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Brown’s tumours
primary hyperPTH
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causes of osteomyletis in all these grousp
adults
children
sickle cell patients
immunocompromsied
congenital
Adults=
S. aureus
Vertebrae, jaw (2o to dental abscess) and toes (2o to diabetic skin ulcer)
Children= Haemophilus influenza, Group B strep
Sickle Cell = Salmonella
`
Immunocompromised =TB
Congenital = Syphilis
.
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Onion skinning of periosteum
ewing's sarcoma
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Histology: Parakeratosis
psoriasis
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most common type of psoriasis ?
* Chronic plaque psoriasis (MOST COMMON) – with salmon pink plaques and silver scales affecting extensor aspects of knees, elbows and scalp
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what is guttate psoriasis ?
* Guttate psoriasis – “rain-drop” plaque distribution, often in children on trunk, usually seen 2 weeks post Group A Beta-haemolytic Strep infection (GABHS)
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types of bullous disease we need to know about ?
Bullous pemphigoid**
IgG Abs and C3 (complement) bind to hemidesmosomes (adhesion molecules) of basement membrane → epidermis lifts off and fluid accumulates in the space
SUBepidermal bulla Large tense bullae on erythematous base.
Often on flexural surfaces (forearms, groin and axillae). ELDERLY.
Bullae do not rupture as easily as pemphigus. EOSINOPHILIA
Linear deposition of IgG along basement membrane
Pemphigus vulgaris**
IgG Abs bind to desmoglein 1 & 3 (adhesion molecules) between keratinocytes in stratum spinosum → acantholysis
INTRAepidermal bulla Bullae are easily ruptured raw red surface.
Found on skin AND mucosal membranes. Nikolsky’s sign +ve.
Mucosal involvement.
Intraepidermal bulla
Netlike pattern of intercellular IgG deposits
Acantholysis
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important prognistic factor for melanoma
o Breslow thickness = most important prognostic factor based off depth (every mm worsens prognosis…)
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most common types of melanoma ?
▪ Superficial spreading (MOST COMMON) – irregular borders with variation in colour
▪ Nodular (2nd COMMONEST) – can occur on all sites, more common in the younger age group
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Salmon pink rash
+
oval macules in Christmas tree distribution
Pityriasis Rosea
* Salmon pink rash appears first (=herald patch) followed by oval macules in Christmas tree distribution
* Appears after HHV-6 and HHV-7 infections.
* Remits spontaneously
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scalp tenderness, temporal headache, jaw claudication --> then proceed to outline this condition
temporal arteritis (GCA)
high ESR / age > 50
Overlap with polymyalgia rheumatica (PMR)
Investigation: ESR (1st) temporal artery biopsy (definitive)
Histology: Granulomatous transmural inflammation + giant cells + skip lesions
Management: oral Pred IMMEDIATELY
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how does Granulomatosis with polyangiitis** present ?
(wegner's)
Triad of:
(1) Upper resp tract: sinusitis, epistaxis, saddle nose
(2) Lower resp tract: cavitation, pulmonary haemorrhage
(3) Kidneys: crescentic glomerulonephritis haematuria & proteinuria
cANCA +ve
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how does Eosinophilic granulomatosis with polyangiitis present ?
Asthma, allergic rhinitis
Eosinophilia
Later systemic involvement
pANCA +ve
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how does Henoch Schonlein Purpura present ?
IgA mediated vasculitis
In children 3-15 yrs
Preceding URTI → glomerulonephritis
Triad of:
* Purpuric rash on lower limb extensors + buttocks
* Abdo pain
* Arthralgia
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how does Microscopic polyangiitis present ?
Pulmonary renal syndrome:
* Pulmonary haemorrhage
* Rapidly progressive glomerulonephritis
pANCA +ve
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different types of amyloid what are they associated with ?
PRIMARY (AL amyloidosis)
* Most common
* Deposition of Ig light chains
* Most associated with multiple myeloma (although most don’t have multiple myeloma)
* Most have monoclonal Ig, free light chains in serum and urine (Bence Jones) and increased bone marrow plasma cells
SECONDARY (AA amyloidosis)
* Amyloid formed from serum amyloid A = acute phase protein, therefore build up occurs secondary to chronic infections / inflammation
o E.g. autoimmune diseases (60%): RA, ankylosing spondylitis, IBD
o E.g. chronic infections: TB osteomyelitis, IVDU (skin infections)
o Non-immune: renal cell carcinoma, Hodgkin’s
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clinicnal features of amyloid and why ?
Clinical features: caused by amyloid deposits in various organs:
* KIDNEY: nephrotic syndrome = most common presentation
* HEART: restrictive cardiomyopathy, conduction defects, heart failure, cardiomegaly
* LIVER/SPLEEN: hepatosplenomegaly
* TONGUE: macroglossia in 10%
* NEUROPATHIES: including carpal tunnel
Think of amyloid proteins either constricting the organ or depositing and making it bigger
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sarcoidosis - features and histo
A multisystem disease of unknown cause, commonly affecting young adults, characterized by non-caseating granulomas in many tissues.
Histology: non-caseating granulomas; also get Schaumann and asteroid bodies (inclusions of protein and calcium)
* More severe disease in Afro-Caribbeans
* F>M, 40-60yrs
* Lungs most commonly involved
* Often detected at routine CXR → bilateral hilar lymphadenopathy (ddx TB, lymphoma, bronchial ca)
* Also see pulmonary infiltrates → fine nodular shadowing in mid zones
* Most seek help with insidious shortness of breath, cough, chest pain and night sweats
High-yield content:
o Bilateral hilar lymphadenopathy on CXR
o Non-caseating granulomas on histology
o High calcium, high ACE
o Treated with steroids
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what ix in sarcoidosis ?
Investigations:
* ↑Ca2+ (ectopic 1-alpha hydroxylase release by activated macrophages),
* ↑ESR,
* ↑ACE
* Transbronchial biopsy → non caseating granuloma
* Spirometry → restrictive,
