Histopath Flashcards
Why do lupus pts have a malar rash
o There is lymphocytic infiltration of the dermis
o You see vacuolisation (dissolution of the cells) of basal epidermis
o Extravasation of red blood cells causes the rash
o Immunofluorescence will show immune complex deposition at the epidermis-dermis junction
Glomerulonephritis histopath
o The glomerular capillaries are thickened (wire-loop capillaries)
o The capillaries are thick due to immune complex deposition in the basement membrane
o Immunofluorescence can be used to visualise the immune complex deposition (electron microscopy will also show dark areas of immune complex deposition)
What sort of endocarditis do you get in lupus?
o This is a non-infective form of endocarditis that is associated with SLE
o Patients may present with emboli, heart failure or murmurs
o The vegetations are made up of lymphocytes, neutrophils, fibrin strands etc
PID causative organism
Usual causes: o Gonococci o Chlamydia o Enteric bacteria Usually starts at the lower genital tract and spreads upwards via the mucosal surface • Other causes: o Staphylococcus o Streptococcus o Coliform bacteria o Clostridium perfringens These tend to occur secondary to abortion Usually starts in the uterus and spreads upwards via lymphatics and blood vessels • Involves the deep tissue layers • Complications o Peritonitis o Intestinal obstructions due to adhesions o Bacteraemia o Infertility
Cx of salpingitis
o Complications • Plical fusion • Adhesions to ovary • Tubo-ovarian abscess • Peritonitis • Hydrosalpinx (enlarged fallopian tube filled with fluid) • Infertility • Ectopic pregnancy
High risk and low risk HPV strains
High risk = 16 and 18
Low risk = 6 and 11
How does HPV cause cervical cancer?
oIn most people with an HPV infection, NOTHING will happen because the immune system will eliminate HPV
oHPV becomes undetectable within 2 years in about 90% of cases
oRelatively few patients develop symptoms
oHowever, persistent infection with high risk HPV types is associated with pre-cancerous and cancerous cervical changes
oTwo proteins (E6 and E7) which is encoded by the virus have transforming genes
oE6 and E7 bind to and inactivate TWO tumour suppressor genes:
• Retinoblastoma (Rb) - E7
• P53 - E6
oThis interferes with apoptosis and increased unscheduled cellular proliferation which contributes to oncogenesis
Cervical cancer screening routine
Screening Intervals • First invitation: 25 years • 25-49 = 3 yearly • 50-62 = 5 yearly • 65+ = only screen those who have not been screened since they were 50 or have recent abnormal tests
Endometrial hyperplasia
o There is an increase in stroma and glands
o Usually driven by oestrogen
o Usually occurs perimenopausal
o Causes
• Persistent anovulation (because of persistently raised oestrogen levels)
• Polycystic ovarian syndrome can also cause persistently elevated levels of oestrogen giving rise to endometrial hyperplasia
• Granuloma cell tumours of the ovary
• Oestrogen therapy
Type II endometrial carcinoma
- SUBTYPES: serous and clear cell tumours
- Older patients
- Less oestrogen-dependent
- Arise in atrophic endometrium
- High grade, deeper invasion and higher stage
- Genetic Mutations
Prognosis of partial and compelte moles in terms of malignancy
- NO partial moles will progress to malignancy
- 2.5% of complete moles progress to malignancy
- 10% of complete moles develop into locally destructive invasive moles
Benign ovarian tumors
- Serous cystadenoma
- Cystadenofibromas
- Mucinous cystadenomas
- Brenner tumour
- Serous cystadenoma
- Cystadenofibromas
- Mucinous cystadenomas
- Brenner tumour
Secondary ovarian tumour
o Krukenberg Tumour
• Bilateral metastases composed of mucin-producing signet ring cells
• Most often from gastric or breast cancer
o Metastatic Colorectal Carcinoma
• Ovaries are prone to metastatic spread of colorectal cancer
Hereditary causes of ovarian cancer
o Up to 10% are familial
o 10% of women with ovarian carcinoma are carriers of a breast/ovarian cancer susceptibility gene
THREE familial syndromes:
1. Familial breast-ovarian cancer syndrome
2. Site-specific ovarian cancer
3. Cancer family syndrome (Lynch type II)
o BRCA1
o Hereditary ovarian cancer occurs at a younger age
o Specific Associations
• Serous = BRCA
• Mucinous = HNPCC
• Endometrioid = HNPCC
Hibernating Myocardium
The concept that chronic sublethal ischaemia leads to lower metabolism (i.e. hibernating) in myocytes which can be reversed with revascularisation
Reperfusion Injury in MI
o This is the consequence of letting blood go back into an area of myocardial necrosis
o The oxidative stress, calcium overload and inflammation can cause further injury
o Arrhythmias are common
o Biochemical abnormalities can last a few days
o It can cause stunned myocardium - reversible cardiac failure lasting several days
MI complications
o Contractile Dysfunction
• 40% of infarcts will go into cardiogenic shock which has a 70% mortality rate
• This tends to be due to an arrhythmia
o Arrhythmia
• Due to myocardial irritability and conduction disturbance
o Myocardial Rupture
o Pericarditis (Dressler’s syndrome)
o RV infarction
o Infarct extension - new necrosis adjacent to old
o Infarct expansion - necrotic muscle stretches
Sudden Cardiac death
- DEFINITION: unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1 hour) after the onset of symptoms
- Usually due to lethal arrhythmia
- Most people will have a background of ischaemic heart disease (90%)
- Acute myocardial ischaemia is the usual trigger
- Causes electrical instability at sites distant from conduction system often near scars from old MIs
- Other associated conditions include aortic stenosis, mitral valve prolapse and pulmonary hypertension
Cardiomyopathy
- Summary: too thin, too thick, too stiff
* Cardiomyopathies are inherent problems with the heart that are not ischaemic or valvular etc.
Different types of cardiomyopathy
Dilated: Caused by progressive loss of myocytes, Leads to a dilated heart
Hypertrophic: Left ventricular hypertrophy, Familial in 50% (autosomal dominant, variable penetrance)
Restrictive cardiomyopathy: Impaired ventricular compliance, Idiopathic or secondary to myocardial disease (e.g. amyloid (image above), sarcoidosis)
Cardiac valve disease
o Caused by immune cross-reactivity with the cardiac valves
o It’s the sequelae of previous rheumatic fever
o Usually the left-sided valves (almost always mitral)
• Mitral > Aortic >Tricuspid > Pulmonary
o Thickening of valve leaflet, especially along the lines of closure (this means that the valve can’t open or close properly)
HIV opportunistic infections
PCP (Pneumonia) CMV (oesophagitis, retina) (causes ulcers in oesophagus, on cytology the have epithelial cells which this large swelling - that is the CMV nuclear inclusion body) Candida TB Cryptococcus meningitis Toxoplasma gondii causing encephalitis JC Papovirus (leukoencephalopath) Herpes Simplex Cryptosporidium
Kaposi Sarcoma cytology
- Dermis shows a mass of spindle shapes cells with blood spaces between them.
Endothelial cells infected with HHV8 undergo altered lymphatic differentiation and manufacture cytokines creating a favorable milieu for angiogenesis.
Slit-like vascular spaces formed by spindled endothelial cells with minimal to moderate atypia; hemorrhage, hemosiderin and plasma cells are key histologic clues
Where can a mycobacterial infection spread too?
Can literally affect ANYWHERE: Lung LN Heart (pericarditis) GIT (peritonitis) Bone (vertebra) CNS (meningitis)
Describe a sarcoid granuloma
Non-caseating granuloma that is a collection of epitheliod macrophages with a border of lymphocytes around the circumference. Giant cells can be present.
IgG4 related disease
•Characterised by large numbers of IgG4 positive plasma cells
o NOTE: as part of a polyclonal response you would expect to have mixed levels of the different IgGs
• May involve the pancreas, bile ducts and almost any other part of the body
• IgG4 related disease is a relatively new phenomenon and is thought to have explained most cases of what has been described as ‘autoimmune pancreatitis’ thus far
• HISTOLOGY (above) - the duct is surrounded by loads of IgG4 expressing plasma cells, inflammatory infiltrative
• These patients respond very well to steroids
Chronic alcohol consumption manifestation
GI: Oesopahgeal varices, ascites, Steatosis -> Steatohepatitis -> fibrosis -> Cirrhosis -> HCC
Pancreatitis
CNS- Werenicke’s and PNS (periphernal neuropathy)
Cardio - dilated cardiomyopathy
FAS
Oral / oesophageal cancer
Types of Renal stones and their relative causes
- Calcium oxalate (Weddelite) - 75% (due to hypercalciuria e.g. increased absorption in gut, decreae reabsorption in PCT)
- Magnesium ammonium phosphate (struvite) - 15%
Form as a consequence of infection with urease-producing organisms (Proteus)
Ammonia produced by the bacteria alkalinises the urine leading to precipitation of magnesium ammonium phosphate salts
They can become LARGE (e.g. staghorn calculus) - Uric acid - 5%
May form in patients with hyperuricaemia
Gout
Rapid cell turnover (e.g. chemotherapy)
HOWEVER, most patients do NOT have hyperuricaemia or increased uric acid excretion in the urine
Thought to be due to a tendency to have slightly more acidic urine
How do stones present?
- Small stones may stay in the kidney and be asymptomatic (may be detected during investigation of haematuria or recurrent UTI)
- Small stones drifting out of the kidney may becomes impacted and cause ureteric colic
Tends to get stuck at places where the urinary tract bends:
• Pelvi-ureteric junction
• Pelvic brim
• Vesico-ureteric junction - Large stones tend to stay in the kidney and can lead to:
• Obstruction
• Risk of infection
• CKD
Types of benign renal neoplasms
Papillary Adenoma
Renal Oncocytoma
Angiomyolipoma
Papillary Adenoma
Benign EPITHELIAL kidney tumour composed of papillae and/or tubules
By definition < 15 mm in size
Well-circumscribed
Trisomy 7, Trisomy 17 or Loss of Y Chromosome
o Frequent incidental finding in nephrectomies and at autopsy
o Especially common in people with CKD and acquired cystic renal disease
Renal Oncocytoma
Often incidental
benign EPITHELIAL kidney tumour composed of oncocytic cells
Well circumscribed
Usually sporadic
Can be seen in Birt-Hogg-Dubé syndrome
o Usually an incidental finding
o Histology (mahogany brown tumour with central scar)
What does an oncocyte look like?
Oncocyte = large cells with VERY PINK granular cytoplasm and a prominent nucleolus (pink due to mitochondria?)
Angiomyolipoma
Angio - vessels
myo - smooth muscle
lipoma - fat
(not necessarily equal proportions)
benign MESENCHYMAL kidney tumour composed of thick-walled blood vessels, smooth muscle and fat.
Derived from PEC cells (perivascular epitheliod cells)
Benign tumour but can be dangerous as can haemorrhage
Again, usually found incidentally
Large tumours (> 4 cm) may present with flank pain, haemorrhage and shock
Renal Cell carcinoma types and how do they present
LOADS of subtypes Top 3: o Clear cell renal cell carcinoma (70%) o Papillary renal cell carcinoma (15%) o Chromophobe renal cell carcinoma (5%)
Half of cases will present with painless haematuria. Most of the remaining cases are only detected on incidental imaging
Small proportion present with metastatic disease
Risk factors for renal CC
o Smoking o Hypertension o Obesity o Long-term dialysis o Genetic syndromes (e.g. von Hippel Lindau)
Clear RCC
appearance, genetics, histology
EPITHELIAL kidney tumour composed of NESTS of clear cells set in a delicate capillary vascular network
o Appears grossly as a GOLDEN-YELLOW tumour with haemorrhagic areas
o Genetics: loss of chromosome 3p is a common finding
The normal renal parenchyma is squashed by the CC and the tumour composed of lots of clear cells.
Papillary RCC
epithelial kidney tumour composed of papillae and/or tubules
• By definition > 15 mm in size
• This is the malignant counterpart of a papillary adenoma
• Genetically shows trisomy 7, trisomy 17 and loss of Y chromosome
• Subdivided into TWO types (type 1 and type 2) based on morphology . Type 2 are quite heterogenous but type 1 is quite well defined.
• Grossly appears as a fragile, friable BROWN tumour
•Type 1-composed of a single layer of small and flat cells. You see lots of islands of cells.
• Type 2 - there is stratification (multi-layering) of the cells. Type 2 tend to do worse than type 1.
Chromophobe
epithelial kidney tumour composed of SHEETS of large cells that display distinct cell BORDERS, reticular cytoplasm and a thick-walled vascular network
o Shows variable genetic aberrations
o Grossly appears as a well-circumscribed solid BROWN tumour
• There are sharply defined cell borders and a thick vascular network - ‘plant like’
Wilm’s
o Malignant TRIPHASIC kidney tumour of childhood
• Blastema (small round blue cells)
• Epithelial
• Stromal
o Typically presents as an abdominal mass in children aged 2-5 years
o 95% of cases show favourable histological features with excellent prognosis
Uroepithelial Carcinoma
AKA transitional cell carcinoma They are a group if malignant epithelial neoplasms arsing in the urothelial tract: o Bladder o Renal pelvis o Ureters Major risk factors: o Smoking o Aromatic amines More present with haematuria THREE main subtypes 1 Non-invasive papillary urothelial carcinoma 2 Infiltrating urothelial carcinoma 3 Flat urothelial carcinoma in situ
Infiltrating Uroepithelial Carcinoma
o Urothelial tumour displaying invasive behaviour
o Once urothelial cells start to invade, the morphology becomes really diverse (e.g. it can be come a squamous cell carcinoma, adenocarcinoma, sarcoma etc.)
o The presence of divergent morphology is associated with a poorer prognosis
o Wide range of subtypes
o Treatment is based on the depth of invasion
• Lamina propria (better prognosis)
• Muscularis propria (worse, requiring extensive surgery)
Flat Urothelial Carcinoma In situ
Most severe of the three
o May be invisible or appear as a reddish area
o This is essentially a high grade in situ lesion
o It is a high grade area that could develop into an invasive tumour
BPH
• Benign enlargement of the prostate as a consequence of increased cell number (hyperplasia)
• VERY COMMON (symptomatic in 25% of men aged > 80 years)
•Aetiology is unclear
?Increased oestrogen in the blood due to ageing may induce androgen receptors and stimulate hyperplasia
Treatment is based on blocking ^:
• 5 alpha-reductase inhibitors
• Alpha-blockers
• Transurethral resection (cores out centre of prostate to ease the flow of urine)
Presents with lower urinary tract symptoms (FUND HIPS)
Alternative presentations include UTI, acute urinary retention of renal failure
What is the other prostate pathology that you need to know?
2 Prostate pathologies covered in this lecture: BPH and Prostate adenocarcinoma
• Malignant epithelial prostate tumour
• MOST COMMON malignant tumour in MEN (25% of all male cancers)
• Arises from prostatic intraepithelial neoplasia
• Identified mutations include PTEN, AMACR, GST-pi and p27
• Usually asymptomatic
• Diagnosed by biopsy following DRE or raised PSA
• May have lower urinary tract symptoms (less likely than in BPH because the tumours tend to lie in the periphery of the gland)
• Rarely may present with metastatic disease (e.g. pathological fracture)
• Gleason score is the most powerful prognostic indicator
What are the types of testicular tumour?
Non-Germ cell (less common)
- Lymphoma (malignant)
- Sertoli Cell Tumour (usually benign)
- Leydig Cell Tumours (usually benign( (may present as pre-pubertal)
Germ Cell (90%) Tumours of the testis arising from germ cells (cells that give rise to gametes). Typically arise in men 20-45 years
Risk Factors: Undescended testes & LBW
Present as painless testicular lumps. 10% will cause symptoms of metastases: Back pain (due to spread to para-aortic nodes) & Cough/ Dyspnoea
5 Histological types.
Treatment: Testicular germ cell tumours are highly sensitive to platinum-based chemotherapy regimes
EXCELLENT prognosis - 98% 5-year survival
5 subtypes of testicular GC tumour
- Seminoma (clear cells with quite a prominent lymphocytic infiltrate) (MOST COMMON)
- Yolk Sac (Smaller cells, Lace-like pattern, there are some pink inclusions)
- Embryonal carcinoma (very high grade, prominent nucleoli)
- Post-pubertal teratoma (this tumour is trying to produce a variety of tissues (e.g. keratin, cartilage, glands) it is malignant- unlike ovarian teratoma). Each counterpart can also become malignant in its own right - malignancy squared
- Choriocarcinoma
Made up of 2 cells: Cytotrophoblasts (clear looking cells)
and Syncytiotrophoblasts (multinucleated cells)
NB both components are needed to call it a choriocarcinoma. (Worsens prognosis)
Paratesticular disease
Epididymal cyst
Epididymitis - Men < 35: related to C. trachomatis or N. gonorrhoeae. Men > 35: related to E. coli
Varicocoele - Dilated venous plexus
Hydrocoele - Fluid accumulating between the layers of the tunica vaginalis
Adenomatoid tumour - Small tubules lined by mesothelial cells
Penile Diseases
Lichen sclerosis/balanitis xerotica obliterans - Inflammatory condition that causes phimosis
Zoon’s balanitis- Inflammatory condition that causes red areas
Condylomas- HPV 6 and 11
Peyronie’s disease– Scarring, inflammation and thickening of corpus cavernosa
Penile carcinoma
•Rare, seen in elderly men
•Smoking, HPV and chronic lichen sclerosus are risk factors
Urethral Diseases
o Urethritis - Neisseria gonorrhoeae, Chlamydia trachomatis
o Prostatic urethral polyp- Papillary lesion in prostatic urethra
o Urethral caruncle - Common lesion at urethral meatus in women
o Urethral carcinoma - RARE, Usually squamous cell carcinoma, More common in women
o Malignant melanoma
Scrotal Diseases
o Epidermoid cyst
• COMMON
o Scrotal calcinosis
• RARE
• May be related to epidermoid cysts
o Angiokeratomas
• Benign vascular lesions
o Fournier’s Gangrene
• Necrotising fasciitis (15-20% mortality)
o Scrotal squamous cell carcinoma
• VERY RARE
• Used to happen to chimney sweeps
Oesophagus histology/microanatomy
Pale, Squamous epithelium which ends at the border of the Z junction (becomes columnar).
Layers of the oesophagus from lumen inwards:
Epithelium - > Submucosa -> Muscularis Externa -> Adventitia
Stomach anatomy
The body and the fundus contain most of the specialised glands that are responsible for producing acid and enzymes . From lumen inwards: Gastric mucosa (columnar, mucin secreting) -> lamina propria (specialised glands) -> muscularis mucosa
How is the walll anatomy of antrum and the body of the stomach different?
Antrum do not have specialised cells in the lamina propria.
NB •In the antrum and pyloric canal, you tend to see H. pylori-associated gastritis
Duodenal wall anatomy
Glandular epithelium with goblet cells made up of villi and crypts.
The crypt is where cells proliferate. They then migrate upwards to the tip of the villous and shed at the top
• In terms of length, there is usually a 2:1 villous to crypt ratio (This is dependent on the height of the villi and the depth of the crypts)
• If the villi are shorter, the crypts take up a bigger proportion of the total length
• When the villi get damaged, the crypts will proliferate to replace the damage villi
IMPORTANT: goblet cells are NOT normally seen in the stomach. The presence of goblet cells in the stomach is a feature of intestinal metaplasia
Acute Oesophagitis
• The redness is a cardinal sign of inflammation
• The histology shows the presence of loads of neutrophils, which is the hallmark of acute inflammation
Cause: usually GORD
It can result in: Ulceration (produces a necrotic slough, inflammatory exudate and granulation tissue) & Fibrosis.
Complications:
• Haemorrhage
• Perforation
• Stricture
• BARRETT’s OESOPHAGUS
Barrett’s oesophagus
• This is a classic metaplastic process by which the normal squamous epithelium of the lower oesophagus gets replaced by columnar epithelium
• This is also known as columnar-lined oesophagus (CLO)
• The metaplasia can go one step further when goblet cells become visible - this is called intestinal metaplasia
• The risk of cancer is MUCH HIGHER in cases of Barrett’s oesophagus with intestinal metaplasia
Metaplasia –> Dysplasia –> Cancer
Metaplasia is NOT technically pre-malignant because it is REVERSIBLE
However, once you have metaplasia you can progress to dysplasia
Adenocarcinoma is when the abnormal cells invade through the basement membrane
NOTE: adenocarcinomas can spread underneath the columnar epithelium - this is a massive issue for surgeons because they don’t know exactly where to stop cutting
Dysplasia definition
changes showing some of the cytological and histological features of malignancy but with no invasion through the basement membrane
SCC Of the oesophagus
• In Africa, squamous cell carcinoma is the most common type of oesophageal cancer
• Classically associated with smoking and alcohol
• Tends to affect the mid/lower oesophagus
• Invades into the submucosa
Histology: cells make keratin (normally, the squamous epithelium of the oesophagus is non-keratinised) and the cells also have intercellular bridges.
These are the hallmarks of squamous cell carcinoma
Causes of acute vs chronic gastritis and how their histology differs
(Inflammation of the gastric mucosa )
ACUTE Gastritis caused by chemical (aspirin, nsaids, OH, corrosives) or by infection ( H pylori commonly. CMV, strongyloides in the immuno/c)
CHRONIC Gastritis is caused by ABC. AI, bacteria and chemical. (chemical also includes bile reflux).
AI (auto-antibodies e.g. anti-parietal cell, Crohn’s)
oThe key inflammatory cells are lymphocytes as this is chronic inflammation
oHowever, be aware as the presence of co-existing acute processes can mean that you may also see a lot of neutrophils
Why does MALT occur?
- Chronic gastritis associated with H. pylori infection induces lymphoid tissue in the stomach
- It induces the development of lymphoid follicles in germinal centres
- If you see lymphoid follicles in a stomach biopsy, it is highly suggestive that the patient has had an H. pylori infection (i.e. the presence of lymphoid follicles is NOT part of the normal stomach mucosa)
- The fact that H. pylori induces MALT formation is important because it is associated with an increased risk of lymphoma
How does H Pylori colonise the gut and what are the long term consequences?
H. pylori can bind to epithelial cells and inject toxins into them but they do NOT directly invade the epithelium
Consequences of H. pylori associated gastritis:
• CLO –> IM –> Dysplasia
• Adenocarcinoma (8 x increased risk)
• Lymphoma (MALToma)
Cag-A positive H. pylori have a needle like appendage that injects toxins into intercellular junctions allowing the bacteria to attach more easily
• Cag-A is a toxin and this strain is associated with more chronic inflammation
IMPORTANT: treatment of H. pylori infection with antibiotics drastically reduces the risk of cancer
pathologies of the stomach covered in this lecture
- Gastritis (acute and chronic)
- Ulcers (acute and chronic)
- Cancer
Gastric Ulcer
• Technical Definition of Ulcer: the depth of the loss of tissue goes beyond the muscularis mucosa (into the submucosa)
o I.e. if you only get loss of the surface epithelium +/- lamina propria, then it is an erosion, not an ulcer
Difference between acute ulceration and chronic ulceration: Chronic ulcers are accompanied by scarring and fibrosis
!IMPORTANT: ALL ULCERS SHOULD BE BIOPSIED TO EXCLUDE MALIGNANCY
Complications:
o Bleeding –> anaemia, shock (massive haemorrhage)
o Perforation –> peritonitis
What is intestinal metaplasia
- The presence of goblet cells in the mucosa of the stomach is intestinal metaplasia
- This occurs in response to long term damage
- Intestinal metaplasia is associated with an increased risk of cancer
Where is there a higher incidence of gastric cancer?
- High incidence in Japan, Chile, Italy, China, Portugal and Russia
- More common in MALES
Gastric Cancer
> 95% of all malignant tumours in the stomach are ADENOCARCINOMAS
• These adenocarcinomas can be split morphologically into:
INTESTINAL (Well-differentiated, Presence of big glands containing mucin)
DIFFUSE (poorly differentiated, composed of single cells with no attempt at gland formation) Subtypes: Linitis plastica & Signet ring cell carcinoma.
Remaining 5% of Gastric Cancers o Squamous cell carcinoma o Lymphoma (MALToma) o Gastrointestinal stromal tumour (GIST) o Neuroendocrine tumours
IMPORTANT: overall survival rate = 15%
Duodenitis
•Caused by increased acid produced in the stomach that spills into the duodenum (almost all causes of duodenal ulcer is H Pylori -> acute denitis -> chronic which can actually develop metaplasia (gastric mucosa)
(The intestinal epithelium will change to look more like gastric epithelium because the gastric epithelium is well designed to deal with acid)
• Chronic inflammation can also lead to duodenal ulceration (same definition of ulcers)
Other pathogens affecting the duodenum
o CMV
o Cryptosporidium
o Giardiasis (unicellular parasite) (Travel hx St. Petersburg in competent, or I/C)
o Whipple’s disease (Tropheryma whippelii) (infection of macropahges)
Malabsorption
1 . Villous atrophy
- Crypt hyperplasia
- Increased intraepithelial lymphocytes (Normal Range: < 20 per 100 enterocytes)
NB: the T cell response to gliadin in Coeliac disease is responsible for the damage to the villi. Crypt hyperplasia occurs in an attempt to regenerate the damaged villi
In coeliac disease, you get architectural changes (loss of villi and crypt hyperplasia) and you get inflammatory changes (increased intraepithelial lymphocytes)
What is Lymphocytic duodenitis?
When you have inflammatory changes (increased intraepithelial lymphocytes) without architectural changes. Many people with this condition either have coeliac disease or are going to develop coeliac disease.
Different types of lymphomas in GIT?
• Patients with coeliac disease have an increased risk of GIT cancers
• MALTomas associated with coeliac disease are found in the duodenum. They are T cell lymphomas
o NOTE: lymphomas in the stomach due to H. pylori are B cell lymphomas
Layers of skin
Epidermis, Dermis and Subcutaneous
Epidermis - kertainocytes and squamous (act as barrier)
Dermis - collage, elastic fibres, blood vessels, sweat glands, hair follicles, sebaceous glands and nerve fibres
Layers of epidermis can be split into:
Come Lets Get Some Beers
Stratum corneum, lucidum, gravidarum, spinosum, basale.
NB Skin is different parts of your body will be slightly different e.g. on your face, you will have a lot more sebaceous glands than on your torso and arms. Different layers will be thicker - corneum will be thicker on your toes/feet. In elderly population will have a thinner epidermis and more fragile
