Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Path MC > Histology MC > Flashcards

Histology MC Flashcards

1
Q

Squamous cell carcinomas - tumour types

A

Histological features:
Keratin production
Intracellular bridges
NO glands

Site: head+neck, skin, oesophagus (squamous cells), anus, cervix, vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Adenocarcinoma - tumour types

A

Histological features:
Form glands, secrete glandular fluid
Mucin production

Site: lung, breast, colon, pancereas, stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Histo chemical stains

A

Fontana + melanin
Congo red + amyloid (apple green briefringence)
Prussian blue + iron (haematochromatosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Immuno histo stains

A

CD45 + lymphoid cells

Cytokeratin epithelial marker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fontana histochemical stain

A

Melanin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Congo Red histochemical stain

A

Amyloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prussian blue histochemical stain

A

Iron (haematochromatosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CD45 +ve immunohisto stain

A

Lymphoid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cytokeratin positive immunohisto stain

A

Epithelial marker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 components of atherosclerotic plaques?

A

Cells - SMC, macrophages, leukocytes
ECM including collagen
Intracellular and extracellular lipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the histological findings of MI chronologically?

A

<6 h - normal histology
6-24 h - loss of nuclei, necrotic cells, homogenous cytoplasm
1-4 days - polymorph infiltration + macrophages
5-10 d - removal of debris
1-2 w - granulation tissue, novo angiogenesis, myofibroblasts
weeks-month strenghtening, scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does nut met liver imply?

A

Congestive hepatopathy, also known as nutmeg liver and chronic passive congestion of the liver, is liver dysfunction due to venous congestion, usually due to congestive heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hyperthrophic cardiomyopathy (HCM)

A

Thick walled, heavy, hyper contracting heart.
Histology: myocyte dissaray +/- arrhytmia
Autosomal dominant mutation in beta MHC gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rheumatic fever

epidemiology, clinical features, ix, tx

A

Peak age 5-15 yo
Multisystem - heart, joints, skin (erythema marginatum), CNS (enchephalopathy)

Clin features: 2-4 weeks post strep throat infection
Lancefield group A strep - main pathogen

May affect mitral valve

Histology: verrucae vegetations, aschoff bodies, antischkov myocytes

Tx: Benzylpenicillin
Erythromycin if allergic to penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the main pathogen associated with Rheumatic fever?

A

Lancefield group A strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the Jones Major Criteria?

A 
Criteria for diagnosis of group A strep infection 
Major criteria: CASES
Carditis
Arthritis
Sydenham's chorea
Erythema marginatum
Subcutaneous nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Erythema marginatum and what is it associated with?

A

pink rings on the torso and inner surfaces of the limbs which come and go for as long as several months. It is found primarily on extensor surfaces.

Group A streptococcal infection, otherwise known as Streptococcus pyogenes infection

Rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for rheumatic fever?

A

Benzylpenicillin
Erythromycin if penicillin allergy (bacteriostatic, binding to the 50s subunit of the bacterial rRNA complex, protein synthesis and subsequent structure and function processes critical for life or replication are inhibited)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the pathology of rheumatic heart disesae

A

young 5-15 yo
antigen mimicry - cross reaction of anti streptococcal antibodies with myocardial antigens
Causes verrucae (beady fibrous vegetations) on mitral valve (70%) or both mitral and aortic (25%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Libman Sacks endocarditis associated with?

A

SLE and antiphospholipid syndrome

Small, warty vegetations, sterile, platelet rich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is non bacterial thrombotic endocarditis associated with?

A

DIC/ Hypercoagulable states

Small vegetations formed of thrombi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the clinical features of bacterial endocarditis

A

Systemic illness
Cardiac murmurs (MR/AR)
Immune response: Roth spots, oslers nodes, haematuria - glomerulonephritis
Thromboembolic phenomena: Janeway lesions, septic abscesses, splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What valves are affected in bacterial endocarditis

A

Tricuspid in IVID

Mitral/aortic otherwise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some of the causative organisms for bacterial endocarditis?

A 
Staph aureus (esp IVID) 
Strep pyogenes

Unusual bacteria
HAECK - haemophilus, aggregatibacter, cardiobacterium, eikenella, kingella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the Duke criteria and what is it used for?

A

Bacterial endocarditis
Major:
- positive blood cultures
- echo confirming vegetation

Minor

  • RF: prosthetic valve, IVDU, congenital heart valve abnormalities
  • fever
  • immune stuff
  • thromboembolic criteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the Rx for bacterial endocarditis

A

Broad spect until cultures confirm
Flucloxacillin (MSSA)
Rifampicin, vancomycin, gentamicin MRSA

Subacute
Benzylpenicillin + gentamicin
Vancomycin 4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which valve issue is associated with rheumatic fever?

A

Mitral stenosis, mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which valve issue is associated with infective endocarditis?

A

Aortic regurgitation,

Mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What histological features do you expect in chronic bronchitis?

A
  1. Dilatation of airways
  2. Goblet cell hyperplasia
  3. Hyperthrophy of mucous glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What histological features do you expect in Bronchiectasis?

A

permanent dilatation of bronchi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What histological features do you expect in asthma?

A

Curschman spirals
Eosinophils
Leyden crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Curschman spirals
Eosinophils
Leyden crystals

What do these histological findings confirm?

A

Asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What RF and pathogen is associated with:

Farmer’s lung

A

mouldy hay/grain/ silage
Saccharopolyspora rectivirgula

Gram-positive rod. It was formerly known as Micropolyspora faeni. Inhalation of the bacteria can cause the disease farmer’s lung, a type of hypersensitivity pneumonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What RF and pathogen is associated with:

Humidifier’s lung

A

Heated water reservoirs

Thermactinomyces spp f Gram-positive endospore-forming bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What RF and pathogen is associated with:
Malt workers lung

+TX

A

Germinated barely
Aspergillus calvatus/ fumigatus

TX: amphotericin B liposomal
caspofungin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What RF and pathogen is associated with:

Cheese washer’s lung

A

mouldy cheese
Aspergillus calvatus
Penicillium casei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q 
Histology report: 
keratinisation
Intracellular prickles (desmosomes) 
Smoker male 
Squamous cells on cytology
A

Squamous cell carcinoma of lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Histology report:
non smoking woman
glandular differentiation (gland formation + mucin production)
cytology: mucin vacuols

A

Adenocarcinoma of lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Management of oesophageal varices

A

Emergency endoscopy -> sclerotherapy / banding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Gastric ulcer vs duodenal ulcer

A

Worse with food vs relieved by food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Gastric lymphoma

Pathology rx

A 
H pylori - chronic antaigen stimulation
Remove cause - H Pylori using triple therapy
PPI 
Clarithromycin
Amoxicillin or Metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Coeliac disease

Pathology

A

T cell mediated autoimmune disease

Gluten intolerance - villous atrophy and malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Coeliac clinical findings

A

Steatorrhoea, abdo pain, failure to thrive
Dermatitis herpetiformis
Chronic blistering skin condition, characterised by blisters filled with a watery fluid that can be very itchy. Despite its name, DH is neither related to nor caused by herpes virus: the name means that it is a skin inflammation having an appearance similar to herpes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What condition are these serological investigations used for
Anti endomysial ab
Anti tissue transglutaminase IgA
Anti gliadin

A

Coeliac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Upper GI endoscopy and duodenal biopsy is the gold standard for?

A

Coeliac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q 
Histological report: 
Skil lesions
cobblestone appearance of mucosa
Rosethorn ulers 
non caseating granulomas 
transmural inflammation
aphthosus ulcer - first lesion
A

Crohn’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Backwas ileitis
no granulomas/fissures/fistulae
islands of regenerating mucosa bulge into lumen causing pseudopolyps

A

Ulcerative cholitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What conditions are the following skin manifestations associated with:
Erythema nodosum, pyoderma gangrenosym, erythema multiforme, clubbing

A

UC and Crohn’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the Mx for Crohn’s disease?

A

Ix Systemic markers of inf (ESR, CRP)
Barium contrast
Endoscopy

Rx:
Mild: Prednisolone
Severe: IV hydrocortisone, metronidazole
Additional: Azathiopine, Infliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the Mx for UC?

A

Ix Rectal biopsy, flexible sig/colonoscopy, AXR, stool culture

Rx:
Mild Prednisolone + Mesalazine (5 ASA)
Moderate Prednisolone + mesalazine + steroid enema bd
Severe: admit, NBM, fluids, IV hydrocortisone, rectal steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which antibiotics are associated with C difficile and why?

A

Ciprofloxacin and Cephtriaxone
Because it kills commensals allowing for C Diff to flourish
Exotoxins cause pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

RX and Ix for C Diff infection?

A

Stool sample
Metronidazole (covers anaerobes)
or
Vancomycin as 2nd line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Carcinoid syndrome

A

Diverse group of tumours
Enterochromaffin cell origin
Produce 5-HT

Carcinoid syndrome: bronchoconstriction, flushing, diarhorrea

Carcinoid crisis: Life threatening, unstable (vasodilation, hypotensive, tachycardic, bronchoconstriction, hyperglycaemia)

IX: 24 hr urine 5HIAA main serotonin metabolite

RX Octreotide somatostatin analogue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Chronic gastritis with lymphocyte infiltration +/- neutrophils suggests?

+/- Marginal B cell lymphoma

A

MALT/Mucosal associated lymphoid tissue
usually associated with H pylori inflammation
Risk of developing into adenocarcinoma or MALT lymphoma
If caught early - triple therapy: PPI, clarithromycin, amoxicillin or metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What cancer is Duke staging used for?

What are the stages ? A-D

A

Colorectal cancer
98% are adenocarcinomas
Ix proctoscopy, sigmoidoscopy, barium enema, bloods
Carcinoembryonic antigen CEA to monitor disease

Duke staging
A, B1, B2, C1, C2, D
A - confined to mucosa
B1 - extending into muscularis propria
B2 -transmural invasion, no lymph node
C1 - muscularis propria, LN mets
C2 - transmural invasion, LN mets
D - distant mets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What marker is used to monitor colorectal cancer?

A

CEA carcioemrbyonic antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is Peutz-Jeghers syndrome?

A

A type of hamartomatous polyp disease.
Multiple polyps, hyperpigmentation of mucosa, freckles everywhere
Autosomal dominant disease - LKB1
risk of intussusception and malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is Familial Adenomatous Polyposis?

A

FAP is a familial syndrome causing colorectal cancer
70% autosomal dominant with APC gene mutation C5Q1
30% autosomal recessive mutation in DNA mismatch repair genes

Presents at around 10-15 yrs with more than 100 adenomatous polyps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

HNPCC - hereditary non polyposis colorectal cancer

A

Autosomal dominant mutation in DNA mismatch repair genes
usually in right colon
few polyps
rapid malignant progression in under 50 yo
associated with endometrial, ovarian, small bowel, transitional cell (bladder) and stomach carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the endocrine functions of the islets of Lnagerhans?

A

Alpha cells - glucagon increases blood glucose
Beta cells: insulin decreases blood glucose
Delta cells: somatostatin, regulates alpha and beta cells
D1: Vasoactive peptide, stimulates secretion of H2O in pancreas
PP: pancreatic polypeptide - self regulates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is metabolic syndrome?

A

cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes.

Fasting hyperglycaemia >6 mmol/L
HTN >140/90
Central obesity
Dyslipidaemia low HDL, high TGs
Microalbuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How do you diagnose diabetes?

A

Fasting plasma glucose >7 mmol/L

Random plasma glucose >11 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Features of T1DM?

A

Autoimmune destruction of beta cells by CD4 + and CD8 + T cells
Complication: DKA - lack of insulin => increased plasma glucose => increase need for muscle ketones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Features of T2DM?

A

linked to obesity and insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the GLASCOW scale and what is it used for?

A

Used to determine severity of acute pancreatitis
PaO₂ <59.3 mmHg (7.9 kPa)

Age >55 years

WBC >15 x 10³/µL (10⁹/L)

Calcium <8 mg/dL (2 mmol/L)

BUN >44.8 mg/dL (serum urea >16 mmol/L)

LDH >600 IU/L

Albumin <3.2 g/dL (32 g/L)

Glucose >180 mg/dL (10 mmol/L)`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is painless jaundice associated with?

A

Pancreatic carcinoma at the head of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is multiple endocrine neoplasia?

A

MEN are a group of syndromes with functioning hormone producing tumours in multiple organs.
MEN1 - PPP parathyroid hyperplasia, pancreatic tumor, pituitary adenoma
MEN 2 A - parathyroid, thyroid, phaeochromocytoma
MEN 2 B medularry thyroid, phaeochromocytoma, neuroma (MARFANOID phenotype)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What does nutmeg liver suggest?

A

hronic passive congestion of the liver, is liver dysfunction due to venous congestion, usually due to congestive heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the investigation of choice for hepatocellular carcinoma?

A

alpha-fetoprotein

USS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is modified child’s pugh score used for?

A 
To indicate prognosis of cirrhosis,
Includes:
Ascites
Enchephalopathy
Bilirubin
Albumin
PTT

Results
Child Pugh A <7 50% 5 yr survival
Child Pugh B 7-9 20% 5 yr survival
Child Pugh C >10 <20% 5 yr survival

71
Q

What are the causes of portal hypertension?

A

Pre hepatic
Portal vein thrombosis (factor V lieden)

Hepatic
Pre-sinusoidal - schoistosomiasis, PBC
Sinusoidal - cirrhosis
Post sinusoidal - veno occlusive disease

Post hepatic
Budd Chiari syndrome - occlusion of hepatic vein
RX thrombolytic

72
Q

Which of the following is now the most common cause for hepatic steatosis?

A

Metabolic syndrome is very common because of obesity. It is defined as central obesity, or BMI >30, with hypertriglyeridemia, decreased HDL cholesterol, hypertension, and hyperglycemia.

Steatosis = fat droplets in hepatocytes

Chronic alcohol abuse may lead to hepatic steatosis. The carbohydrate deficient transferrin (CDT) test measures isoforms of iron transport protein transferrin. Consumption of ethanol more than 50 to 80 g/day for 2-3 weeks may increase serum CDT. The CDT may be higher in chronic heavy drinkers than light social drinkers.

Steatosis is reversible over weeks to months. Reduce alcohol consumption. Adopt a diet and exercise program to lose weight (a 10% weight reduction helps to prevent progression of steatosis to steatohepatitis and to cirrhosis).

73
Q

Case:
40 yo obsese man shows mild to moderately elevated serum alanine transferase (ALT) on bloods and no other signs on examination.
What is the most likely diagnosis?

A

Non alcoholic fatty liver disease from metabolic syndrome aka obesity

The lipid accumulates in the hepatocytes as vacuoles. These vacuoles have a clear appearance with H&E staining

74
Q

What genetic factors may cause liver steatosis?

A

Polymorphisms in the patatin-like phospholipase domain containing 3 (PNPLA3) gene encoding for a triacylglycerol lipase involved in lipid regulation may explain greater propensity to develop steatosis in some populations.

75
Q

Histology - what might the following histological findings suggest?
Hepatocyte ballooning,
Hepatocyte necrosis
Mallory bodies

A

Alcoholic liver cirrhosis
Mallory body, Mallory-Denk body, and Mallory’s hyaline, is an inclusion found in the cytoplasm of liver cells. Mallory bodies are damaged intermediate filaments within the hepatocytes.

Can be seen acutely after a binge episode

76
Q

What are some causes for macronodular cirrhosis?

A

Hepatitis B and C - most common
Alpha 1 anti trypsin deficiency
Wilsons disease

77
Q

What are transaminase values with alcoholic liver disease?

A

AST and ALT high
AST > ALT

On CT: micronodular signs of cirrhosis + spleen enlargement from portal hypertension

78
Q

Which of the following cells plays the greatest role in fibrogenesis of the liver?
A Bile duct epithelial cell

B Endothelial cell

C Hepatocyte

D Ito cell

E Kupffer cell

A

The hepatic stellate (Ito) cell, which resides in the space of Disse, normally stores vitamin A. However, it can respond to injury and express alpha-smooth muscle actin as well as differentiate into myofibroblasts.

79
Q

What are the histological findings in primary biliary cholangitis?

A

loss of bile duct associated with chronic inflammation

early stages - granulomas

80
Q

What antibody is used to diagnose primary biliary cholangitis?

A

Anti mitochondrial antibodies AMA

81
Q

What do you use to treat primary biliary cholangitis?

A

ursodeoxycholic acid

82
Q

What are the histological findings in primary sclerosing cholangitis?

A

inflammation of extrahepatic and intrahepatic bile ducts forming multiple strictures.
The sclerosis of surrounding tissue squeezes life out of bile ducts
associated with UC

83
Q

What IX are needed to confirm primary sclerosing cholangitis?

A

USS - bile duct dilation

ERCP gold standard shows beading of bile duct due to many strictures

84
Q

What is haemochromatosis?

A

Genetic condition which increases absorption of iron from the gut
Causes chocolate brown organs
Autosomal recessive mutation
Signs: bronze, diabetes, hepatomegaly

HHC results from a mutation involving the hemochromatosis gene (HFE) that leads to increased iron absorption from the gut. The prevalence is between 1:200 and 1:500 persons in the U.S. About 1 in 10 persons of northern European ancestry carries the abnormal recessive HFE gene, and most of these are the C282Y mutation.

TX
venesetion
desferrioxamine

85
Q

What is wilsons disease?

A

Failure to excrete copper
autosomal recessive defect in chr 13
low levels of ceruloplasmin

KEYSER FLEISCHER RINGS

Rhodanine stain on histology - mallory bodies and fibrosis seen on microscopy

TX lifelong penicillamine

86
Q

Alpha 1 antitrypsin deficiency ?

A

Failure to secrete alpha 1 antitripsin
autosomal dominant - accumulates in hepatocyytes causing inclusions in cytoplasm

Intra cytoplasmic inclusions of A1AT which stain with periodic acid schiff

Kids: neonatal jaundice
Adults: emphysema and Chronic liver disease

87
Q

What does Periodic acid schiff stain for?

A

alpha 1 antitrypsin intra cytoplasmic inclusions for A1AT deficiency

88
Q

What antibodies are used to diagnose autoimmune hepatitis?>

A

Anti smooth muscle actin Anti SMA

89
Q

What is the most common cause of cystitis ?

A

80% caused by Gram -ve bacilli from gut

E coli
Proteus
Klebsiella
Enterobacter

90
Q

What is the treatment for cystitis?

A

Trimethoprim or Nitrofurantoin

91
Q

What are the RF, clin features and diagnosis of transitional cell tumours?

A 
bladder cancer
male
>50
smoking
painless haematuria
DX: cystoscopy + biopsy
92
Q

Bladder suqamous cell carcinoma is associated with?

A

Schistosomiasis in endemic regions

93
Q

BPH tx?

A

TURP, 5 alpha reductase inhibitors

94
Q

What grading system is used for prostate cancer?

A

Gleason system based on degree of differentiation and glandular patterns

95
Q

What is the cut off of PSA for prostate cancer?

A

4 ng/ML

96
Q

What are the biological markers for teratomas?

A

AFP, HCG, LDH

97
Q

What stain is used for histology in haemochromatosis?

A

Prussian blue

98
Q

What organs are affected in haemochromatosis and what does it cause?

A

Excessive iron deposition in persons with HH can affect many organs, but heart (congestive failure), pancreas (diabetes mellitus), liver (cirrhosis and hepatic failure), and joints (arthritis) are the most severely affected.

99
Q

What are RF for liver adenomas?

A

Oral contraceptive use is the most common risk for hepatic adenoma, but even then it is rare. Anabolic steroid usage may increase the risk in men. Congenital glycogen storage diseases are a risk as well.

100
Q

What is the most likely tumor marker detected in the blood of a patient with hepatocellular carcinoma?

A

AFP alpha feto protein
biomarker found in up to 80% of hepatocellular carcinomas. It is also a biomarker of the testicular carcinomas with a ‘yolk sac’ element, including yolk sac carcinomas and embryonal carcinomas.

101
Q

What are some tx for Hep B?

A

Pegylated interferon alfa (PEG-IFN-a), entecavir (ETV), and tenofovir disoproxil fumarate (TDF) are the agents primarily used for treatment of chronic active hepatitis B, suppressing, but not clearing the virus. Interferons have antiviral, antiproliferative, and immunomodulatory effects. Entecavir is a guanosine analogue inhibitor of hepatitis B viral polymerase. Tenofovir is a nucleotide analogue reverse transcriptase and HBV polymerase inhibitor.

102
Q

What histological changes may you see in viral hepatitis?

Actue stage and chronic stage findings

A

Individual hepatocytes are affected by viral hepatitis. Viral hepatitis A rarely leads to signficant necrosis, but hepatitis B can result in a fulminant hepatitis with extensive necrosis. A large pink cell undergoing “ballooning degeneration” is seen below the right arrow. At a later stage, a dying hepatocyte is seen shrinking down to form an eosinophilic “councilman body” below the arrow on the left.

103
Q

What stain can be used in histology for viral hepatitis?

A

This trichrome stain demonstrates the collapse of the liver parenchyma with viral hepatitis. The blue-staining areas are the connective tissue of many portal tracts that have collapsed together.

104
Q

What do you use to treat paracetamol overdose?

A

N-acetylcysteine helps regenerate glutathione stores to counteract the effect of toxic metabolites generated from acetaminophen poisoning.

105
Q

What are the most common causes of renal calculi?

A 
Calcium oxalate (or phosphate)	75%
Magnesium ammonium phosphate (struvite, or "triple phosphate")	12%
Uric acid	6%
Cystine	1%
Other	6%

Struvite refers to bacterial calculi, usually caused by proteus bacteria

Uric acid stones may be associated with gout

Urinary tract calculi are usually unilateral and about 1 to 3 mm in size. Their passage is marked by intense abdominal or back or flank pain. This pain can be paroxysmal, known as renal or ureteral “colic”. Hematuria may also be present. Larger stones that cannot pass may produce hydronephrosis or hydroureter.

106
Q

What is an example of a complex renal calculi and how does this affect the kidney?

A

“staghorn calculus” is a massive stone that nearly fills the calyceal system, rendering the kidney non functional. needs nephrectomy as this is a risk to infection.

Leucocytes ++
Blood ++
Protein trace
Nitrite ++

107
Q

What is nephrotic syndrome? What are the characteristics?
Key words in EMQ - swelling (face of kids, feet of adults)
KEY WORDS: Frothy urine

A

Nephrotic syndrome is the breakdown of glomerular filtration barrier. It is one step away from end stage kidney failure.

4 clinical features:

  1. Oedema
  2. Proteinuria (>3.5 mg/day)
  3. Hypoalbuminaemia
  4. Hyperlipidaemia - liver produces lipoproteins to compensate for loss of albumin)
108
Q

What are some of the primary causes for nephrotic syndrome?

A

Minimal change disease (children, podocytes, prednisolone)

Membranous glomerular disease (podocytes only in basement membrane, spikey subepithelial deposits)
1ry associated with phospholipase A2 receptor on podocytes
2ry associated with SLE, infection, drugs, malignancy

Focal segmental glomerulosclerosis (podocytes, scars, immunosuppresion)

109
Q

What are the histological findings associated with diabetic glomerulosclerosis?

A

Diffuse glomerular basement membrane thickening.
Kimmelstein Wilson nodules - where mesangial matrix takes over the whole glomerulus
EMQ KEY WORD ASIAN

110
Q

What are the histological findings associated with amyloid inducing nephrotic syndrome?

A

Deposition of extracellular proteinaceous material. Seen as apple green under polarised light due to Congo red stain.

Commonest proteins associated:
Amyloid associated protein and amyloid light.

111
Q

What are the most common proteins associated with amyloid deposition in the kidneys?

A

Serum amyloid associated protein - AA
from chronic inflammation such as rheumatoid arhtritis, chronic infections TB

Amyloid light protein - derived from immunoglobulin light chains
associated with multiple myeloma

112
Q

What are some of the clinical findings in amyloidosis

A

Macroglossia - large tongue
Heart failure
Hepatomegaly

113
Q

What is amyloid light protein associated with?

A

Multiple myeloma - blood cancer arising from plasma cells
Patients with plasma cell dyscrasias (multiple myeloma) can have an excess of immunoglobulin light chains that form the AL amyloid.

114
Q

What is nephritic syndrome and what is it characterised by?

A 
Manifestation of glomerular inflammation i.e. glomerulonephritis 
Characteristics PHAROH
Proteinuria 
Haematuria
Azootemia high urea and creat
Red cell casts in urine
Oliguria
HTN
115
Q

What is trichrome stain used for?

A

3 colours
A trichrome stain can colour the muscle tissue red, and the collagen fibres green or blue. Liver biopsies may have fine collagen fibres between the liver cells, and the amount of collagen may be estimated based on the staining method. Trichrome methods are now used for differentiating muscle from collagen, pituitary alpha cells from beta cells, fibrin from collagen, and mitochondria in fresh frozen muscle sections, among other applications. It helps in identifying increases in collagenous tissue

116
Q

What 3 serologic tests have high sensitivity for post-streptococcal GN?

A

Anti streptolysin O ASOT
anti hyalouridase
anti DNase B

117
Q

What are the characteristics of post streptococcal GN?

A

occurs 1-3 weeks post strep infection (throat or impetigo, usually Group A alpha haemolytic strep = pyogenes)
Immune complex deposition
Haematuria, proteinuria, oedema, HTN
High anti streptolysin O titre

On microscopy - granular depositions of IgG, subendothelial lumps
The deposits are seen here with bright breen fluorescence in a granular, bumpy pattern because of the focal nature of the immune complex deposition process. In type III hypersensitivity, antigen-antibody complexes tend to filter out and become trapped along basement membranes, such as those in glomerular capillaries.

118
Q

What type of hypersensitivity reaction is post strep GN?

A

Type 3 hypersensitivity

119
Q

What is the most common cause of nephrotic syndrome?

A

Membranous glomerular disease
In most cases there is no underlying condition present (idiopathic). However, some cases of membranous GN can be linked to a chronic infectious disease such as hepatitis B, a carcinoma, or SLE.

Diffuse BM thickening in glomerulus
IgG and complement deposits along entire GBM

Urianalysis: frothy cloudy urine, proteinuria

Membranous nephropathy is an immunologically mediated disease in which deposts of mainly IgG and complement collect in the basement membrane and appear in a diffuse granular pattern by immunofluorescence, as seen here. Membranous nephropathy can be secondary to an underlying malignancy, infection, drug ingestion, or SLE. It can be idiopathic. About 3/4 of persons with the idiopathic form have antibodies to phospholipase A2 receptor, a transmembrane cell surface receptor. Levels of this antibody can indicate the severity of disease.

120
Q

What antibodies can be associated with membranous glomerular disease (nephrotic syndrome)?

A

Phospholipase A2 receptor antibodies - transmembrane cell surface receptor
Can indicate severity of disease

121
Q

What is the commonest cause of glomerulonephritis?

A

IgA nephropathy (BERGER disease)

122
Q

What are the characteristics of IgA nephropathy?

A

Deposition of IgA immune complexes in glomeruli
1-2 d post URTI with frank haematuria
May progress to end stage renal failure
Biopsy - fluorescent microscopy shows deposition of IgA in glomeruli and complenment in mesangium

May also cause isolated microscopic haematuria with no associated sx

123
Q

What is the pathogenesis of IgA nephropathy

A

In IgA nephropathy, there is abnormally glycosylated IgA1. Anti-glycan antibodies form and lead to immune complexes deposited within the mesangium of the glomeruli. These complexes attach to fibronectin or type IV collagen in the extracellular matrix and activate mesangial cells to produce extracellular matrix, leading to mesangial hypercellularity, segmental glomerulosclerosis or adhesion, tubular atrophy, and interstitial fibrosis.

The IgA is deposited mainly within the mesangium, which then increases mesangial cellularity as shown at the arrow. Patients with IgA nephropathy usually present with hematuria (nephritic syndrome). Older adults may also have proteinuria, microscopic hematuria, and hypertension. Most cases are idiopathic. Some cases occur when there is defective clearance of IgA with liver disease. Some cases occur in patients with celiac disease.

124
Q

What is rapidly progressive glomerulonephritis? (crescentic GN)

A

Aggressive form of nephritic syndrome that may develop into end stage renal failure within weeks.
Main clinical features:
oliguria = urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL or 500 mL per 24h in adults - this equals 17 or 21 mL/hour.
renal failure

Classified based on immunological findings
Type 1 - Anti GBM (Goodpastures syndrome)
Type 2 - immune complex mediates (SLE, IgA nephropathy, post infectious GN)
Type 3- ANCA associated (c ANCA, p ANCA)

Present of crescents on light microscopi in glomeruli

crescents composed of proliferating epithelial cells

125
Q

What are the characteristics of type 1 rapidly progressive/crescentic GN?

A

Type 1 = Anti GBM antibody against collagen type 4
Goodpasture syndrome most common cause
Can see crescents on light microscopy with proliferating epithelial cells
Fluorescent microscopy: linear deposition of IgG in GBM (* immunofluorescence pattern shows positivity with antibody to IgG and has a smooth, diffuse, linear pattern that is characteristic for deposition of glomerular basement membrane antibody with Goodpasture syndrome)
May see lung involvement - pulmonary haemorrhage

126
Q

If Goodpasure syndrome is suspected, what serologic test should be obtained?

A

Anti GBM antibody

127
Q

What are the characteristics of type 2 rapidly progressive/crescentic GN?

A

Immune complex mediated - SLE, IgA, post infectious
Crescents on light microscopy
Fluorescent microscopy: granular IgG complexes on GBM and mesangium

128
Q

What are the characteristics of type 3 rapidly progressive/crescentic GN?

A

Pauci immune - no Anti GBM no immune complex

ANCA associated - cANCA Wegners granulomatosis
pANCA microscopic polyangiitis

Crescent on light microscopy

nothing on fluorescent microscopy

Usually associated with vasculitis - presenting with skin rashes or pulmonary haemorrhage

129
Q

What is Wegner’s granulomatosis?

A

It is a type of rapidly progressive crescentic glomerulonephritis associated with c-ANCA. has kidney + URT involvement.
anuria (increase creat and urea)
oliguria
Inflamed glomerular capillaries
Associated with vasculitis - skin rashes and pulmonary haemorrhages.
rare multisystem autoimmune disease of unknown etiology. Its hallmark features include necrotizing granulomatous inflammation and pauci-immune vasculitis in small- and medium-sized blood vessels

130
Q

What does ANCA stand for and what is is associated with?

A

anti-neutrophil cytoplasmic autoantibody
C-ANCA - Wegner’s granulomatosis - vasculitis in skin and lung
P-ANCA - microscopic polyangitis

131
Q

What is Alport syndrome?

A

Hereditary nephritis - X linked condition where there is a mutation in Collagen alpha 5 chain
Causes nephritic syndrome, deafness, eye disorder (lens dislocation + cataract)
Young onset - 5-20 yo
Progresses to ESRF

This is a type of hereditary nephritis known as Alport syndrome in which patients may also manifest nerve deafness and eye problems. The glomeruli show irregular thickening and thinning and splitting of basement membranes due to an inherited abnormality in collagen. Most cases are X-linked and have mutations of the COL4A5 gene. In addition, as shown below, the renal tubular cells appear foamy because of the accumulation of neutral fats and mucopolysaccharides.

132
Q

What is benign familial haematuria?

A

Thin basement disease
Rare cause of nephritic syndrome
Autosomal dominant condition where there is thinning of GBM leading to isolated haematuria with no functional defect of the kidneys

133
Q

What drugs may cause acute interstitial nephritis?

A

Antibiotic: meticillin, penicillin, cephalosporins
NSAIDS
Thiazide diuretics (furosemide)
H2 blocker cimetide
Allopurinol - GOUT medication used to decrease high blood uric acid levels. It is specifically used to prevent gout, prevent specific types of kidney stones and for the high uric acid levels that can occur with chemotherapy. It is taken by mouth or injected into a vein
Sulphonamides - antibacterial sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthase (DHPS), an enzyme involved in folate synthesis. Sulfonamides are therefore bacteriostatic and inhibit growth and multiplication of bacteria, but do not kill them.

134
Q

What do you expect to find on U&E in acute renal failure?

A

Reduced GFR, increase creat and urea

135
Q

What are the histological findings for membranoproliferative glomerulonephritis? What serologic test is often positive with MPGN?

A

Silver stain showing tram track BM, double contour BM

C3 nephritic factor autoantibody that targets C3 convertase

136
Q

What are the inflammatory disorders causing tubulointerstitial nephritis?

A
  1. Acute pyelonephritis - E coli (leukocytic casts in urine)
  2. Chronic pyelonephritis + reflux nephropathy
    Chronic inflam + scarring from recurrent or persistent infection.
    Urine reflux
  3. Acute interstitial nephritis - hypersensitivity 1 or 4 reaction to drugs (antbx: methicillin, cephalosporins; NSAIDs; diuretics e.g thiazide)
  4. Chronic interstitial nephritis/ Analgesic nephritis (old using NSAIDs or paracetamol)
137
Q

What are the 2 thrombotic microangiopathies?

A

HUS (haemolytic uraemic syndrome) and TTP (thrombotic thrombocytopenic purpura)

138
Q

What is HUS?

A

Haemolytic uraemic syndrome
in children
triad: uraemia, thrombocytopaenia, MAHA (haemolytic anaemia)
Associated with diarrhorea caused by E coli O157:H7
Thrombi is confined to kidneys

can present with bleeding due to low platelets from MAHA

139
Q

What is TTP?

A

Thrombotic thrombocytopaenia purpura
Adults
Pentat: uraemia, thrombocytopaenia, MAHA (haemolytic syndrome), neuro signs (headache/coma), fever
can present with bleeding due to low platelets (petichae)

140
Q

What are some of the diagnostic signs of HUS or TTP?

A

Low HB, Low Plt
signs of haemolysis - increased bilirubin, increased reticulocytes
fragmented RBC on blood smear
COOMBS TEST NEGAIVE NO AIHA

141
Q

Causes and complications of Acute renal failure?

A

Pre renal - sepsis, hypovolaemia, burns

Renal - Acute tubular necrosis, acute glomerulonephritis, thrombotic microangiopathy (HUS, TTP)

Post renal - obstruction - stones, tumours, BPH

Complications: metabolic acidosis, hyperkalcaemia, fluid overload, HTN, uraemia

142
Q

What is chronic renal failure?

A

Progressive, irreversible loss of renal function. Sx of uraemia (itching, fatigue, anorexia)

Causes:
Diabetes, glomerulonephritis, HTN, vascular changes, reflux nephropathy, PCKD

143
Q

What are the stages of chronic renal failure? How is it classified?

A 
By GFR
>90 kidney damage, N function
60-89 Mild
30-59 moderate
15-29 Severe
<15 - renal failure - needs replacement therapy
144
Q

Adult PCKD?

A

Autosomal dominant
PKD1 on chr 16 - multiple renal cysts, liver cysts, beryr aneurysm
PKD2 on Chr 4
Clinical manifestation as complication of cyst rupture

145
Q

What are the 2 types of amyloidosis? What is amyloidosis?

A

Multisystem disorder caused by abnormal folding of proteins + deposition of amyloid fibrils in tissue, disrupting normal function.

Primary AL amyloidosis
Associated with multiple myeloma
Amyloid L proteins forming free light chains in serum and urine (Bence Jones) 
monoclonal Ig
increased bone marrow plasma cell

Secondary AA amyloidosis

Amyloid formed from serum amyloid A - acute phase protein, so 2ry to infection/ inflam
Autoimmune - rheumatoid arthritis
Chronic inf - TB
Non immune- renal carcinoma, hodgkins

146
Q

What proteins are associated with haemodialysis amylodosis?

A

Deposition of beta 2 microglobulin

147
Q

What is familial amyloidosis?

A

Diff kinds of genetic amyloidosis
Most common - Familial mediterranean fever

Production of IL-1 CAUSING FEVER AND INFLAMMATION of serosal surfaces
AA amyloid - renal deposition

148
Q

What are the clinical features of Amyloidosis?

A 
Organ specific:
Kidney - nephrotic syndrome 
1. . Oedema
2. Proteinuria (>3.5 mg/day)
3. Hypoalbuminaemia
4. Hyperlipidaemia

Heart - conduction, HF
Liver/spleen - hepatosplenomegaly
Tongue - MACROGLOSSIA
neuropathies - carpal tunnel

149
Q

What stain would you use for Amyloidosis and what do you expect to see?

A

Congo red stain showing apple green birefringence under polarised light/fluorescent microscopy.

If pink/red - caused by beta pleated sheet configuration

150
Q

What is sarcoidosis?

A

Multisystem disease of unknown cause, usually found in young patients.
Non-caseating granulomas.

Multi organ involvement
Skin - erythema nodosum
Lung - bilateral lymph adenopathy on CXR
Joins - arthritis
Eyes - uveitis, visual loss, keratoconjunctivitis, Heerfordt's Syndrome)
Hepatosplenomegaly
Hear - rythm disturbance
CNS involvement

DIAGNOSIS OF EXCLUSION

151
Q

What investigations should you do to diagnose sarcoidosis?

A

Calcium high
ESR high
ACE high
Transbronchial biopsy

152
Q

What are the histological findings in Alzheimers? What is the gross pathology?

A 
Gross pathology: 
Widened sulci
Narrow gyri
Enlarged ventricles
Generalised atrophy

Histological:
Senile beta amyloid plaques - cause inflammatory reaction
Neurofibrilary tangles of Tau protein

*intracellular beta amyloid misfolding may be more toxic than extracellular

153
Q

What are some of the treatments available for AD?

A

Anti-cholinesterases
nAChR agonists
Glutamate antagonists

154
Q

What are the diagnostic characteristics of dementia?

A 
Impaired cognitive function and personality without impariment of consciousness. 
Memory impairment + 1 of the following:
Aphasia - language disorder
Apraxia - no tasks done
Agnosia - losing recognition ability
155
Q

Which pathological proteins are associated with AD?

A

Neurofibrilary tangles of tau

beta amyloid

156
Q

Which pathological proteins are associated with Dementia with Lewy bodies?

A

Alpha synuclein - aggregates called lewy bodies

Ubiquitin

157
Q

Which pathological proteins are associated with Corticobasal degeneration?

A

Tau in astrocytes (post mortem diagnosis)

Parkinsonism

158
Q

Which pathological proteins are associated with frontotemporal dementia?

A

Tau

159
Q

Which pathological proteins are associated with Pick’s disease?

A

Tau

160
Q

Which pathological proteins are associated with Progressive supranuclear palsy?

A

Tau in astrocytes ( post mortem diagnosis)

Parkinsonism

161
Q

Which pathological proteins are associated with Multiple system atrophy?

A

Alpha synuclein in oligodendrocytes- clinically similar to PD, can be diagnosed when alive

162
Q

What are the Parkinson plus syndromes?

A

Lewy Body dementia - fluctuating cognition, visual hallucination, early dementia
Progressive supranuclear palsy -limited vertical gaze, early falls
Corticobasal syndrome - unilateral parkinsonism
Multiple system atrophy - may be cerebellar predominant or parkinsonims predominant - early autonomic dysfunction
Vascular parkinsonism - multi infarct presentation with gait instability and lower body parkinsonism

163
Q

What is Lewy Body dementia?

A

A type of parkinsonism where you have fluctuating cognition and may have visual disturbances.
Alpha synuclein aggregates

164
Q

What is characteristic to Progressive supranuclear palsy?

A

Tautopathy with limited downgaze, early falls

165
Q

What is characteristic to Corticobasal syndrome ?

A

Tautopathy

Classical unilateral parkinsonysm, apraxia +/- alien limb

166
Q

What is characteristic to Multiple system atrophy?

A

Synucleinopathy
Cerebellar predominant
or
Parkinsonism predominant

Associated with early autonomic dysfunction

167
Q

What is characteristic to Vascular Parkinsonism?

A

Multiple infarct presentation
Gait instability
Lower body parkinsonism
Rare - tremour

168
Q

Why is Tau important?

A

gene responsible for frontotemporal dementia proteins on chr 17 q 21

a bunch of pathologies

169
Q

What is characteristic to Pick’s disease?

A

Tau positive pick bodies
Fronto temporal atrophy
Marked gliosis and neuronal loss = WALNUT APPEARANCE
Balloon neurons

170
Q

Histological findings:
Walnut appearance of gliosis and neuronal loss
Balloon neurons

What is it?

A

Pick’s disease

171
Q

What is Braak’s staging used for?

A

Parkinsons and AD

172
Q

What is characteristic to Multiple sclerosis?

A

Autoimmune demyelinating disease
young onset - F 20-40 yo
Relapsing remitting - better between episodes, progressive
Primary progressive - just keeps getting worse

173
Q

What pathology is associated with MS?

A

MS plaques showing sharp margins of myelin loss

Myelin Basic Protein
Proteo-lipid protein

174
Q

What is prion disease and how does it work?

A

Proteinaceous infectious disease. Transmissible by infected protein.
Misfolding of alpha prion protein into beta, which potentiates further misfolding.
Humans - variable CJD - linked to bovine spongiform enchephalopathy - late incubation period of years
Deposits in cerebellum and motor cortices

Other syndromes:
Kuru - Papa new guinea
fatal familial insomnia

Path MC (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions